Crush injury and rhabdomyolysis

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 [1-4]. 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]. Large numbers of patients with crush injuries and rhabdomyolysis have been reported after the collapse of mines [6,7], severe beatings [8], and earthquakes [9-15]. In the United States, alcohol intoxication associated with prolonged muscle compression and seizures is the most common etiology of rhabdomyolysis [16]. Serum creatine kinase (CK) levels correlate with the degree of muscle injury [14] and can be used to assess the severity of rhabdomyolysis. Acute renal failure (ARF) is one of the most serious consequences of rhabdomyolysis and occurs in 4% to 33% of cases, carrying with it a mortality rate of 3% to 50% [17]. Rhabdomyolysis accounts for 5% to 7% of all cases of ARF in the United States [18]. This article focuses on the pathophysiology and treatment of myoglobinuric renal failure caused by traumatic rhabdomyolysis and crush injuries.