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Exertional Rhabdomyolysis

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Other Names

  • Rhabdomyolysis
  • Rhabdo
  • Exertional Rhabdomyolysis (ER)

Background

  • This page refers to Rhabdomyolysis, a phenomenon of muscle necrosis and release of intracellular contents into circulation
    • Although there are many causes of rhabdomyolysis, this page focuses on exertional rhabdomyolysis (ER) seen in athletes

History

Epidemiology

  • Incidence
    • Among military personal, 29.9 per 100,000 person years[1]
  • There is an estimated 12,000 cases annually in the United States[2]

Pathophysiology

  • General
    • Muscle necrosis and release of intracellular contents following exertional activity
    • Clinical syndrome: muscle weakness, swelling, pain +/- myoglobinuria
    • Symptoms and Creatinine Kinase (CK) 5 times upper limit of normal is required for diagnosis
    • Most cases are self limited and resolve with hydration, however end organ dysfunction can occur
  • Definition of Exertional Rhabdomyolysis (ER):
    • Presence of muscle related symptoms preceded by exercise
    • Elevation of CK greater than 5x the upper limit of normal (ULN)

Etiology

  • Exertional
    • Exercise with hyperthermia
    • Exercise with Sickle Cell Trait
    • Exercise with hypokalemia
    • Hyperkinetic states (seizure, stimulant or sympathomimetic use)
  • Non-exertional
    • Trauma (crush syndrome, immobilization, compartment syndrome, electrical injuries)
    • Drugs/Tox (sedatives, alcohol, statins, colchicine, carbon monoxide poisoning, mushroom ingestion)
    • Infection (viral, bacterial, toxic shock syndrome)
    • Endocrine (hypothyroidism)
    • Inflammatory myopathies
    • Other (status asthmaticus)

Mechanism

  • General
    • Characterized by breakdown and necrosis of skeletal muscle after engaging in physical activity[3]
    • Common final pathway: increased intracellular calcium much higher than normal
    • Trauma: caused by direct injury, rupture of cell membrane
  • Exertional Rhabdo (ER)
    • Overproduction of heat, results in increased intracellular calcium via depletion of ATP
    • Loss of ATP, dysfunction of Na/K–ATPase and Ca2+ATPase pumps, increase of intracellular calcium
    • Intracellular calcium leads to activation of proteases, reaction oxygen species, culminating in cell death
    • Cell death leads to release of intracellular contents, causing pain, swelling and potentially end organ damage
    • Intracellular contents includes potassium, myoglobin, creatine kinase, and LDH
    • Release of myoglobin leads to the commonly noted "coca cola" colored urine (psuedo-hematuria)

Associated Conditions

  • Acute Compartment Syndrome
    • In one American football camp, 43 players had ER and 3 were also diagnosed with compartment syndrome[4]
  • Delayed Onset Muscle Soreness (DOMS)
    • Considered by some to be the extreme end of DOMS[5]
    • Affected individuals typically complain of pain, tenderness, weakness and swelling in the muscles utilized during the activity

Risk Factors


Differential Diagnosis


Clinical Features

  • History
    • There should be a clear history of exertion preceding symptoms
    • Symptoms tend to occur in the muscle group(s) that were overworked
    • Mild cases may be asymptomatic
    • Moderate-to-severe cases may include myalgias, stiffness, weakness, malaise
    • Severe cases can include nausea, vomiting, abdominal pain, hemodynamic instability, mental status changes
    • Fever, typically mild
    • Self reported dark colored urine
  • Physical Exam
    • Swelling or tenderness to the associated muscle grups
    • Patients urine may be dark or red colored

Evaluation

Laboratory

  • General
    • Workup will depend on degree of illness and clinical picture
  • Total CK
    • Diagnosis based on 5x the upper limit of normal (~2000)
    • Begins to rise around 2-12 hours from injury, peaks at 24-72 hours
    • Quantitative value correlates with muscle injury but not renal failure
  • Urinalysis
    • Classically myoglobinuria
    • The presence of myoglobinuria does not correlate with severity of ER[10]
    • May see hematuria without RBC (80% sensitive) (need citation)
  • Serum Myoglobin
    • Elevated
    • Levels due not accurately predict risk or degree of renal injury[11]
  • CK-MB
    • May be normal or slightly elevated
  • Metabolic Panel/ Electrolytes
    • Renal: renal failure can occur, BUN/Creatinine will increase
    • Hyperkalemia
    • Hyperphosphatemia
    • Hypocalcemia
    • Hyperuricemia
  • Consider depending on severity of illness
    • CBC
    • Uric Acid
    • Liver function Tests (intramuscular AST/ALT can rise, AST>ALT)[12]
    • Blood gas
    • DIC panel (coags, fibrinogen, dimer)

Electrocardiogram

  • Strongly consider if suspicious of electrolyte abnormalities

Classification

  • No widely accepted classification system exists
    • ER can be loosely divided into physiologic and clinically significant categories.[2]
  • Physiologic ER:
    • CK level is less than 50x the upper limit of normal (CK elevation deemed a physiologic response to the exercise)
    • Patient lacks muscle weakness/swelling
    • No noted myoglobinuria or signs of ARF
  • Clinically significant ER:
    • Muscle symptoms more than simple myalgia
    • Significant comorbidities
    • Myoglobinuria
    • CK level greater than 50x the upper limit of normal
    • Prior episodes of rhabdomyolysis
    • Concomitant heat stroke

Management

  • Mild cases (physiologic ER)
    • Often go undiagnosed
    • Can be treated on an outpatient basis with oral hydration and rest[13]
    • Recheck CK and Urinalysis at 72 hours
  • Moderate/ Severe cases
    • Athletes with CK > 5 times upper limit of normal, hospital admission should be considered
    • It is important to demonstrate CK is trending down, electrolytes are normalizing
  • Trend
    • Volume/ fluid status
    • Follow urine pH, chemistry, CK, electrolytes, LFTs
  • PO/IV Fluids
    • Mild cases can orally hydrate
    • 1-2 liters per hour of IV fluid if needed
    • Goal urinate output is 200-300 ml/HR
  • Urinary alkalinization
    • Controversial, no clear benefit in the literature
    • Consider bicarbonate
    • Contraindications (severe hypocalcemia, pH > 7.50, bicarb > 30 meq/L)
    • Discontinue when (urine pH does not rise about 6.5 at 3-4 hours, symptomatic hypocalcemia, pH > 7.50, bicarb > 30 meq/L)
  • Hemodialysis
    • Indicated if patient cant maintain appropriate volume or electrolyte balance
  • Drugs to avoid
    • Mannitol or other diuretics can worsen dehydration, oliguria

Disposition

  • Discharge if
    • Clearly exertional
    • Otherwise healthy
    • No comorbidities (heat stress, dehydration, other risk factors)
    • Downtrending CK
  • Admit if they do not meet the above criteria

Rehab and Return to Play

High- and Low-risk athletes (click to enlarge)[14]

Rehabilitation

  • No specific rehabilitation guidelines exist

Return to Play/ Work

  • General
    • There are no evidence based guidelines for return to play after ER
    • Athletes should be characterized as high risk or low risk (see table)
    • High risk athletes should under go testing
      • Consider electromyogram, genetic, muscle biopsy, exercise challenge, caffeine halothane test
    • Low risk athletes can begin a gradual return when:
      • Afebrile, symptom free, well hydrated, CK levels normal, resolution of myoglobinuria

CHAMP Guidelines

  • Phase 1[15]
    • Rest for 72 hours, encourage oral hydration
    • 8 hours of sleep nightly
    • Remain in a thermally controlled environment if the episode of ER was in relation to heat illness
    • Follow-up after 72 hours with a repeat serum CK level and UA
    • If the CK has dropped to below 5 times the upper limit of normal and the UA is negative, the athlete can progress to phase 2; if not, reassessment in 72 additional hours is warranted
    • Should the UA remain abnormal or the CK remain elevated for 2 weeks, expert consultation is recommended
  • Phase 2
    • Begin light activities, no strenuous activity
    • Physical activity at own pace/distance
    • Follow-up with a care provider in 1 week
    • If there is no return of clinical symptoms, the athlete can progress to phase 3; if not, the athlete should remain in phase 2 checking with the health care professional every week for reassessment; if muscle pain persists beyond the fourth week, consider expert evaluation to include psychiatry
  • Phase 3
    • Gradual return to regular sport/physical training
    • Follow-up with care provider as needed

Complications and Prognosis

Prognosis

  • Self limited disease in most cases
    • Recurrent cases will require workup

Complications

  • Acute Renal failure
    • Difficult to predict; neither myoglobinuria or total CK reliably predict ARF
    • Rare in exertional rhabdo without presence of dehydration or heat illness
    • Oliguria is common
  • Cardiac Dysrhythmias
  • Hyperkalemia
    • Related to kidney injury more than intra-cellular potassium release
    • Treat aggressively, may require ICU/ dialysis
  • Hypocalcemia (early)
    • Treat if symptomatic or if severe hyperkalemia (2/2 rebound hypercalcemia)
  • Hypercalcemia (recovery phase)
  • Hyperphosphatemia
    • Treat cauctiously
    • Consider phosphate binders if level >7
  • Disseminated intravascular coagulation (DIC)
    • Usually self limited
  • Compartment syndrome
  • Peripheral nerve injury
    • Usually resolves within days to weeks

See Also


References

  1. Armed Forces Health Surveillance Center. Update: exertional rhabdomyolysis, active component, U.S. Armed Forces. MSMR. 2012;19(3):17-19
  2. 2.0 2.1 Scalco R. et al. Exertional rhabdomyolysis: physiological response or manifestation of an underlying myopathy? BMJ Open Sport & Exercise Medicine. 2016; 2(1).
  3. Giannoglou G, Chatzizisis YS, Misirili G. The syndrome of rhabdomyolysis: pathophysiology and diagnosis. Eur J Intern Med. 2007;18:90-100
  4. 4.0 4.1 Oh JY, Laidler M, Fiala SC, Hedberg K. Acute exertional rhabdomyolysis and triceps compartment syndrome during a high school football camp. Sports Health. 2012;4:57-62
  5. Mougios V. Reference intervals for serum creatine kinase in athletes. Br J Sports Med. 2007;41:674-678
  6. Harmon KG, Drezner JA, Klossner D, Asif M. Sickle cell trait associated with a RR of death of 37 times in National Collegiate Athletic Association football athletes: a database with 2 million athlete-years as the denominator. Br J Sport Med. 2012;46:325-330
  7. Galvez R, Stacy J, Howley A. Exertional rhabdomyolysis in seven division-1 swimming athletes. Clin J Sports Med. 2008;18:366-368
  8. Do KD, Bellabarba C, Bhananker SM. Exertional rhabdomyolysis in a bodybuilder following overexertion: a possible link to creatine overconsumption. Clin J Sports Med. 2007;17:78-79
  9. Clarkson P. Exertional rhabdomyolysis and acute renal failure in marathon runners. Sports Med. 2007;37:361-363
  10. Schiff HB, MacSearraigh ET, Kallmeyer JC. Myoglobinuria, rhabdomyolysis and marathon running. Q J Med. 1978;47:463-472
  11. Schiff HB, MacSearraigh ET, Kallmeyer JC. Myoglobinuria, rhabdomyolysis and marathon running. Q J Med. 1978;47:463-472
  12. Mayo Clin Proc 2017;92[1]:e1; J Med Toxicol 2010;6[3]:294
  13. ’Connor FG, Campbell WW, Heled Y, et al. Clinical practice guideline for the management of exertional rhabdomyolysis in warfighters. CHAMP USU Consortium for Health and Military Performance. http://www.usuhs.mil/mem/pdf/ExertionalRhabdomyolysis.pdf Accessed February 3, 2014
  14. Tietze, David C., and James Borchers. "Exertional rhabdomyolysis in the athlete: a clinical review." Sports Health 6.4 (2014): 336-339.
  15. O’Connor FG, Brennan FH, Jr, Campbell W, Heled Y, Deuster P. Return to physical activity after exertional rhabdomyolysis. Curr Sports Med Rep. 2008;7:328-331
Created by:
John Kiel on 30 September 2022 21:47:36
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Last edited:
1 October 2022 22:11:41
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