Rhabdomyolysis is a condition where striated muscle tissue breaks down, releasing the cellular constituents into the extracellular fluid and circulation. The etiology of rhabdomyolysis is diverse and causation ranges from extreme crushing muscle trauma to disease and drug toxicity (13,14,25). Exertional rhabdomyolysis is a form of muscle damage that can be brought about from overexertion exercise. Renal (kidney) failure can be a consequence of rhabdomyolysis; hospitalization is often warranted to prevent it. Myoglobin released from the damaged muscle cells can precipitate within the kidneys, which can obstruct the renal tubules, leading to tubular necrosis and ultimately renal failure (13,14). Rhabdomyolysis, if left untreated, can be fatal (6,7,15,16,23,28).
Rhabdomyolysis has been well documented in case studies of otherwise healthy individuals (1,20,21). Early descriptions of rhabdomyolysis were from incidences that occurred during military training, which entailed extremely rigorous physical training under strict instruction and was often associated with heat stress and dehydration (1,5,7-9,11). However, rhabdomyolysis occurring in the absence of heat stress or dehydration, while less common, has also been documented (3,10,12,21). The classic symptoms of exertional rhabdomyolysis have been well described and include dark reddish-brown urine, muscle pain and stiffness, muscle weakness, and general fatigue (11,13,14,25). The myoglobin released by the damaged muscle will discolor the urine to a reddish brown color (5,19,25). During rhabdomyolysis, massive quantities of creatine kinase (CK) and other muscle proteins are also released by the damaged muscle into the bloodstream (19,20,25); CK in the blood serves as a surrogate for myoglobin because it is less expensive and easier to measure. Diagnosis of rhabdomyolysis generally includes urine tests to detect myoglobin and blood tests to detect CK levels (19,20,25). Circulating CK levels are also used to chart progression of treatment, as CK levels will decrease as the rhabdomyolysis resolves (25).
Here we present a case of exertional rhabdomyolysis occurring in a healthy, fit 18-year-old placekicker following a practice session led by the National Collegiate Athletic Association (NCAA) Division 1-A football team strength and conditioning coach. This case is important because it demonstrates and supports that, although rare (3,10,12,21), rhabdomyolysis can occur in the absence of dehydration and heat stress and helps to disprove the erroneous and common belief that dehydration is necessary for rhabdomyolysis to occur. This belief is troubling and potentially dangerous because of the potential negative consequences that can occur with a delay or misdiagnosis of rhabdomyolysis. Furthermore, this case illustrates that there may be a lack of knowledge regarding the hallmark signs of rhabdomyolysis: brown urine and severe pain. Details of the precipitating exercise session and actual hospital records were provided by the patient and his parents with the understanding that the information would be used for publication with personal identities protected. The University of Massachusetts Internal Review Board was notified and provided with a copy of this case report.
The incidental training session occurred during late summer, after 4 weeks of participation in a summer intensive team training camp. The NCAA Division 1-A football team players, including the patient, were living on campus, were training strenuously daily, and were conditioned. During the incidental training session, the football team players, including the patient, performed the following exercises after a brief stretching session. The players were instructed by the strength and conditioning coach to perform 10 sets of 30 repetitions of squat exercises (300 total) using resistance bands attached to a platform beneath the feet and stretched over the shoulders. There was a 1-minute break between each set. The patient recalled that this was the most painful exercise he had ever performed. After the 10 sets of squats, the players were next instructed to perform 30 Romanian dead lifts using 40-lb dumbbells. Finally, they all performed 30 shoulder shrug bicep curls using 80-lb dumbbells. The training session was held in the late afternoon and the room was not air-conditioned. At the time of the training session, the patient reported that the temperature of the room was very warm but not hot, somewhere in the range of 78-84° F. The patient reported that during the incidental training session that he consumed water (6-8 oz each time) between each set of exercises. Following the exercise session, the patient reported that he felt dizzy and was experiencing pain in the quadriceps group. The patient also reported that several other players were stressed by the session and were vomiting during the training.
Following the practice, the patient reported that the pain in his quadriceps interfered with ambulation as he returned to his dorm room. He continued to consume water over the course of the evening. The severe pain in the quadriceps muscles continued throughout the night, and the patient reported difficulty sleeping. The following day, the patient continued to experience such severe pain that he became concerned and discussed his situation with the assistant athletic trainer, and reported that he was experiencing dark brown urine and requested crutches as he had difficulty walking. The patient reported that he was instructed to continue to drink water and to prepare for the 5 pm pregame practice. The patient attended the game and stood on the sidelines using crutches due to the severe pain and inability to bend his legs. The team athletic trainers and team physician were present. The following morning at 3 am, still experiencing severe pain, the patient sought treatment at the emergency room of the local hospital, where he was diagnosed with rhabdomyolysis as a result of overtraining.
At the time of admittance, (approximately 36 hours after the incidental exercise), the patient's CK values were measured at 130,899 IU·L−1 with urine positive for myoglobin and occult blood. The laboratory results performed at the time of admittance are presented in Table 1. The patient's urine had a normal range specific gravity of 1.025, and a normal range blood osmolality of 281 mosm·Kg−1. In addition, the admitting physician noted that the patient had moist mucus membranes. All factors were indicative of sufficient hydration. The patient had a pulse of 68 beats per minute, a blood pressure of 108/64 mmHg, and a temperature of 98.6° F. The patient was unable to bend his knees, and the physician could not test his gait due to the inability of the patient to walk. Besides the severe pain in the patient's quadriceps muscles, he was otherwise alert and healthy with no fever or viral infection. The patient had no history of sickle cell trait and tests for sickle cell were not performed. The patient did not have a history of muscular dystrophy. The patient was diagnosed with rhabdomyolysis secondary to exertion and hospitalized.
The patient remained hospitalized and was given intravenous (IV) fluids (250 mL·hr−1). Sodium bicarbonate (1 ampule·L−1) was added to the IV fluids to alkalinize the urine to prevent myoglobin from precipitating in the kidney tubules. Electrolyte levels were monitored and telemetry used to screen for cardiac abnormalities. CK values, measured at 24-hour intervals over the course of the hospitalization, are summarized in Table 2. The patient had neither previous nor familial history of rhabdomyolysis or muscle disease. The patient had no history of seizures or previous exercise intolerance. The physician noted that the patient did not drink alcohol or use illicit drugs, and that this claim was supported by routine drug testing required by the team. The physician also noted there was no extreme heat stress, no history of sickle cell trait, and no current infections or diseases requiring medication. A second examination by another hospital physician approximately 48 hours after admittance was performed and reaffirmed the original diagnosis of exertional rhabdomyolysis brought about by overtraining. At this examination, the patient's CK values were measured at 84,629 IU·L−1 with urine clearing. The physician also noted that there were no symptoms of compartment syndrome, and that kidney function was normal. The consulting physician confirmed the treatment of aggressive IV fluids. A basic metabolic profile was repeated daily and urinalysis performed approximately every 48 hours over the course of hospitalization, with those results presented in Tables 2 and 3, respectively. The patient had normal electrolyte levels at admittance and those levels remained within normal range over the entire course of the hospitalization (Table 3). Blood osmolality and urine specific gravity were within normal levels at the time of admittance, indicative of sufficient levels of hydration.
Three days after admittance, further chemistry profiles showed the patient to have elevated levels of aspartate aminotransferase (AST, 2466 IU·L−1) and alanine aminotransferase (ALT, 773 IU·L−1). Levels of both these enzymes decreased over the remaining course of hospitalization (Table 2). Like CK, these indicate muscle damage. The patient also had elevated levels of CKMB (13.6 ng·mL−1) 6 days after admittance (Table 2); however, the normal EKG suggests that this increase is from skeletal muscle.
Eight days after admittance, the patient was discharged; his urine had cleared and his CK values were down to 4620 IU·L−1. One full month after the incidental exercise, the patient was declared able to resume normal activities with no restrictions. The diagnosis remained exertional rhabdomyolysis occurring as an isolated incidence related to overtraining, with no indication of future rhabdomyolysis being expected to repeat.
This case is interesting in that it involves a rhabdomyolysis situation where neither dehydration nor extreme heat stress were contributing factors. Rhabdomyolysis has been well documented as occurring in combination with dehydration and heat stress (2,18,26,27); however, dehydration is not by any means a sole causation. Rhabdomyolysis occurs when muscle membranes become ruptured and fail to contain the cellular contents. Myoglobin is a major protein constituent of muscle and when released from the muscle, can overwhelm the kidneys (13,14). In this scenario, dehydration will directly affect the ability of the body to deal with or recover from overexertion exercise; however, dehydration is not a prerequisite to cause rhabdomyolysis (13,19,25). Treatment with IV fluids is standard rhabdomyolysis therapy and is aimed at preserving renal function and aiding in flushing myoglobin to prevent renal failure (19).
Rhabdomyolysis has been documented in highly fit as well as novice exercisers (13,22,24,29). A common thread to developing rhabdomyolysis is overexertion, whether as a result of unaccustomed novice exercise or from an overly vigorous and strenuous (unaccustomed) workout by a well-conditioned individual (13). Other factors, such as viral infections, alcohol, and drug use, can also play a role in the development of rhabdomyolysis (5,14,20,25,27). In the case presented here, we had a healthy young man at collegiate athlete level of physical conditioning develop rhabdomyolysis following a training session. During this training session, the patient performed a large number of resistance squats, an exercise with an eccentric contraction bias. Stretching the muscle while it contracts (eccentric contractions) can disrupt the sarcomeric organization of the individual muscle fibers resulting in muscle damage (4,17,20). Indicative of the effect that this exercise had upon the patient was the fact that he experienced severe pain and muscle weakness following the exercise and brown urine shortly thereafter, all classic symptoms of muscle damage and rhabdomyolysis (3,4,11,19,20,22) that were missed by the patient's coaches and athletic trainers. This patient had no family history of rhabdomyolysis, was not dehydrated, was not using alcohol or drugs, and was not a novice to exercise.
The patient reported that when presented with diagnosis from the hospital, the team's representatives still maintained that a lack of hydration was the cause of the patient's rhabdomyolysis. This indicates a belief that rhabdomyolysis is caused by dehydration during exercise. When the patient was admitted, his medical records indicate an alert and otherwise healthy young man with moist mucus membranes, no difficulty urinating, normal glomular filtration rates, and a normal blood osmolality level-all suggesting that hydration was not a factor. The patient reported that he consumed water prior to and throughout the exercise as well as after training. Indeed, his hydration levels may have played a role in attenuating the effects of his rhabdomyolysis and may have enhanced his recovery.
While uncommon, rhabdomyolysis, a potentially life-threatening condition, can occur from significant overexertion. Athletic trainers and coaches who are responsible for monitoring and training young athletes should recognize the hallmark signs of rhabdomyolysis; an educational summary module that provides basic rhabdomyolysis information is presented in Table 4. We noted from inspection of many athletic training and exercise physiology texts that there was either no mention of rhabdomyolysis or the description did not include the hallmark signs. Although obviously important, hydration alone is not sufficient to prevent the development of rhabdomyolysis. The training catalyst that caused the patient's rhabdomyolysis may not have been preventable or foreseeable; however, the follow-up and concern for this young player reporting significant red-flag symptoms of rhabdomyolysis (severe muscular pain, dark brown urine) after the training was lacking and troubling.
The authors thank the patient and his parents for providing this information and cooperating with this publication.
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Keywords:© 2009 National Strength and Conditioning Association
exertional rhabdomyolysis; dehydration; creatine kinase; symptom recognition