Pathophysiology

Crush injury and syndrome

Crush injury is associated with the direct injury resulting from the incident, for example, a car running over a person’s legs may result in broken bones and lacerations, bleeding, etc.

Crush syndrome is associated with the systemic effect of muscle cell damage from crushing pressure.

There are 3 common factors that 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.

The clinical features of crush syndrome are mainly due to the result of traumatic rhabdomyolysis and subsequent release of muscle cell contents. The mechanism behind this is the leakiness of the sarcolemmal membrane caused by pressure or stretching. 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 such as myoglobin, phosphate, and urate.

The result of these events can lead to shock, hyperkalaemia, hypocalceamia, metabolic acidosis, compartment syndrome, acute renal failure. Later on, issues that can result from crush syndrome include Acute Respiratory Distress Syndrome (ARDS), coagulopathy, and sepsis.

Physical signs of crush syndrome can include:

  • Mottled/Blistered skin
  • Oedema
  • Reddish/Brown urine
  • Absent/Diminished pulses
  • Paralysis/Paresis
  • Pain