Rhabdomyolysis | Hyperkalemia | Myoglobinuria | Acute Kidney Injury
CRUSH INJURY VS CRUSH SYNDROME
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
Clinical 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
The Killer You Must Anticipate
Crush syndrome kills at the moment of release, not while the patient is trapped. Never extricate a long-entrapped limb without intravenous (or intraosseous) fluids running and a plan for hyperkalaemia. Treat hyperkalaemia and hypovolaemia before any orthopaedic intervention.
Memory Aids
CBIGKDC-BIG-K-DROP (Hyperkalaemia)
| C | Calcium gluconate - membrane stabilisation (does NOT lower K+) Calcium gluconate - membrane stabilisation (does NOT lower K+) |
| B | Bicarbonate - shifts K+ intracellularly Bicarbonate - shifts K+ intracellularly |
| I | Insulin + glucose - shifts K+ intracellularly Insulin + glucose - shifts K+ intracellularly |
| G | Glucose (with insulin, to avoid hypoglycaemia) Glucose (with insulin, to avoid hypoglycaemia) |
| K | Kayexalate/resonium - removes K+ via gut Kayexalate/resonium - removes K+ via gut |
| D | Dialysis - definitive K+ removal Dialysis - definitive K+ removal |
| C | Calcium gluconate - membrane stabilisation (does NOT lower K+) Calcium gluconate - membrane stabilisation (does NOT lower K+) | I | Insulin + glucose - shifts K+ intracellularly Insulin + glucose - shifts K+ intracellularly | K | Kayexalate/resonium - removes K+ via gut Kayexalate/resonium - removes K+ via gut |
| B | Bicarbonate - shifts K+ intracellularly Bicarbonate - shifts K+ intracellularly | G | Glucose (with insulin, to avoid hypoglycaemia) Glucose (with insulin, to avoid hypoglycaemia) | D | Dialysis - definitive K+ removal Dialysis - definitive K+ removal |
Hook:Stabilise the heart first, then shift, then remove the potassium.
FLUSHFLUSH (Crush Priorities)
| F | Fluids before release - start before extrication Fluids before release - start before extrication |
| L | Lethal triad - hyperkalaemia, acidosis, hypocalcaemia Lethal triad - hyperkalaemia, acidosis, hypocalcaemia |
| U | Urine output target 200-300 mL/h to flush myoglobin Urine output target 200-300 mL/h to flush myoglobin |
| S | Saline, not Hartmann's (avoid potassium load) Saline, not Hartmann's (avoid potassium load) |
| H | Hyperkalaemia kills - treat as the immediate threat Hyperkalaemia kills - treat as the immediate threat |
| F | Fluids before release - start before extrication Fluids before release - start before extrication | S | Saline, not Hartmann's (avoid potassium load) Saline, not Hartmann's (avoid potassium load) |
| L | Lethal triad - hyperkalaemia, acidosis, hypocalcaemia Lethal triad - hyperkalaemia, acidosis, hypocalcaemia | H | Hyperkalaemia kills - treat as the immediate threat Hyperkalaemia kills - treat as the immediate threat |
| U | Urine output target 200-300 mL/h to flush myoglobin Urine output target 200-300 mL/h to flush myoglobin |
Hook:FLUSH the myoglobin and FLUSH the potassium before it stops the heart.
CCCC4 Cs of Muscle Viability
| C | Colour - dusky/grey muscle is non-viable Colour - dusky/grey muscle is non-viable |
| C | Contractility - no twitch to stimulus is non-viable Contractility - no twitch to stimulus is non-viable |
| C | Consistency - friable/mushy muscle is non-viable Consistency - friable/mushy muscle is non-viable |
| C | Capacity to bleed - fails to bleed when cut is non-viable Capacity to bleed - fails to bleed when cut is non-viable |
| C | Colour - dusky/grey muscle is non-viable Colour - dusky/grey muscle is non-viable | C | Consistency - friable/mushy muscle is non-viable Consistency - friable/mushy muscle is non-viable |
| C | Contractility - no twitch to stimulus is non-viable Contractility - no twitch to stimulus is non-viable | C | Capacity to bleed - fails to bleed when cut is non-viable Capacity to bleed - fails to bleed when cut is non-viable |
Hook:Assessed at fasciotomy; extensive non-viable muscle driving toxicity may mandate amputation.
AEIOUDialysis Triggers (AEIOU)
| A | Acidosis - severe, refractory (pH under 7.1) Acidosis - severe, refractory (pH under 7.1) |
| E | Electrolytes - refractory hyperkalaemia Electrolytes - refractory hyperkalaemia |
| I | Intoxication - overwhelming myoglobin/uraemic toxin load Intoxication - overwhelming myoglobin/uraemic toxin load |
| O | Overload - fluid overload/pulmonary oedema Overload - fluid overload/pulmonary oedema |
| U | Uraemia/Oliguria despite resuscitation Uraemia/Oliguria despite resuscitation |
| A | Acidosis - severe, refractory (pH under 7.1) Acidosis - severe, refractory (pH under 7.1) | O | Overload - fluid overload/pulmonary oedema Overload - fluid overload/pulmonary oedema |
| E | Electrolytes - refractory hyperkalaemia Electrolytes - refractory hyperkalaemia | U | Uraemia/Oliguria despite resuscitation Uraemia/Oliguria despite resuscitation |
| I | Intoxication - overwhelming myoglobin/uraemic toxin load Intoxication - overwhelming myoglobin/uraemic toxin load |
Hook:The classic dialysis vowels, applied to the crush patient.
Overview & Epidemiology
Definitions
Crush injury is the direct local tissue damage caused by sustained mechanical compression of a body part. Crush syndrome (traumatic rhabdomyolysis) is the systemic sequelae - rhabdomyolysis, electrolyte disturbance and acute kidney injury (AKI) - that follow compression and, critically, the moment of reperfusion when the limb is released. The condition was first characterised by Bywaters and Beall during the London Blitz of 1941, who linked limb crush to dark urine and fatal renal failure.
Who Gets It
Crush syndrome occurs after earthquakes and building collapse (the leading cause of mass-casualty crush), industrial and motor-vehicle entrapment, and prolonged immobilisation ("long-lie" after collapse, overdose, or being found-down). Risk rises sharply with entrapment beyond roughly 4-6 hours, large muscle-mass involvement (thigh, trunk, bilateral limbs), and delayed or absent pre-extrication resuscitation. After major earthquakes a significant minority of rescued survivors develop crush-related AKI, and the proportion requiring dialysis depends heavily on rescue speed and access to renal services.
Pathophysiology
The Compression-Reperfusion Mechanism
Pathophysiological Cascade
Direct pressure plus arterial occlusion produces myocyte ischaemia. ATP depletion disables the Na+/K+ and Ca2+ pumps, so sodium, water and calcium flood into cells while potassium and myoglobin leak out. Muscle is relatively protected from acute systemic toxicity while still compressed because the venous outflow is occluded.
On extrication, restored blood flow flushes accumulated potassium, myoglobin, phosphate, urate, lactate and creatine kinase into the systemic circulation. This sudden potassium and acid load can precipitate ventricular fibrillation within minutes - the classic "smiling death" or extrication death.
Reperfused muscle sequesters massive volumes of fluid (litres per limb), causing profound hypovolaemia, hypotension and worsening renal hypoperfusion. Compartment pressures rise, perpetuating ischaemia.
AKI results from three converging mechanisms - renal vasoconstriction (hypovolaemia plus scavenging of nitric oxide by myoglobin), intratubular cast formation (myoglobin precipitating with Tamm-Horsfall protein in acidic urine), and direct myoglobin/ferrihaemate tubular toxicity with oxidative injury.
Why Reperfusion Is the Danger Point
The single most examined concept: the patient is often haemodynamically deceptive while trapped, then deteriorates or arrests on release. This is why intravenous fluids must be running before the crushing force is removed - to dilute the potassium load and pre-empt the reperfusion washout.
Clinical Presentation
Recognising Crush Syndrome
Local Signs
- Swollen, tense, often pulseless limb
- Pain out of proportion; pain on passive stretch
- Sensory loss, paraesthesia, motor weakness
- Skin necrosis, blistering, fixed compression marks
Systemic Signs
- Hypovolaemic shock after release (third-spacing)
- Dark tea/cola-coloured urine (myoglobinuria)
- Cardiac arrhythmia from hyperkalaemia
- Oliguria progressing to anuria
- Nausea, confusion, features of metabolic acidosis
Deceptive Early Stability
A trapped patient may look stable with a normal blood pressure because the compressed limb is not yet reperfused. Do not be reassured - the metabolic load is building and will be released the moment compression ends.
Differential Diagnosis
Distinguishing Crush Syndrome from Mimics
| Condition | Distinguishing Features | Key Discriminator |
|---|---|---|
| Crush syndrome | Prolonged compression, rising CK, hyperkalaemia, myoglobinuria, AKI after release | History of entrapment plus systemic rhabdomyolysis |
| Acute compartment syndrome (isolated) | Tense compartment, pain on passive stretch, usually after fracture/reperfusion | Local limb-threat without the systemic metabolic load (they overlap) |
| Arterial injury / acute limb ischaemia | Pulseless, cold, pale limb; hard signs of vascular injury | Vascular imaging and absent distal flow rather than diffuse muscle necrosis |
| Non-traumatic rhabdomyolysis | Statins, exertion, seizures, NMS, toxins; high CK without crush history | No mechanical entrapment |
| Haemoglobinuria / haemolysis | Dipstick blood positive, plasma pink, low haptoglobin | Plasma colour and haemolysis markers, not muscle injury |
| Septic shock with AKI | Fever, vasodilatation, infection source | Sepsis markers and absence of massive CK rise |
Investigations & Imaging
Imaging Gallery
Crush Care Algorithm
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
1-1.5L/hour of 0.9% saline starting before release. Continue through extrication. If delayed extrication, may need 1L every 30 minutes.
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.
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).
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.
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.
| Indication | Threshold | Urgency |
|---|---|---|
| Absolute pressure | Greater than 30mmHg | Emergency fasciotomy |
| Delta pressure | Less than 30mmHg (DBP - CP) | Emergency fasciotomy |
| Clinical diagnosis | Pain on passive stretch, tense compartment | Emergency fasciotomy |
| Prolonged ischemia greater than 6h | Before reperfusion | Prophylactic fasciotomy |
| Severe crush with swelling | High clinical suspicion | Low 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.
Complications
Complications of Crush Syndrome
| Complication | Incidence | Timing | Management |
|---|---|---|---|
| Acute Kidney Injury | 50% (30-50% need dialysis) | 24-72 hours | Fluids, dialysis if refractory |
| Cardiac arrhythmias | 30-40% | Minutes to hours (at extrication) | Calcium, insulin, dialysis |
| Compartment syndrome | 20-30% | Hours to days | Emergency fasciotomy |
| Disseminated intravascular coagulation | 15-20% | 24-48 hours | Treat underlying cause, FFP, platelets |
| Sepsis/wound infection | 10-20% | Days to weeks | Debridement, antibiotics |
| ARDS | 10-15% | 24-72 hours | Ventilatory support, lung protective strategy |
| Multi-organ dysfunction | 10-20% | Days | ICU support, treat underlying cause |
| Amputation | 10-15% | Days to weeks | For non-viable limb, uncontrolled infection |
| Death | 10-20% | Variable | Prevention 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
Management of Crush-Related Injuries After Disasters (Landmark Review)
- Definitive review of disaster-related crush injury drawing on the Renal Disaster Relief Task Force experience
- Establishes pre-extrication and early intravenous fluid loading as the central preventive intervention against crush-induced AKI
- Frames hyperkalaemia, hypovolaemia and myoglobinuric AKI as the principal early killers
- Calls for early mobilisation of dialysis and intensive-care resources in mass-casualty settings
Marmara Earthquake - Largest Crush Syndrome Renal Series
- 639 patients with crush-related acute renal failure across 35 hospitals after the 1999 Marmara earthquake
- 477 patients (74.6%) received one or more dialysis treatments
- Overall mortality 15.2% (17.2% in dialysed vs 9.3% in non-dialysed patients)
- Death was driven by sepsis, thrombocytopenia, DIC, ARDS and thoraco-abdominal trauma rather than renal failure alone
Exam Viva Scenarios
Use these scenarios to practise clinical reasoning and management decisions
Scenario 1: Building Collapse with Prolonged Entrapment
"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?"
Scenario 2: Post-Extrication Cardiac Arrest
"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?"
Scenario 3: Crush Injury with Compartment Syndrome
"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?"
Guidelines, Registries & Global Practice
Global Epidemiology
Crush syndrome arises in three broad contexts worldwide: natural disasters (earthquakes are the dominant cause of mass-casualty crush, e.g. Marmara 1999, Kashmir 2005, Haiti 2010, Turkey-Syria 2023), industrial and motor-vehicle entrapment (mining, construction, building collapse, prolonged extrication after road traffic collisions), and prolonged immobilisation (collapse with "long-lie", drug overdose, the elderly found-down). After a major earthquake, crush-related AKI develops in a substantial minority of rescued survivors; the proportion needing dialysis varies enormously with rescue speed and access to renal services - illustrated by the Marmara series (74.6% of renal victims dialysed) versus the rural Kashmir earthquake, where far fewer reached dialysis at all.
Side-by-Side Guidance
| Source | Emphasis | Key Position |
|---|---|---|
| ISN Renal Disaster Relief Task Force / Sever (NEJM) | Disaster nephrology | Pre-extrication and early high-volume isotonic fluids; early dialysis mobilisation; avoid potassium-containing fluids |
| KDIGO (AKI) | Renal protection | Volume expansion as primary renoprotection; routine bicarbonate/mannitol not supported by strong evidence |
| AO / orthopaedic trauma teaching | Limb & compartment | Low threshold for fasciotomy; serial compartment assessment; damage-control surgery |
| ATLS / military (e.g. JTS-type guidance) | Pre-hospital & field | IV/IO access and fluids before release; cardiac monitoring; treat hyperkalaemia empirically in the field |
| Resuscitation councils (ERC/AHA/ARC) | Cardiac arrest | Hyperkalaemia is a reversible cause of arrest; give calcium early, consider dialysis |
High- vs Limited-Resource Practice Variation
In well-resourced settings, rapid extrication, point-of-care potassium, continuous renal replacement therapy and intensive care allow aggressive support and comparatively low renal-cause mortality. In limited-resource or austere disaster settings, delayed rescue, scarce dialysis and limited transport drive higher rates of hyperkalaemic death and amputation; field priorities shift toward early fluids, empirical hyperkalaemia treatment, and triage of who can be transferred for renal replacement. International coordination (e.g. deploying mobile dialysis capacity after earthquakes) materially changes outcomes.
Controversies & Areas of Uncertainty
Fluid Type & Rate
Isotonic saline is favoured to avoid potassium, but large-volume saline risks hyperchloraemic acidosis; some advocate balanced (low-potassium) crystalloid once hyperkalaemia is controlled. Optimal rate (commonly cited 1-1.5 L/h, titrated to urine output) is consensus-based, not trial-proven.
Urinary Alkalinisation
Bicarbonate to raise urine pH above 6.5 is widely taught, but Brown et al. and others show no clear added benefit over volume alone; alkalinisation risks worsening hypocalcaemia and metabolic alkalosis.
Mannitol
Once routine, now largely abandoned - no proven benefit and potential harm (osmotic nephrosis, volume shifts) in hypovolaemic patients. Reserve, if ever, for well-hydrated patients with persistent oliguria.
Prophylactic vs Therapeutic Fasciotomy
Routine prophylactic fasciotomy in crush limbs is debated: it can prevent ischaemic necrosis but converts a closed injury into an open wound with infection and bleeding risk, especially in disaster settings with limited sterility. Decompress on clear indication; individualise the prophylactic decision.
Crush Syndrome - Exam Day Quick Reference
Clinical 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