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Crush syndrome

Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find one of our health articles more useful.

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What is crush syndrome?

Crush injury is commonly found in victims of earthquakes, mine disasters, explosions, terrorist attacks, local wars, and other accidents. The complications that arise due to the crush injury inflicted on victims give rise to crush syndrome1 .

The 'Diseases Database' defines crush syndrome as2 :

"Severe systemic manifestation of trauma and ischaemia involving soft tissues, principally skeletal muscle, due to prolonged severe crushing. It leads to increased permeability of the cell membrane and to the release of potassium, enzymes and myoglobin from within cells. Ischaemic renal dysfunction secondary to hypotension and diminished renal perfusion results in acute tubular necrosis and uraemia."


  • Crush injury can follow prolonged continuous pressure on muscle tissue. Crush injury can lead to crush syndrome.

  • Ischaemia reperfusion (when the pressure is released from the crushed limb) is the main mechanism of muscle injury in crush syndrome. There is traumatic rhabdomyolysis.

  • Muscle injury causes large quantities of potassium, phosphate, myoglobin, creatine kinase and urate to leak into the circulation.

  • Myoglobin levels in the plasma are normally very low. If a significant amount of skeletal muscle is damaged (>100 g),excess myoglobin is filtered by the kidneys and can cause renal tubular obstruction and renal damage: the excess myoglobin is nephrotoxic.

  • Intravascular volume depletion and renal hypoperfusion, combined with myoglobinuria, result in renal dysfunction.

Crush syndrome is characterised by4 :

This can also lead to:

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Who is affected by crush syndrome? (Epidemiology)

Crush syndrome has been described in numerous settings, most commonly after earthquakes, during war and after explosions that have caused buildings to collapse. It is also seen following industrial accidents, such as those occurring in mining and after road traffic accidents. The incidence of crush syndrome has been reported as 2% to 15% in all trauma patients and it can be as high as 30% in earthquake victims5 .

Crush syndrome symptoms

The key clinical features of crush syndrome are:

  • Crushing injury to a large mass of skeletal muscle.

  • Sensory and motor disturbances in the compressed limbs, which subsequently become tense and swollen. The limb/body part may be pulseless.

  • Myoglobinuria and/or haemoglobinuria, which may make the urine tea-coloured quite early on.

  • There may be oliguria with profound hypovolaemic shock.

  • Nausea, vomiting, confusion and agitation may occur as consequences of disturbed body chemistry; urea, creatinine, uric acid, potassium, phosphate and creatine kinase are elevated. There may also be hypocalcaemia.

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Crush syndrome treatment and initial management

If not treated in time, the mortality rate of crush syndrome is very high. The most important measure that can be taken to reduce mortality in such situations is immediately to start treatment. However, the traditional treatment methods such as fluid resuscitation, diuresis, and hemodialysis are not feasible enough to be carried out at the disaster scene1 .

  • Check for safety of self and others.

  • The patient must be assessed in keeping with the usual criteria for assessing a severely injured person.

  • Assessment of 'Airway, Breathing and Circulation' should be carried out.

  • Monitor vital signs and oxygen saturation level.

  • Administer oxygen through a non-rebreather mask.

  • Assess limbs using the '5 Ps' of acute limb ischaemia - pain, paraesthesia, paralysis, pallor and pulselessness - to estimate extent of ischaemic injury.

  • Attention should be given to life-threatening injuries.

  • Venous access should be obtained as early as possible, ideally before the trapped limb is freed and decompressed.

  • Preserve body heat.

  • Prior to release, consider an arterial tourniquet if compression has been less than 30 minutes. Apply a tourniquet if compression has been more than 30 minutes.

  • In the adult, a saline infusion of 1,500 ml/hour should be initiated during extrication. Early, vigorous hydration (≥10 litres/day) helps preserve renal function6 .

  • Because of the very high risk of acute kidney injury, a catheter should be inserted at an early stage and urine output monitored.

  • Because of the need to maintain fluid balance, a central venous line is usually required.

  • Analgesia should be provided. Entonox® may be more suitable than IV or oral analgesia due to the dangers of hypotension.


Blood tests

These should include:

  • U&Es, including potassium.

  • Creatinine.

  • Calcium (there may be hypocalcaemia).

  • Phosphate.

  • Creatine kinase (rhabdomyolysis has been defined as total creatine kinase levels 5-10 times above normal in a patient with typical symptoms and/or risk factors)7 .

  • Uric acid (may be raised).

  • FBC and clotting studies (to look for evidence of DIC).

  • LFTs (may show hepatic dysfunction).

  • Blood gases.

Other investigations

  • Urine dipstick for myoglobin (but this is only positive in 50-80% of cases of rhabdomyolysis so a negative dipstick does not exclude it)8 .

  • ECG may show changes secondary to hyperkalaemia.

  • The usual assessment for trauma, including X-rays, should be performed.

  • Assessment of compartment pressures (see 'Complications', below).

Further management

Medical4 6

  • Urine output should be maintained at 300 ml/hour until myoglobinuria has ceased9 .

  • A forced mannitol-alkaline diuresis may help to protect the kidneys against damage from myoglobin and may reduce the risk of hyperkalaemia. Mannitol protects the kidney by enhancing renal perfusion and may reduce muscle injury as well.

  • Urinary alkalinisation with sodium bicarbonate may help to prevent acute kidney injury.

  • Hyperkalaemia will need treatment.

  • Hypocalcaemia does not generally need treatment.

  • Renal dialysis may be needed.

  • DIC will need treatment with fresh frozen plasma, cryoprecipitate and platelets.


It may be necessary to amputate crushed limbs. Amputation at an early stage may prevent crush syndrome.

Crush syndrome complications5

  • Hyperkalaemia and infection are the most common causes of death. Hyperkalaemia can lead to arrhythmia and arrest.

  • Infection is a major cause of death in disaster zones.

  • Acute kidney injury can occur.

  • Compartment syndrome can occur because of the uptake of fluid into muscle cells contained within a tight compartment. Fasciotomy is useful in reducing muscle damage from compartment syndrome10 . It should be done early.

  • DIC can occur with massive tissue damage3 .

  • Creatine kinase levels peak within 24 hours and should then decrease by 30-40% per day. Serial measurements will be needed. If levels continue to elevate, consider ongoing muscle injury or compartment syndrome11 .


  • Adequate fluid support improves prognosis12 .

  • The mortality rate for crush syndrome following the earthquake in northern Turkey in 1999 was 15.2%13 . However, rates in subsequent quakes have varied and it is thought that many factors may affect survival, such as hampered rescue and transport, destroyed medical facilities, availability or not of sophisticated therapeutic options and the method of construction of the collapsed buildings.

  • Time under the rubble does not have an adverse effect on outcome but this may be because those who survive have been less severely injured. It has been recommended that recovery of survivors should continue for at least five days14 .

  • Anyone who has been buried under rubble for a length of time will be dehydrated and hence more susceptible to renal damage.

Crush syndrome prevention

  • In any major disaster, adequate triage must carried out to identify those in need of urgent attention. This may have a marked effect on morbidity and mortality15 .

  • Adequate rehydration reduces the risk of acute kidney injury in crush syndrome.

  • In acute kidney injury, peritoneal dialysis may be life-saving. To this end, the Renal Disaster Relief Task Force (RDRTF) has offered support for renal problems in the aftermath of several disasters - eg, the Marmara earthquake (1999) in Turkey, the Bam earthquake (2003) in Iran and, more recently, the earthquake in Eastern Turkey (2011)16 .

Further reading and references

  • Song J, Ding H, Fan HJ, et al; Canine model of crush syndrome established by a digital crush injury device platform. Int J Clin Exp Pathol. 2015 Jun 1;8(6):6117-25. eCollection 2015.
  1. Li N, Wang X, Wang P, et al; Emerging medical therapies in crush syndrome - progress report from basic sciences and potential future avenues. Ren Fail. 2020 Nov;42(1):656-666. doi: 10.1080/0886022X.2020.1792928.
  2. Crush syndrome; Diseases database, Unified Medical Language System
  3. Sever MS, Vanholder R; Management of crush syndrome casualties after disasters. Rambam Maimonides Med J. 2011 Apr 30;2(2):e0039. doi: 10.5041/RMMJ.10039. Print 2011 Apr.
  4. Reperfusion Injury/Crush Injury; Wheeless' Textbook of Orthopaedics
  5. Li W, Qian J, Liu X, et al; Management of severe crush injury in a front-line tent ICU after 2008 Wenchuan earthquake in China: an experience with 32 cases. Crit Care. 2009;13(6):R178. doi: 10.1186/cc8160. Epub 2009 Nov 6.
  6. Crush Injury; University of California Medical School, 2013
  7. Abrahamsen SO, Stilling M; Life-threatening rhabdomyolysis after prolonged hypoperfusion of the lower legs. BMJ Case Rep. 2013 May 20;2013. pii: bcr2012008305. doi: 10.1136/bcr-2012-008305.
  8. Nemiroff L, Cormier S, LeBlanc C, et al; Don't you forget about me: considering acute rhabdomyolysis in ED patients with cocaine ingestion. Can Fam Physician. 2012 Jul;58(7):750-4.
  9. Ganeshram P, Goundan PN, Jeyachandran V, et al; Five factors contributing to severe rhabdomyolysis in a 21 yr old IV drug abuser: a case report. Cases J. 2009 Jul 7;2:6479. doi: 10.4076/1757-1626-2-6479.
  10. Atef-Zafarmand A, Fadem S; Disaster nephrology: medical perspective. Adv Ren Replace Ther. 2003 Apr;10(2):104-16.
  11. Valdez C, Schroeder E, Amdur R, et al; Serum creatine kinase levels are associated with extremity compartment syndrome. J Trauma Acute Care Surg. 2013 Feb;74(2):441-5; discussion 445-7. doi: 10.1097/TA.0b013e31827a0a36.
  12. Better OS, Abassi ZA; Early fluid resuscitation in patients with rhabdomyolysis. Nat Rev Nephrol. 2011 May 17.
  13. Sever MS, Erek E, Vanholder R, et al; Lessons learned from the catastrophic Marmara earthquake: factors influencing the final outcome of renal victims. Clin Nephrol. 2004 Jun;61(6):413-21.
  14. Sever MS, Erek E, Vanholder R, et al; Lessons learned from the Marmara disaster: Time period under the rubble. Crit Care Med. 2002 Nov;30(11):2443-9.
  15. Song J, Ding H, Fan HJ, et al; Canine model of crush syndrome established by a digital crush injury device platform. Int J Clin Exp Pathol. 2015 Jun 1;8(6):6117-25. eCollection 2015.
  16. Vanholder R, Van Biesen W, Lameire N, et al; The role of the International Society of Nephrology/Renal Disaster Relief Task Force in the rescue of renal disaster victims. Contrib Nephrol. 2007;156:325-32.

Article history

The information on this page is written and peer reviewed by qualified clinicians.

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