Crush Syndrome

The 'Diseases Database' defines crush syndrome as:¹

"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."

It is also known as Bywaters' syndrome. Crush syndrome was first described by Bywater 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. Rhabdomyolysis is the breakdown of muscle fibres with the leakage of potentially toxic cellular contents into the systemic circulation.³
• 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),⁴ excess myoglobin is filtered by the kidneys and can cause renal tubular obstruction and renal damage: the excess myoglobin is nephrotoxic.⁵
• Intravascular volume depletion and renal hypoperfusion, combined with myoglobinuria, result in renal dysfunction.²

Crush syndrome is characterised by:⁶

• Hypovolaemic shock (due to sequestration of water in the injured muscle cells)³
• Hyperkalaemia (release of cellular potassium by the injured muscle cells)³

This can also lead to:³

• Metabolic acidosis (release of cellular phosphate and sulphate by the injured muscle cells)
• Acute renal failure
• Disseminated intravascular coagulation (DIC)

• 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, as well as after road traffic accidents.
• The incidence of crush syndrome following earthquakes has been estimated as at least 2 to 5% of those who are buried under rubble.

Clinical features can include:

• Obvious muscle injury with pain, swelling, bruising and tenderness
• Tea-coloured urine may be an early sign
• Nausea, vomiting, confusion and agitation
• Profound hypovolaemic shock
• There may be loss of sensation and muscle power in the affected body part
• The limb/body part may be pulseless

Compartment syndrome can occur after crush because of the uptake of fluid into muscle cells contained within a tight compartment. Once compartment pressure exceeds capillary perfusion pressure at about 30 mmHg, the tissue inside the compartment becomes ischaemic, and compartment syndrome develops.

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)³
• Uric acid (may be raised)
• Full blood count and clotting studies (to look for evidence of DIC)
• Liver function tests (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)³
• ECG may show changes secondary to hyperkalaemia
• The usual assessment for trauma, including X-rays should be performed
• Assessment of compartment pressures may be needed if compartment syndrome is a concern (focal muscle tenderness and firm muscle compartment)³

Medical

• Urine output should be maintained at 300 ml/hour until myoglobinuria has ceased.⁵
• 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.²
• 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.
• DIC will need treatment with fresh frozen plasma, cryoprecipitate and platelets.³

Surgical

• Fasciotomy is useful in reducing muscle damage from compartment syndrome.⁷ It should be done early.
• It may be necessary to amputate crushed limbs. Amputation at an early stage may prevent crush syndrome.

• Hyperkalaemia and infection are the commonest causes of death.⁸ Hyperkalaemia can lead to arrhythmia and arrest. Infection is a major cause of death in disaster zones.⁸
• Acute renal failure can occur.
• Disseminated intravascular coagulation 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.³

• Adequate fluid support improves prognosis.
• The earthquake in Marmara, Northern Turkey in 1999 has been well documented. The mortality rate for crush syndrome was 15.2%.⁹
• 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 5 days.¹⁰
• 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 like 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.¹¹
• Adequate rehydration reduces the risk of acute renal failure in crush syndrome.
• Amputation at an early stage may prevent crush syndrome.