The importance of brown urine is stressed as a key factor in the diagnosis of AER in much of the literature on the condition.1-10 It is suggested that brown urine is pathognomonic for this condition. However, the urine for the individuals presented here with significant AER was not brown or even tinged. In a field evaluation, an inexperienced HCP might miss an AER diagnosis in the absence of urine findings. In addition, given that AER can occur in stages, it is essential that the HCP have a situational awareness of this condition in today’s culture of fitness and exercise.
Cocaine is a common cause of rhabdomyolysis, namely, in urban patient populations. Prolonged vasoconstriction of intramuscular arteries may result in muscle ischemia and acute rhabdomyolysis, but there also is a direct toxic effect that can produce acute skeletal myofibrillar degeneration.
A number of prescription drugs have been implicated in cases of rhabdomyolysis, including colchicine, zidovudine, isoniazid, benzodiazepines, opiates, corticosteroids, statins, and fibric acid derivatives. One particular interaction that is clinically significant is the interaction between statins and fibrates.16
The pathogenesis of rhabdomyolysis precipitated by infections (whether bacterial, viral, or fungal) is thought to be the result of direct cell invasion of striated muscle and cellular degeneration by the pathogen. Substantial morbidity (57% of cases with acute renal failure) and mortality (death in almost 40% of cases) are linked to bacterial causes of rhabdomyolysis.
In adult patients, Legionella species most often are associated with rhabdomyolysis. Other bacteria linked to rhabdomyolysis include group A β-hemolytic streptococci, Salmonella species, Francisella tularensis and Escherichia coli. Viruses, such as influenza, parainfluenza, coxsackievirus, Epstein-Barr virus, adenovirus, HIV, and cytomegalovirus also have been associated with this condition.
Rhabdomyolysis also can be observed in septic patients without direct muscle infection when the damage is caused by a toxin, associated fever, dehydration, and rigors. Electrolyte disorders, such as hyponatremia or hypernatremia, hypokalemia, and hypophosphatemia can result in rhabdomyolysis, distorting the permeability and the functions of sarcolemma in the muscles. Some endocrine disorders (ie, pheochromocytoma and thyrotoxicosis) also are able to potentiate rhabdomyolysis due to hypermetabolism.
A workout program should progress gradually according to the individual’s current level of fitness, whether it’s cardiovascular, circuit training, or weight training. Fluid intake should be monitored, particularly when the workout is long, intense, or hot and especially when the workout meets all 3 conditions. Fluid replacement is important, and for strenuous and longer training evolutions, electrolyte replacement should be considered. Hard exercise while maintaining a low-calorie diet or after long fasting periods should be avoided. Sufficient caloric and fluid intake to allow muscles to work efficiently during strenuous workout period is needed. Recreational drugs, including alcohol should be limited before exercise, and illicit recreational or performance-enhancing drugs should be avoided.
Acute exertional rhabdomyolysis is more common in the lower extremities and in males. Extremely rigorous upper-extremity training can result in AER. The presentation usually is clear with an inciting event and muscle pain in the extremity. Besides identifying associated risk factors and performing a thorough examination, the patient should be examined for compartment syndrome. Early diagnosis and comprehensive management are crucial to ensure full recovery and avoidance of complications, such as acute tubular necrosis, renal failure, cardiac arrhythmias from hyperkalemia, and death. As in most cases with early diagnosis and aggressive management, these patients fully recovered and experienced no sequelae at 8 weeks postevent.