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Rhabdomyolysis (Rhabdo– meaning rod, myo– meaning muscle, lysis– meaning breakdown or dissolution) is a potentially lethal syndrome that follows striated muscle breakdown.

Rhabdomyolysis can follow direct or indirect muscle injury and the injured muscle cells release their intracellular contents into the circulatory system. These muscle breakdown products are ultimately filtered in the kidney, and potentially lead to acute or permanent kidney injury.1,2


Rhabdomyolysis can occur because of physical or nonphysical causes.1–6

  • Physical causes include trauma, compression, excessive physical activity, prolonged bedrest, vascular occlusion, hypoperfusion, electrical current, neuroleptic malignant syndrome, and sepsis.
  • Nonphysical causes include metabolic myopathies (e.g., Carnitine palmitoyl transferase deficiency, McArdle disease)7, medications (e.g., statins, corticosteroids)8, alcohol, illicit drugs, toxins, infections, electrolyte abnormalities, endocrine disorders, polymyositis, and dermatomyositis.


The annual prevalence of rhabdomyolysis based on the National Hospital Discharge Survey in 1995 was 26,000 cases.9

The incidence of rhabdomyolysis is not well described in literature. A study of patients treated by the Department of Neurology in one hospital in Vienna, Austria identified 248 patients with rhabdomyolysis from 2000 to 2017 with median age of 49.6 years and males as 60.5% of the cohort.10 Upon further analysis of the patients in the study, the rhabdomyolysis incidence rate was highest in myopathies (49.8/1,000 person-years, followed by epilepsy (16.4/1,000 person-years), stroke (11.9/1,000 person-years), multiple sclerosis (6.7/1,000 person-years), and polyneuropathies (4.1/1,000 person-years).10 The highest of recurrent rhabdomyolysis episodes was in patients with myopathies (20.7%).10

Per a retrospective review of patients presenting to emergency departments in the US over a 20-year period between 2000 and 2019, the incidence of exertional rhabdomyolysis was 0.66 per 100,000 population and included a 10-fold increase in the incidence of exertional rhabdomyolysis from the first decade of study to the second decade of study.11

Rhabdomyolysis is more common in adults, with a higher incidence in men than women. In a study of 2371 adults with rhabdomyolysis, the most frequently associated clinical conditions include trauma (26%), immobilization (18%), sepsis (10%), vascular surgery (8%) and cardiac surgery (6%).12 Another study of 475 adults showed the most common causes were exogenous toxins (46%) including alcohol and illicit drugs (34%) and medical drugs (11%).13 Underlying myopathy or muscle metabolic defects are seen in 10% of cases, and when present, these patients are at risk for recurrent rhabdomyolysis.7,12,14 Up to 60% of patients with rhabdomyolysis had more than one etiologic factor, while no etiology was identified in 7% of patients.12,14

Common causes in the pediatric population include infections, trauma, metabolic conditions, and muscle diseases. Viral myositis is more common between 0 and 9 years of age, and trauma is more common between 9 and 18 years of age.15

Acute kidney injury is the most common systemic complication of rhabdomyolysis. An estimated 10%-40% of patients with rhabdomyolysis develop acute kidney injury (AKI), and up to 15% of all cases of AKI can be attributed to rhabdomyolysis.16 The mortality for those who develop AKI is estimated at 7%.4–6,16


Both the physical and non-physical etiologies of rhabdomyolysis lead to adenosine triphosphate (ATP) depletion which disrupts the balance of intracellular electrolyte concentration and creates an excessive intracellular influx of sodium ions and calcium ions. The increased intracellular sodium drives water into the cell. Increased intracellular calcium activates sustained myofibrillar contraction, further depleting ATP. Elevation in calcium activates calcium-dependent proteases and phospholipases, which causes breakdown and lysis of the cellular membrane. Lysis of the cellular membrane releases intracellular muscle contents into the bloodstream and extracellular space. These intracellular contents include potassium, myoglobin, uric acid, creatine kinase, aldolase, lactate dehydrogenase, alanine aminotransferase and aspartate aminotransferase.

The combination of increased concentration of myoglobin, hypovolemia/dehydration, and aciduria will precipitate the myoglobin in the glomerular filtrate, producing pigmented casts, and cause tubular obstruction with the potential for renal failure.1–6

Specific secondary or associated conditions and complications

  • Early complications: electrolyte abnormalities, cardiac arrest and arrhythmias, compartment syndrome, hyperkalemia, hypocalcemia, elevated liver enzymes, acute renal failure, and disseminated intravascular coagulation.1–6
  • Late complications: fatigue, muscle contractures, and nerve damage related to compartment syndrome.

Essentials of Assessment


Rhabdomyolysis is a syndrome which can range from asymptomatic laboratory elevations of muscle enzymes to severe muscle injury with subsequent renal failure and death.

The classic triad of symptoms of clinical rhabdomyolysis includes muscle pain, muscle weakness and dark-colored urine due to myoglobinuria.

However, the classic triad is observed in less than 10% of patients. More than 50%> of patients do not report muscle pain or weakness. Likewise, dark or tea-colored urine is reported in only 3.6% of cases.16

Both upper and lower limbs could be affected during rhabdomyolysis for both exertional and non-exertional rhabdomyolysis.17

Specifically in pediatric rhabdomyolysis, common presenting symptoms may include muscle pain, fever and viral prodromes. 2,4,5,16

A high degree of suspicion for possible muscle injury should be kept during evaluation of a patient with typical risk factors for rhabdomyolysis such as trauma, prolonged immobilization, in the case of alcohol, cocaine, narcotic, diuretic or statin use, toxin exposure, inflammatory disorders, genetic disorders (e.g., sickle cell disease), metabolic disorders, signs or symptoms of dehydration, and history of extreme heat/cold exposure, history of recent physical exertion, or in a patient with altered mental status or in a post-ictal state.

The differential diagnoses depend on the presenting symptoms for the patient, but should include cardiac etiologies (e.g. myocardial infarction), other causes of red or brown urine, inflammatory myopathies, and local causes of pain (e.g. renal colic, deep vein thrombosis).

Physical examination

  • General manifestations include malaise, fever, tachycardia, nausea, and vomiting.
  • Musculoskeletal manifestations include myalgias, weakness, cramping, and tenderness. Muscle pain when present is typically most prominent in proximal muscles groups such as the thigh, lower back, and shoulders. Swelling may also be present, and may be of the muscles themselves, which would be nonpitting and either at onset or with rehydration, or of peripheral edema, which usually occurs with rehydration.
  • Skin changes of ischemic tissue injury or pressure necrosis are seen in less than 10% of patients but may include non-blanchable erythema of intact skin, partial or full thickness skin loss, and necrotic tissue. Further out from the acute insult, contractures may develop.5,6
  • Clinical manifestations of AKI, disseminated intravascular coagulation, and multi-organ failure may subsequently appear. A high index of suspicion is important in the initial presentation of the disease.

Functional assessment

In some patients, the history is nonspecific and unreliable for a diagnosis. Caregivers may provide additional information. With muscle weakness and pain, one needs to assess to what degree mobility and self-care and independent living skills are affected. It is important to determine the patient’s prior functional status regarding ADLs and IADLs, current residence status (e.g., home vs. apartment, stairs to enter, stairs inside the home, first floor set-up) and family/friend/caregiver support.

Laboratory studies

Studies to confirm the diagnosis or complications include the following:4,5,16

  • Creatine kinase (CK) also known as creatine phosphokinase (CPK): Normal CK enzyme levels are 45–260 U/L. Elevated CK levels are the most sensitive test for diagnosis, however there is no formally established cut-off level diagnostic of rhabdomyolysis. However, concentrations of CK greater than 5 times the upper limit or 1000U/L is often used. CK rises in rhabdomyolysis within 12 hours of the onset of muscle injury, peaks in 1–3 days, and declines 3–5 days after the cessation of muscle injury. The half-life is 1.5 days.  In terms of prognosis, patients who initially present with CK levels greater than 5000U/L on admission, AKI is likely present. However, patients who initially present with CK levels below 40,000 U/L on admission are unlikely to ultimately need hemodialysis.18
  • Urinalysis or urine/serum levels of myoglobin: Myoglobin becomes elevated early during the course of rhabdomyolysis but normalizes after 6-8 hours due to its short half-life (2-3 hours). Myoglobin turns urine into a dark red–brown color when the concentration exceeds 100 mg/dL. It can be detected by urine dipstick when it exceeds concentrations of only 0.3 mg/dL in the serum. However, urine dipstick evaluation may be negative in up to half of patients with rhabdomyolysis in part due to myoglobin’s short half-life.19
  • Urine dipstick and urine microscopy: Urine can be examined for the presence of protein, brown casts, and uric acid crystals. Cast formation and tubular obstruction from myoglobinuria and uric acid crystals can contribute to AKI.
  • Complete metabolic profile (CMP): This is important to assess for degree of dehydration, monitor renal function, correct electrolyte and acid base abnormalities, and to monitor AST and ALT for impending liver failure.
  • Complete blood count (CBC): A decrease in hemoglobin and platelets may be seen.
  • Prothrombin time (PT) and activated partial thromboplastin time (aPTT): If clinical presentation is suggestive of DIC.
  • Lactate dehydrogenase (LDH): Elevated due to release from destroyed muscle cells.” 4,5,16

Supplemental assessment tools 4,5,16

Additional tests may be necessary to monitor for possible complications.

  • Electrocardiographic (EKG) evaluation is needed in patients with hyperkalemia or hypocalcemia to determine if there are any acute changes on EKG and treated appropriately.
  • Muscle intracompartment pressure should be monitored in the affected limb after trauma and in non-traumatic patients with acute pain and paresthesia. This is especially true for patients whose CK levels do not decline as expected. A delta pressure of < 30 mmHg between diastolic blood pressure and intracompartmental pressure is considered abnormal and warrants an emergent surgical evaluation for fasciotomy. Delayed recognition of compartment syndrome may lead to severe nerve injury and/or amputation.20
  • Electromyography may help to differentiate rhabdomyolysis from polymyositis (acute denervation changes such as sharp waves and fibrillation potentials are usually not present in rhabdomyolysis, myopathic motor unit action potentials may be seen).21
  • New markers of acute kidney injury include urine/serum neutrophil gelatinase-associated lipocalin (NGAL). This polypeptide is one of the substances most rapidly released from the kidney after an ischemic or toxic event before changes in creatinine occur.5 More recent studies have recommended using elevated NGAL to risk stratify patients who are at risk of AKI and AKI requiring dialysis.22
  • Muscle biopsy and genetic testing may be helpful in the diagnosis of congenital metabolic, inflammatory, and toxic myopathies.7

Early predictions of outcomes

  • Hypovolemia and aciduria are risk factors for the development of renal failure in patients with rhabdomyolysis.6 The early administration of intravenous fluids therapy decreases the probability of renal injury. Delaying fluid replacement increases the risk of renal failure. The outcome of patients with rhabdomyolysis with renal failure is worse than rhabdomyolysis without renal compromise, as previously mentioned.
  • Abnormal coagulation times (PT, PTT, international normalized ratio) and low platelet counts are indicators for DIC and indicate a worse prognosis.2,4–6,16
  • Rhabdomyolysis and multiorgan dysfunction syndrome with renal failure and DIC have higher mortality rates and worse outcomes.

Social role and social support system

Falls in adults who are unable to get up after the fall are one preventable etiology of rhabdomyolysis. Older adults who live alone should be recommended to purchase an alert alarm system in case they fall and cannot stand up. Also, family, friends and neighbors should frequently check on the well-being of older adults living by themselves.

Professional Issues

The list of potential medications which may cause rhabdomyolysis is extensive (e.g., amitriptyline, haloperidol, thiazides, benzodiazepines, diphenhydramine, hyperlipidemic agents). Patients taking these medications who have additional risk factors for rhabdomyolysis (alcohol, immobilization, dehydration, and others noted above) will have a higher chance of potentiating the process of muscle breakdown. Prescribers should keep this in mind when prescribing these medications and encourage their patients to always stay well hydrated to reduce the risk of complications developing.4,5,16

If the patient has developed renal insufficiency, a nephrology consultation will assist to determine the need for possible temporary dialysis.

Rehabilitation Management and Treatments

Available or current treatment guidelines

The two most important goals in the treatment of rhabdomyolysis are treating the underlying cause and preventing renal failure.1,6,15,23,24 It is important to identify high-risk groups of patients and then implement preventive measures, such as promotion of fluid intake, avoidance of nonsteroidal medications, follow-up of CK levels, kidney function tests, and urine dipstick.

Patients with severe trauma will benefit from an early and adequate fluid resuscitation to prevent renal failure. However, a careful evaluation for the development of fluid overload must be implemented at the same time.

Monitoring of electrolyte abnormalities is critical and should be implemented as soon as rhabdomyolysis is suspected.

For patients who develop acute compartment syndrome requiring lower extremity fasciotomy, most patients will need surgical clearance by the surgeon for early weight bearing as tolerated and range of motion (ROM) exercises. Initial therapy may be focused more on ROM and prevention of contracture. Some patients with poor outcomes may benefit from rehabilitation if they have resulting weakness and gait abnormalities. These patients may require orthotics such as ankle foot orthoses.20

For athletes who have had exertional rhabdomyolysis, return to play is an important consideration, although there are no formal guidelines established for this. Cleary et al. suggest that return to play is safe when the athlete is asymptomatic, afebrile, their CK levels have normalized, and myoglobin is no longer present in the serum and urine. When athletes do return to sport, types of exercise that are associated with rhabdomyolysis such as eccentric exercise should be avoided initially. Additionally, a gradual or graded increase in activity is recommended. Aquatic exercise has been suggested as an optimal means of return to activity for strengthening with less muscle strain although limited evidence exists as to best exercise modality for athletes with prior rhabdomyolysis.25

Management goals at different disease stages

New onset/acute 13,23,24,26

  • Goal is for early rather than late fluid replacement with crystalloids with the goal of normovolemia. There is no clear quality evidence on whether liberal vs. conservative fluid administration prevents rhabdomyolysis-induced AKI.IVF type should be based on the clinical context (i.e., sepsis, traumatic bleeding, severe acidosis) rather than the mere presence of rhabdomyolysis, and providers should take into consideration that normal saline’s chloride content may worsen acidosis while balanced fluids may be inappropriate in hyperkalemic patients.5
  • Monitoring of CK levels and myoglobin.
  • Correction of electrolyte and acid base balance.
  • In the presence of metabolic acidosis, a bolus of acetazolamide may be helpful. Alkalinization of urine with sodium bicarbonate has been used to prevent nephrotoxic effects of myoglobinuria and hyperuricosuria. However, there have been no studies that clearly show that alkalinization helps prevent AKI.5,24
  • Muscle decompression with fasciotomies.
  • It is important to maintain adequate urine output (> 0.5 ml/kg/hr for 6-8 hours) and monitor for signs of dehydration.
  • In the presence of disseminated intravascular coagulation (DIC) and hemorrhagic complications, platelets, vitamin K, and fresh frozen plasma may be necessary.4,5


  • Continued monitoring of electrolyte and acid balance.
  • Continued monitoring of CK levels and myoglobin and renal function.
  • Administration of allopurinol will reduce the production of uric acid and acts as a free radical scavenger.
  • If renal failure or severe hyperkalemia or acidosis has been established, continuous hemodialysis or hemofiltration should be implemented.


  • Recurrent rhabdomyolysis has been described. Patient must be mindful of risks if performing strenuous activities.
  • Patients who have had fasciotomies may require skin grafting.
  • Physical therapy and occupational therapy: initially, a prevention of contractures program with range of motion exercises (active and passive) occurs, followed by aerobic training and gradual resistance training to maintain functional activity. The current best evidence supports a submaximal strengthening program to prevent a recurrent exertional rhabdomyolysis.26

Coordination of care

Appropriate and early fluid resuscitation in the field by rescue teams, continued by emergency room personnel, will assure a lower rate of complications in patients who had severe trauma, or patients with risk factors for rhabdomyolysis.23 There is the need to prevent secondary sequelae, such as contractures, and work on strengthening muscles in a gentle fashion that involves nursing, therapists, and the patient and the family when the patient is out of the hospital.

Patient & family education

Athletes, family, and coaching staff must be aware of signs and symptoms of heat exhaustion (e.g., heaving sweating, cold clammy skin, fast and weak pulse, nausea, cramps, dizziness, fainting). Adequate hydration during games or practices is needed to reduce the risk of rhabdomyolysis.

Patients and families with inherited metabolic disorders have an increased risk for rhabdomyolysis. They need counseling and careful follow-up after physical activities.27

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  • High index of suspicion in patients with risk factors.
  • Vigorous fluid resuscitation in patients with crush injuries, severe trauma, or with risk factors for rhabdomyolysis.
  • Proper hydration during games and practices.
  • Be aware of signs and symptoms of exhaustion.
  • Patients with recurrent rhabdomyolysis should undergo investigation for an underlying cause such as sickle cell trait or metabolic myopathies, although in many cases an underlying cause will not be identified.

Cutting Edge/ Emerging and Unique Concepts and Practice

Antioxidant therapy with L-carnitine, bicarbonate, or other oxygen free radical scavengers have been studied in animals as a treatment for rhabdomyolysis.13 Other antioxidants, such as vitamin E, vitamin C, lazaroids, minerals, such as zinc, manganese, and selenium, are being studied as oxygen free radical scavengers in rhabdomyolysis.6 Pentoxifylline is a xanthine derivative and has been used to improve microvascular blood flow.16

One study enrolled 50 hospitalized patients with rhabdomyolysis and found that ultrasound played an important role in early diagnosis of exercise-induced rhabdomyolysis but had limited diagnostic value in rhabdomyolysis caused by other etiologies such as trauma, infection, drugs, alcohol, and heat stroke. Changes of muscles under ultrasound indicative of rhabdomyolysis included thickening of the muscle, edge thickening of fascia and traits of edema, blurred muscle fiber structure and ground glass-like changes, and heterogenous echo.28 Another study has examined the use of MRI in rhabdomyolysis and found that multiplicity of MRI changes within a compartment may be a predictor of the development of peripheral neuropathy.29

More recently, genetic screening has been used especially in those with recurrent rhabdomyolysis of unknown etiology and recurrent exertional rhabdomyolysis.30 Mutations in genes known to cause rhabdomyolysis include CPT2, RYR1, PFKM, and others suggest a wide heterogeneity of rhabdomyolysis. Additionally epigenetic modifications of a variety of genes have also been showed to be related to exertional rhabdomyolysis. Growth in genetics, epigenetics, proteomics allows for individualized preventative medicine for those who are at constant occupational risk of developing exertional rhabdomyolysis.30

There have also been several cases of rhabdomyolysis associated with COVID-19.31–33 This is an area of developing research.

Gaps in the Evidence-Based Knowledge



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  32. Chedid NR, Udit S, Solhjou Z, Patanwala MY, Sheridan AM, Barkoudah E. COVID-19 and Rhabdomyolysis. Journal of General Internal Medicine. 2020;35(10):3087-3090. doi:10.1007/s11606-020-06039-y
  33. Gefen AM, Palumbo N, Nathan SK, Singer PS, Castellanos-Reyes LJ, Sethna CB. Pediatric COVID-19-associated rhabdomyolysis: a case report. doi:10.1007/s00467-020-04617-0/Published

Original Version of the Topic

German Ojeda Correal, MD, Jose Mena, MD. Rhabdomyolysis. 9/20/2013

Previous Revision(s) of the Topic

Dominique Vinh. MD, Daniel Sova, MD. Rhabdomyolysis. 7/18/2017

Author Disclosure

Nova Hou, MD
Nothing to Disclose

Ziva Petrin, MD
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