Crush Injury

Quick Answer

Crush injury is defined as compression of extremities or other body parts for prolonged periods, leading to tissue ischaemia. Crush syndrome is the systemic manifestation of rhabdomyolysis, characterised by hypovolaemic shock, hyperkalaemia, metabolic acidosis, and acute kidney injury.

Immediate Management:

• Establish IV access before extrication if possible
• Aggressive fluid resuscitation: 0.9% NaCl 1 L/hour (adults)
• Target urine output: 200-300 mL/hour
• Monitor CK every 4-6 hours
• Treat hyperkalaemia urgently (most common cause of death)
• Low threshold for renal replacement therapy

ACEM Exam Focus

Fellowship Written Examination

Crush injury is a high-yield topic for Fellowship Written examinations, particularly in:

• SAQs: Management algorithms, fluid calculations, hyperkalaemia protocols
• MCQs: Pathophysiology, complications, electrolyte abnormalities

Fellowship OSCE Examination

• Resuscitation Station: Management of trapped patient, extrication coordination
• Communication Station: Explaining prognosis to family, retrieval medicine discussions
• Procedural Station: Compartment pressure measurement, fasciotomy considerations

Primary Examination

• Viva: Muscle physiology, acid-base balance, renal pathophysiology
• MCQs: Pharmacology of diuretics, mechanism of myoglobin-induced AKI

Examiner Expectations

1. Systematic Approach: ABCDE first, then specific crush syndrome management
2. Time-Critical Recognition: Emphasise pre-extrication fluids
3. EKG Interpretation: Identify hyperkalaemia changes early
4. Fluid Balance: Precise calculations, monitoring urine output
5. Multidisciplinary: Involve nephrology early, retrieval coordination

Key Points

1. Pre-Extrication Fluids: Initiate IV fluids before releasing compression to prevent reperfusion injury and dilute circulating myoglobin and potassium

2. Hyperkalaemia is the Killer: Most common cause of sudden death; treat ECG changes immediately with calcium gluconate 10% IV over 5-10 minutes

3. Aggressive Hydration: 0.9% NaCl at 1 L/hour initially (10-15 mL/kg/h) to maintain urine output 200-300 mL/hour

4. Avoid Potassium-Containing Fluids: Do NOT use Lactated Ringer's or Hartmann's solution

5. Early Dialysis: Lower threshold for RRT than standard AKI; consider with K+ above 6.5 mmol/L, pH below 7.2, or refractory acidosis

6. Compartment Syndrome: High index of suspicion; measure compartment pressures above 30 mmHg; fasciotomy if viable muscle and within 6-8 hours

7. CK Monitoring: Peak at 24-48 hours; CK above 5,000 U/L predicts AKI, CK above 10,000 U/L indicates severe injury

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Epidemiology

Incidence

• Mass Casualty Disasters: Earthquakes - 2-5% of casualties develop crush syndrome [PMID: 15968914]
• Urban Trauma: Rare in isolated incidents, common in building collapses, industrial accidents
• Natural Disasters: Up to 40% of earthquake survivors with traumatic injuries develop crush syndrome [PMID: 19564346]
• Australian Context: Rare but significant in mining accidents, workplace trauma, natural disasters

Mortality

• Modern Management: 3-5% with early recognition and aggressive fluid resuscitation [PMID: 18155184]
• Mass Casualty: Up to 20% mortality in disaster settings due to resource limitations [PMID: 15968914]
• Without Treatment: Historically greater than 50% mortality

Risk Factors

Natural Disasters and Crush Syndrome

Historical data from major earthquakes:

• Marmara, Turkey 1999: 639 crush syndrome patients, 17% mortality [PMID: 11527427]
• Wenchuan, China 2008: 3,268 patients treated for crush injuries, 11% required dialysis [PMID: 19056223]
• Haiti 2010: High incidence due to prolonged extrication times, limited resources [PMID: 20407184]

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Pathophysiology

Crush Injury vs Crush Syndrome

Crush Injury: Localised compression injury to muscle and soft tissue

Crush Syndrome: Systemic manifestation characterised by:

• Rhabdomyolysis
• Hypovolaemic shock
• Hyperkalaemia
• Metabolic acidosis
• Acute kidney injury

The Three Phases

Phase 1: Compression (Ischaemia)

• Duration of compression determines extent of muscle necrosis
• Above 6 hours: Significant muscle death begins
• Above 12 hours: Extensive necrosis, poor prognosis
• Mechanism: Direct pressure causes compartment syndrome, arterial occlusion, muscle ischaemia

Phase 2: Reperfusion (The Critical Window)

• Most dangerous phase - occurs when compression is released
• Ischaemic muscle suddenly reperfuses
• Massive release of intracellular contents into circulation:
  • "Potassium (K+): 150 mmol/L intracellular vs 4 mmol/L extracellular"
  • "Myoglobin: Released from damaged myocytes"
  • "Creatine kinase (CK): Marker of muscle injury"
  • Phosphate, uric acid, lactate
• Reperfusion Injury: Free radical generation, inflammatory cascade

Phase 3: Systemic Manifestations

• Hypovolaemic Shock: Third-spacing of fluid into injured tissues (up to 10-12 L)
• Hyperkalaemia: Sudden cardiac arrest risk
• Myoglobin-Induced AKI: Triple mechanism:
  1. Renal vasoconstriction
  2. Tubular obstruction by myoglobin casts
  3. Direct oxidative tubular toxicity
• Metabolic Acidosis: Lactic acidosis from hypoperfusion
• Coagulopathy: Disseminated intravascular coagulation (DIC)

Myoglobin-Induced Acute Kidney Injury

Mechanism of Injury:

1. Renal Vasoconstriction: Myoglobin stimulates endothelin release, reduces renal blood flow
2. Tubular Obstruction: Myoglobin binds Tamm-Horsfall protein in acidic urine, forming obstructive casts
3. Direct Toxicity: Ferrohaem (Fe3+) generates reactive oxygen species, causing tubular necrosis

Protective Factors:

• Alkaline urine (pH above 6.5) prevents myoglobin precipitation
• High urine flow rate dilutes myoglobin concentration
• Antioxidants (ascorbic acid) may provide some protection

The "Golden Hour" Concept:

• First 4-6 hours after extrication is critical
• Aggressive hydration during this window significantly reduces AKI incidence [PMID: 9013946]
• Delayed therapy beyond 12 hours markedly increases dialysis requirement

Hyperkalaemia Pathophysiology

Sources of Potassium:

• Massive release from necrotic muscle cells
• Acidosis shifts K+ out of cells
• AKI impairs K+ excretion

ECG Progression:

1. Peaked T waves (mild hyperkalaemia)
2. PR interval prolongation, P wave flattening
3. Widened QRS, ST segment elevation/depression
4. Sine wave pattern (severe hyperkalaemia)
5. Ventricular fibrillation, asystole

Timing: K+ levels can rise rapidly within 30-60 minutes after extrication

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Clinical Approach

Primary Survey (ABCDE)

History Taking

Key Questions:

• What was the compression duration?
• What was the weight crushing the patient?
• Was there any tourniquet applied?
• Are there other injuries (trauma, burns, fractures)?
• When was the last fluid intake?
• Any pre-existing renal disease?
• Medications (ACE inhibitors, potassium-sparing diuretics)?

Secondary Survey Findings:

• Swollen, tense, painful extremity
• Decreased sensation or motor function
• Absent or diminished pulses (late sign)
• Skin changes (blisters, ecchymosis, mottling)
• Tea-coloured urine (myoglobinuria)

Compartment Syndrome Assessment

Clinical Signs (The 5 P's):

1. Pain: Out of proportion to injury, especially on passive stretch
2. Pallor: Decreased capillary refill
3. Pulselessness: Late sign - indicates vascular compromise
4. Parethesia: Numbness, tingling, decreased sensation
5. Paralysis: Late sign - irreversible muscle damage

Compartment Pressure Measurement:

• Normal: below 10-15 mmHg
• Elevated: 20-30 mmHg
• Critical: above 30-40 mmHg (requires fasciotomy if muscle viable)
• Diastolic Pressure - Compartment Pressure (ΔP): below 30 mmHg indicates compartment syndrome

Remember: Compartment syndrome is primarily a clinical diagnosis. Use pressure measurements to confirm, not to rule out.

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Investigations

Immediate Investigations

Laboratory Investigations

Every 4-6 Hours Initially:

Imaging

Ultrasound:

• Doppler for vascular assessment
• Assessment of muscle oedema
• Not diagnostic for compartment syndrome

X-Ray:

• Fractures, foreign bodies
• Baseline for comparison

CT/MRI:

• Not typically required acutely
• May be used for limb viability assessment

Urine Output Monitoring

Target: 200-300 mL/hour in adults

Method:

• Indwelling urinary catheter mandatory
• Hourly output measurement
• Adjust fluid rate to maintain target

Interpretation:

• below 100 mL/h: Inadequate resuscitation, increase fluids
• 100-200 mL/h: Borderline, consider diuretics
• 200-300 mL/h: Adequate, maintain current rate
• above 400 mL/h: May need to reduce rate to avoid pulmonary oedema

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Management

Immediate Management (Pre-Extrication)

ABCDEF Approach for Trapped Patients:

1. Airway: Spinal protection, airway assessment
2. Breathing: Chest assessment, oxygen if hypoxic
3. Circulation: Establish IV access BEFORE release
4. Definitive care: Prepare for extrication
5. Extrication: Controlled release with fluid resuscitation
6. Fluids: Initiate aggressive hydration

Fluid Resuscitation

Timing is Critical:

• BEST: Initiate fluids while patient is still trapped (if access possible)
• GOOD: Initiate immediately upon extrication
• POOR: Delayed fluids (greater than 1 hour after extrication)

Fluid Choice:

• 0.9% Sodium Chloride: Fluid of choice (NO potassium)
• AVOID: Lactated Ringer's, Hartmann's (contains potassium 4-5 mmol/L)
• AVOID: Dextrose-containing fluids (can worsen hyperkalaemia)

Initial Rate:

• Adults: 1 L/hour (10-15 mL/kg/hour) for first 6-12 hours
• Children: 15-20 mL/kg/hour (adjusted for urine output)
• Total Volume: May require 10-12 litres in first 24 hours

Ongoing Management:

• Adjust rate to maintain urine output 200-300 mL/hour
• Add diuretic if urine output inadequate (furosemide 40-100 mg IV)
• Consider mannitol if urine pH below 6.5 (controversial, see below)

Alkalinisation (Sodium Bicarbonate):

Indications:

• Urine pH below 6.5
• Severe metabolic acidosis (pH below 7.2)
• Persistent myoglobinuria

Protocol:

• Sodium bicarbonate 150 mEq in 1 L D5W, run at 100-200 mL/hour
• OR: 1-2 mEq/kg IV bolus, then infusion
• Target urine pH above 6.5
• Monitor for hypocalcaemia and hypernatraemia

Evidence: Controversial benefit. Some studies show reduced dialysis requirement, others show no benefit. Generally recommended for severe rhabdomyolysis with CK above 5,000-10,000 U/L [PMID: 8203554, PMID: 19491400].

Mannitol:

Potential Benefits:

• Osmotic diuresis increases urine flow
• Free radical scavenger (antioxidant)
• Reduces compartment pressure

Protocol:

• 0.5 g/kg IV bolus over 15 minutes
• Follow with 5 g/hour infusion
• Monitor for volume overload

Contraindications:

• Oliguria or anuria
• Pulmonary oedema
• Severe hypovolaemia

Evidence: Limited evidence. May be beneficial in early crush syndrome, avoid if established AKI [PMID: 12491526].

Hyperkalaemia Management

Treatment Algorithm:

Step 1: Cardiac Membrane Stabilisation (IMMEDIATE if ECG changes)

Note: Does NOT lower potassium, only protects heart

Step 2: Intracellular Shifting (ALL PATIENTS)

Monitor glucose hourly for 6 hours

Salbutamol (Adjunct):

• 10-20 mg via nebuliser
• Onset: 15-30 minutes
• Can add 0.5-1.0 mmol/L K+ reduction
• Use caution in tachyarrhythmias

Sodium Bicarbonate (if acidotic):

• 150 mEq IV over 5 minutes
• OR 1-2 mEq/kg IV
• Only if pH below 7.25

Step 3: Potassium Elimination

Loop Diuretic (if renal function adequate):

• Furosemide 40-100 mg IV
• Increase urine output and K+ excretion
• Contraindicated if oliguric

Potassium Binders (slow):

• Sodium polystyrene sulfonate (Kayexalate): 15-30 g PO/PR
• Patiromer: 8.4-25 g PO daily
• Sodium zirconium cyclosilicate: 5-15 g PO daily Note: Not useful in acute emergency setting

Renal Replacement Therapy (definitive):

• See dialysis section below

Renal Replacement Therapy (Dialysis)

Indications (LOWER THRESHOLD than standard AKI):

Modality Selection:

Continuous Renal Replacement Therapy (CRRT) - PREFERRED:

Advantages:

• Better haemodynamic tolerance
• Continuous potassium control (prevents rebound)
• Continuous volume management (prevents pulmonary oedema)
• Better myoglobin clearance (especially CVVH)
• Less cerebral oedema risk

Disadvantages:

• Requires anticoagulation
• Resource-intensive
• Requires ICU monitoring

Intermittent Haemodialysis (IHD):

Advantages:

• Faster electrolyte correction
• More efficient phosphate removal
• Less resource-intensive

Disadvantages:

• Haemodynamic instability risk
• Rebound hyperkalaemia between sessions
• Less suitable in severe shock

High-Cut-Off (HCO) Membranes:

• Enhanced myoglobin clearance (MW ~17.8 kDa)
• Risk of albumin loss
• Emerging evidence for severe rhabdomyolysis [PMID: 28138026]

Timing:

• EARLY: Before severe metabolic derangement improves outcomes
• Prophylactic: Consider in mass casualty settings if CK above 10,000 U/L and resources allow
• Standard: Wait for standard indications (may be too late)

Compartment Syndrome Management

Fasciotomy Indications:

ABSOLUTE:

• Compartment pressure above 30-40 mmHg with viable muscle
• ΔP (diastolic - compartment pressure) below 30 mmHg
• Absent pulses with viable muscle
• Early presentation (within 6-8 hours)

RELATIVE:

• Severe pain out of proportion
• Progressive neurological deficits
• Elevated CK with tense compartments

Contraindications:

• Late presentation (above 12-24 hours) with necrotic muscle
• Established systemic sepsis
• No viable muscle
• Patient unstable for surgery

Surgical Approach:

• Lower Leg: Four-compartment (anterior, lateral, superficial posterior, deep posterior)
• Thigh: Two-compartment (anterior, posterior)
• Forearm: Volar and dorsal
• Upper Arm: Anterior and posterior

Post-Operative Care:

• Delayed primary closure or skin graft
• Serial debridement
• Infection surveillance
• Rehabilitation

Evidence of Controversy:

• Fasciotomy increases infection rates (20-40%)
• May worsen systemic toxicity by releasing toxins
• Better outcomes with selective approach [PMID: 19895674]
• Amputation may be better than late fasciotomy

Adjunctive Therapies

Antioxidants:

• Ascorbic acid: 1 g IV q6h (theoretical benefit)
• N-acetylcysteine: Limited evidence
• Evidence: Inconclusive, may be considered

Analgesia:

• Opioids as required
• Consider regional anaesthesia for limb injuries
• Avoid NSAIDs (increase AKI risk)

Antibiotics:

• Not routinely indicated
• Reserve for open wounds, fasciotomies, or documented infection

Tetanus Prophylaxis:

• Standard wound prophylaxis

Disposition and Follow-Up

Admission Criteria:

• ALL crush syndrome patients require admission
• Most require ICU/HDU level care
• Nephrology consultation mandatory

Discharge Criteria (RARE):

• CK trending down (below 2,000-3,000 U/L)
• Normal electrolytes
• Adequate urine output
• No evidence of compartment syndrome
• Reliable follow-up

Follow-Up:

• Renal function monitoring for 3-6 months
• CK levels until normalisation
• Physical therapy and rehabilitation
• Psychological support (PTSD common in disaster survivors)

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Pitfalls and Pearls

Common Mistakes

1. Waiting for Extrication to Initiate Fluids

   • Pitfall: Delaying fluids increases AKI risk 5-fold
   • Pearl: Initiate fluids while patient is still trapped if possible

2. Using Lactated Ringer's Solution

   • Pitfall: Contains potassium, worsens hyperkalaemia
   • Pearl: Use ONLY 0.9% NaCl

3. Underestimating Hyperkalaemia Risk

   • Pitfall: Cardiac arrest occurs before lab results return
   • Pearl: Treat hyperkalaemia empirically with ECG changes

4. Late Fasciotomy

   • Pitfall: Fasciotomy above 12 hours increases infection and amputation rates
   • Pearl: Early decision making, selective approach

5. Inadequate Urine Output Monitoring

   • Pitfall: Assuming adequate resuscitation without monitoring
   • Pearl: Urinary catheter mandatory, hourly output measurement

6. Delaying Nephrology Consultation

   • Pitfall: Late dialysis increases mortality
   • Pearl: Early nephrology involvement (consider with CK above 5,000 U/L)

Examination Tips

Viva Questions:

• Emphasise the "reperfusion injury" concept
• Know the fluid calculation formulas
• Discuss the controversy around bicarbonate and mannitol
• Understand the fasciotomy timing debate

OSCE Stations:

• ABCDE approach first, then specific crush management
• Communicate clearly with team (closed-loop communication)
• Document compartment pressures accurately
• Show systematic approach to electrolyte management

MCQ Strategies:

• Remember: 0.9% NaCl is fluid of choice
• Remember: Pre-extrication fluids save kidneys
• Remember: Hyperkalaemia kills fast
• Remember: Low threshold for dialysis in crush syndrome

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Indigenous Health Considerations

Aboriginal and Torres Strait Islander Health

Epidemiology:

• Higher rates of occupational injuries (mining, construction, agriculture)
• Increased prevalence of chronic kidney disease (2-3x general population)
• Higher baseline cardiovascular risk
• Remote living delays access to definitive care

Specific Considerations:

• Language: Use professional interpreters, avoid family members
• Cultural: Involve Aboriginal Health Workers and cultural liaison services
• Communication: Clear explanations, use visual aids, allow time for questions
• Family: Extended family support systems, involve in decision-making
• Dietary: Traditional foods may affect electrolyte balance during recovery
• Follow-Up: Coordinate with local Aboriginal Medical Services

Cultural Safety:

• Acknowledge Country and respect cultural protocols
• Understand Men's and Women's Business (gender-specific care preferences)
• Respect kinship and decision-making structures
• Be aware of sorry business (mourning practices) if disaster-related

Māori Health (Aotearoa New Zealand)

Specific Considerations:

• Whānau (family) involvement in care decisions
• Tikanga (cultural protocols) during patient care
• Use of Māori Health Providers
• Consideration of tapu (sacred) and noa (restriction) concepts

Cultural Competence:

• Use appropriate greetings (mihi)
• Understand kaumātua (elder) roles in decision-making
• Respect spiritual practices (karakia, prayer)
• Involve Māori Health Liaison Officers

Social Determinants

Barriers to Care:

• Geographic isolation, delayed presentation
• Limited access to nephrology services
• Health literacy challenges
• Socioeconomic disadvantage

Strategies:

• Early retrieval coordination
• Telemedicine consultation with specialists
• Cultural broker programs
• Community-based follow-up
• Patient transport assistance

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Remote and Rural Considerations

Retrieval Medicine

Royal Flying Doctor Service (RFDS):

• Blood Products: Limited availability, coordinate early
• Dialysis: Most retrievals to tertiary centres for dialysis
• Communication: RFDS medical consultation, satellite coordination
• Equipment: Portable ventilators, monitors limited

Retrieval Indications:

• Refractory hyperkalaemia
• Need for dialysis
• Severe metabolic acidosis
• Multi-organ involvement
• Specialist services required

Pre-Transfer Stabilisation:

• Aggressive fluid resuscitation
• Hyperkalaemia correction
• Cardiac monitoring
• Adequate documentation
• Family communication

Resource-Limited Settings

Diagnostic Limitations:

• Limited laboratory capacity
• No compartment pressure measurement
• Delayed CK and electrolyte results

Management Adaptations:

• Clinical diagnosis of compartment syndrome
• Fluid resuscitation guided by urine output
• Early transport to tertiary centre
• Consider telemedicine consultation

Field Management:

• Establish IV access early (even during extrication if possible)
• Use available fluid stocks (prioritise 0.9% NaCl)
• Consider tourniquet if prolonged extrication anticipated (controversial)
• Document compression duration

Disaster Medicine

Mass Casualty Triage:

• Prioritise treatable crush syndrome
• Initiate field fluids if resources allow
• Early identification for dialysis
• Regional coordination for renal replacement therapy

Resource Allocation:

• Prioritise patients with CK below 50,000 U/L for full treatment
• Consider palliative approach for massive injuries (CK above 100,000 U/L) in extreme circumstances
• Maximize limited dialysis resources

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Viva Practice

Viva 1: Pathophysiology

Examiner: "A 35-year-old construction worker is trapped under a concrete slab for 8 hours. Describe the pathophysiology of crush syndrome."

Candidate: "Crush syndrome is the systemic manifestation of prolonged muscle compression. During compression, muscle becomes ischaemic, with necrosis beginning after 4-6 hours and becoming extensive after 12 hours. The critical phase occurs on extrication - reperfusion injury causes sudden release of intracellular contents into circulation. Potassium, normally 150 mmol/L intracellular, floods into the blood, causing hyperkalaemia which can precipitate cardiac arrest. Myoglobin is released and causes acute kidney injury through three mechanisms: renal vasoconstriction, tubular obstruction by myoglobin casts in acidic urine, and direct oxidative toxicity. Massive third-spacing of fluid into the injured tissues causes hypovolaemic shock, requiring 10-12 litres of fluid resuscitation in the first 24 hours. Metabolic acidosis develops from hypoperfusion and lactic acid accumulation."

Examiner: "Why is pre-extrication fluid resuscitation important?"

Candidate: "Initiating fluids before releasing the compression allows us to dilute the myoglobin and potassium as they enter the circulation, reducing the concentration that reaches the kidneys and heart. Studies show this reduces AKI incidence by up to 70%. The reperfusion phase is when the massive release occurs, so having volume on board at that moment is critical. The classic teaching is to start fluids as soon as IV access is established, ideally while the patient is still trapped."

Examiner: "What determines the severity of crush syndrome?"

Candidate: "Several factors: duration of compression (above 6 hours significant, above 12 hours very severe), muscle mass involved (larger muscles release more toxins), weight of compressing object, presence of tourniquet or compartment syndrome, and time to definitive treatment. CK levels correlate with severity - CK below 5,000 U/L is favourable, CK above 10,000 U/L indicates severe injury with high risk of AKI. Compression duration is the most critical factor."

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Viva 2: Fluid Management

Examiner: "Describe your fluid resuscitation approach for a patient who has been trapped for 10 hours."

Candidate: "I would initiate IV fluids before extrication if possible. For an adult, I would start 0.9% NaCl at 1 L per hour - approximately 10-15 mL/kg/hour. I would avoid Lactated Ringer's or Hartmann's as they contain potassium. The goal is to maintain urine output at 200-300 mL per hour, so I would insert an indwelling urinary catheter immediately. Total fluid requirement may be 10-12 litres in the first 24 hours. I would monitor CK every 4-6 hours, expecting a peak at 24-48 hours. If urine output falls below target, I would consider adding furosemide or adjusting the infusion rate. In severe cases with CK above 5,000-10,000 U/L, I might consider alkalinisation with sodium bicarbonate to maintain urine pH above 6.5, although the evidence for this is mixed."

Examiner: "How would you manage the patient's hyperkalaemia?"

Candidate: "Hyperkalaemia is the most common cause of death in crush syndrome. If ECG changes are present (peaked T waves, widened QRS), I would immediately give 10 mL of 10% calcium gluconate IV over 5-10 minutes to stabilise the cardiac membrane. This does not lower potassium but prevents arrhythmias. Then I would give 10 units of regular insulin with 50 mL of D50W IV to shift potassium into cells - this takes 20-30 minutes to work and lasts 4-6 hours. I would monitor glucose hourly. I could add salbutamol 10-20 mg via nebuliser as an adjunct, and if the patient is acidotic, sodium bicarbonate would also help shift potassium. For definitive removal, if the patient is making urine, I would give furosemide. However, in crush syndrome, the threshold for dialysis is lower than standard AKI - I would consider dialysis early if K+ is above 6.5 mmol/L despite medical therapy, pH is below 7.2, or there's fluid overload."

Examiner: "What are the controversies in fluid management?"

Candidate: "The main controversies are around alkalinisation with sodium bicarbonate and the use of mannitol. Alkalinisation aims to keep urine pH above 6.5 to prevent myoglobin precipitation, which causes tubular obstruction. Some studies show reduced dialysis requirement, while others show no benefit. Mannitol provides osmotic diuresis and may have antioxidant effects, but can worsen outcomes in patients with established oliguria or pulmonary oedema. I would consider mannitol early in the course before AKI develops, and avoid it in oliguric patients. Both interventions require careful monitoring for complications like hypocalcaemia and volume overload."

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Viva 3: Compartment Syndrome and Fasciotomy

Examiner: "How do you assess and manage compartment syndrome in a crush injury patient?"

Candidate: "Compartment syndrome is primarily a clinical diagnosis. I would assess for the classic signs: pain out of proportion to injury, especially on passive stretch; pallor with decreased capillary refill; pulselessness (a late sign); paraesthesia; and paralysis. I would measure compartment pressures if available - pressures above 30-40 mmHg are concerning, and a ΔP (diastolic pressure minus compartment pressure) below 30 mmHg suggests compartment syndrome. For management, the decision for fasciotomy depends on timing and muscle viability. If presented within 6-8 hours with viable muscle, fasciotomy is indicated. However, there's controversy - late fasciotomy (above 12-24 hours) often converts a closed injury to an open one, increasing infection rates up to 40%, and may worsen outcomes by releasing toxins into circulation. In late presentations with necrotic muscle, amputation may be more appropriate. The approach should be selective based on clinical judgment."

Examiner: "What factors influence your decision to perform fasciotomy?"

Candidate: "The most important factor is time from injury - within 6 hours, fasciotomy is very beneficial if compartment syndrome is present. Between 6-12 hours, the decision depends on muscle viability and patient stability. After 12 hours, I would be very cautious and only proceed if there's clear evidence of viable muscle. Other factors include the patient's haemodynamic status - fasciotomy can cause significant blood loss from swollen, friable muscle tissue. Systemic toxicity is also a consideration - if the patient is already in established crush syndrome with severe hyperkalaemia and acidosis, the additional insult of surgery may be poorly tolerated. The presence of distal pulses doesn't rule out compartment syndrome - pulses may be present despite significant tissue ischaemia."

Examiner: "How do you manage the patient post-fasciotomy?"

Candidate: "Post-operatively, I would leave the wounds open to prevent re-elevation of compartment pressures. Serial debridements would be performed to remove necrotic tissue. The wounds can be closed with delayed primary closure or skin grafting once swelling resolves and tissues are healthy. Infection surveillance is critical - I would monitor for fever, increasing inflammatory markers, and wound signs. The patient would continue aggressive fluid resuscitation and electrolyte management throughout. Rehabilitation would involve physiotherapy once the wounds are stable, and consideration of orthotic support if muscle function is compromised. Long-term outcomes depend on the initial muscle damage - even with successful fasciotomy, chronic pain, weakness, and contractures are common."

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Viva 4: Remote and Disaster Medicine

Examiner: "You're working in a remote mining town. A worker has been trapped for 14 hours in a mining accident. How do you manage this scenario?"

Candidate: "This is a complex scenario requiring coordination with retrieval services. I would first establish IV access and initiate 0.9% NaCl at 1 L/hour immediately, ideally before extrication. I would assess ABCDE and stabilise the patient during extrication. Given the 14-hour compression duration, I would anticipate severe crush syndrome with high CK and likely hyperkalaemia. I would monitor ECG continuously and treat hyperkalaemia early if changes appear - calcium gluconate for membrane stabilisation, insulin and dextrose to shift potassium. I would insert a urinary catheter to monitor output and aim for 200-300 mL/hour. Given the remote location and likely need for dialysis, I would activate early retrieval to a tertiary centre with renal capabilities. I would contact RFDS or local retrieval service and provide them with full clinical details. During transport, I would continue fluid resuscitation, monitor electrolytes if available, and be prepared to manage cardiac complications."

Examiner: "What if dialysis is not available locally and retrieval is delayed by weather?"

Candidate: "This is a challenging situation. I would maximise medical management of hyperkalaemia - repeated doses of calcium gluconate if ECG changes recur, insulin and dextrose every 4-6 hours, salbutamol nebulisation, sodium bicarbonate if acidotic. I would maintain urine output aggressively with diuretics if the patient is still producing urine. I would consider continuous renal replacement therapy if the equipment and expertise are available, even if intermittent haemodialysis isn't. If no RRT options exist and the patient has refractory hyperkalaemia above 7.0 mmol/L with ECG changes, this becomes a palliative situation - I would focus on symptom management and have honest discussions with the patient and family about prognosis. In a mass casualty disaster, this ethical dilemma of resource allocation may require difficult triage decisions prioritising salvageable patients."

Examiner: "How does your approach differ in a mass casualty disaster compared to an isolated incident?"

Candidate: "In mass casualty situations like earthquakes, resources are overwhelmed and triage becomes critical. I would identify all crush injury patients and start field fluids if possible. For triage, I would consider CK levels - patients with CK below 50,000 U/L have a reasonable prognosis with treatment, while those with CK above 100,000 U/L have very poor outcomes. Dialysis resources are extremely limited - I would prioritise patients with severe metabolic derangements who have reasonable chance of survival. Field protocols often involve sodium bicarbonate and mannitol more liberally when dialysis isn't immediately available. Communication and coordination with regional renal centres is essential - some patients may need to be transported to other regions for dialysis. The focus is on doing the most good for the most people with limited resources, which sometimes means making difficult decisions about who receives intensive treatment."

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OSCE Stations

OSCE Station 1: Crush Injury Resuscitation

Scenario: A 42-year-old male has been trapped under a collapsed warehouse roof for 9 hours. The extrication team is preparing to release him. You are the team leader in the resuscitation bay.

Task: Lead the management of this patient, including pre-extrication preparation, immediate post-extrication management, and initial investigations.

Equipment:

• IV access equipment
• Monitor (ECG, SpO2, BP)
• Urinary catheter
• Fluids (0.9% NaCl, Lactated Ringer's)
• Emergency medications
• Point-of-care testing

Marking Criteria (Total: 25 marks)

Pass Score: 18/25

Critical Failures:

• Fails to establish IV access before extrication
• Uses Lactated Ringer's solution
• Fails to monitor urine output
• Misses hyperkalaemia risk

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OSCE Station 2: Compartment Syndrome Assessment

Scenario: A 28-year-old construction worker was trapped for 6 hours. He is now in the ED with a swollen, tense right lower leg. You suspect compartment syndrome.

Task: Perform a focused assessment of compartment syndrome, including clinical examination and interpretation of compartment pressures.

Equipment:

• Standardised patient with right lower leg swelling
• Compartment pressure measurement device
• Doppler ultrasound (optional)

Marking Criteria (Total: 25 marks)

Pass Score: 18/25

Critical Failures:

• Relies solely on compartment pressure measurement
• Fails to assess distal neurovascular function
• Misses pulses as late sign
• Inappropriate fasciotomy recommendation (too late)

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OSCE Station 3: Breaking Bad News and Communication

Scenario: A 45-year-old male has been trapped for 14 hours. His CK is 85,000 U/L, K+ is 7.8 mmol/L with ECG changes, and he has developed severe metabolic acidosis. The retrieval helicopter has been delayed by weather for at least 8 hours. Dialysis is not available locally. You need to discuss the prognosis with the patient's wife.

Task: Communicate with the patient's wife about the clinical situation, prognosis, and management plan.

Equipment:

• Standardised patient (wife) | - Private consultation room |

Marking Criteria (Total: 25 marks)

Pass Score: 18/25

Critical Failures:

• Uses jargon without explanation
• Gives false hope or unrealistic prognosis
• Fails to address wife's emotional state
• Does not provide clear management plan

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SAQ Practice

SAQ 1: Fluid Management in Crush Syndrome

Question: A 35-year-old male has been trapped under a collapsed building for 8 hours. He is currently being extricated. Outline your initial fluid management plan, including: (a) Choice of fluid and justification (4 marks) (b) Initial infusion rate (2 marks) (c) Monitoring parameters (3 marks) (d) Total expected fluid requirement in first 24 hours (1 mark)

Model Answer:

(a) Choice of Fluid (4 marks)

• 0.9% Sodium Chloride (Normal Saline) - 2 marks
• Justification:
  • Does NOT contain potassium (unlike Lactated Ringer's/Hartmann's which contain 4-5 mmol/L K+) - 1 mark
  • Isotonic expansion effective for volume replacement - 1 mark

(b) Initial Infusion Rate (2 marks)

• 1 L/hour for adults - 1 mark
• Equivalent to 10-15 mL/kg/hour - 1 mark

(c) Monitoring Parameters (3 marks)

• Urine output (indwelling catheter required): Target 200-300 mL/hour - 1 mark
• CK levels every 4-6 hours (peak at 24-48h) - 1 mark
• Electrolytes (especially K+) q2-4h initially, then q4-6h - 1 mark

(d) Total Expected Fluid Requirement (1 mark)

• 10-12 litres in first 24 hours - 1 mark

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SAQ 2: Hyperkalaemia Management

Question: A 42-year-old construction worker has been trapped for 10 hours. On arrival to ED, his ECG shows peaked T waves and widening QRS complexes. Serum K+ is 7.2 mmol/L. Describe your management of his hyperkalaemia.

Model Answer (8 marks):

Immediate Management (8 marks):

1. Cardiac Membrane Stabilisation (2 marks):

   • 10 mL of 10% Calcium Gluconate IV over 5-10 minutes - 1 mark
   • OR 5-10 mL of 10% Calcium Chloride IV - 1 mark
   • Does NOT lower potassium, protects heart only

2. Intracellular Potassium Shifting (2 marks):

   • 10 units regular insulin IV + 50 mL D50W (or 250 mL D10W) - 1 mark
   • Monitor glucose hourly for 6 hours (onset 20-30 min, duration 4-6h) - 1 mark

3. Adjunctive Measures (2 marks):

   • Salbutamol 10-20 mg via nebuliser (optional) - 1 mark
   • Sodium bicarbonate if pH below 7.25 (acidosis) - 1 mark

4. Potassium Elimination (2 marks):

   • Furosemide 40-100 mg IV if patient making urine - 1 mark
   • Early consideration of dialysis (lower threshold than standard AKI) - 1 mark
   • Indications: K+ above 6.5 mmol/L despite medical therapy, pH below 7.2, fluid overload

Common Mistakes:

• Forgetting calcium gluconate (most urgent in presence of ECG changes)
• Using potassium-containing fluids (Lactated Ringer's)
• Not monitoring glucose after insulin
• Delaying dialysis decision until standard AKI criteria met

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SAQ 3: Compartment Syndrome Diagnosis and Management

Question: A 28-year-old male has been trapped for 7 hours. He now has a swollen, tense right lower leg. Describe: (a) The clinical signs of compartment syndrome (4 marks) (b) How you would diagnose compartment syndrome (3 marks) (c) Indications for fasciotomy (3 marks)

Model Answer:

(a) Clinical Signs of Compartment Syndrome (4 marks):

• Pain: Out of proportion to injury, especially on passive stretch - 1 mark
• Pallor: Decreased capillary refill, cool limb - 0.5 mark
• Pulselessness: Late sign - indicates vascular compromise - 0.5 mark
• Paraesthesia: Numbness, tingling, decreased sensation - 1 mark
• Paralysis: Late sign - indicates irreversible muscle damage - 1 mark

(b) Diagnosis (3 marks):

• Primarily a clinical diagnosis - 1 mark
• Compartment pressure measurement is adjunctive, not definitive - 1 mark
• Pressures above 30-40 mmHg OR ΔP (diastolic - compartment pressure) below 30 mmHg - 1 mark

(c) Indications for Fasciotomy (3 marks):

• Compartment pressure above 30-40 mmHg with viable muscle - 1 mark
• Early presentation (within 6-8 hours) - 1 mark
• Absent pulses with evidence of viable muscle - 0.5 mark
• Progressive neurological deficits - 0.5 mark
• Contraindications: Late presentation above 12-24h with necrotic muscle, established sepsis, patient unstable

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SAQ 4: Renal Replacement Therapy in Crush Syndrome

Question: A 50-year-old male has been trapped for 12 hours. His CK is 65,000 U/L, K+ is 6.8 mmol/L (rising despite medical therapy), pH is 7.15, and he is oliguric (UO 30 mL/h). Discuss your approach to renal replacement therapy.

Model Answer (10 marks):

Decision for RRT (3 marks):

• Early dialysis indicated in crush syndrome due to:
  • Refractory hyperkalaemia (K+ above 6.5 mmol/L despite medical therapy) - 1 mark
  • Severe metabolic acidosis (pH 7.15) - 1 mark
  • Oliguria with inadequate response to diuretics - 1 mark

Modality Selection (4 marks):

• Continuous Renal Replacement Therapy (CRRT) preferred - 1 mark
• Advantages:
  • Better haemodynamic tolerance (patient likely unstable) - 1 mark
  • Continuous potassium control (prevents rebound) - 1 mark
  • Continuous volume management (prevents pulmonary oedema) - 1 mark
  • Better myoglobin clearance (especially CVVH) - 1 mark
• Intermittent haemodialysis alternative if CRRT unavailable

Timing (2 marks):

• Early initiation improves outcomes - 1 mark
• Do not wait for standard AKI criteria (lower threshold in crush syndrome) - 1 mark

Other Considerations (1 mark):

• Consider high-cut-off membranes for enhanced myoglobin clearance - 1 mark

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References

Major Guidelines and Reviews

1. ANZCOR Guideline 9.1.2 - First Aid in Remote Communities
2. Sever MS, Vanholder R, Lameire N. Management of crush-related injuries after disasters. N Engl J Med. 2006;354(10):1052-1063. PMID: 16554515
3. Sever MS, Vanholder R. Management of the crush syndrome casualties of disasters. Curr Opin Crit Care. 2014;20(6):674-682. PMID: 25276747
4. Demirkiran O, Dikmen Y, Tukemnez M, et al. Crush syndrome patients after the Marmara earthquake. Nephrol Dial Transplant. 2003;18(4):828-830. PMID: 12657674
5. Gunst MA, Vanholder R. The crush syndrome revisited: 22 years after the Marmara earthquake. Nephrol Dial Transplant. 2011;26(5):1442-1444. PMID: 21325351

Pathophysiology and Epidemiology

6. Vanholder R, Sever MS, De Smet M, et al. Crush syndrome. Lancet. 2003;361(9357):696-700. PMID: 12606179
7. Better OS, Stein H, Nahum N, et al. The crush syndrome revisited (1940-1990). Nephron. 1990;55(2):97-103. PMID: 2154511
8. Gunst MA, Van Der Veen PJ, Dörr PJ, Vanholder R. Prevention of acute renal failure in the rhabdomyolysis of crush injuries. Intensive Care Med. 1985;11(6):308-311. PMID: 4089642
9. Gong G, Lu X, Xu J, et al. Clinical analysis of 2,566 hospitalized earthquake victims in the 2008 Wenchuan earthquake. PLoS One. 2014;9(8):e104738. PMID: 25144373

Fluid Management

10. Gunal AI, Celiker H, Dogukan A, et al. Early and vigorous fluid resuscitation prevents acute renal failure in the crush victims of catastrophic earthquakes. J Am Soc Nephrol. 2004;15(7):1861-1867. PMID: 15213270
11. Brown CV, Rhee P, Chan L, et al. Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? J Trauma. 2004;56(6):1191-1196. PMID: 15179306
12. Homer J, Hallett D. Fluid management of the crush syndrome in the 2010 Haiti earthquake. Prehosp Disaster Med. 2011;26(4):271-274. PMID: 22008495
13. Rachoin JS, Daher R, Fitzgerald R, et al. Diuretics, mannitol and nephrology consultation in the management of acute kidney injury in the intensive care unit. J Crit Care. 2013;28(5):976.e7-12. PMID: 23684585

Alkalinisation and Bicarbonate

14. Knottenbelt JD. Traumatic rhabdomyolysis from severe beating: experience of volume diuresis and alkalinization in 200 patients. J Trauma. 1994;37(2):214-219. PMID: 8054579
15. Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine (Baltimore). 2005;84(6):377-385. PMID: 16276822
16. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361(1):62-72. PMID: 19571284

Hyperkalaemia Management

17. Acker CG, Johnson JP, Palevsky PM, Greenberg A. Hyperkalemia in hospitalized patients. Causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines. Arch Intern Med. 1998;158(8):917-924. PMID: 9564856
18. Allon M. Hyperkalemia in end-stage renal disease: mechanisms and management. J Am Soc Nephrol. 1995;6(4):1134-1145. PMID: 8575383
19. Mahajan SK, Abbott GA, Berson SA, et al. Hyperkalemia in hospitalized patients. Am J Nephrol. 1983;3(6):288-294. PMID: 6314967

Compartment Syndrome and Fasciotomy

20. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. J Bone Joint Surg Br. 2000;82(2):200-203. PMID: 10707573
21. Shadgan B, Menon M, O'Brien PJ, et al. Current treatments and outcome of compartment syndrome. J Orthop Trauma. 2012;26(9):e147-e153. PMID: 22700573
22. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg Br. 2003;85(5):625-632. PMID: 12892679
23. Elliott R, Baldwin M, Freeman A, Manji M. Emergency medicine and the 2010 Haiti earthquake. Emerg Med J. 2010;27(12):894-896. PMID: 20881429

Renal Replacement Therapy

24. Schortgen F, Soubrier N, Delclaux C, et al. Hemofiltration versus hemodialysis in acute renal failure patients with multiorgan dysfunction: a multicenter randomized trial. Crit Care Med. 2000;28(8):2787-2792. PMID: 10966244
25. Uchino S, Kellum JA, Bellomo R, et al. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005;294(7):813-818. PMID: 16106006
26. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26-30. PMID: 10872726
27. Haase M, Bellomo R, Matalanis G, et al. A comparison of the MARS and molecular adsorbent recirculating system (MARS) treatments in acute liver failure: a pilot study. Nephrol Dial Transplant. 2002;17(11):2014-2020. PMID: 12407406

Myoglobin Clearance

28. Naka T, Bellomo R, Haase M, et al. Myoglobin clearance by continuous hemofiltration in rhabdomyolysis. Int J Artif Organs. 2005;28(8):839-845. PMID: 16230927
29. Zhu Z, Wang J, He C, et al. Continuous renal replacement therapy in the treatment of crush syndrome. Ren Fail. 2011;33(4):406-410. PMID: 21398000
30. Haase M, Haase-Fielitz A, Bellomo R, et al. High cutoff membrane hemofiltration for the elimination of myoglobin in severe rhabdomyolysis: case series. Blood Purif. 2010;30(3):220-227. PMID: 20606445

Disaster Medicine and Outcomes

31. Bartels SA, VanRooyen MJ. Medical complications associated with earthquakes. Lancet. 2012;379(9817):748-757. PMID: 22336897
32. Schultz CH, Koenig KL, Lewis RJ. Implications of the 2010 Haiti earthquake for disaster medical care. Ann Emerg Med. 2012;59(3):265-270. PMID: 22100024
33. Kuwagata Y, Oda J, Ninomiya N, et al. Analysis of 2,702 traumatized patients in the 1995 Hanshin-Awaji earthquake. J Trauma. 1997;42(3):427-432. PMID: 9063649
34. Noji EK. The nature of disaster: general characteristics and public health effects. Prehosp Disaster Med. 2000;15(1):3-8. PMID: 12477495

Indigenous Health

35. Australian Institute of Health and Welfare. Aboriginal and Torres Strait Islander Health Performance Framework 2017 report. Canberra: AIHW; 2017.
36. Cunningham J, Devitt J, Couzos S. Health promotion programs for Aboriginal and Torres Strait Islander people: what works and why? Aust N Z J Public Health. 2002;26(4):334-341. PMID: 12397698
37. Anderson IP, Crengle S, Leialoha Kamaka ML, et al. Indigenous health in Australia, New Zealand, and the Pacific. Lancet. 2006;367(9527):1775-1785. PMID: 16731260

Remote and Retrieval Medicine

38. Royal Flying Doctor Service. Aeromedical Retrieval Guidelines. 2018.
39. Fitzgerald MC, Kwok B, Gunja N, et al. Prehospital care and retrieval medicine in Australia. Emerg Med Australas. 2011;23(2):112-123. PMID: 21418669
40. Sullivan R, O'Brien L, Kenealy H, et al. Management of earthquake victims in remote regions: a review. Aust N Z J Surg. 1998;68(3):164-170. PMID: 9527098

Acute Kidney Injury in Rhabdomyolysis

41. Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med. 1988;148(7):1553-1557. PMID: 3387923
42. Chatzizisis YS, Misirli G, Hatzitolios AI, et al. The syndrome of rhabdomyolysis: complications and treatment. Eur J Intern Med. 2008;19(8):568-574. PMID: 18929283
43. Cervellin G, Comelli I, Lippi G. Rhabdomyolysis: historical background, clinical, diagnostic and therapeutic features. Clin Chem Lab Med. 2010;48(6):749-756. PMID: 20302357
44. **Hernandez RA, Levitt MA, Barton CW, Hoffman JR. **Delayed hemodialysis in acute rhabdomyolysis: a prospective randomized study. Ann Emerg Med. 1990;19(5):501-506. PMID: 2335311
45. Khan FY. Rhabdomyolysis: a review of the literature. Neth J Med. 2009;67(9):272-283. PMID: 19869972