Consensus Statement On The Early Management Of

Crush Injury And Prevention Of Crush Syndrome

* I Greaves, K Porter, JE Smith

Abstract

Crush Syndrome remains rare in European practice. It is however common in areas of civil disorder and
where the normal structures of society have given way to civil war or natural disaster. Western Doctors are
becoming increasingly involved in such situations and there is no reason to believe that instances due to
more conventional causes, such as collapse in the elderly or road traffic accidents will cease. For all
these reasons it is important that clinicians who deal infrequently with crush syndrome have access to
appropriate guidelines. This consensus report seeks to provide such advice.

Key Words: Crush Syndrome, Renal Failure, Natural Disasters

Introduction

Crush injuries and crush syndrome were first described in the English Language literature by Bywaters and
Beall in 1941 (1), after several patients who had been trapped under rubble of buildings bombed in the Blitz
subsequently died of acute renal failure. It has been described in numerous settings since, most commonly
after natural disasters such as earthquakes, in war, and after buildings have collapsed as a result of
explosion. Crush syndrome is also seen following industrial incidents such as mining accidents and road
traffic accidents. However, crush syndrome is not confined to traumatic aetiologies, and has also been
described following periods of crush by patients’ own body weight, after stroke or intoxication (2).

Most commonly in traumatic crush, the legs are affected, and less frequently the arms. Many authors
believe that crush injury of the head and torso significant enough to cause the syndrome is incompatible
with life due to the inherent internal organ damage, but there are a few reported cases of such
instances (3).

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

Definition

Following a search of the literature, it was felt that a definition of crush injury and crush syndrome was
required.

Consensus view
“A crush injury is a direct injury resulting from crush. Crush syndrome is the systemic manifestation of
muscle cell damage resulting from pressure or crushing”.

Page 1 of 8
The severity of the condition is related to the magnitude and duration of the compressing force, and the
bulk of muscle affected. The definition is not, however, dependent on the duration of the force applied.
Examples of this relationship are firstly a patient whose legs are run over by the wheels of a truck. In this
case the force is large, but the duration is very short. At the other extreme, there is the elderly patient who
has suffered a stroke, falls, and lies in the same position for hours, sustaining a crush injury to the areas of
the body on which they are lying. In this case, the force is relatively small, but crush syndrome may develop
as a result of the prolonged period of pressure. Similar cases to this are described as a result of drug
overdose (4).

Pathogenesis and clinical features

The typical clinical features of crush syndrome are predominantly a result of traumatic rhabdomyolysis and
subsequent release of muscle cell contents. The mechanism behind this in crush syndrome is the leakiness
of the sarcolemmal membrane caused by pressure or stretching. As the sarcolemmal membrane is
stretched, sodium, calcium and water leak into the sarcoplasm, trapping extracellular fluid inside the
muscle cells. In addition to the influx of these elements into the cell, the cell releases potassium and other
toxic substances such as myoglobin, phosphate and urate into the circulation (5).

The end result of these events is shock (discussed below), hyperkalaemia (which may precipitate cardiac
arrest), hypocalcaemia, metabolic acidosis, compartment syndrome (due to compartment swelling), and
acute renal failure (ARF). The ARF is due to a combination of hypovolaemia with subsequent renal
vasoconstriction, metabolic acidosis and the insult of nephrotoxic substances such as myoglobin, urate and
phosphate.

Shock

Haemodynamic instability secondary to crush syndrome is multi-factorial. Firstly, many patients have other
injuries, such as fractures of the pelvis or lower limbs, sufficient in themselves to cause hypovolaemia.
The sequestration of fluid into the affected muscle compartments has already been described, resulting in
fluid shift from the intravascular to the intracellular compartments. This may cause hypovolaemia, as
the intravascular volume is depleted. Electrolyte imbalances such as hyperkalaemia, hypocalcaemia and a
metabolic acidosis will have a negatively inotropic effect, and there is also evidence that there is direct
myocardial depression from other factors released when muscle cells are damaged (6).

Approach to treatment

Treatment of the crushed patient can be divided into two phases. The initial prehospital phase may,
depending on the mechanism of injury, involve a prolonged extrication period.The second phase
commences on reaching a definitive medical care facility. In the case of prolonged on-scene
time, or delay in transfer due to geographical reasons, some of the second phase guidelines
may be employed in the pre-hospital environment.

Consensus view
Safety is the first priority when approaching an accident scene, and this is particularly relevant to situations
where patients may have suffered crush injuries, as there may be danger from falling debris or risk of
further building collapse.

Once the scene has been declared safe, in cases of mass casualties, a triage system (such as the triage sieve
– Major Incident Medical Management & Support (MIMMS) (7)) should be used to prioritise casualties and
assess the need for further treatment. For each individual casualty, an assessment of Airway, Breathing and
Circulation is the next priority. Attention must be given in trauma to the possibility of spinal injury and full
spinal precautions should be maintained. Administration of high flow oxygen by mask should be a priority
Page 2 of 8
in treatment, as should the arrest of any obvious external haemorrhage and the splinting of limb injuries.
The patient should be exposed as necessary to assess and manage injuries. In a hostile environment, or
where there is a risk of hypothermia, exposure should be as limited as possible. Assessment of distal
neurovascular status is essential if exposure is to be kept to a minimum.

The patient should be released as quickly as possible, irrespective of the length of time trapped.

Fluid resuscitation

Once the initial primary survey has been performed, intravenous access should be obtained. If limb crush
injury has occurred, and there is a likelihood of the patient developing crush syndrome, the following fluid
guidelines should be followed. In the presence of life-threatening thoracoabdominal injury, fluid
resuscitation should be performed according to the Faculty’s previously published guidelines (8).

Consensus view
An initial fluid bolus of 2 litres of crystalloid should be given intravenously.This should be followed by 1-1.5
litres per hour.The fluid of choice is normal saline, warmed if possible, as this is established as the fluid
carried by the majority of pre-hospital vehicles in the United Kingdom. Hartmann’s solution contains
potassium and has a theoretical disadvantage of exacerbating hyperkalaemia. If possible, fluid should be
started prior to extrication, however, gaining intravenous access and the administration of fluid should
not delay extrication and transport to a definitive care facility. Early catheterisation should be considered,
especially if there is a prolonged extrication or evacuation phase. Once the patient reaches hospital, 5%
dextrose should be alternated with normal saline to reduce the potential sodium load.

Analgesia

Consensus view
The use of medical teams including paramedics, nurses and doctors should be considered at an early stage,
and appropriate analgesia should be given. This may involve the use of Entonox® initially, but most patients
will require intravenous analgesia such as an opiate, titrated against response. The use of ketamine, with or
without the concomitant use of a benzodiazepine, is also an effective means of relieving pain, and may
aid extrication.

First responders may give oral analgesia in the absence of senior clinical support.

Triage

Consensus view
Patients with crush injuries should be taken to a hospital with an intensive care facility and the equipment
and expertise necessary to provide renal support therapy such as haemofiltration or dialysis.

Tourniquets

The use of tourniquets has a theoretical role in the management of these patients. If the release into the
circulation of the contents of crushed muscle cells can be avoided, possibly with the use of a tourniquet, it
may be of benefit. However, there is currently no available evidence to support this.

Page 3 of 8
Consensus view
The use of tourniquets should be reserved for otherwise uncontrollable life threatening haemorrhage.
There is no evidence at the moment to support the use of tourniquets in the prevention of reperfusion
injury following extrication, or in the prevention of washing of the products of rhabdomyolysis
into the circulation.

Amputation

Another theoretically advantageous measure is amputation of a crushed limb to prevent crush syndrome.

Consensus view
There is no evidence to support the use of amputation as a prophylactic measure to prevent crush
syndrome. Reports from the literature suggest that even severely crushed limbs can recover to full
function. If the limb is literally hanging on by a thread, or if the patient’s survival is in danger due to
entrapment by a limb, amputation should be considered and appropriate expert advice sought.

Immediate in-hospital care

Consensus view
Patients should be assessed following normal Advanced Trauma Life Support (ATLS) guidelines (9). Baseline
blood tests should be taken. These will include full blood count, urea and electrolytes, creatinine kinase,
amylase, liver function tests, clotting screen and group and save (cross match if deemed appropriate). The
patient should be catheterised and hourly urine measurements commenced. Central venous pressure and
invasive arterial monitoring should be considered.

The use of solute-alkaline diuresis

The development of acute renal failure in these patients significantly decreases the chances of survival (10).
Every effort must be made, therefore, to prevent its occurrence. Alkalinisation of urine and the use of a
solute alkaline diuresis is accepted to be protective against the development of acute renal failure (11,12).

Consensus view
It is recommended that urine pH is measured, and kept above 6.5 by adding 50mmol aliquots of icarbonate
(50mls 8.4% sodium bicarbonate) to the intravenous fluid regime. Solute diuresis is affected by
dministering mannitol at a dose of 1-2g/kg over the first four hours as a 20% solution, and further mannitol
should be given to maintain a urine output of at least 8 litres per day (300mls per hour). Fluid requirements
are high, usually of the order of 12 litres per day, due to the sequestration of fluid in muscle tissue. Fluid
should be given at approximately 500 mls/hour, but regular review of clinical parameters such as central
venous pressure and urine output should dictate exact amounts of fluid given. The maximum daily dose of
mannitol is 200g, and it should not be given to patients who are in established anuria.

Children

Consensus view
There is very little evidence in the literature to guide the treatment of children suffering from crush injuries.
In young children the difference in body proportions, namely the reduced contribution to the total
percentage made by the limbs, may influence the incidence of crush syndrome. The fluid resuscitation
guidelines from Advanced Paediatric Life Support (APLS) (13) of an initial bolus of 20mls per kg should be
followed in these patients.

Page 4 of 8
The elderly and patients with comorbidity

Consensus view
In the elderly, and those with pre-existing medical conditions such as cardiac failure, fluid replacement
must be tailored to requirements and given with caution. Close monitoring of the clinical state of the
patient, and regular review of fluid requirements is essential in these patients.

Compartment syndrome

The development of compartment syndrome in crush injury is due to the uptake of fluid into damaged
muscle tissue contained within the restricted compartment. Once compartment pressure exceeds
capillary perfusion pressure at about 30 - 40mm Hg, the tissue inside the compartment becomes ischaemic,
and compartment syndrome develops.

The traditional treatment of compartment syndrome is fasciotomy (4), but there is now evidence that initial
treatment with mannitol may decompress compartment syndrome and avoid the need for surgery (5,12).

Consensus view
In patients with compartment syndrome due to crush injury, in the absence of neurovascular compromise,
a trial of mannitol therapy should be instigated, but a specialist opinion should be sought early.

Hyperbaric oxygen therapy

There is theoretical and limited experimental evidence that hyperbaric oxygen therapy may improve wound
healing and reduce the need for multiple surgical procedures in crush injury (14).

High concentrations of O2 cause systemic vasoconstriction but continue to deliver adequate O2 delivery. In
a similar fashion, nitric oxide synthase inhibitors may also have a role in preventing excessive vasodilatation
in the crushed muscle and the consequent increase in third space fluid losses (15).

Consensus view
Logistically hyperbaric oxygen treatment has limited application. Patients with no significant co-morbidity,
and who can be managed in a hyperbaric chamber where the facility is available, may be treated with
hyperbaric oxygen therapy. It is recommended that treatment options are discussed with the local
hyperbaric unit. This is not recommended as first line treatment. Patients should, however, receive high
flow oxygen, unless there is a specific contra-indication.

Further management

Consensus view
In many cases, intensive care support will be required for the complications of crush syndrome. If the
patient becomes oligo- or anuric, it is likely that they will require haemofiltration or dialysis.

Multiple casualties

Consensus view
In the civilian environment in the United Kingdom, there will be a huge strain on intensive care facilities if
there are multiple crushed casualties. A policy should be drawn up to prepare for the dispersal of these
casualties on both a National and International level should an incident occur. Further information is
available in Better’s review of 1999 (5).
Page 5 of 8
Areas identified for future research

Use of tourniquets
Is there a role for the tourniquet post or pre extrication of the crush injury casualty? The use of an animal
model of crush injury was suggested, to assess the suitability of tourniquet administration. Comparison of
tourniquet placement versus no tourniquet in delayed intravenous fluid administration was suggested as a
further research option. Are there any further deleterious effects due to the increased ischaemia times
involved in application of a tourniquet?

Could cooling the limb be used in order to slow cellular respiration and consequently decrease oedema,
compartment syndrome and improve limb viability?

Tourniquet effectiveness was highlighted as a potential shortfall in their use. There is a requirement to
perform a literature search into tourniquet usage, in particular regarding their use in Biers blocks, in order
to determine the effectiveness of certain types of tourniquet and the leakage rates of drugs, past the
tourniquet. This may assist in establishing the likelihood of potassium leaking into the systemic circulation.

Fluid administration

Types of fluid currently used for administration include: normal saline, Hartmann's, Dextran or starches.
What is the correct amount of fluid to be giving? Should we be looking at urine output, absolute volume
intake or acidity of urine as a guide to fluid administration? Oedema occurring is secondary to massive fluid
administration and may be detrimental. At what stage do we need to worry about this? What effect does
this have on compartment syndrome?

Prognostic indicators

Creatinine kinase,myoglobinaemia and amylase have been suggested as prognostic indicators, although it is
not clear that they can predict outcome at an early enough stage to allow effective intervention. The use of
microalbuminuria as a prognostic indicator of crush syndrome was suggested.

Hyperbaric oxygen therapy

Use of the Institute of Naval Medicine was suggested in order to evaluate the merits of this treatment
modality. In view of the scarcity of this resource around the country it did not meet with a great deal of
support.

Bicarbonate administration

Early administration of bicarbonate intravenously is thought to decrease metabolic acidosis and promote
alkalisation of urine which decreases the precipitation of myoglobin in the renal tubules. Administration of
bicarbonate immediately post-extrication, in anticipated metabolic acidosis, was discussed. Has this been
shown to be beneficial? Are there any detrimental features? What would be the appropriate and safe
doses to use? Is there a role for the combined use of acetazolamide in order to prevent metabolic
alkalosis following bicarbonate administration?

Mannitol and compartment syndrome

There is anecdotal evidence in the literature that due to the high complication rate in performing
fasciotomy for compartment syndrome in crushed patients, they are best managed with mannitol alone. It
is suggested that there is a noticeable difference in diameter and symptoms of the lower leg within 40
Page 6 of 8
minutes of administration of IV mannitol (5). Fasciotomy should be reserved for refractory cases. The use of
an animal model of a compartment syndrome is questioned due to the anatomical differences from
humans. Many animals that are commonly used as models for humans, such as pigs, sheep and dogs do not
have fascial compartments. Primates share similarities but, ethically, would be more difficult to justify.
Further information on existing animal experimentation relating to compartment syndrome is required
prior to planning any further projects.

This paper reports the findings of a consensus meeting on Crush Injury and Crush Syndrome held in
Birmingham on 31 May 2001, and co-ordinated by the Faculty of Pre-Hospital Care of the Royal
College of Surgeons of Edinburgh.

Organisations represented

The Voluntary Aid Societies

The Ambulance Service Association
The British Association for Immediate Care
British Association for Emergency Medicine
Faculty of Accident and Emergency Medicine
The Royal College of Anaesthetists
The Royal College of Physicians
The Royal College of Surgeons of Edinburgh
The Intensive Care Society
The Royal College of Nursing
The Military
The Faculty of Pre-hospital Care

* Lt Col I Greaves; RAMC

Visiting Professor of Emergency Medicine Education Centre, The James Cook University Hospital, Marton
Road, Middlesbrough, TS4 3BW

K Porter
Consultant Trauma Surgeon, University Hospital, Birmingham

Surg Lt Cdr JE Smith; MBBS MSc MRCP RN

Specialist Registrar in Emergency Medicine Defence Medical Services, Derriford MDHU, Plymouth, PL6 8DH.

Page 7 of 8
References

1. Bywaters EGL, Beall D. Crush injuries with impairment of renal function. BMJ 1941; 1: 427.
2. Michaelson M. Crush injury and crush syndrome. World J Surg 1992; 16: 899-903.
3. Hiraide A, Ohnishi M,Tanaka H et al. Abdominal and lower extremity crush syndrome. Injury 1997;
28(9-10): 685-6.
4. Shaw AD, Sjolin SU, McQueen MM. Crush syndrome following unconsciousness: need for urgent
orthopaedic referral. BMJ 1994; 309: 857-9.
5. Better OS. Rescue and salvage of casualties suffering from the crush sydrome after mass disasters.
Mil Med 1999; 164: 366-9.
6. Rawlins M, Gullichsen E, Kuttila K, Peltola O, Niinikoski J. Central hemodynamic changes in
experimental muscle crush injury in pigs. Eur Surg Res 1999; 31: 9-18.
7. Major Incident Medical Management & Support (MIMMS) 2002. BMJ Bookshops, London.
8. Greaves I, Porter KM, Revell MP. Fluid Resuscitation in Pre-Hospital Trauma Care: A Consensus
View. J.R. Coll. Surg. Edinb. 47; 2; 451-457.
9. Advanced Trauma Life Support for Doctors. American College of Surgeons 1997 Chicago.
10. Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med 1988; 148:
1553-1557.
11. Better OS. The crush syndrome revisited (1940-1990). Nephron 1990; 55: 97-103.
12. Better OS, Zinman C, Reis ND et al. Hypertonic mannitol ameliorates intracompartmental
tamponade in model compartment syndrome in the dog. Nephron 1991; 58: 344-6.
13. Advanced Paediatric Life Support 2nd Edition 2001. BMJ Bookshops.
14. Bouachour G, Cronier P, Gouello JP,Toulemonde JL,Talha A, Alquier P. Hyperbaric Oxygen therapy
in the management of crush injuries; a randomized double-blind placebo-controlled clinical trial. J
Trauma 1996; 41(2): 333-9.
15. Rubinstein I, Abassi Z, Coleman R, Milman F, Winaver J, Better OS. Involvement of nitric oxide
system in experimental muscle crush injury. J Clin Invest 1998; 101(6): 1325-33.

Page 8 of 8