Crush injury and rhabdomyolysis

Abstract

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.

The Relationship Between Skeletal Muscle Serum Markers and Primary THA: A Pilot Study

“…Reported use of blood enzyme markers is common throughout the surgical literature [9,12,[16][17][18][20][21][22][23][24]. Rhabdomyolysis has numerous etiologies and includes local crush injury, vascular compromise, soft tissue infections, electrical injuries, excessive steroid use, seizures, surgery, and heat stroke [1,19,22].…”

“…Rhabdomyolysis has numerous etiologies and includes local crush injury, vascular compromise, soft tissue infections, electrical injuries, excessive steroid use, seizures, surgery, and heat stroke [1,19,22]. Whether these changes occur after differing hip approaches is unknown.…”

“…Creatine kinase is a naturally occurring enzyme with the greatest concentrations found in skeletal muscle, cardiac muscle, and the brain [9,19]. Myoglobin also is found in cardiac and skeletal muscle and is released into the circulation when muscle is damaged through disease, exertion, or trauma and is excreted in the urine [9,16,19,20,22]. The use of serum markers, including CK, CPK, and serum myoglobin, may allow for an objective evaluation of the potential advantages among various MIS techniques.…”

Amputations in natural disasters and mass casualties: staged approach

“…1 Extensive lower limb injuries as a result of land-mine explosion Fig. 2 Late presentation of the lower extremity injuries due to crushing trauma presentation after the crush [51]. And there are some good results reported in cases of crush syndrome of a single extremity with early presentation [52,53].…”

Review article: Acute kidney injury in critical illness

“…The following mechanisms lead to myoglobinuric AKI: intravascular volume depletion due to fluid sequestration in injured muscle; renal hypoperfusion and ischemia; intratubular heme pigment cast formation; uric acid crystallization and obstruction along with secondary renal injury due to oxidative stress from ironmediated free radical production; myoglobin-induced nitric oxide scavenging; circulation of inflammatory mediators; and activation of innate immune system. 91 The epidemiology of myoglobinuric AKI is poorly characterized; however, estimates resulting from small studies have indicated that 20-50% of patients with rhabdomyolysis develop AKI. 92,93 The proposed diagnostic criteria are based on a small clinical study showing high positive predictive value for AKI requiring RRT in at-risk patients who fulfilled the following criteria: 1) SCr [ 133 lmoLÁL -1 ; 2) base deficit of B -4 mEqÁL -1 ; 3) creatine kinase C 5,000 UÁL -1 ; and 4) myoglobinuria.…”