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Journal of Strength & Conditioning Research:
doi: 10.1519/JSC.0b013e318216302f
Brief Review

Exertional Rhabdomyolysis in an Adolescent Athlete during Preseason Conditioning: A Perfect Storm

Cleary, Michelle A1; Sadowski, Kelsey A2; Lee, Samuel Y-C3; Miller, Gretchen L4; Nichols, Andrew W5

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Author Information

1Department of Kinesiology and Rehabilitation Science, Human Performance Research Laboratory, University of Hawaii at Manoa, Honolulu, Hawaii; 2Department of Athletics, Bonner Physical Therapy/Sandpoint High School, Sandpoint, Idaho; 3Department of Athletics, Hawaii Baptist Academy, Honolulu, Hawaii; 4Department of Athletics, Castle High School, Kaneohe, Hawaii; and 5Division of Sports Medicine, Family Medicine and Community Health, John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, Hawaii

Address correspondence to Dr. Michelle A. Cleary, mcleary@hawaii.edu.

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Abstract

Cleary, MA, Sadowski, KA, Lee, SY-C, Miller, GL, and Nichols, AW. Exertional rhabdomyolysis in an adolescent athlete during preseason conditioning: a perfect storm. J Strength Cond Res 25(12): 3506–3513, 2011—The purpose of this brief review is to present a case of a healthy, male adolescent athlete (age = 16 years, body mass = 67.9 kg, height = 165.5 cm) who participated in a 3-day preseason wrestling camp which resulted in hospitalization for exertional rhabdomyolysis. As part of the preseason conditioning program directed by the coaches, the athlete completed 60 minutes of short, intense intervals of wall-sits, squats, sit-ups, push-ups, lunges, and plyometric jumps. The following day, the athlete continued his vigorous training consisting of running drills. That night he noticed voiding dark brown urine the color of cola. The day after the camp ended, the athlete reported to his Athletic Trainers with the chief complaint of severe bilateral leg pain in his quadriceps. Two days after the initial assessment, he was admitted to the hospital where he was diagnosed with exertional rhabdomyolysis based on creatine kinase (CK) levels that peaked at 146,000 IU·L−1, elevated far beyond normal (normal range = 58–280 IU·L−1). The athlete was hospitalized for 6 days where he received intravenous normal saline for rehydration, and his CK levels were assessed daily. Athletic Trainers, personal trainers, physical education teachers, and coaches should be aware that exertional rhabdomyolysis is the most common form of rhabdomyolysis and affects individuals who participate in novel and intense exercise to which they are unaccustomed. Stressful ambient conditions may lead to dehydration and exacerbation of the condition, particularly when the individual is not accustomed to the exercise intensity.

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Introduction

Exertional or exercise-induced rhabdomyolysis is a serious, potentially life-threatening condition that can develop unexpectedly under supervised training conditions (25). Rhabdomyolysis is a general or “umbrella” term that refers to injury to skeletal muscle cells that leads to leakage of muscle cell contents, including the muscle proteins myoglobin and creatine kinase (CK or CPK) (23). General rhabdomyolysis is reported in 26,000 cases each year in the United States (5) with 47% meeting the criteria for diagnosis as exercise-induced rhabdomyolysis (32). Rhabdomyolysis results from the disruption in the integrity of muscle membranes, which may come from a variety of conditions; however, exercise-induced or exertional rhabdomyolysis can be diagnosed using the following criteria: a history of strenuous exercise, CK level >5 times normal (range 58–280 IU·L−1) or 290–1,400 IU·L−1 (23,27), and urine dipstick positive for blood (often described as tea or cola colored) (9,27). Although the clinical signs and symptoms vary widely, practitioners should be aware of this condition because the damaged muscle can swell excessively and lead to compartment syndrome requiring surgical intervention (23,25,29) or acute renal failure caused by myoglobin precipitating into the renal tubules (8,9,20). Although compartment syndrome and acute renal failure may be rare in cases of exertional rhabdomyolysis, hospital admission is still reasonable and prudent (32). The purpose of this brief review is to increase awareness of Athletic Trainers, personal trainers, physical education teachers, and coaches about exercise-induced or exertional rhabdomyolysis (rhabdomyolysis) so that these practitioners can prevent this condition in individuals who participate in novel and intense exercise to which they are unaccustomed. Specifically, this instructive case report will be used to focus on the causes of exertional rhabdomyolysis, how to recognize it in the field, appropriate referral and management of the condition, and how to prevent this condition in adolescent athletes during preseason conditioning.

The primary pathophysiology of rhabdomyolysis typically involves strenuous eccentric exercises at an intensity to which individuals are unaccustomed or in individuals that are unprepared or underprepared for a physically demanding task. Cases of rhabdomyolysis have been often associated with “high stakes testing” for important outcomes such as firefighter candidates (5), law enforcement trainees, or military cadets (16). Previous incidences of rhabdomyolysis have involved extremely rigorous physical training under strict instruction, often combined with heat stress and dehydration; however, the condition has also occurred in the absence of heat stress or dehydration (25). To our knowledge, there have been no previously reported cases in an adolescent performing preseason wrestling activity.

Cases of rhabdomyolysis have been previously reported in young people trying out for team sports (11,21,25) or students participating in physical education classes (7,24). Clearly, additional knowledge is needed because the condition is continuing to plague youths involved in physical activity. Most recently in summer of 2010, 10 high-school football players in Oregon were hospitalized with rhabdomyolysis after intense preseason summer training. Three of these athletes developed compartment syndrome requiring surgical decompression (21). Similarly, high-school preseason football training combined with dehydration led to a case of rhabdomyolysis in a 16-year-old Hispanic male quarterback. On the second day of practice, the athlete initially presented to the Athletic Trainer with severe muscle cramps throughout his legs to trunk. He was hospitalized for 2 days with rhabdomyolysis with blood levels of CK peaking at 3,363 IU·L−1. This relatively low CK level, about 12 times normal, was attributed to the muscle breakdown after the intense cramping in the large muscles of the legs and trunk secondary to dehydration and extreme exercise in the heat. After vigorous intravenous (IV) rehydration, the athlete was discharged from the hospital and gradually returned to football within 2 weeks (11). Also, in a football practice session supervised by the team's strength and conditioning coach, an 18-year-old place kicker developed rhabdomyolysis. The athlete experienced extreme pain and dark urine and sought treatment at a local emergency department (ED) where he was hospitalized with rhabdomyolysis based on myoglobinuria, muscle pain, and extremely elevated circulating CK values of 130,000 IU·L−1. After 8 days of hospitalization with IV fluids, the patient recovered without complications. It is important to appreciate that rhabdomyolysis can occur after strenuous exercise in otherwise conditioned and healthy athletes and does not necessarily require dehydration or heat stress (25).

Physical educators should also be aware that excessive exercise can elicit rhabdomyolysis. Numerous cases (7,24) have been reported in the literature involving students in physical education classes being led through exercise that far exceeds the physical capacity of the child. Specifically, a case involving a 12-year-old boy described his participation in an indoor physical education class during which he was required to perform excessive (>250) repetitive squat jumps as punishment for talking in class. The boy reported intense muscle soreness in his thighs and dark urine 2 days postexercise, and his parents brought him to the ED. He was hospitalized with serum CK rising to 244,006 IU·L−1 at 4 days postexercise (7). A similar scenario involving numerous children in a physical education class included 119 high-school students aged 17–18 years who performed 120 push-ups in 5 minutes (24). Many of the students developed muscle pain and dark urine 2–4 days after the exercise with serum CK values as high as 174,260 IU·L−1. Most were treated as outpatients with oral hydration, but 20 students were admitted to the hospital and were later discharged without organ damage. Fortunately, all of these cases resulted in a positive outcome with hospitalization and treatment of vigorous IV hydration. With knowledge about the previously reported cases involving adolescents performing excessive physical activity (7,11,21,24,28), future cases are preventable.

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Case Report

This case involved a male adolescent athlete (age = 16 years, body mass = 67.9 kg, height = 165.5 cm) participating in wrestling preseason conditioning supervised by his coach. Details of the precipitating exercise event 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 Hawaii Institutional Review Board, Committee on Human Subjects was notified and provided with a copy of this case report. The timeline of events is presented in Table 1. This athlete participated in a 3-day preseason wrestling camp over winter break during which he was allowed noncontact participation until cleared by his physician for a non–sports-related concussion (skateboarding accident). The wrestling camp consisted of 3 practices per day in an off-site non–air conditioned gymnasium in a subtropical environment with average December temperature = 70° F or 21 °C (range = 60–79° F or 16–26° C) and relative humidity ranging from 65 to 85%. On the second day of the camp, his physician cleared him for participation, and he performed noncontact drills during the second half of practice under the direction of the coach. The athlete felt that he had fallen behind his peers who had been training without him. Supervised by his coach, he attempted to “catch up” to his peers by completing 60 minutes of short, intense intervals of wall-sits, squats, sit-ups, push-ups, lunges, and plyometric jumps. The following day, the athlete continued his vigorous training consisting of running drills. On the night of the third day of training, he noticed voiding dark brown urine the color of cola. On the fourth day (the day after the camp ended), the athlete reported to his Athletic Trainers with the chief complaint of severe bilateral leg pain in his quadriceps. He had reduced knee flexion because of pain and tightness with moderate swelling superior to the patella bilaterally. He denied a history of any medical conditions and did not mention any medications or his dark-colored urine. Additionally, he denied taking supplements or being dehydrated but did mention there were limited water breaks during which he drank less than a half cup of water.

Table 1
Table 1
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Upon initial clinical evaluation, the primary Athletic Trainer recognized the athlete had pain in both his quadriceps and a small amount of swelling in the distal quadriceps superior to the patella. Because of the athlete's inactivity for a month before the episode of injury, bilateral quadriceps swelling, pain, and tightness; the Athletic Trainer related the signs and symptoms to delayed-onset muscle soreness (DOMS). The Athletic Trainers advised the athlete to apply ice for 20 minutes before and after practice to reduce swelling and pain, and he was released to practice as tolerated. During practice, the athlete had a constant feeling of tightness and asked the coach to stretch his quadriceps after practice, which was exceedingly painful.

Within 2 days after the initial assessment, the patient's parents became concerned about the cola-colored urine. His parents brought him to the ED where he was evaluated and admitted to the hospital. Upon initial triage in the ED, vital signs were within normal limits, but the patient's chief complaint was extremely severe (10/10) pain levels in his bilateral anterior thighs with walking and knee flexion, swelling, and tenderness to palpation. The patient was self-medicating by taking ibuprofen (Motrin®, McNeil PPC, Inc., Skillman, NJ, USA) for pain and reported taking loratadine (Claritin®, Merck Inc., Whitehouse Station, NJ, USA) for seasonal allergic rhinitis. Blood and urine samples were obtained, and the ED physician ordered clinical laboratory tests on metabolic, hepatic, and renal function for analysis. The differential diagnosis for this patient included DOMS, exercise-related muscle cramps, exertional rhabdomyolysis, myositis, and dehydration.

The patient's laboratory results (summarized in Table 2) revealed serum CK levels that peaked at 146,000 IU·L−1, elevated far above normal limits (normal range = 58–280 IU·L−1). Additionally, other enzymes indicative of damage to skeletal muscle tissue, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were elevated in response to strenuous physical exercise. The AST and ALT in a 3:1 ratio suggested elevation of these enzymes secondary to muscle breakdown. The patient's urine analysis revealed myoglobinuria and mild dehydration based on urine specific gravity (Usg) = 1.025 μg·L−1. All other metabolic panels, hepatic tests, blood clotting tests (albumin, coagulants), and renal function tests indicated no hepatic or renal insufficiency at this time. The athlete was hospitalized for 6 days while he was administered IV normal saline titrated to maintain an adequate urine output, and he was prescribed IV morphine for his pain (Table 2). His CK levels were checked daily, and improvement was noticed each day. His myalgia in his bilateral thighs, stiffness, and tenderness decreased each day; however, after 6 days of hospitalization, he still had muscle pain while ambulating, and he was walking with a limp. At the time of discharge, the patient's CK level was 2,433 IU·L−1 (no other clinical data available).

Table 2
Table 2
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Upon discharge from the hospital, the patient still had muscle pain while ambulating and was still limping when he walked. He was prescribed 300 mg of acetaminophen with 30 mg of codeine (Tylenol No. 3®, McNeil PPC, Inc.) by mouth every 4 hours or as needed and home physical therapy for 3 weeks. The patient was prescribed outpatient home-based physical therapy for 1 month twice per week including plans for improving ambulation. His discharge instructions consisted of limited walking, no cardiovascular exercise, and no weight training exercises (even with upper body exercises) to avoid additional muscle damage. He was provided a handout with instructions for gentle stretching emphasizing hip and knee flexion within his pain-free range of motion. He was sent home with a wheelchair and crutches with plans for classes, particularly because there were stairs and no elevator at the school. Because ambulating at school would be difficult and he could complete his class work at home, the athlete did not return to school for 2 months while he recovered. His goals for physical therapy were to (a) increase knee flexion range of motion to 90° and (b) progress to independent ambulation with crutches. The patient was provided no other physical therapy and was not allowed to return to wrestling until cleared by his primary care physician. The athlete was highly motivated to recover, and within weeks, he progressed rapidly from the wheelchair to ambulating without crutches. Within 3 months, the athlete was participating in light wrestling activities, weight training, and recreational sports such as roller hockey. By the following Fall, the patient had recovered fully and enjoyed a successful senior wrestling season, taking fourth place in the state championships in the 145-lb weight class.

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Discussion

This case is described to educate Athletic Trainers, coaches, personal trainers, and physical educators about how strenuous, unaccustomed exercise can cause damage of striated muscle resulting in either DOMS or in extreme cases, exertional rhabdomyolysis. We will present the characteristics of DOMS and the diagnostic criteria for rhabdomyolysis. In addition, we will describe the contributing factors that can lead to a diagnosis of rhabdomyolysis after intense, unaccustomed physical activity. Rhabdomyolysis can exist as a physiologic or benign condition in which the clinical picture is essentially that of muscle damage characterized by DOMS with elevated CK, with no other evidence of rhabdomyolysis. However, the condition becomes “clinically relevant” when there is clinical sequelae from muscle damage including severe muscle pain, muscle swelling or weakness, and most specifically myoglobinuria (27). Muscle damage may be induced by repetitive eccentric contraction exercise over a long period of time in untrained or undertrained individuals. Exercise that is particularly damaging usually involves eccentric loading, lengthening contractions, lowering weight against gravity, or “negatives” (27). Strenuous exercise that damages skeletal muscle is manifested by delayed-onset pain and soreness, weakness, and increased circulation of muscle proteins such as CK, lactate dehydrogenase, and myoglobin (9). The pathophysiology of eccentric muscle damage, recognizing rhabdomyolysis in the field, and factors that precipitate the development of this condition will be described.

Any exercise that includes a strong eccentric (muscle lengthening) component is likely to cause muscle damage and DOMS. Stretching the muscle while it is attempting to contract (“lengthening contraction”) creates a tensile stress on the muscle fibers resulting in disruption of the sarcomeric structures of the fiber (26). The sensation of pain and stiffness in the muscles that occurs from 1 to 5 days after unaccustomed exercise and peaks 72 hours after activity is characteristic of DOMS. Exertional rhabdomyolysis appears to be a complication relating to factors that exacerbate a benign condition of DOMS. Although temporary, DOMS adversely affects muscular performance, both from voluntary reduction of effort and from inherent loss of capacity of the muscles to produce force (2). A number of clinical correlates are associated with DOMS, including elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure. In the present case, the patient performed an excessive volume of body weight exercises against gravity (squats, lunges, plyometric jumping, etc.) that lead to eccentric loading and skeletal muscle damage in the quadriceps muscle group. Initially, his primary complaint was DOMS resulting from muscle damage caused by the strenuous eccentric loading and weight-bearing activity to which he was unaccustomed.

Eccentric exercises, where the muscle is lengthening while trying to contract, are a particularly damaging exercise on muscle fibers because of the increase strain placed on muscle tissue. Examples of eccentric exercises are squats, lunges, push-ups, plyometrics, or running downhill (2,4). When the damage to muscle is extensive, myoglobin is released from the muscle into the blood and filtered through the kidney. If myoglobin levels reach a threshold level in the blood, glomerular filtration rate cannot compensate for the increase in volume, and myoglobin enters the urine. Considerable muscle damage must occur for this to happen, because each kilogram of muscle contains only 4 g of myoglobin, and the kidney is able to filter approximately 300 ng·ml−1 (31). If the myoglobin proteins are absorbed by the nephron, the renal tubules produce clear urine; however, if there is sufficient muscle damage to release high levels of myoglobin, it will “spill over” into the urine causing dark urine or myoglobinuria, which is an indication of rhabdomyolysis.

The classic symptoms of rhabdomyolysis have been well described and include muscle pain and stiffness, muscle weakness, and general fatigue (3,6,10,23,34). Movement may cause severe pain, and the muscles are tender and usually “doughy” feeling often with redness, ecchymosis, and edema. If the process is sufficiently severe, paresthesia may be present or deep tendon reflexes may be absent secondary to neurovascular compression (23). The clinician should be concerned about compartment syndrome if the muscles affected are contained within a tight fascial compartment such as the anterior tibial muscles, the soleus, or the lateral muscles of the thigh (23). Compartment syndrome was reported in 3 of 10 high-school football athletes hospitalized after intense preseason conditioning requiring surgical decompression as a consequence of rhabdomyolysis (21). To identify this potentially catastrophic condition, the Athletic Trainer should complete a neuromuscular assessment with the affected limbs and if a developing compartment syndrome is identified, the patient must be referred to the ED as soon as possible. Fortunately in the present case, although the patient was suffering from intense quadriceps muscle pain, swelling, and tenderness, the patient was neurovascularly intact and was able to ambulate although with difficulty.

Practitioners should be aware that a hallmark of rhabdomyolysis that can be identified in the field setting is myoglobin that presents itself as myoglobinuria (dark tea color or cola-colored urine) (27,29). Myoglobin, the oxygen-binding protein in muscle, is increased with skeletal muscle injury and excreted through the kidneys (29). Myoglobin is filtered through the renal tubules into the urine and is responsible for myoglobinuria or increased urinary excretion of myoglobin, the most important consequence of significant muscle breakdown (24,35). The myoglobin released by the damaged muscle will discolor the urine to a reddish brown color (30,34). Myoglobinuria cannot occur without rhabdomyolysis, which in the broad spectrum of etiologies is very common in the hospital setting (32). If rhabdomyolysis is suspected, a urine sample should be provided by the patient and visually analyzed for color and for protein with a urine reagent strip or “dipstick.” For myoglobin (or hemoglobin) to be visible in urine, it requires a concentration of at least 100 mg·dl−1. The common dipstick method of analyzing urine in the Athletic Training setting does detect the heme portion of the molecule but does not differentiate between myoglobin and hemoglobin. Nonetheless, this simple test is satisfactory in nearly all instances when considered in light of an appropriate history and physical findings for rhabdomyolysis and myoglobinuria. Dipstick sensitivity for detecting the heme pigment ranges from 1 to 10 × 10−6 g·ml−1 (23). The only test more sensitive than the dipstick test is a radioimmunoassay procedure (24), which must be completed in a hospital laboratory setting once the patient is referred to the ED or admitted to the hospital. Referral to a physician is necessary for confirmation of the diagnosis of rhabdomyolysis.

Once rhabdomyolysis is suspected, the athlete must be referred to the ED for follow-up testing. Specifically, the laboratory study used to differentially diagnose rhabdomyolysis is CK secreted into the bloodstream from the damaged skeletal muscle. Analysis of CK level is the best laboratory test that is specific and reliable in assessing damage to the muscle tissue (29). In cases of rhabdomyolysis, CK is used as a surrogate measure of myoglobin because it is released from muscle proportionately with myoglobin and can be assessed more quickly and with less cost (8). Serum CK levels are commonly used to judge the severity of muscle damage and to determine when to hospitalize patients who present with symptoms of rhabdomyolysis to prevent renal failure (9,29). However, no CK standard exists because of the limited information available regarding exercise-induced CK elevation and renal function (9). Currently, there is no commonly accepted algorithm for determining when to hospitalize and treat individuals who present with elevated CK. During rhabdomyolysis, massive quantities of CK and other muscle proteins are released by the damaged muscle into the bloodstream (34); CK in the serum can reach levels near 100,000 IU·L−1 where normal range is less than 280 IU·L−1 (23,27). O'Connor et al. (27) and others (19,29) consider serum CK levels 5 times greater than normal to be an indication to suspect rhabdomyolysis. Serum CK rises 2–12 hours after the injury or insult occurs, then peaks in 1–3 days and starts to decline in 3–5 days (29). Circulating CK levels are also used to chart progression of treatment, because CK levels will decrease as the rhabdomyolysis resolves (34). Once rhabdomyolysis is suspected, the following additional laboratory tests should be performed for differential diagnosis: serum electrolytes, hepatic function tests, and renal function tests (19,23,34). Because assessment of CK levels is the most important aspect of diagnosis of rhabdomyolysis, a referral to a physician to rule out the condition is crucial for appropriate management.

Rhabdomyolysis may be exacerbated with confounding factors such as heat stress, dehydration, nonsteroidal anti-inflammatory drugs (NSAIDs) or other drug use, or sickle cell trait combine to create a situation of the ‘perfect storm’ (8,15,17,27). The possibility of developing rhabdomyolysis is most commonly increased in athletes who perform strenuous exercise in a dehydrated condition. Dehydration occurs in active individuals when there is inadequate or insufficient replacement of sweat losses during and after training or while performing vigorous exercise with environmental heat stress (18). For dehydration levels as low as 2% body mass loss, inadequate replacement of electrolytes and fluids may impede the physical performance and disrupt fluid homeostasis and impair kidney function (25). In any extreme environment, it is essential that athletes replace the fluids lost through sweat by drinking quantities of fluid equal to sweat loss. For example, an athlete that loses 2 kg of body mass during exercise (when weighed before and after exercise) should replace the sweat losses with 2 L of fluid (water or carbohydrate–electrolyte beverage).

Dehydration is common during physical activity, particularly in the heat without clinical sequelae. However, dehydration becomes “‘clinically relevant”’ when there is severe muscle pain, muscle swelling or weakness, myoglobinuria, and other manifestations typically considered part of rhabdomyolysis. Muscle damage and necrosis are exacerbated by dehydration especially in untrained participants performing unaccustomed exercise in high temperature ambient environments (25). Hyperthermic (13) and dehydrated individuals (12) who perform eccentric exercise may exacerbate skeletal muscle damage resulting from structural, contractile, and enzymatic protein denaturation, in addition to the myofiber and connective damage resulting from the eccentric muscle tension (12,13). Individuals performing novel exercise, particularly with a significant eccentric component, should use caution when training in a hot, humid environment and implement frequent rest and rehydration breaks. Although dehydration alone may not be a sole causative factor, when muscle membranes become ruptured and fail to contain the cellular contents, rhabdomyolysis may occur.

The use of NSAIDs during exercise has been cited as leading to reduced kidney function (15) and has been associated with exertional rhabdomyolysis after the marathon (8). Clarkson postulated that likely candidates for factors provoking renal failure in cases of exertional rhabdomyolysis in a marathon situation are a pre-existing viral or bacterial infection and the use of analgesics and NSAIDs. Nonsteroidal anti-inflammatory drugs can reduce renal perfusion, leading to a depressed glomerular filtration rate (8). In the current case, the athlete had been recovering from a non–sport-related concussion and may have been taking NSAIDS for the symptoms of that injury before beginning his preseason conditioning program. He admitted to taking ibuprofen for his symptoms of DOMS within the first day of conditioning while he continued to train in warm, humid environmental conditions without consuming sufficient water. It is likely that the athlete's ibuprofen use was associated with significantly greater reductions in glomerular filtration rate during exercise in his volume-depleted condition. Under conditions where the exercise intensity might be greater or the degree of dehydration might be more severe, ibuprofen use could potentially precipitate acute renal deficiencies or possibly failure (15).

As a limitation of this case study, the medical records for the patient in this case did not report the sickle cell trait status, so it is impossible to determine if erythrocyte sickling was involved in the pathogenesis of his rhabdomyolysis. However, sickle cell trait has been reported in the literature as a contributory factor to the fatal collapses of military personnel (16) and college football players in training (1,30). In these related cases, the clinical course and the pathological correlation strongly suggest that exertional sickling was the cause of these collapses in otherwise healthy young adults. These cases involved the “perfect storm” of intense exercise often in the heat, dehydration, and sickle cell trait. Sickled red blood cells can accumulate in the bloodstream during intense exercise bouts causing a “logjam” in blood vessels and lead to collapse from ischemic rhabdomyolysis, which is a potentially fatal medical emergency (14). In patients with sickle cell trait, it appears that sickling can begin within 2–3 minutes of maximal sprinting—or any other all-out, sustained exertion—and can reach grave levels very soon thereafter if the athlete struggles on or is urged on by coaches despite warning signs. Heat, dehydration, altitude, and asthma can increase the risk for and worsen exertional sickling (1,14). The clinical course of exertional rhabdomyolysis concomitant with sickle cell trait illustrates the importance of laboratory evaluation to identify common laboratory features of acute renal failure and rhabdomyolysis and the increased risk of exercise-related death in those with sickle cell trait (16). With the limitations of clinical case report data, it is impossible to rule out the involvement of sickle cell trait in the present case. All considered, the outcome of the case was fortunate in that this patient survived with no long-term deficits.

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Practical Applications

Personal trainers, physical education teachers, coaches, and others responsible for monitoring and training young athletes should be aware of the causes and recognize the hallmark signs of rhabdomyolysis. Practitioners should be aware that rhabdomyolysis is a preventable but potentially life-threatening condition with the most common cause being extreme muscular exertion at a level that the individual is unaccustomed (25,33). Unfortunately, many athletic training and exercise physiology texts either have no mention of rhabdomyolysis or the description did not include the hallmark signs for identification of the condition (25). Although rhabdomyolysis is rare in young children, it can occur when excessive exercise is spurred on by an adult (7,21). Practitioners should be aware that, as in the current case, children who have unexpectedly high exercise volume, especially when pushed or prodded by an adult to complete more exercise than the child is prepared to complete. Team sports and coaching curricula should incorporate educational material on the potential danger of excessive exercise in children (7). The training catalyst that caused this patient's rhabdomyolysis may not have been foreseeable; however, coaches and physical educators should identify any young athletes reporting significant red-flag symptoms of rhabdomyolysis: myalgia or muscular aches, muscle weakness, and brown or tea or cola-colored urine that develop within 12–36 hours after the damaging exercise training (19,21,25) and refer the athlete to the Athletic Trainer or a physician.

Because the signs and symptoms of rhabdomyolysis are nonspecific and may not always be present, practitioners should have a high level of suspicion for rhabdomyolysis in an athlete who has any of the hallmark signs combined with a history of intense or strenuous physical activity to which they are unaccustomed. Referral to a physician is necessary to rule out other differential diagnosis and to confirm any abnormal laboratory values. An elevated plasma CK level is the most sensitive laboratory finding pertaining to muscle injury, whereas acute renal failure and compartment syndrome represent the major life-threatening complications (22,35). When identified early by the practitioner and referred to the Athletic Trainer or physician for referral to the ED and aggressive IV hydration (29), this condition may cause little or no damage to the kidneys or other organs and, as in this case, lead to a full recovery.

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Acknowledgments

The authors thank the patient and his parents for providing this information and cooperating with this publication.

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References

1. Anzalone, ML, Green, VS, Buja, M, Sanchez, LA, Harrykissoon, RI, and Eichner, ER. Sickle cell trait and fatal rhabdomyolysis in football training: A case study. Med Sci Sports Exerc 42: 3–7, 2010.

2. Armstrong, RB. Mechanisms of exercise-induced delayed onset muscular soreness: A brief review. Med Sci Sports Exerc 16: 529–538, 1984.

3. Brudvig, TJ and Fitzgerald, PI. Identification of signs and symptoms of acute exertional rhabdomyolysis in athletes: A guide for the practitioners. Strength Cond J 2007;29: 10–14.

4. Byrne, WC, Clarkson, PM, White, JS, Hsieh, SS, Frykman, PN, and Maughan, RJ. Delayed onset muscle soreness following repeated bouts of downhill running. J Appl Physiol 59: 710–715, 1985.

5. Centers for Disease Control MMWR Weekly. 39: 751–756, 1990. Available at: www.cdc.gov/MMWR/preview/mmwrhtml/00001812.htm. Accessed October 16, 2005.

6. Chatzizisis, YS, Misirli, G, Hatzitolios, AI, and Giannoglou, GD. The syndrome of rhabdomyolysis: Complications and treatment. Eur J Intern Med 19: 568–574, 2008.

7. Clarkson, PM. Case report of exertional rhabdomyolysis in a 12-year-old boy. Med Sci Sports Exerc 38: 197–200, 2006.

8. Clarkson, PM. Exertional rhabdomyolysis and acute renal failure in marathon runners. Sports Med 37: 361–363, 2007.

9. Clarkson, PM, Kearns, AK, Rouzier, P, Rubin, R, and Thompson, PD. Serum creatine kinase levels and renal function measures in exertional muscle damage. Med Sci Sports Exerc 38: 623–627, 2006.

10. Cleary, MA. Sickle cell trait and exertional rhabdomyolysis. Athl Ther Today 6: 66–67, 2003.

11. Cleary, MA, Ruiz, D, Eberman, LE, Binkley, HM, and Mitchell, ID. Dehydration, cramping, and exertional rhabdomyolysis: A case report with suggestions for recovery. J Sport Rehab 16: 244–259, 2007.

12. Cleary, MA, Sitler, MR, and Kendrick, ZV. Dehydration does not affect symptoms of delayed onset muscle soreness in normothermic males. J Athl Train 41: 36–45, 2006.

13. Cleary, MA, Sweeney, LA, Sitler, MR, and Kendrick, ZV. Dehydration and symptoms of delayed onset muscle soreness in hyperthermic males. J Athl Train 40: 288–297, 2005.

14. Eichner, ER. Sickle cell trait. J Sport Rehab 16: 197–203, 2007.

15. Farquhar, B and Kenney, LW. Anti-inflammatory drugs, kidney function, and exercise. Sports Sci Exch II: 1–5, 1997.

16. Gardner, JW and Kark, JA. Fatal rhabdomyolysis presenting as mild heat illness in military training. Mil Med 159: 160–163, 1994.

17. Giannoglou, GD, Chatzizisis, YS, and Misirli, G. The syndrome of rhabdomyolysis: Pathophysiology and diagnosis. Eur J Intern Med 18: 90–100, 2007.

18. Gonzalez-Alonso, J, Jose, AL, Nielsen, C, and Nielsen, B. Muscle blood flow is reduced with dehydration during prolonged exercise in humans. J Physiol 513: 895–905, 1998.

19. Harriston, S. A review of rhabdomyolysis. Dimens Crit Care Nurs 23: 155–161, 2004.

20. Huerta-Alardín, AL, Varon, J, and Marik, PE. Bench-to-bedside review: Rhabdomyolysis—An overview for clinicians. Crit Care 9: 158–169.

21. Johnson M. Football players at McMinnville H. S. rushed to hospital. KATU News. Available at: http://www.katu.com/news/101125979.html. Accessed October 30, 2010.

22. Khan, FY. Rhabdomyolysis: A review of the literature. Neth J Med 67: 272–283, 2009.

23. Knochel, JP. Rhabdomyolysis and myoglobinuria. Ann Rev Med 33: 435–443, 1982.

24. Lin, CM, Wang, TL, and Leu, JG. Rhabdomyolysis in 119 students after repetitive exercise. Br J Sports Med 39: 1, 2005.

25. Moeckel-Cole, SA and Clarkson, PM. Rhabdomyolysis in a collegiate football player. J Strength Cond Res 23: 1055–1059, 2009.

26. Morgan, DL and Proske, U. Sarcomere popping requires stretch over a range where total tension decreases with length. J Physiol 15; 574: 627–628, 2006.

27. O'Connor, FG, Brennan, FH Jr, Campbell, W, Heled,Y, and Deuster, P. Return to physical activity after exertional rhabdomyolysis. Curr Sports Med Rep 7: 328–331, 2008.

28. Rosenthal, MA and Parker, DJ. Collapse of a young athlete. Ann Emerg Med 21: 1493–1498, 1992.

29. Rupert, SA. Pathogenesis and treatment of Rhabdomyolysis. Clin Case Study 14: 82–87, 2002.

30. Russell, T. Acute renal failure related to rhabdomyolysis: Pathophysiology, diagnosis, and collaborative management. Nephr Nurs J 32: 409–419.

31. Sayers, SP and Clarkson, PM. Exercise-induced rhabdomyolysis. Curr Sports Med Rep 1: 59–60, 2002.

32. Sinert, R, Kohl, L, Rainone, T, and Scalea, T. Exercise-induced rhabdomyolysis. Ann Emerg Med 23: 1301–1306, 1994.

33. Springer, BL and Clarkson, PM. Two cases of exertional rhabdomyolysis precipitated by personal trainers. Med Sci Sports Exerc 35: 1499–1502, 2003.

34. Vanholder, R, Sever, MS, Erek, E, and Lameire, N. Rhabdomyolysis. J Am Soc Nephrol11: 1553–1561, 2000.

35. Warren, JD, Blumbergs, PC, and Thompson, PD. Rhabdomyolysis: A review. Muscle Nerve 25: 332–347, 2002.

Keywords:

creatine kinase; dehydration; myalgia

© 2011 National Strength and Conditioning Association

 

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