Although clinical syndromes consistent with rhabdomyolysis were recognized in the
late 19th and early 20th centuries, the modern history of the crush syndrome begins
with Bywaters' and Beal's classic description of the entrapped bombing victims of
London during World War II [
1
,
2
,
3
,
4
]. They reported five cases of crush injury, in which victims had one or more of their
extremities trapped under debris for prolonged periods of time. All five patients
presented in shock, had swollen extremities, developed dark urine, progressed to renal
failure, and eventually died. Histologic examination of the kidney revealed tubular
necrosis and pigmented casts. In 1944, Bywaters and Stead identified myoglobin as
the urinary pigment and proposed its role in the development of renal failure [
[5]
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