Crush Injury and Syndrome part 1

Crush Injury and Syndrome:

Although the likelihood of attending a patient with a crush injury or syndrome is uncommon, a patient presenting with crush injury or syndrome will cause significant challenge to the clinician on scene. There will be multiple factors to attend with, from personal safety, extrication and evacuation, treatment, joint agency response, and more. A crush injury patient can pose a significant challenge.


Crush injury and syndrome presentation remains a rare occurrence within European practice. Crush injury and syndrome is often seen in events of:

  • Natural disasters, such as earthquakes
  • In war settings
  • Building collapses following explosions
  • Industrial accidents
  • Road traffic collisions
  • Sometimes following collapses of patients where their own bodyweight has been trapping a limb over an extended period

Within the traumatic crush setting, statistically the legs are most commonly affected, with the arms being less frequent. Any crush injury to the head and/or torso often causes significant injury and destruction, resulting in trauma incompatible with life. This is often the scenario, however, there are some cases where patients have survived following a head or torso crush.


In the pathophysiology, crush injury and crush syndrome are different:

Crush injury is associated with the direct injury resulting from the incident. The injury itself can cause significant pathophysiological issues affecting multiple systems of the body depending on the MOI, location of injury, and amount of tissue involved. If the patient isn’t immediately killed from the initial injury and tissue destruction, further complications will start to arise. The patient may begin to haemorrhage internally or externally from the trauma, organs may be injured and begin to fail, major blood vessels may be disrupted, and further complications may develop. In chest injury, a pneumo/haemothorax may develop, cardiac tamponade, etc.

Crush syndrome is associated with the systemic effect of muscle cell damage from the crushing pressure. The are 3 common factors which lead to the development of crush syndrome, these include;

  • The degree of compressive force
  • The amount of muscle mass involved
  • The duration of the compression

When attending a potential crush syndrome patient, recognition of these 3 factors can help in determining the severity of crush syndrome and how adversely affected the patient may be. For example, a patient with a large concrete pillar crushing both legs over 4 days will be severely affected by crush syndrome compared to a patient crushing their finger in a vice for 2 hours.

The onset of crush syndrome usually occurs following reperfusion of injured muscle when the compressive force is released and the affected tissue’s toxins, etc, re-enter the body’s circulation. Depending on the factors above, this may result in acute and/or delayed-onset of clinical symptoms and presentations.

The clinical features of crush syndrome are mainly due to the result of traumatic rhabdomyolysis and subsequent damage and release of muscle cell contents. The mechanism behind this is the leakiness of the sarcolemmal membrane caused through the pressure or stretching from the incident. The Sarcolemma is the cell membrane which surrounds and contains skeletal muscle cells. Within this containment there is also the cytoplasm, or Sarcoplasm, mitochondria, myoglobin, calcium, and other components. As the membrane is stretched, sodium, calcium, and water leak into the sarcoplasm which traps extracellular fluid inside the muscle membrane. Additional to the influx of these substances into the cell, the cell releases potassium, and other toxic substances into circulation of the affected area such as myoglobin, phosphate, and urate.

From crush syndrome, a cascade of pathophysiological processes occur which can negatively affect numerous organs and homeostatic function. These numerous pathologies can present numerous opportunities of death to the patient. For example, when a patient is trapped from a significant crush injury, the crushed area increases permeability of the sarcolemmal membranes, allowing an influx of sodium and calcium creating a pressure head for water to follow by osmosis. The entire extracellular fluid volume may penetrate into the injured muscles within hours to days of injury. This leads to a rapid depletion of intravascular fluid, hypovolaemic shock and cardiac arrest.

On the release of the crushing object, the release of toxins, dead tissue cells, etc, will return to the body’s circulation. This sudden influx of toxic material on the body’s organs and tissues can result in numerous pathophysiology’s such as shock, hyperkalaemia, hypocalcaemia, metabolic acidosis, Acute Kidney Injury, cardiac arrhythmias, etc. Later on issues which can result from crush syndrome include Acute Respiratory Distress Syndrome (ARDS), coagulopathy, sepsis, and renal failure.