ReviewNon-traumatic rhabdomyolysis: Background, laboratory features, and acute clinical management
Section snippets
Historical background
The first “reference” on rhabdomyolysis is thought to be found in the Pentateuch, the first five books of the Bible, which describes an episode of mass poisoning afflicting the Jews soon after the ingestion of quails caught during their staying in the Sinai desert (“And while the flesh was yet between their teeth, ere it was chewed, the wrath of the Lord was kindled against the people, and the Lord smote the people with a very great plague”; Numbers 11.33) [1]. The description is somehow
Definition and epidemiology
Although there is no consensus on the precise definition of this condition, the term rhabdomyolysis describes the rapid breakdown of striated, or skeletal, muscle. It is hence characterized by the rupture and necrosis of muscle fibers, resulting in release into the bloodstream and extracellular space of cell products. Since skeletal muscles comprises ~ 40% of body weight (i.e., several kg), and the destruction of just 100 g of muscle tissue is capable to induce the clinical syndrome of
Etiology
Direct muscle injury remains the most common cause of rhabdomyolysis, although the etiology includes up to four leading mechanisms, that are frequently overlapped: i) hypoxic, ii) physical, iii) chemical, iv) biological. Each one of these etiologic categories may have intrinsic or extrinsic causes, as follows (only citing the most frequent). Hypoxic mechanisms: i) extrinsic (carbon monoxide or cyanide poisoning), ii) intrinsic (compartment syndrome; compression; immobilization; vascular
Pathophysiology
All the aforementioned mechanisms capable to produce muscle damage converge in a final common pathway that triggers a cascade of events leading to a rapid influx of calcium ions into muscle cells. This fact can trigger the pathophysiological cascade, resulting in a pathological interaction between actin and myosin and activation of cell protease, with subsequent necrosis of muscle fibers, and release of intracellular metabolites (potassium, phosphates, and urates) and intracellular proteins
Clinics
The classic triad of symptoms of rhabdomyolysis includes muscle pain, weakness and dark urine. Muscle weakness and muscle pain can occur in any body region, but the muscle groups mostly involved are those of the proximal leg, calf and lumbar region [17], [31]. These muscles may appear tense and swollen, sometimes associated with bed sores. However, this classic triad is observed in < 10% of patients only, and up to 50% of the patients do not complain of muscle pain or weakness, only complaining
Laboratory diagnostics
The laboratory diagnosis of rhabdomyolysis is still essentially based on the measurement of serum or plasma CK, which is considered the most sensitive test despite being only regarded as a “surrogate” marker. Although there is no established cut-off threshold, a concentration five to ten times the URL (i.e., ~ 1000 U/L) is commonly used [17], [82]. In the case of a single event (i.e., mostly trauma), CK levels tend to rise in the first 12 h, peak on the second or third day and return to baseline
Emergency department treatment and management
After establishing a definitive diagnosis of rhabdomyolysis, or even when is strongly suspected it (e.g., in case of crush syndrome), fluid infusion should be promptly initiated, with the goal of maintaining a urinary flow of 200–300 mL/h. In order to avoid volume overload, it is highly recommended to alternate 500 mL of sterile saline solution with 500 mL of 5% glucose solution, adding 50 mmol of sodium bicarbonate for each subsequent 2–3 L of solution (usually 200–300 mmol on the first day) and
Conclusions
Overall, rhabdomyolysis remains a relatively rare condition, but it clinical consequences are frequently dramatic in terms of both morbidity and mortality. Unlike many other human diseases the triggering factors are often unrecognized, so that clinical prevention strategies are frequently ineffective. Therefore, a deepened knowledge of triggering factors, clinical and laboratory features along with the appropriate treatment in the ED remains pivotal for the clinical management of patients with
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