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Crush Syndrome

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Crush Syndrome

Comprehensive guide to crush syndrome - rhabdomyolysis, hyperkalemia, myoglobinuria, pre-hospital IV fluids before extrication, fasciotomy indications, and renal protection strategies for orthopaedic fellowship exam

complete
Updated: 2025-01-08
High Yield Overview

CRUSH SYNDROME - SYSTEMIC LIFE-THREATENING EMERGENCY

Rhabdomyolysis | Hyperkalemia | Myoglobinuria | Acute Kidney Injury

20%Mortality rate overall
50%Develop AKI requiring dialysis
4-6hEntrapment threshold for syndrome
1L/hFluid resuscitation rate pre-extrication

CRUSH INJURY VS CRUSH SYNDROME

Crush Injury
PatternLocalized tissue damage from compression
TreatmentStandard trauma care
Crush Syndrome
PatternSystemic manifestation after release
TreatmentAggressive IV fluids BEFORE extrication
Reperfusion Injury
PatternMetabolic derangement upon release
TreatmentPrevent with pre-extrication fluids
Lethal Triad
PatternHyperkalemia, acidosis, hypocalcemia
TreatmentCardiac monitoring, dialysis

Critical Must-Knows

  • Crush syndrome = systemic manifestation after release; crush injury = localized damage
  • IV fluids MUST start BEFORE extrication - prevents reperfusion cardiac arrest
  • Lethal triad: Hyperkalemia (cardiac arrest), metabolic acidosis, hypocalcemia
  • Target urine output 200-300mL/hour to flush myoglobin and prevent AKI
  • Fasciotomy threshold: Compartment pressure greater than 30mmHg or delta pressure less than 30mmHg

Examiner's Pearls

  • "
    Pre-hospital IV fluids before release distinguishes survivors from non-survivors
  • "
    Hyperkalemia kills in minutes - treat before other priorities if K+ greater than 6.5
  • "
    Dark tea-colored urine = myoglobinuria until proven otherwise
  • "
    Hypocalcemia from calcium sequestration in damaged muscle - do NOT aggressively replace

Clinical Imaging

Imaging Gallery

Clinical photograph of lower leg fasciotomy wound showing open longitudinal incision with exposed anterior compartment musculature - post-decompression for compartment syndrome.
Click to expand
Clinical photograph of lower leg fasciotomy wound showing open longitudinal incision with exposed anterior compartment musculature - post-decompressioCredit: PMC Open Access via Open-i (NIH) (CC-BY 4.0)
Clinical photograph comparing bilateral lower legs - affected leg shows marked swelling and tense compartments compared to normal contralateral leg, classic compartment syndrome presentation.
Click to expand
Clinical photograph comparing bilateral lower legs - affected leg shows marked swelling and tense compartments compared to normal contralateral leg, cCredit: PMC Open Access via Open-i (NIH) (CC-BY 4.0)
Bilateral lower leg fasciotomies with vessel loop shoelace closure technique - yellow vessel loops creating tension-controlled wound approximation for delayed primary closure.
Click to expand
Bilateral lower leg fasciotomies with vessel loop shoelace closure technique - yellow vessel loops creating tension-controlled wound approximation forCredit: PMC Open Access via Open-i (NIH) (CC-BY 4.0)

Management Algorithm

📊 Management Algorithm
Crush Syndrome Management Algorithm
Click to expand
Visual Sketchnote Management Algorithm: Key actions involve pre-extrication fluids and preventing reperfusion injury.Credit: OrthoVellum

Management

Management Priorities

1. Pre-extrication fluids (prevents cardiac arrest at release) 2. Treat hyperkalemia (immediate life threat) 3. Massive IV fluid resuscitation (prevents AKI) 4. Cardiac monitoring (continuous) 5. Consider dialysis early (if oliguria persists)

Volume Resuscitation Protocol

Fluid Management

Pre-ExtricationField Fluid Loading

1-1.5L/hour of 0.9% saline starting before release. Continue through extrication. If delayed extrication, may need 1L every 30 minutes.

First 6 HoursAggressive Resuscitation

1-1.5L/hour continuing in hospital. Target urine output 200-300mL/hour. May require 10-12L in first 24 hours. Central line and arterial line recommended.

AlkalinizationSodium Bicarbonate

Add 50-100mEq sodium bicarbonate to each liter of half-normal saline. Target urine pH greater than 6.5. Monitor serum pH (avoid greater than 7.50).

OngoingTitrated Fluid Therapy

Adjust based on urine output, electrolytes, and clinical status. May continue high-volume fluids for 48-72 hours. Monitor for fluid overload.

Why Normal Saline?

Normal saline is preferred because it does not contain potassium (unlike Hartmann's/Ringer's lactate). Lactated solutions should be avoided in crush syndrome due to the potassium content.

Emergency Management of Hyperkalemia

TreatmentDoseMechanismOnset
Calcium gluconate 10%10-20mL IV over 2-5 minMembrane stabilization1-3 minutes
Insulin + Dextrose10 units insulin + 50mL 50% dextroseShifts K+ intracellularly15-30 minutes
Sodium bicarbonate50-100mEq IVShifts K+ intracellularly15-30 minutes
Salbutamol10-20mg nebulizedBeta-2 mediated K+ shift15-30 minutes
Calcium resonium15-30g PO or 30g PRGI K+ binding/removal1-2 hours (slow)
HemodialysisContinuous or intermittentDefinitive K+ removalWithin minutes of starting

Calcium Chloride vs Gluconate

Calcium gluconate 10% is preferred over calcium chloride as it is less irritant to peripheral veins. Calcium chloride requires central access. Both provide membrane stabilization but do NOT lower potassium levels - they buy time for other treatments.

Preventing Myoglobin-Induced AKI

Protective Measures

  • Volume expansion: Primary protective measure
  • Urinary alkalinization: Bicarbonate to pH greater than 6.5
  • Maintain UO: Target 200-300mL/hour (3mL/kg/hr)
  • Avoid nephrotoxins: No NSAIDs, aminoglycosides, contrast

Dialysis Indications

  • Refractory hyperkalemia: K+ greater than 6.5 despite treatment
  • Severe acidosis: pH less than 7.1
  • Fluid overload: Pulmonary edema despite diuretics
  • Oliguria: Less than 0.5mL/kg/hr despite fluids
  • Uremic symptoms: Encephalopathy, pericarditis

Mannitol Controversy

Mannitol was traditionally used for osmotic diuresis and free radical scavenging. Current evidence does NOT support routine use - it may worsen AKI if patient is hypovolemic. Only consider in well-hydrated patients with persistent oliguria.

Intensive Care Management

SystemMonitoringIntervention
CardiovascularContinuous ECG, invasive BP, CVPTreat arrhythmias, volume optimize
RenalHourly urine output, daily weightsFluids, bicarbonate, dialysis if needed
Metabolic4-hourly electrolytes initiallyCorrect K+, avoid Ca2+ unless symptomatic
HematologicDaily coagulation studiesFFP, platelets for DIC
InfectionTemperature, WCC, culturesAntibiotics if sepsis; wound care

Surgical Management

Compartment Syndrome in Crush Injury

Fasciotomy Decision

Crush injuries carry high risk of compartment syndrome. Fasciotomy is indicated if: compartment pressure greater than 30mmHg, delta pressure (DBP - compartment pressure) less than 30mmHg, or clinical signs present. Do not delay for pressure measurements if clinical picture is clear.

IndicationThresholdUrgency
Absolute pressureGreater than 30mmHgEmergency fasciotomy
Delta pressureLess than 30mmHg (DBP - CP)Emergency fasciotomy
Clinical diagnosisPain on passive stretch, tense compartmentEmergency fasciotomy
Prolonged ischemia greater than 6hBefore reperfusionProphylactic fasciotomy
Severe crush with swellingHigh clinical suspicionLow threshold for fasciotomy

Prophylactic Fasciotomy

For prolonged entrapment (greater than 6 hours) or severe crush injury with anticipated massive swelling, consider prophylactic fasciotomy at time of extrication or early in hospital course. This prevents the devastating consequences of delayed compartment syndrome.

Clinical presentation of compartment syndrome showing leg swelling
Click to expand
Clinical photograph comparing both lower legs demonstrating acute compartment syndrome. One leg shows significant tense swelling while the contralateral leg appears normal. This comparative view illustrates the classic presentation - a tense, swollen limb requiring urgent fasciotomy to prevent muscle necrosis and systemic complications.Credit: PMC - CC BY 4.0

Four-Compartment Fasciotomy of Leg

Two-Incision Technique

Step 1Anterolateral Incision

15-20cm incision centered between tibial crest and fibula. Identify anterior intermuscular septum. Release anterior compartment (tibialis anterior, extensors). Release lateral compartment (peronei) through same incision by incising lateral septum.

Step 2Posteromedial Incision

15-20cm incision 2cm posterior to posteromedial tibial border. Incise fascia to release superficial posterior compartment (gastrocnemius, soleus). Detach soleus from tibia to access deep posterior compartment (tibialis posterior, FHL, FDL).

Step 3Wound Management

Assess muscle viability (4 Cs: Color, Contractility, Consistency, Capacity to bleed). Debride non-viable tissue. Leave wounds open with loose dressings or VAC therapy.

Step 4Second Look

Return to OR in 48-72 hours for reassessment, washout, and consideration of delayed primary closure or split-thickness skin graft.

Bilateral leg fasciotomies with vessel loop shoelace closure technique
Click to expand
Clinical photograph demonstrating bilateral lower leg fasciotomies with vessel loop 'shoelace' technique for gradual wound closure. Yellow vessel loops are criss-crossed across both fasciotomy wounds, allowing progressive tightening as limb swelling subsides. This technique enables delayed primary closure while maintaining wound edge approximation, avoiding the need for skin grafting in many cases.Credit: PMC - CC BY 4.0

Forearm Fasciotomy

Volar Compartment Release

  • Curvilinear incision from antecubital fossa to palm
  • Cross wrist crease obliquely (avoid contracture)
  • Release superficial flexors (FDS, FCR, FCU, PL)
  • Release deep flexors (FDP, FPL, pronator quadratus)
  • Carpal tunnel release is mandatory

Dorsal Compartment Release

  • Straight incision over mobile wad
  • Release extensor compartments
  • Usually required if volar compartments affected
  • Assess for ongoing swelling

Thigh Fasciotomy

CompartmentIncisionContents
AnteriorLateral longitudinal incisionQuadriceps (rectus femoris, vastus muscles)
MedialMedial longitudinal incisionAdductors (gracilis, adductor longus/brevis/magnus)
PosteriorPosterior longitudinal incisionHamstrings (biceps femoris, semitendinosus, semimembranosus)

Thigh Anatomy

The thigh has significant muscle mass and can sequester large volumes of fluid. Three-compartment release is typically performed. Be aware of femoral vessels and sciatic nerve. Thigh crush injuries carry highest risk of systemic complications.

Complications

Complications of Crush Syndrome

ComplicationIncidenceTimingManagement
Acute Kidney Injury50% (30-50% need dialysis)24-72 hoursFluids, dialysis if refractory
Cardiac arrhythmias30-40%Minutes to hours (at extrication)Calcium, insulin, dialysis
Compartment syndrome20-30%Hours to daysEmergency fasciotomy
Disseminated intravascular coagulation15-20%24-48 hoursTreat underlying cause, FFP, platelets
Sepsis/wound infection10-20%Days to weeksDebridement, antibiotics
ARDS10-15%24-72 hoursVentilatory support, lung protective strategy
Multi-organ dysfunction10-20%DaysICU support, treat underlying cause
Amputation10-15%Days to weeksFor non-viable limb, uncontrolled infection
Death10-20%VariablePrevention through early aggressive treatment

Mortality Predictors

Poor prognostic factors include: greater than 6 hours entrapment, trunk or bilateral limb involvement, CK greater than 75,000 U/L, delayed fluid resuscitation, DIC, and multi-organ failure. Early aggressive management significantly improves survival.

Evidence Base

Sever Earthquake Crush Syndrome - Armenian Experience

3
Sever MS et al. • NEJM (2006)
Key Findings:
  • 1988 Armenian earthquake - 600 crush syndrome patients
  • Dialysis required in 50% of patients with AKI
  • Mortality 20% overall, 60% in those requiring dialysis
  • Pre-hospital fluid therapy significantly improved outcomes
Clinical Implication: Early aggressive fluid therapy and access to dialysis are the cornerstones of crush syndrome management. Pre-hospital intervention is crucial.
Limitation: Retrospective analysis, resource-limited setting.

Marmara Earthquake - Largest Crush Syndrome Series

3
Sever MS et al. • Nephrol Dial Transplant (2002)
Key Findings:
  • 639 crush syndrome patients from 1999 Marmara earthquake
  • 477 (75%) developed AKI
  • 314 (49%) required renal replacement therapy
  • Mortality 15% with dialysis support available
Clinical Implication: Large-scale disasters require immediate mobilization of dialysis resources. International coordination essential for optimal outcomes.
Limitation: Single event analysis, unique circumstances.

Fluid Resuscitation in Crush Syndrome

4
Better OS et al. • J Am Soc Nephrol (1997)
Key Findings:
  • Pre-extrication fluid loading reduces cardiac arrest risk
  • Target urine output 200-300mL/hour optimal for myoglobin clearance
  • Alkalinization reduces myoglobin toxicity in renal tubules
  • Normal saline preferred to avoid potassium-containing solutions
Clinical Implication: The key intervention in crush syndrome is aggressive pre-extrication and ongoing fluid therapy. This prevents the majority of deaths.
Limitation: Expert opinion and case series, no RCT possible.

Role of Mannitol in Rhabdomyolysis

3
Brown CV et al. • J Trauma (2004)
Key Findings:
  • Retrospective study of 2,083 rhabdomyolysis patients
  • Mannitol and bicarbonate did not reduce AKI incidence
  • Volume of crystalloid was the only protective factor
  • Aggressive saline resuscitation is the primary intervention
Clinical Implication: Mannitol should not be routinely used. Aggressive crystalloid resuscitation remains the cornerstone of renal protection.
Limitation: Retrospective, heterogeneous population, various etiologies.

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: Building Collapse with Prolonged Entrapment

EXAMINER

"You are called to a building collapse where a 35-year-old construction worker has been trapped under concrete debris for 5 hours. His right leg is crushed. Rescue teams are preparing to extricate him. What is your management?"

EXCEPTIONAL ANSWER
This patient is at high risk for crush syndrome given greater than 4 hours of entrapment. My priority is to establish IV access and begin fluid resuscitation BEFORE extrication. I would initiate **1-1.5L/hour of normal saline** immediately. If IV access is difficult, intraosseous access is acceptable. I would ensure continuous cardiac monitoring is available if possible. Once fluids are running, I would coordinate with rescue teams to proceed with extrication. During and after extrication, I would continue high-volume fluids. I would transport to a facility with ICU and dialysis capability, notifying them in advance. I would avoid Hartmann's/lactated Ringer's due to potassium content. On arrival, I would check ECG for hyperkalemia (peaked T waves), send bloods for K+, CK, creatinine, blood gas, and assess compartments of the affected limb. If K+ is elevated or ECG changes present, I would treat immediately with calcium gluconate, insulin/dextrose, and salbutamol.
KEY POINTS TO SCORE
IV fluids MUST start before extrication - 1-1.5L/hour normal saline
Entrapment greater than 4-6 hours significantly increases crush syndrome risk
Avoid potassium-containing fluids (Hartmann's/Ringer's)
Continuous cardiac monitoring if available
Early notification to receiving facility with dialysis capability
COMMON TRAPS
✗Extricating patient without establishing IV access first
✗Using Hartmann's or lactated Ringer's (contains potassium)
✗Underestimating fluid requirements - may need 10-12L in 24 hours
✗Not anticipating hyperkalemia at moment of extrication
LIKELY FOLLOW-UPS
"What if his potassium is 7.2 on arrival and ECG shows peaked T waves?"
"What are the indications for dialysis in crush syndrome?"
"Should you perform prophylactic fasciotomy?"
VIVA SCENARIOChallenging

Scenario 2: Post-Extrication Cardiac Arrest

EXAMINER

"A 28-year-old woman was trapped in a car accident for 3 hours with her legs crushed. She was extricated by paramedics and appeared stable initially. Ten minutes after extrication, she develops VF arrest. What is the likely cause and how would you manage this?"

EXCEPTIONAL ANSWER
The most likely cause of cardiac arrest 10 minutes post-extrication is **hyperkalemia-induced ventricular fibrillation**. Upon release, potassium from the crushed muscle flooded her circulation, causing lethal arrhythmia. This is the classic presentation of 'extrication death.' Management follows ALS protocol with modifications: Continue CPR and defibrillation per standard algorithm. Administer **calcium gluconate 10% 30mL IV** (3 ampules) as a push - this stabilizes cardiac membranes. Give **sodium bicarbonate 50-100mEq IV** to shift potassium intracellularly. Give **insulin 10 units + 50mL 50% dextrose IV**. Give **nebulized salbutamol 10-20mg** if return of circulation. Continue high-volume **normal saline**. If ROSC achieved, check potassium urgently and repeat treatments. **Early dialysis** is indicated for refractory hyperkalemia. Prevention of this scenario requires pre-extrication IV fluids - this patient likely did not receive adequate fluid loading before release.
KEY POINTS TO SCORE
Hyperkalemia is the most likely cause of post-extrication cardiac arrest
Calcium gluconate stabilizes cardiac membranes - give early in arrest
Continue standard ALS algorithm alongside hyperkalemia treatment
Prevention is key - pre-extrication fluids would have prevented this
Early dialysis for refractory hyperkalemia
COMMON TRAPS
✗Not considering hyperkalemia as the cause of arrest
✗Not giving calcium early in resuscitation
✗Stopping at one round of hyperkalemia treatment if no ROSC
✗Assuming standard arrest causes (MI, PE) without considering context
LIKELY FOLLOW-UPS
"How would you have prevented this scenario?"
"What is the mechanism of hyperkalemia in crush syndrome?"
"If ROSC is achieved but potassium remains 7.5, what next?"
VIVA SCENARIOCritical

Scenario 3: Crush Injury with Compartment Syndrome

EXAMINER

"A 40-year-old man is admitted following a mining accident. His right thigh was crushed for 4 hours. He is hypotensive, has dark urine, and his thigh is massively swollen and tense. Potassium is 6.8, CK is 85,000, creatinine is rising. His leg is pulseless. How would you manage him?"

EXCEPTIONAL ANSWER
This is a life-threatening combination of crush syndrome with severe metabolic derangement and likely thigh compartment syndrome with vascular compromise. Management priorities are: **First**, treat hyperkalemia immediately - calcium gluconate 10% 20mL IV, insulin 10 units + dextrose, bicarbonate 100mEq, salbutamol nebulizer. Continuous ECG monitoring. **Second**, aggressive fluid resuscitation with normal saline 1.5L/hour, targeting UO 200-300mL/hour. Insert urinary catheter and central/arterial lines. **Third**, the pulseless leg with tense compartments requires **emergency thigh fasciotomy** - all three compartments (anterior, medial, posterior). This is both diagnostic and therapeutic. Assess muscle viability intraoperatively. **Fourth**, given rising creatinine, CK 85,000, and likely oliguria, prepare for **dialysis** - contact nephrology urgently. **Fifth**, assess limb viability post-fasciotomy. If muscle is non-viable and limb unsalvageable, amputation may be required to prevent ongoing systemic toxicity. This is a damage-control situation requiring multidisciplinary ICU care.
KEY POINTS TO SCORE
Life-threatening hyperkalemia is the immediate priority
Pulseless swollen limb needs emergency fasciotomy - all compartments
CK 85,000 and rising creatinine almost certainly needs dialysis
Assess muscle viability - may need amputation if non-viable
Multidisciplinary approach: trauma, orthopedics, vascular, nephrology, ICU
COMMON TRAPS
✗Focusing on limb before treating lethal hyperkalemia
✗Delaying fasciotomy while waiting for angiography
✗Not considering amputation for non-viable limb causing ongoing systemic toxicity
✗Underestimating fluid requirements - thigh can sequester massive volumes
LIKELY FOLLOW-UPS
"If at fasciotomy the quadriceps is non-contractile and grey, what would you do?"
"What are the indications for amputation in crush injury?"
"How would you manage this patient in ICU over the next 48 hours?"

Australian Context

Epidemiology in Australia

Crush syndrome in Australia occurs primarily in the context of industrial accidents (mining, construction), road traffic accidents with prolonged entrapment, and natural disasters (earthquakes less common, but floods and building failures can occur). Mining accidents in remote areas present unique challenges due to distance from tertiary care and dialysis facilities.

Pre-Hospital Care

Australian paramedic services are well-trained in crush syndrome management. The Australasian Triage Scale (ATS) would typically classify these patients as Category 1 (immediately life-threatening). Retrieval services (RFDS, state-based helicopter services) are essential for transport from remote locations. Pre-hospital protocols emphasize IV access and fluid loading before extrication. Intraosseous access is increasingly available in Australian ambulance services.

Tertiary Care and Dialysis Access

Major trauma centers in Australian capital cities have ICU and dialysis capabilities. Rural and remote areas may require coordination with retrieval services for transport to appropriate facilities. The Australian and New Zealand Intensive Care Society (ANZICS) provides guidelines for ICU management of multi-organ failure. Telehealth consultation with nephrology is available for remote locations. In mass casualty events, state health emergency plans include provisions for dialysis surge capacity.

Crush Syndrome - Exam Day Quick Reference

High-Yield Exam Summary

Definitions

  • •Crush injury = localized tissue damage from compression
  • •Crush syndrome = SYSTEMIC manifestation after release (rhabdomyolysis, AKI, hyperkalemia)
  • •Develops after greater than 4-6 hours of compression
  • •Reperfusion injury = metabolic derangement at moment of release

Lethal Triad

  • •Hyperkalemia - causes cardiac arrest (K+ greater than 6.5 is dangerous)
  • •Metabolic acidosis - lactic + phosphoric acid
  • •Hypocalcemia - sequestered in muscle (do NOT aggressively replace)

Pre-Extrication Protocol

  • •IV access BEFORE release - never extricate without IV
  • •Normal saline 1-1.5L/hour (NOT Hartmann's - contains K+)
  • •Cardiac monitoring if available
  • •Intraosseous access if IV impossible

Fluid Targets

  • •Urine output 200-300mL/hour (3mL/kg/hr)
  • •May need 10-12L in first 24 hours
  • •Alkalinize urine to pH greater than 6.5 with bicarbonate
  • •Avoid nephrotoxins (NSAIDs, aminoglycosides, contrast)

Hyperkalemia Treatment (C-BIG-K-DROP)

  • •Calcium gluconate 10% 10-20mL IV (membrane stabilization)
  • •Bicarbonate 50-100mEq IV (K+ shift)
  • •Insulin 10U + Dextrose 50mL 50% (K+ shift)
  • •Salbutamol 10-20mg nebulized (K+ shift)
  • •Kayexalate/Dialysis (K+ removal)

Fasciotomy Indications

  • •Compartment pressure greater than 30mmHg
  • •Delta pressure (DBP - CP) less than 30mmHg
  • •Clinical: pain on passive stretch + tense compartment
  • •Prophylactic for prolonged ischemia greater than 6 hours

Dialysis Indications

  • •Refractory hyperkalemia (K+ greater than 6.5 despite treatment)
  • •Severe acidosis (pH less than 7.1)
  • •Fluid overload/pulmonary edema
  • •Oliguria (less than 0.5mL/kg/hr despite fluids)

Key Numbers

  • •CK greater than 5,000 U/L = high risk AKI
  • •CK greater than 15,000-20,000 U/L = almost certain dialysis
  • •Entrapment greater than 4-6 hours = high risk crush syndrome
  • •20% overall mortality; 50% of AKI need dialysis
Quick Stats
Reading Time62 min
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