Clinical meaning
Crush syndrome is a systemic manifestation of muscle cell damage (rhabdomyolysis) resulting from prolonged compression of skeletal muscle (typically >1 hour). During compression, ischemia causes ATP depletion, disrupting Na+/K+-ATPase and Ca2+-ATPase pumps. Intracellular calcium rises, activating proteases and lipases that destroy the sarcolemma. Upon release of the compressive force (extrication), reperfusion delivers oxygen to damaged cells, generating reactive oxygen species that amplify cellular injury. Simultaneously, the contents of destroyed myocytes flood the systemic circulation: potassium (life-threatening hyperkalemia and cardiac arrest), myoglobin (precipitates in renal tubules causing AKI), phosphorus (hyperphosphatemia, binds calcium), uric acid, creatine kinase, and lactic acid. The triad of crush syndrome is: hyperkalemia (most immediately lethal), myoglobinuric AKI, and hypovolemic shock (third-spacing of fluid into damaged muscle -- up to 12 liters in bilateral lower extremity crush).