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  • Updated 10.10.2023
  • Released 09.06.1993
  • Expires For CME 10.10.2026

Rhabdomyolysis (myoglobinuria)



Rhabdomyolysis refers to the breakdown of striated muscle that is followed by leakage of the muscle protein myoglobin into the blood, leading to its excretion in the urine. This phenomenon is called myoglobinuria. The etiology of rhabdomyolysis is diverse and includes hereditary (metabolic diseases, dystrophinopathies, channelopathies) and acquired disorders (excessive muscular stress, ischemia, toxic damage, infections). Epidemiologic studies have shown that the etiology of a significant percentage of patients with recurrent rhabdomyolysis remains unknown. It is thought that these patients may have undiscovered muscle metabolism disorders. In this article, the authors review the epidemiology of rhabdomyolysis in the adult and pediatric populations, the metabolic causes leading to recurrent rhabdomyolysis, and some preventive and treatment strategies employed for this condition.

Key points

• Extensive work-up for rhabdomyolysis is indicated for recurrent or family history of rhabdomyolysis and myalgia or muscle cramps, especially at rest.

• The most common cause of the first episode of rhabdomyolysis in an adult who does not report a history of earlier significant exertion is drugs.

• The most common etiologies of rhabdomyolysis in the pediatric population are trauma and viral myositis.

• It is always recommended to wait 4 to 6 weeks after an episode of rhabdomyolysis is resolved to obtain a muscle biopsy.

• Knowing the baseline creatinine kinase (CK) in a patient who has known chronic muscle disease with recurrent rhabdomyolysis is important.

Historical note and terminology

Muscle tissues contain the oxygen-binding protein myoglobin. When striated muscles break down or rhabdomyolysis occurs, muscle cell content leaks into the blood, including myoglobin, leading to the excess amount excreted into the urine. This phenomenon is called myoglobinuria (18). The clinical presentation is variable. The classical features are myalgia, weakness, pigmenturia, or dark tea-colored urine. However, this triad is seen in only 10% to 18% of patients (51). The urine becomes pigmented with a brownish color when myoglobin concentration is over 100 µg/mL (09).

The term rhabdomyolysis has been employed increasingly since the 1960s to denote the abrupt muscle injury that causes myoglobinuria. Thus, myoglobinuria and rhabdomyolysis are used interchangeably because myoglobinuria would not occur without rhabdomyolysis (18; 55). In a systematic review by Chavez and colleagues, there was heterogeneity in the diagnostic criteria of rhabdomyolysis (16). However, most studies defined rhabdomyolysis as an elevation of serum creatine kinase (CK) level of at least five times the upper limit of normal (greater than 1000 U/L) followed by its decrease to (near) normal values. Some use a CK level greater than 10 times the upper limit of normal to guide the need for hospitalization (55). However, as CK level may be affected by other factors, there should be caution in diagnosing acute rhabdomyolysis in patients with cardiac diseases, chronic kidney disease, stroke or status epilepticus, and chronic neuromuscular disease (84). Having a baseline CK in these settings would be of high value.

Pigmenturia, in association with symptoms of muscle injury, was recognized in the German literature in the late 19th century as a disorder that affected horses and humans (32). Over the first half of the 20th century, biochemical studies led to the identification and characterization of the muscle heme protein, myoglobin and elucidation of its role in transporting oxygen from hemoglobin to mitochondria (40). Parallel clinical observations established more firmly the link between muscle injury and the urinary excretion of myoglobin and began to outline the epidemiology of this syndrome. Of special note are the studies of Bywaters, which identified rhabdomyolysis as a complication of muscle crush injuries sustained in the Battle of Britain in World War II; he described acute renal failure as a rhabdomyolysis complication and performed seminal experimental studies implicating myoglobin (rather than other constituents of injured muscle) in the pathogenesis of renal injury (12).

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