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. Ischemic renal dysfunction secondary to hypotension and diminished renal perfusion results in acute tubular necrosis and uraemia

It is also known as Bywaters' syndrome. He first described it in the BMJ in 1941 after the London Blitz. Many of the references used here relate to experience from the Mamara earthquake in Turkey in 1999.

Crush syndrome is a reperfusion injury as a result of traumatic rhabdomyolysis. Rhabdomyolysis follows prolonged continuous pressure on muscle tissue. It has been described in numerous settings, most commonly after earthquakes, in war, and after explosions have caused buildings to collapse. Crush syndrome is also seen following industrial incidents such as mining and road traffic accidents.

Crush syndrome is common in earthquakes of disastrous proportions.

The diagnostic criteria for crush syndrome are:

• Crushing injury to a large mass of skeletal muscle.
• There are sensory and motor disturbances in the compressed limbs, which subsequently become tense and swollen.
• Myoglobinuria and/or haematuria.
• Peak creatine kinase (CK) >1000 U/L.
• Renal problems are common with one of the following characteristics;
  • Oliguria (urine output <400 ml/24 h)
  • Elevated levels of blood urea, creatinine, uric acid, potassium, phosphate, or decreased calcium.

The incidence of crush syndrome following earthquakes has been estimated as at least 2 to 5% of those who are buried under rubble. Approximately 50% of these patients develop acute renal failure, and approximately 50% of these will need dialysis.

Risk factors

Time under the rubble does not have an adverse effect on outcome but that may be because those that survived had been less severely injured. It was recommended that recovery of survivors should continue for at least 5 days.² Those with oliguria, raised creatinine, low platelets and albumin and hypotension had adverse outcomes. Other adverse factors were high body temperature, high potassium, amputations and thoracic or abdominal trauma.³ 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.

Symptoms

The patient will be very distressed. The immediate concern will be the injury. They may have symptoms of hypovolaemia. Rhabdomyolysis is a major concern. Early symptoms are weakness, myalgia and tea-coloured urine.⁴

Signs

This condition is characterised by profound shock. If a limb has been trapped, it will be pulseless on release. Later, it will become red, swollen and blistered. There may be loss of sensation and muscle power.

It is possible to assess the area of burns with the rule of nines but more recently a rule of thirds has been suggested to assess the severity of crush injury.⁵

Compartment syndrome occurs 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.

The patient must be assessed in keeping with the usual criteria for assessing a severely injured person including the assessment of airway, circulation and other injuries including to abdominal organs and the spine.

Crush syndrome must be distinguished from simple hypovolaemia. The presence of haemoglobin or myoglobin in the urine suggests crush syndrome. CK will be elevated.

Because of the very high risk of acute renal failure a catheter should be inserted at an early stage and urine output monitored. Once in hospital, U&E, creatinine, Ca, PO4, CK and blood gases should be monitored. Because of the need to maintain fluid balance and possible renal impairment a CVP line may be required.

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

It is useful to understand the pathogenesis of the condition to know what to look for. As the membrane of the sarcolemma is stretched, sodium, calcium and water leak into the sarcoplasm, trapping extracellular fluid inside the muscle cells leading to hypovolaemia and associated features. In addition the cell releases potassium and other toxic substances such as myoglobin, phosphate and urate into the circulation. When water enters the damaged muscle, hypovolemia and haemodynamic shock may occur with acute renal failure. Hypocalcemia, hyperkalaemia and hypovolaemia, especially with hypotension all predispose to cardiac arrhythmias or arrest.

Infection is a major cause of death,⁶ especially in disaster zones.

Disseminated intravascular coagulation can occur.

Non-drug

Early, vigorous hydration helps preserve renal function in rhabdomyolysis. Get venous access as early as possible. In the adult, a saline infusion of 1000-1500 ml/h should be initiated during extrication. When a urine flow has been established, a forced mannitol-alkaline diuresis up to 8 L/day should be maintained (urine pH greater than 6.5). This helps to protect the kidneys against damage from myoglobin and reduces the risk of hyperkalaemia.⁷ Once the patient reaches hospital, 5% dextrose should be alternated with normal saline to reduce the potential sodium load. A relatively smaller amount is used in children.⁸ Mannitol protects the kidney and may reduce muscle injury too.⁷

Drugs

Allopurinol can reduce urate levels and protect the myocardium.

Surgical

Fasciotomy is useful in reducing muscle damage from compartment syndrome.⁹ It should be done early.

It may be necessary to amputate crushed limbs.

Hyperkalaemia and infection are the commonest causes of death.⁶ The former may require dialysis.

Disseminated intravascular coagulation can occur with massive tissue damage. Acute renal failure will require appropriate management.

Peak levels of CK have important prognostic implications. Levels in excess of 100,000 presage haemodialysis or death. Children with extensive injuries do very poorly.⁸ Adequate rehydration improves prognosis. The earthquake in Marmara, Northern Turkey in 1999 has been well documented. The mortality rate for crush syndrome was 15.2%.³

If there has been a substantial crush it may be necessary to amputate the limb at an early stage to prevent this syndrome. Amputation can never be taken lightly, especially in children, but a severely damaged limb may not be amenable to salvage and it can cause death. It is better to have a live patient with an amputated limb than a patient who is intact but dead.

In a major disaster triage must be done to identify those in need of urgent attention. This may have a marked effect on morbidity and mortality.¹⁰ The area of crush and signs of shock are important criteria. Adequate rehydration reduces acute renal failure.