Crush Syndrome

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

The 'Diseases Database' defines crush syndrome as:

"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."[1]

It is also known as Bywaters' syndrome. Crush syndrome was first described by Bywaters in the British Medical Journal in 1941 after the London Blitz.

  • 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.[2] 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.[3][4]
  • Intravascular volume depletion and renal hypoperfusion, combined with myoglobinuria, result in renal dysfunction.[2]

Crush syndrome is characterised by:[5]

  • Hypovolaemic shock (due to sequestration of water in the injured muscle cells).
  • Hyperkalaemia (release of cellular potassium by the injured muscle cells).

This can also lead to:[6]

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.

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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.
  • 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.
  • 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.[4]
  • 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 function.[7]
  • 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.

Blood tests

These should include:

  • Urea and electrolytes, 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).[6]
  • Uric acid (may be raised).
  • FBC and clotting studies (to look for evidence of disseminated intravascular coagulation (DIC)).
  • LFTs (may show hepatic dysfunction).
  • Blood gases.

Other investigations

  • Urine dipstick for myoglobin (but this is only positive in 50% of cases of rhabdomyolysis so a negative dipstick does not exclude it).[6]
  • 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).

Medical

  • Urine output should be maintained at 300 ml/hour until myoglobinuria has ceased.[4]
  • A forced mannitol-alkaline diuresis may help to protect the kidneys against damage from myoglobin and may reduce the risk of hyperkalaemia.[2] 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 renal failure.
  • Hyperkalaemia will need treatment.
  • Hypocalcaemia does not generally need treatment.
  • Renal dialysis may be needed.
  • Disseminated intravascular coagulation (DIC) will need treatment with fresh frozen plasma, cryoprecipitate and platelets.

Surgical

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

  • Hyperkalaemia and infection are the most common causes of death.[8] Hyperkalaemia can lead to arrhythmia and arrest.
  • Infection is a major cause of death in disaster zones.[8]
  • 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 syndrome.[9] It should be done early.
  • Disseminated intravascular coagulation (DIC) can occur with massive tissue damage.
  • 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 syndrome.[6]
  • Adequate fluid support improves prognosis.[10]
  • The mortality rate for crush syndrome following the earthquake in northern Turkey in 1999 was 15.2%.[11] 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 that survive have been less severely injured. It has been recommended that recovery of survivors should continue for at least five days.[12]
  • Anyone who has been buried under rubble for a length of time will be dehydrated and hence more susceptible to renal damage. There may be other injuries, eg chest compression and spinal injury.
  • 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 mortality.[13]
  • Adequate rehydration reduces the risk of acute renal failure in crush syndrome.

Further reading & references

  1. Diseases database; Crush syndrome; Unified Medical Language System
  2. Malinoski DJ, Slater MS, Mullins RJ; Crush injury and rhabdomyolysis.; Crit Care Clin. 2004 Jan;20(1):171-92.
  3. Melli G, Chaudhry V, Cornblath DR; Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine (Baltimore). 2005 Nov;84(6):377-85.
  4. Sauret JM, Marinides G, Wang GK; Rhabdomyolysis. Am Fam Physician. 2002 Mar 1;65(5):907-12.
  5. Reperfusion Injury/Crush Injury, Wheeless' Textbook of Orthopaedics
  6. Craig S; Rhabdomyolysis in Emergency Medicine, Medscape, Dec 2010
  7. Vanholder R, Sever M et al; Oxford Journals online. Acute renal failure related to the crush syndrome: towards an era of seismo-nephrology? Oct 2000.
  8. Kazancioglu R, Cagatay A, Calangu S, et al; The characteristics of infections in crush syndrome.; Clin Microbiol Infect. 2002 Apr;8(4):202-6.
  9. Atef-Zafarmand A, Fadem S; Disaster nephrology: medical perspective.; Adv Ren Replace Ther. 2003 Apr;10(2):104-16.
  10. Better OS, Abassi ZA; Early fluid resuscitation in patients with rhabdomyolysis. Nat Rev Nephrol. 2011 May 17.
  11. 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.
  12. 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.
  13. Bulut M, Fedakar R, Akkose S, et al; Medical experience of a university hospital in Turkey after the 1999 Marmara earthquake.; Emerg Med J. 2005 Jul;22(7):494-8.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Michelle Wright
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Last Checked:
19/08/2011
Document ID:
1230 (v23)
© EMIS