Crush Injury & Crush Syndrome
Summary
Crush injury is compressive trauma to body parts causing direct tissue damage. Crush syndrome is the systemic manifestation that occurs on reperfusion after release — myoglobin, potassium, phosphate, and lactate enter the systemic circulation causing hyperkalaemia, AKI, DIC, and potentially fatal cardiac arrest. The risk of cardiac arrest is highest at the moment of release. Pre-hospital IV fluid resuscitation before extrication can be life-saving.
Key Facts
- Mechanism: Compression → ischaemia → toxin accumulation → reperfusion injury on release
- Life-threatening components: Hyperkalaemia (cardiac arrest), AKI (myoglobinuria)
- Critical timing: Risk is highest at moment of release — cardiac monitoring essential
- Triad: Rhabdomyolysis + hyperkalaemia + AKI
- Treatment: Aggressive IV saline (1L/hr), treat hyperkalaemia, anticipate AKI/RRT
- Pre-hospital: IV fluids BEFORE extrication if entrapment over 1 hour
Clinical Pearls
Cardiac arrest risk is HIGHEST at the moment of release — continuous ECG monitoring is mandatory
Start IV fluids BEFORE extrication if possible in prolonged entrapment (pre-hospital 4.5%)
Calcium is cardioprotective — give early if hyperkalaemia suspected (even prophylactically)
Why This Matters Clinically
Crush syndrome is a major cause of death in disasters (earthquakes, building collapse). Understanding the pathophysiology guides treatment — the goal is to prevent hyperkalaemic arrest at release and protect the kidneys from myoglobin-induced AKI. Every clinician involved in trauma or disaster response must understand these principles.
Visual assets to be added:
- Crush syndrome pathophysiology flowchart
- Pre-hospital management algorithm
- Hyperkalaemia ECG changes progression
- Fluid resuscitation protocol diagram
Incidence
- Rare in routine practice but common in disasters
- Major earthquakes: Up to 20% of trapped survivors develop crush syndrome
- Building collapse: High incidence
- Road traffic collisions: Entrapment scenarios
Demographics
- Age: All ages; more common in working-age adults
- Occupation: Construction workers, industrial settings
- Disasters: Earthquakes, terrorist attacks, building collapse
Risk Factors for Crush Syndrome
| Factor | Notes |
|---|---|
| Duration of entrapment | Over 1 hour = significant risk |
| Mass of tissue compressed | Large muscle mass (thigh, torso) = higher risk |
| Extremity involved | Lower limbs most common |
| Age | Elderly at higher risk |
| Pre-existing renal disease | Reduces capacity to handle load |
| Dehydration | Worsens outcome |
Phase 1: Compression & Ischaemia
- Direct mechanical injury to muscle
- Ischaemia from vessel compression
- ATP depletion → membrane pump failure
- Cell swelling and oedema
Phase 2: Toxin Accumulation (During Entrapment)
- Potassium accumulates (intracellular reserves released)
- Myoglobin released from damaged myocytes
- Phosphate released
- Lactate and organic acids accumulate
Phase 3: Reperfusion Injury (On Release)
| Released Substance | Effect |
|---|---|
| Potassium | Hyperkalaemia → cardiac arrhythmias → VF/arrest |
| Myoglobin | Precipitates in renal tubules → AKI |
| Phosphate | Precipitates with calcium → hypocalcaemia |
| Lactate/acids | Metabolic acidosis |
| Free radicals | Ongoing cellular damage |
The "Lethal Cocktail"
On release, the trapped limb releases:
- Hyperkalaemia → cardiac arrest within minutes
- Hypovolaemia → third-spacing into injured tissue
- Acidosis → worsens hyperkalaemia effects
- Myoglobinuria → AKI within hours
Renal Injury Mechanism
- Myoglobin filters into tubules
- In acidic urine, myoglobin precipitates
- Cast formation → tubular obstruction
- Direct tubular toxicity
- Renal vasoconstriction
- Result: Acute tubular necrosis and AKI
Pre-Release
Immediate Post-Release
Delayed (Hours to Days)
Red Flags Requiring Immediate Action
| Red Flag | Action |
|---|---|
| Peaked T waves on ECG | Immediate calcium gluconate |
| Cardiac arrest at release | CPR, treat hyperkalaemia |
| Dark urine | Aggressive fluid resuscitation |
| Anuria | Anticipate RRT |
Pre-Hospital Assessment
- Duration of entrapment
- Body parts trapped
- Level of consciousness
- Signs of life in trapped limbs
Post-Release Assessment
| System | Assessment |
|---|---|
| Cardiovascular | BP, HR, ECG (hyperkalaemia changes) |
| Limb | Swelling, pulses, sensation, compartment tension |
| Urine | Colour (dark = myoglobinuria), output |
| Metabolic | Acidosis, hyperkalaemia |
ECG Changes in Hyperkalaemia (Progressive)
- Peaked T waves
- Flattened P waves
- Widened QRS
- Sine wave pattern
- VF/asystole
Immediate (Pre-Hospital/ED)
| Investigation | Purpose |
|---|---|
| ECG | Hyperkalaemia detection — MOST URGENT |
| VBG/ABG | K+, pH, lactate |
| Blood glucose | Often deranged |
| Urine dipstick | Blood positive but no RBCs = myoglobin |
Hospital Investigations
| Investigation | Finding in Crush Syndrome |
|---|---|
| CK | Massively elevated (>10,000, often >00,000 U/L) |
| Potassium | Elevated (life-threatening >.0) |
| Creatinine/Urea | Rising (AKI) |
| Phosphate | Elevated |
| Calcium | Low (binds to phosphate) |
| Uric acid | Elevated |
| Coagulation | Prolonged PT/APTT, low fibrinogen (DIC) |
| Urinalysis | Myoglobinuria (blood + but no RBCs) |
Risk Stratification by Entrapment Duration
| Duration | Risk | Action |
|---|---|---|
| Under 1 hour | Low risk of systemic syndrome | Standard trauma care |
| 1-4 hours | Moderate risk | IV fluids, monitor for syndrome |
| Over 4 hours | High risk | Aggressive pre-release fluids, anticipate dialysis |
AKI Staging (Post-Crush)
Use KDIGO criteria based on:
- Serum creatinine rise
- Urine output
Pre-Hospital / Before Extrication
If entrapment over 1 hour:
- Establish IV access early
- Start 0.9% saline 1L/hr BEFORE release
- Continuous ECG monitoring
- Consider calcium gluconate 10ml 10% IV prophylactically
- Tourniquet on trapped limb (controversial — rescue amputation scenario)
At Point of Release
- Continue aggressive IV fluids
- Immediate 12-lead ECG — look for hyperkalaemia
- Treat hyperkalaemia if present
- Continue cardiac monitoring
In Hospital
Fluid Resuscitation:
- Target: Urine output 200-300 ml/hr
- Typically requires 1-1.5 L/hr crystalloid initially
- Avoid lactated solutions (lactate adds to metabolic burden)
Urinary Alkalinisation:
- Add sodium bicarbonate to IV fluids
- Target urine pH >6.5 (prevents myoglobin precipitation)
- Monitor for hypokalaemia with bicarbonate use
Treat Hyperkalaemia:
| Treatment | Mechanism |
|---|---|
| Calcium gluconate 10ml 10% | Cardioprotection |
| Insulin 10 units + 50ml 50% glucose | Shifts K+ intracellularly |
| Salbutamol 10-20mg nebulised | Shifts K+ intracellularly |
| Dialysis | Definitive removal |
Renal Replacement Therapy (RRT):
- Early threshold for dialysis in crush syndrome
- Indications: Refractory hyperkalaemia, severe acidosis, volume overload, anuria
Limb Management
- Elevation to heart level (not above)
- Monitor for compartment syndrome
- Fasciotomy if compartment syndrome develops
Immediate
- Cardiac arrest (hyperkalaemia)
- Hypovolaemic shock
- Metabolic acidosis
Early (Hours to Days)
- AKI (50-70% of cases)
- Compartment syndrome
- DIC
- Hypocalcaemia (symptomatic in severe cases)
Late
- Chronic kidney disease
- Ischaemic limb loss/amputation
- Contractures
- PTSD
Mortality
- Without treatment: Up to 50% from hyperkalaemic arrest
- With aggressive management: <10% in resourced settings
- Disaster settings: Higher mortality due to delayed treatment, resource constraints
Renal Outcomes
- 50-70% develop AKI
- 50% of those require RRT
- Most recover renal function if survive acute phase
Limb Outcomes
- Depends on severity and compartment syndrome development
- Fasciotomy may be limb-saving
- Amputation may be required if severe ischaemic necrosis
Key Guidelines
- ICRC War Surgery Manual: Crush Syndrome
- JESIP/UK HART Guidance for Entrapment
- Renal Disaster Relief Task Force Guidelines
Key Evidence
- Pre-release IV fluid administration reduces mortality in prolonged entrapment
- Alkalinisation reduces myoglobin-induced AKI (animal studies, clinical consensus)
- Early dialysis improves outcomes
What is Crush Syndrome?
Crush syndrome happens when part of your body is trapped for a long time (usually over an hour). When released, harmful chemicals from damaged muscles enter the blood and can affect the heart and kidneys.
Warning Signs
- Dark urine (like cola or tea)
- Reduced urination
- Numbness or weakness in the affected limb
- Irregular heartbeat
Treatment
- IV fluids to flush out the harmful chemicals
- Medications to protect the heart
- Sometimes kidney dialysis is needed
Resources
Primary Guidelines
- ICRC. War Surgery: Working with Limited Resources in Armed Conflict and Other Situations of Violence. Chapter on Crush Syndrome. icrc.org
- Sever MS, Vanholder R. Recommendation for the management of crush victims in mass disasters. Nephrol Dial Transplant. 2012;27 Suppl 1:i1-67. PMID: 22287695
Key Studies
- Better OS. Rescue and salvage of casualties suffering from the crush syndrome after mass disasters. Mil Med. 1999;164(5):366-369. PMID: 10332179
- Michaelson M. Crush injury and crush syndrome. World J Surg. 1992;16(5):899-903. PMID: 1462628