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Crush injury

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  • 3 chapters

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Through Injury, Compression (physics) and Human body

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Complications

  • Hypovolaemic shock. Loss of plasma volume across damaged cell membranes and capillary walls can lead directly to severe hypovolaemia. Shock can develop from myocardial depression following release of intracellular electrolytes. In addition, as a result of the mechanism of injury, blood loss from pelvic or long bone fractures may also co-exist.
  • Hyperkalaemia and electrolyte imbalance. Disruption of cell membranes can result in a significant release of potassium, which is a largely intracellular cation that can precipitate cardiac arrest. Sequestration of plasma calcium into injured tissue can lead to a relative hypocalcaemia, which may worsen disruption of clotting abilities and shock. Metabolic acidosis may result from reperfusion injury and hypoperfusion related to shock.
  • Compartment syndrome. Compartment syndrome is a common complication of crush injury as a consequence of oedematous tissue injury, redistribution of fluid into the intracellular compartment and bleeding. Established compartment syndrome may result in worsened systemic crush syndrome and irreversible muscle cell death.
  • Acute kidney injury. Release of myoglobin by injured muscle leads to rhabdomyolysis coupled with shock leads to a significant rate of acute kidney injury, estimated as up to 15%. Acute kidney injury leads to a significantly higher mortality.

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