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DOI: 10.1191/1460408602ta228oa 2002; 4; 129 Trauma

Ian Greaves, Keith Porter and Jason Smith Consensus statement on crush injury and crush syndrome

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Consensus statement on crush injury and crushsyndromeIan Greavesa, Keith Porterb and Jason Smithc

Crush syndrome remains rare in European practice. It is however common in areasof civil disorder and where the normal structures of society have given way to civilwar or natural disaster. Western doctors are becoming increasingly involved insuch situations and there is no reason to believe that instances due to moreconventional causes, such as collapse in the elderly or road traf® c accidents, willcease. For all these reasons it is important that clinicians who deal infrequentlywith crush syndrome have access to appropriate guidelines. This consensusreport seeks to provide such advice. It reports the ® ndings of a consensusmeeting on crush injury and crush syndrome held in Birmingham on 31 May2001, and coordinated by the Faculty of Pre-Hospital Care of the Royal College ofSurgeons of Edinburgh.

Key words: crush syndrome; renal failure; natural disasters

Introduction

Crush injuries and crush syndrome were ®rst describedin the English language literature by Bywaters andBeall (1941) after several patients who had beentrapped under rubble of buildings bombed in theBlitz subsequently died of acute renal failure. It hasbeen described in numerous settings since, most com-monly after natural disasters such as earthquakes, inwar, and after buildings have collapsed as a result of

explosion. Crush syndrome is also seen followingindustrial incidents such as mining and road traf®caccidents. However, crush syndrome is not con®ned totraumatic aetiologies, and has also been describedfollowing periods of crush by patients’ own bodyweight, after stroke or intoxication (Michaelson,1992).

Most commonly in traumatic crush, the legs areaffected, and less frequently the arms. Many authorsbelieve that crush injury of the head and torso signi®-cant enough to cause the syndrome is incompatiblewith life due to the inherent internal organ damage, butthere are a few reported cases of such instances(Hiraide et al., 1997).

Crush syndrome bears many similarities to, but isdistinct from, the syndrome caused by heat illness.

De� nition

Following a search of the literature, it was felt that ade®nition of crush injury and crush syndrome wasrequired.

Trauma 2002; 4: 129±134

# Arnold 2002 10.1191=1460408602ta228oa

aProfessor of emergency medicine, University of Teeside, JamesCook University Hospital, Middlesbrough, UK.bConsultant trauma and orthopaedic surgeon, University Hos-pital, Selly Oak Hospital, Birmingham, UK.cSpecialist Registrar in emergency medicine, Defence MedicalServices.Address for correspondence: Keith Porter, Selly Oak Hospital,Raddlebarn Road, Birmingham, B29 6JD, UK.Organisations represented: The Voluntary Aid Societies, TheAmbulance Service Association, The British Association forImmediate Care, British Association for Emergency Medicine,Faculty of Accident and Emergency Medicine, The RoyalCollege of Anaesthetists, The Royal College of Physicians,The Royal College of Surgeons of Edinburgh, The IntensiveCare Society, The Royal College of Nursing, The Military, andThe Faculty of Pre-hospital Care.

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Consensus view

`A crush injury is a direct injury resulting from crush.Crush syndrome is the systemic manifestation of musclecell damage resulting from pressure or crushing’.

The severity of the condition is related to the magni-tude and duration of the compressing force, and thebulk of muscle affected. The de®nition is not, however,dependent on the duration of the force applied.

Examples of this relationship include a patientwhose legs are run over by the wheels of a truck. Inthis case the force is large, but the duration is veryshort. At the other extreme, there is the elderly patientwho has suffered a stroke, falls, and lies in the sameposition for hours, sustaining a crush injury to theareas of the body on which they are lying. In this case,the force is relatively small, but crush syndrome maydevelop as a result of the prolonged period of pressure.Similar cases to this are described by Shaw et al. (1994)as a result of drug overdose.

Pathogenesis and clinical features

The typical clinical features of crush syndrome arepredominantly a result of traumatic rhabdomyolysisand subsequent release of muscle cell contents. Themechanism behind this in crush syndrome is the leaki-ness of the sarcolemmal membrane caused by pressureor stretching. As the sarcolemmal membrane isstretched, sodium, calcium and water leak into thesarcoplasm, trapping extracellular ¯uid inside themuscle cells. In addition to the in¯ux of these elementsinto the cell, the cell releases potassium and other toxicsubstances such as myoglobin, phosphate and urateinto the circulation (Better, 1999).

The end result of these events is shock (discussedbelow), hyperkalaemia (which may precipitate cardiacarrest), hypocalcaemia, metabolic acidosis, compart-ment syndrome (due to compartment swelling), andacute renal failure (ARF). The ARF is caused by acombination of hypovolaemia with subsequent renalvasoconstriction, metabolic acidosis and the insult ofnephrotoxic substances such as myoglobin, urate andphosphate.

Shock

Haemodynamic instability secondary to crush syn-drome is multifactorial. First, many patients have

other injuries, such as fractures of the pelvis or lowerlimbs, suf®cient in themselves to cause hypovolaemia.The sequestration of ¯uid into the affected musclecompartments has already been described, resultingin ¯uid shift from the intravascular to the intracellularcompartments. This may cause hypovolaemia, as theintravascular volume is depleted. Electrolyte imbal-ances such as hyperkalaemia, hypocalcaemia and ametabolic acidosis will have a negatively inotropiceffect, and there is also evidence that there is directmyocardial depression from other factors releasedwhen muscle cells are damaged (Rawlins et al., 1999).

Approach to treatment

Treatment of the crushed patient can be divided intotwo phases. The initial prehospital phase may, depend-ing on the mechanism of injury, involve a prolongedextrication period. The second phase commences onreaching a de®nitive medical care facility.In the case of prolonged on-scene time, or delay intransfer due to geographical reasons, some of thesecond phase guidelines may be employed in the pre-hospital environment.

Consensus viewSafety is the ®rst priority when approaching an acci-dent scene, and this is particularly relevant to situa-tions where patients may have suffered crush injuries,as there may be danger from falling debris or risk offurther building collapse.

Once the scene has been declared safe, in cases ofmass casualties a triage system, such as the triagesieveÐMajor Incident Medical Management & Sup-port (MIMMS, 2002)Ðshould be used to prioritizecasualties and assess the need for further treatment.For each individual casualty, an assessment of airway,breathing and circulation is the next priority. Atten-tion must be given in trauma to the possibility of spinalinjury, and full spinal precautions should be main-tained. Administration of high-¯ow oxygen by maskshould be a priority in treatment, as should the arrest ofany obvious external haemorrhage and the splinting oflimb injuries. The patient should be exposed as neces-sary to assess and manage injuries. In a hostile envir-onment or where there is a risk of hypothermia,exposure should be as limited as possible. Assessmentof distal neurovascular status is essential if exposure isto be kept to a minimum.

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Fluid resuscitation

Once the initial primary survey has been performed,intravenous access should be obtained. If limb crushinjury has occurred, and there is a likelihood of thepatient developing crush syndrome, the following ¯uidguidelines should be followed. In the presence oflife-threatening thoraco-abdominal injury, ¯uidresuscitation should be performed according to theFaculty’s previously published guidelines (Greaves etal., 2002).

Consensus viewAn initial ¯uid bolus of 2 l of crystalloid should begiven intravenously. This should be followed by 1±1.5 lper hour. The ¯uid of choice is normal saline, warmedif possible, as this is established as the ¯uid carried bythe majority of prehospital vehicles in the UK. Hart-mann’s solution contains potassium and has a theore-tical disadvantage of exacerbating hyperkalaemia. Ifpossible, ¯uid should be started prior to extrication,however gaining intravenous access and the adminis-tration of ¯uid should not delay extrication and trans-port to a de®nitive care facility. Early catheterisationshould be considered, especially if there is a prolongedextrication or evacuation phase.

Once the patient reaches hospital, 5% dextroseshould be alternated with normal saline to reduce thepotential sodium load.

Analgesia

Consensus viewThe use of medical teams including paramedics, nursesand doctors should be considered at an early stage, andappropriate analgesia should be given. This mayinvolve the use of Entonox1 initially, but most patientswill require intravenous analgesia such as an opiate,titrated against response. The use of ketamine, with orwithout the concomitant use of a benzodiazepine, isalso an effective means of relieving pain, and may aidextrication.

Triage

Consensus viewPatients with crush injuries should be taken to ahospital with an intensive care facility and the equip-

ment and expertise necessary to provide renal supporttherapy such as haemo®ltration or dialysis.

Tourniquets

The use of tourniquets has a theoretical role in themanagement of these patients. If the release into thecirculation of the contents of crushed muscle cells canbe avoided, possibly with the use of a tourniquet, itmay be of bene®t. However, there is currently noavailable evidence to support this.

Consensus viewThe use of tourniquets should be reserved for otherwiseuncontrollable life threatening haemorrhage. There isno evidence at the moment to support the use oftourniquets in the prevention of reperfusion injuryfollowing extrication, or in the prevention of washingof the products of rhabdomyolysis into the circulation.

Amputation

Another theoretically advantageous measure is ampu-tation of a crushed limb to prevent crush syndrome.

Consensus viewThere is no evidence to support the use of amputationas a prophylactic measure to prevent crush syndrome.Reports from the literature suggest that even severelycrushed limbs can recover to full function. If the limb isliterally hanging on by a thread, or if the patient’ssurvival is in danger due to entrapment by a limb,amputation should be considered and appropriateexpert advice sought.

Immediate in-hospital care

Consensus viewPatient should be assessed following normal AdvancedTrauma Life Support (ATLS) 1997 guidelines. Base-line blood tests should be taken. These will include fullblood count, urea and electrolytes, creatinine kinase,amylase, liver function tests, clotting screen and groupand save (cross match if deemed appropriate). Thepatient should be catheterized and hourly urine mea-surements commenced. Central venous pressure andinvasive arterial monitoring should be considered.

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The use of solute-alkaline diuresis

The development of acute renal failure in these patientssigni®cantly decreases the chances of survival (Ward,1988). Every effort must be made, therefore, to preventits occurrence. Alkalinisation of urine and the use of asolute-alkaline diuresis is accepted to be protectiveagainst the development of acute renal failure (Better,1990, 1999).

Consensus viewIt is recommended that urine pH is measured, and keptabove 6.5 by adding 50 mmol aliquots of bicarbonate(50 ml 8.4% sodium bicarbonate) to the intravenous¯uid regime. Solute diuresis is affected by administer-ing mannitol at a dose of 1±2 g=kg over the ®rst fourhours as a 20% solution, and further mannitol shouldbe given to maintain a urine output of at least 8 l perday (300 ml=hour). Fluid requirements are high,usually of the order of 12 l per day, due to the seques-tration of ¯uid in muscle tissue. Fluid should be givenat approximately 500 ml=hour, but regular review ofclinical parameters such as central venous pressure andurine output should dictate exact amounts of ¯uidgiven.

The maximum daily dose of mannitol is 200 g, and itshould not be given to patients who are in establishedanuria.

Children

Consensus viewThere is very little evidence in the literature to guide thetreatment of children suffering from crush injuries. Inyoung children the difference in body proportions,namely the reduced contribution to the total percen-tage made by the limbs, may in¯uence the incidence ofcrush syndrome. The ¯uid resuscitation guidelinesfrom Advanced Paediatric Life Support (APLS,2001) of an initial bolus of 20 ml=kg should be followedin these patients.

The elderly and patients withco-morbidity

Consensus viewIn the elderly, and those with pre-existing medicalconditions such as cardiac failure, ¯uid replacementmust be tailored to requirements and given with cau-

tion. Close monitoring of the clinical state of thepatient, and regular review of ¯uid requirements isessential in these patients.

Compartment syndrome

The development of compartment syndrome in crushinjury is due to the uptake of ¯uid into damaged muscletissue contained within the restricted compartment.Once compartment pressure exceeds capillary perfu-sion pressure at about 30±40 mmHg, the tissue insidethe compartment becomes ischaemic, and compart-ment syndrome develops.

The traditional treatment of compartment syn-drome is fasciotomy (Shaw et al., 1994), but there isnow evidence that initial treatment with mannitol maydecompress compartment syndrome and avoid theneed for surgery (Better et al., 1991; Better, 1999).

Consensus viewIn patients with compartment syndrome due to crushinjury, in the absence of neurovascular compromise, atrial of mannitol therapy should be instigated, but aspecialist surgical opinion should be sought early.

Hyperbaric oxygen therapy

There is theoretical and limited experimental evidencethat hyperbaric oxygen therapy may improve woundhealing and reduce the need for multiple surgicalprocedures in crush injury (Bouachour et al., 1996).

High concentrations of oxygen cause systemic vaso-constriction but continue to deliver adequate oxygendelivery. In a similar fashion, nitric oxide synthaseinhibitors may also have a role in preventing excessivevasodilatation in the crushed muscle and the conse-quent increase in third space ¯uid losses (Rubinsteinet al., 1998).

Consensus viewLogistically hyperbaric oxygen treatment has limitedapplication. Patients with no signi®cant co-morbidity,and who can be managed in a hyperbaric chamberwhere the facility is available, may be treated withhyperbaric oxygen therapy. It is recommended thattreatment options are discussed with the local hyper-baric unit. This is not recommended as ®rst-line treat-ment. Patients should, however, receive high-¯owoxygen, unless there is a speci®c contraindication.

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Further management

Consensus viewIn many cases, intensive care support will be requiredfor the complications of crush syndrome. If the patientbecomes oligo- or anuric, it is likely that they willrequire haemo®ltration or dialysis.

Multiple casualties

Consensus viewIn the civilian environment in the United Kingdom,there will be a huge strain on intensive care facilities ifthere are multiple crushed casualties. A policy shouldbe drawn up to prepare for the dispersal of thesecasualties on both a national and international levelshould an incident occur. Further information is avail-able in Better’s review (1999).

Areas identi� ed for future research

Use of tourniquetsIs there a role for the tourniquet post- or pre-extrica-tion of the crush injury casualty? The use of an animalmodel of crush injury was suggested, to assess thesuitability of tourniquet administration. Comparisonof tourniquet placement versus no tourniquet indelayed intravenous ¯uid administration was sug-gested as a further research option. Are there anyfurther deleterious effects due to the increased ischae-mia times involved in application of a tourniquet?

Could cooling the limb be used in order to slow cell-ular respiration and consequently decrease oedema=

compartment syndrome=improve limb viability?Tourniquet effectiveness was highlighted as a poten-

tial problem with their use. There is a requirement toperform a literature search into tourniquet usage, inparticular regarding their use in Biers blocks, in orderto determine the effectiveness of certain types of tour-niquet and the leakage rates of drugs, past the tourni-quet. This may assist in establishing the likelihood ofpotassium leaking into the systemic circulation.

Fluid administrationTypes of ¯uid currently used for administrationinclude: normal saline, Hartmann’s, Dextran, orstarches. What is the correct amount of ¯uid to begiving? Should we be looking at urine output, absolute

volume intake, or acidity of urine as a guide to ¯uidadministration? Oedema occurring secondary to mas-sive ¯uid administration may be detrimental. At whatstage do we need to worry about this? What effect doesthis have on compartment syndrome?

Prognostic indicatorsCreatinine kinase, myoglobinaemia, and amylase havebeen suggested as prognostic indicators, although it isnot clear that they can predict outcome at an earlyenough stage to allow effective intervention. The use ofmicroalbuminuria as a prognostic indicator of crushsyndrome was suggested.

Hyperbaric oxygen therapyUse of the Institute of Naval Medicine was suggested inorder to evaluate the merits of this treatment modality.In view of the scarcity of this resource around thecountry it did not meet with a great deal of support.

Bicarbonate administrationEarly administration of bicarbonate intravenously isthought to decrease metabolic acidosis and promotealkalisation of urine, which decreases the precipitationof myoglobin in the renal tubules. Administration ofbicarbonate immediately post-extrication, in antici-pated metabolic acidosis, was discussed. Has thisbeen shown to be bene®cial? Are there any detrimentalfeatures? What would be the appropriate and safedoses to use? Is there a role for the combined use ofacetazolamide in order to prevent metabolic alkalosisfollowing bicarbonate administration?

Mannitol and compartment syndromeThere is anecdotal evidence in the literature that, owingto the high complication rate in performing fasciotomyfor compartment syndrome in crushed patients, theyare best managed with mannitol alone. It is suggestedthat there is a noticeable difference in diameter andsymptoms of the lower leg within 40 minutes of admin-istration of IV mannitol (Better, 1999). Fasciotomyshould be reserved for refractory cases. The use of ananimal model of a compartment syndrome is ques-tioned due to the anatomical differences from humans.Many animals that are commonly used as models forhumans, such as pigs, sheep and dogs do not havefascial compartments. Primates share similarities but,ethically, such experiments would be more dif®cult tojustify. Further information on existing animal experi-mentation relating to compartment syndrome isrequired prior to planning any further projects.

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Better OS. 1990. The crush syndrome revisited (1940±1990).Nephron 55: 97±103.

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