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Emergency War Surgery NATO Handbook: Part III: General Considerations of Wound Management: Chapter XVII: Crush Injury

Pathogenesis

United States Department of Defense
Peer Review Status: Internally Peer Reviewed


Sustained compression of a limb impedes perfusion, which results in hypoxia progressing to anoxia, muscle injury, and increased capillary permeability. The crush syndrome is a reperfusion injury. When the extremity is extricated from the compressing rubble, the damaged muscle liberates muscle pigment, potassium, creatinine, lactic acid, and other intracellular substances into the general circulation. The trapped victim may also be suffering from other severe injuries that contribute to or of themselves result in shock. After release from compression, the extravasation of plasma results in swelling of the affected part. When this happens, oligemic shock is precipitated or aggravated. Untreated oligemic shock contributes to acute renal insufficiency. Liberated myoglobin, which accumulates in the renal tubules, also contributes to the development of renal failure. Liberated phosphate and uric acid aggravate an already developing metabolic acidosis. Hyperkalemia can result in sudden cardiac arrest and death. Coagulopathies not uncommonly develop. This combination of hypovolemic shock coupled with myoglobinuric acute renal failure carries a grave prognosis.

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