Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Crush injury and rhabdomyolysis
Musculoskeletal medicine and orthopaedics · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Crush release can precipitate hyperkalaemic collapse
Compressed ischaemic muscle accumulates potassium, acids and myoglobin; release can abruptly return these products to the circulation, causing arrhythmia, shock, compartment swelling and pigment-associated acute kidney injury.
Action: Use trauma ABCDE, establish ECG and intravenous or intraosseous access when feasible without delaying safe extrication, control catastrophic bleeding, release compression as early as safely possible, check blood gas potassium and renal markers repeatedly, treat hyperkalaemia to Resuscitation Council UK doses, and obtain early orthopaedic, critical-care and renal input.
Overview
Manage crushing trauma as multisystem injury, coordinate safe early release without prophylactic tourniquet delay, recognise evolving muscle necrosis, treat hyperkalaemia immediately, individualise fluid and renal support, and identify compartment or unsalvageable-limb surgery.
Crush injury describes local damage from compression; crush syndrome is the systemic metabolic and renal consequence of substantial muscle injury. Record the compressing object, muscle mass, estimated duration, temperature, associated blast or burn, fluids, urine and deterioration during release. Risk increases with greater force, duration and muscle bulk but cannot be predicted by a single time threshold. Small or older people and those with cardiac or renal disease have less physiological reserve.
Extrication is a treatment. Ensure scene safety, relieve compression as early as safely possible and provide analgesia. Establish ECG and vascular access beforehand when practicable, but do not postpone release merely to infuse a fixed volume. Control catastrophic bleeding using trauma principles. A tourniquet can be placed loosely in readiness when major haemorrhage is plausible, but there is no evidence for tightening it to prevent metabolite washout. Prevent hypothermia and communicate release time to the receiving team.
Practice
Two practice questions
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Musculoskeletal medicine and orthopaedicsOriginal SBA
Crush-release wide QRS
Minutes after release from prolonged thigh compression, a patient becomes bradycardic and the ECG shows absent P waves with marked QRS widening. What should be given first to protect the myocardium?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Continue a complete major-trauma survey. Crush mechanisms produce pelvic, spinal, thoracic, abdominal and multiple limb injuries, degloving, burns and blast effects. Use blood components rather than crystalloid for haemorrhagic shock. Check every compressed limb for wounds, pulses, named nerves and compartment findings before and after release and splintage. A dysvascular limb needs immediate vascular care; new swelling and passive-stretch pain needs the compartment pathway, not prophylactic fasciotomy in the absence of diagnosis.
Rhabdomyolysis can lag. Obtain ECG, blood gas, potassium, bicarbonate, ionised calcium, phosphate, CK, urea and creatinine, glucose, coagulation and urine dipstick early and repeat according to risk. CK commonly rises for the first day or longer, so one low result soon after release is not reassuring. A haem-positive dipstick with few red cells supports myoglobin, but urine can look normal. Track measured urine output, fluid balance and body weight while avoiding urinary catheterisation without a clinical indication.
Fluid is individualised. Establish euvolaemia with warmed isotonic crystalloid when bleeding is controlled, reassessing perfusion, lungs, pressure and urine after each increment. Evidence does not support a rigid pre-release volume or indiscriminate high-rate infusion in a well-resourced system. Reduce volumes and involve critical care earlier in heart failure, renal impairment, frailty and pregnancy. Stop escalating fluid when pulmonary oedema or established oliguric renal failure makes further loading harmful.
Treat potassium before the laboratory trajectory worsens. Calcium stabilises myocardium but does not lower serum potassium; repeat ECG and calcium according to the resuscitation algorithm if toxic changes persist. Insulin with glucose shifts potassium intracellularly, salbutamol is an adjunct and neither removes potassium. Check glucose frequently for at least six hours after insulin. Seek renal and critical-care support early because dialysis is definitive removal when hyperkalaemia, acidosis, overload or uraemic complications remain refractory.
Routine urine alkalinisation and mannitol are not recommended for crush injury because outcome benefit is unproven and each can cause harm. Treat hypocalcaemia only when symptomatic or required for hyperkalaemic membrane stabilisation, because calcium can deposit in injured muscle and later rebound. Avoid nephrotoxins and adjust renally cleared medicines. Anaesthesia should know that significant crush and hyperkalaemia make suxamethonium hazardous; airway strategy belongs with the experienced anaesthetic team.
Surgery treats defined tissue threats. Compartment syndrome needs immediate complete decompression, but preventative fasciotomy can convert closed devitalised tissue into an infected wound. Debride open necrotic tissue through orthoplastic care. When a limb is physiologically dangerous and structurally unsalvageable, early amputation may reduce ongoing systemic burden, but the decision requires prompt multidisciplinary consultant assessment rather than a severity score alone. Rehabilitation addresses fractures, muscle loss, nerve damage, renal recovery, pain and psychological trauma.
Key points
Release the crushing force as early as safely possible; do not use a tourniquet merely to delay reperfusion, although one may be loosely pre-positioned for rapid use if catastrophic bleeding begins.
Establish monitoring and IV or IO access during prolonged extrication when practicable, but do not delay release solely to deliver a predetermined fluid volume.
Use blood products for haemorrhagic shock and individualised warmed isotonic crystalloid for hydration and rhabdomyolysis risk, reassessing pressure, lungs and urine rather than chasing a universal urine target.
Obtain an early venous or arterial blood gas, ECG, potassium, bicarbonate, calcium, phosphate, CK, creatinine and urinalysis, then repeat because initial values may be normal.
A urine dipstick positive for blood with few or no red cells supports myoglobinuria; dark urine increases suspicion but its absence does not exclude muscle breakdown.
For moderate or severe hyperkalaemia, give 10 units soluble insulin with 25 g glucose intravenously; add nebulised salbutamol 10–20 mg and monitor glucose closely.
For severe hyperkalaemia with ECG change, give 10 mL of 10% calcium chloride IV over 5 minutes, or 30 mL of 10% calcium gluconate over 10 minutes if chloride is unavailable.
Aetiology
01
Prolonged external compression
Building collapse, industrial entrapment or immobility compresses large muscle masses and impairs arterial inflow and venous outflow before release.
02
High-energy direct trauma
Road collision, machinery and blast directly disrupt muscle, bone and vessels and can produce rhabdomyolysis without prolonged entrapment.
03
Non-traumatic muscle injury
Seizures, hyperthermia, extreme exertion, prolonged unconsciousness, drugs, toxins and metabolic myopathy can cause the same systemic muscle-breakdown syndrome.
04
Reperfusion and surgery
Restored flow after arterial occlusion, limb replantation or prolonged tourniquet use can release accumulated metabolites and amplify oedema.
Pathophysiology
1
Myocyte membrane failure
Mechanical and ischaemic injury depletes ATP, disrupts calcium handling and ruptures muscle cells, releasing CK, myoglobin, potassium and phosphate.
2
Hyperkalaemic cardiotoxicity
Extracellular potassium impairs myocardial membrane conduction, causing peaked T waves, PR prolongation, QRS widening, ventricular arrhythmia and arrest.
3
Pigment kidney injury
Filtered myoglobin obstructs tubules and promotes oxidative injury, especially during hypovolaemia and aciduria, producing acute kidney injury.
4
Capillary sequestration
Damaged muscle traps large fluid volumes, worsening intravascular depletion and limb swelling despite increasing total tissue water.
5
Compartment amplification
Bleeding and reperfusion oedema raise fascial pressure, further reducing perfusion and creating additional necrosis and systemic metabolite release.
Clinical features and red flags
Local crush injury
Bruising, swelling, fractures and weakness remain confined to the compressed region without current systemic electrolyte, renal or shock manifestations.
Crush syndrome
Large-muscle injury with hyperkalaemia, acidosis, hypovolaemia, myoglobinuria or acute kidney injury marks systemic metabolic disease.
Evolving rhabdomyolysis
Increasing CK, muscle swelling, weakness and haem-positive urine with few erythrocytes may appear hours after an initially reassuring test.
Hyperkalaemic toxicity
Peaked T waves, PR prolongation, QRS widening, bradycardia or ventricular arrhythmia around release requires immediate membrane stabilisation and potassium shifting.
Compartment evolution
Increasing pain, passive-stretch pain, tension and nerve change after reperfusion signals local pressure ischaemia despite distal pulse restoration.
Renal failure pattern
Falling urine output, rising creatinine, persistent potassium, acidosis or fluid overload indicates renal support may be required rather than further blind crystalloid.
Red flags requiring action
Bradycardia, broad QRS, absent P waves, sine-wave change, ventricular arrhythmia or cardiac arrest around crush release is hyperkalaemia until urgently assessed and treated.
Oliguria, dark brown urine, rapidly rising potassium, acidosis, CK or creatinine after muscle injury predicts crush syndrome and possible renal replacement therapy.
Investigations
01First-line ECGFirst stepFirst line
Why
Detect potassium cardiotoxicity before or during biochemical confirmation.
Interpretation and limitations
Peaked T waves, PR prolongation, absent P waves, broad QRS or arrhythmia triggers immediate RCUK treatment; a normal ECG does not exclude biochemical hyperkalaemia.
02Immediate blood gas potassium
Why
Provide rapid electrolyte and acid-base assessment around extrication and deterioration.
Interpretation and limitations
Confirm with laboratory testing when possible but treat a plausible toxic pattern without delay; exclude obvious sample haemolysis without ignoring the patient.
03Serial CK
Why
Quantify muscle breakdown trajectory and support renal-risk assessment.
Interpretation and limitations
An early normal or modest value can rise substantially over 24–72 hours; trend until clearly falling with stable renal and electrolyte status.
04Renal and mineral profile
Why
Detect AKI and released intracellular solutes.
Interpretation and limitations
Trend creatinine, urea, potassium, bicarbonate, calcium and phosphate and interpret against urine output, fluid balance and baseline kidney function.
05Urinalysis and microscopy
Differential diagnosis
01
Haemorrhagic shock
Tachycardia, hypotension and acidosis after crush may reflect occult chest, abdominal, pelvic or limb bleeding and requires immediate source search and blood products.
02
Acute limb ischaemia
A cold pulseless limb indicates macrovascular injury requiring emergency revascularisation, which can itself worsen reperfusion chemistry and compartment pressure.
03
Haemoglobinuria
Intravascular haemolysis also produces a blood-positive dipstick with few red cells, distinguished by plasma appearance, blood count and haemolysis markers.
04
Drug or toxin hyperkalaemia
Renal failure, medicines, acidosis and sample haemolysis may contribute to potassium elevation and should be corrected without delaying ECG-directed treatment.
05
Sepsis or heat illness
Hyperthermia, infection and shock can cause muscle breakdown and multiorgan failure and require source-specific care alongside rhabdomyolysis treatment.
Management
01EntrappedPrepare but do not delay releaseFirst stepA person remains compressed by debris, machinery or body position.+
1Ensure scene safety, perform accessible ABCDE care, give analgesia and control catastrophic bleeding while planning earliest safe release.
2Establish ECG and IV or IO access when feasible and consider loosely positioning a tourniquet only for possible catastrophic haemorrhage.
3Use individualised warmed fluid according to trauma physiology and do not require a fixed volume before extrication.
4DefinitiveRecord release time, reassess immediately for collapse, bleeding, dysvascularity and compartment findings and transfer to definitive care.
02MetabolicProtect the heart and kidneysPotassium, ECG, urine or renal findings indicate crush syndrome or rhabdomyolysis.+
Complications
01
Hyperkalaemic cardiac arrest
Rapid potassium release causes conduction failure and lethal arrhythmia before CK or creatinine reaches its later peak.
02
Acute kidney injury
Hypoperfusion and myoglobin cause oliguria, fluid overload, uraemia and dialysis requirement, with risk evolving over several days.
03
Acute compartment syndrome
Reperfusion swelling can convert injured but viable muscle into a closed-space ischaemic emergency requiring complete fasciotomy.
04
Disseminated coagulopathy
Severe tissue injury, shock and systemic inflammation consume clotting factors and worsen bleeding and organ perfusion.
05
Limb loss and chronic impairment
Extensive muscle, vessel, nerve and bone destruction may require amputation or leave contracture, weakness, pain and prolonged rehabilitation.
Monitoring and follow-up
Maintain continuous ECG during significant crush syndrome and repeat twelve-lead assessment after calcium, potassium change or any rhythm deterioration.
Repeat potassium and blood gas promptly after treatment and serially thereafter, recognising rebound when intracellular-shift therapies wear off.
Monitor bedside glucose frequently for at least six hours after insulin and continue longer with renal failure, repeat dosing or hypoglycaemia.
Chart urine output, fluid balance, weight, respiratory examination, creatinine, bicarbonate, calcium, phosphate and CK until renal and muscle trajectories recover.
Repeat limb pulse, nerve and compartment examinations after release, reperfusion, splintage and swelling changes and escalate defined surgical threats immediately.
Follow renal recovery, muscle strength, joint motion, fractures, wounds, pain, mental health and return to mobility or prosthetic goals after discharge.
Special situations
Release is not the enemy
Evidence does not support keeping a patient trapped or applying a tourniquet merely to postpone metabolite washout.
CK is a delayed witness
Cardiotoxic potassium can rise around release while CK has not yet reached its later peak, so ECG and gas come first.
Calcium buys electrical time
Membrane stabilisation acts quickly but leaves serum potassium unchanged and must be paired with shifting and removal.
Fluid can become harmful
Once oliguric renal failure or pulmonary oedema develops, further unmeasured crystalloid worsens overload without flushing closed kidneys.
Dark urine is neither required nor specific
Myoglobin may be present without visible colour, while haemoglobin and true haematuria also produce a positive dipstick.
Fasciotomy needs a diagnosis
Preventative opening of crushed tissue can increase infection and bleeding, whereas confirmed compartment syndrome requires immediate complete release.
Common pitfalls
01
Delaying safe extrication until a fixed fluid volume is infused or applying a tourniquet solely to prevent reperfusion.
02
Focusing on rhabdomyolysis while missing pelvic, abdominal or thoracic haemorrhage, burns, blast injury and hypothermia.
03
Waiting for CK or a formal laboratory potassium before treating convincing ECG-toxic hyperkalaemia.
04
Giving calcium without insulin-glucose and definitive potassium-removal planning or failing to monitor delayed hypoglycaemia.
05
Using routine bicarbonate, mannitol, diuretics or preventative fasciotomy despite absent supporting evidence.
06
Continuing large crystalloid volumes despite oliguria and pulmonary overload instead of escalating renal replacement assessment.
Do not use routine bicarbonate, mannitol, loop diuretics, prophylactic hyperkalaemia drugs or preventative fasciotomy; involve renal and critical care early for refractory potassium, acidosis, overload or oliguria.
Disproportionate pain, passive-stretch pain, tense swelling or progressive neurological change suggests acute compartment syndrome and requires immediate surgical assessment; preventative fasciotomy without evidence is not supported.
Catastrophic haemorrhage, unstable pelvic or torso injury, hypothermia, blast injury, burns and entrapment-related trauma can kill before rhabdomyolysis and must remain within the primary survey.
Why
Identify pigment suggestive of myoglobin and alternative urinary pathology.
Interpretation and limitations
Dipstick haem with few red cells supports myoglobinuria, but sensitivity varies and absence does not exclude rhabdomyolysis.
06Trauma imaging
Why
Define fractures and torso, vascular or blast injury after immediate threats are managed.
Interpretation and limitations
Use mechanism-appropriate trauma CT and limb radiographs, avoiding imaging delay in uncontrolled bleeding, dysvascularity or compartment syndrome.
07Compartment pressure assessment
Why
Support diagnosis when swelling evolves and clinical examination is incomplete.
Interpretation and limitations
Use serial clinical findings first; concurrent pressure measurement assists uncertainty but cannot justify preventative release without a diagnosis.
08Renal replacement assessment
Why
Identify refractory indications for dialysis or filtration.
Interpretation and limitations
Escalate persistent hyperkalaemia, severe acidosis, pulmonary oedema, uraemic complication or ongoing oliguric deterioration rather than using CK alone.
1
Treat ECG-toxic hyperkalaemia with intravenous calcium and moderate or severe elevation with insulin-glucose plus adjunct salbutamol.
2Recheck ECG, potassium and glucose at protocol intervals because calcium wears off and insulin can cause delayed hypoglycaemia.
3Restore euvolaemia with reassessed isotonic crystalloid while avoiding overload and stop routine bicarbonate, mannitol or diuretic protocols.
4Involve critical care and renal teams early for refractory potassium, acidosis, oliguria, overload or likely renal replacement therapy.
03LimbTreat defined surgical threatsCrush injury causes open necrosis, arterial compromise, compartment syndrome or an unsalvageable limb.+
1Activate arterial repair for persistent dysvascularity and perform complete fasciotomy immediately when compartment syndrome is diagnosed.
2Avoid preventative fasciotomy and debride open devitalised tissue through a planned orthoplastic approach.
3Use two-consultant multidisciplinary judgement for early amputation when structural destruction and systemic burden make salvage unsafe.
4Coordinate renal, wound, fracture, nerve, pain, prosthetic and psychological recovery through a written rehabilitation plan.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Stabilises the cardiac membrane rapidly while potassium-shifting and removal treatments take effect.
Calcium for severe hyperkalaemia with ECG changes
Give 10 mL of 10% calcium chloride intravenously over 5 minutes; if calcium chloride is unavailable, give 30 mL of 10% calcium gluconate intravenously over 10 minutes, then reassess the ECG and repeat through the resuscitation algorithm if toxicity persists.
Calcium does not lower potassium; use a secure line, avoid extravasation, separate calcium from bicarbonate by different lines or flushing and do not wait for CK results when ECG toxicity is present.
Moves potassium into cells temporarily while renal excretion or renal replacement removes potassium from the body.
Insulin-glucose for moderate or severe hyperkalaemia
Give 10 units soluble insulin with 25 g glucose intravenously for potassium 6.0–6.4 mmol/L or above 6.5 mmol/L; if pre-treatment glucose is below 7 mmol/L, follow with 10% glucose at 50 mL/hour for 5 hours.
Check glucose repeatedly for at least 6 hours and treat hypoglycaemia promptly; effect is temporary, so repeat potassium and ECG and involve renal care for rebound or refractory elevation.
Beta-2 stimulation adds intracellular potassium shift while definitive elimination is arranged.
Nebulised salbutamol adjunct
Give 10–20 mg by nebuliser for moderate or severe hyperkalaemia as an adjunct to insulin-glucose, not as sole emergency treatment.
Response is variable and may cause tachycardia or tremor; do not
rely on it alone, particularly with beta-blockade, arrhythmia or ECG-toxic