Bombings: Injury Patterns and Care Seminar Curriculum Guide



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Objective

  1. Explain the pathophysiology of crush injury.







Crush Injury: Pathophysiology
#75,76,77


The anatomical areas most commonly affected are:


  • lower extremities

  • upper extremities

  • pelvis

  • gluteal region

  • abdominal muscles

Early mortality in untreated crush injury is due to hyperkalemia and hypovolemia. Late mortality is due to renal failure, coagulopathy and hemorrhage, and sepsis.




Crush Syndrome

#78

The systemic effects of crush injuries are due to rhabdomyolysis and reperfusion of hypoxic and damaged tissues. In rhabdomyolysis, breakdown of muscle fibers result in an efflux of potassium, purines, lactic acid, urate, phosphate, myoglobin, thromboplastin, and creatinine from damaged muscle cells; and an influx of sodium, calcium, and extracellular fluid into the muscle cells.



#79

Reperfusion of an affected body part results in the systemic effects of crush injury. Patients may appear well until extricated, and then precipitously decompensate.


  • Skeletal muscle damage is greatest after reperfusion.

  • Super-oxide radicals produced during reperfusion attack free fatty acids, producing cellular edema, death, and necrosis.

  • Na-K-ATP pump exchanges intracellular sodium for calcium with further derangement of intracellular metabolism.

There is cardiovascular instability due to massive fluid shift, electrolyte abnormalities, and direct myocardial toxicity.






#80


Resultant effects of derangements due to rhabdomyolysis and reperfusion
Potassium  Hyperkalemia  Arrythmias

Calcium  Hypocalcemia  Arrythmias

Phosphate  Hyperphosphatemia  Renal damage

Myoglobin  Myoglobinemia  Renal damage

Fluid shifts  Hypovolemia  Renal failure

Reperfusion  Free radicals  Renal damage

Purines  Hyperuricemia  Renal damage

Hypoxemia  Lactic acid  Acidosis

Thromboplastin  Complement system  DIC

Creatinine  Elevated serum levels



Sodium  Azotemia


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