Crush Syndrome - Wikipedia

Seigo Minami, a Japanese physician, first reported the crush syndrome in 1923.[2][3][4] He studied the pathology of three soldiers who died in World War I due to kidney failure. The renal changes were due to the buildup of excess myoglobin, resulting from the destruction of muscles from lack of oxygen. The progressive acute kidney failure is because of acute tubular necrosis.

The syndrome was later described by British physician Eric Bywaters in patients during the 1941 wartime bombing of London (the Blitz).[5][6] It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products—notably myoglobin, potassium and phosphorus—that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions).

The specific action on the kidneys is not understood completely, but may be due partly to nephrotoxic metabolites of myoglobin.

The most devastating systemic effects can occur when the crushing pressure is suddenly released, without proper preparation of the patient, causing reperfusion syndrome. In addition to tissue directly suffering the crush mechanism, tissue is then subjected to sudden reoxygenation in the limbs and extremities. Without proper preparation, the patient, with pain control, may be cheerful before recovery, but then may suddenly die shortly thereafter. This sudden failure is called the "smiling death".[7]

These systemic effects are caused by a traumatic rhabdomyolysis. As muscle cells die, they absorb sodium, water, and calcium; the rhabdomyolysis releases potassium, myoglobin, phosphate, thromboplastin, creatine, and creatine kinase.[citation needed]

Crush syndrome can directly come from compartment syndrome, if the injury is left untreated.[8] Symptoms include the 5 Ps: pain, pallor, paresthesias (pins and needles), paralysis, and pulselessness.[9]