Author(s): Nova Hou, MD, Ziva Petrin, MD
Originally published: September 20, 2013 Last updated: July 10, 2025
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Disease/Disorder

Definition

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

Rhabdomyolysis is a clinical syndrome that can follow direct or indirect muscle injury and occurs when injured muscle cells release their intracellular contents into the circulatory system. The muscle breakdown products are ultimately filtered in the kidney, and potentially lead to acute or permanent kidney injury.1,2

Etiology

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.

Epidemiology

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, stroke, multiple sclerosis, and polyneuropathies.10 The highest rates of recurrent rhabdomyolysis episodes occurred in patients with myopathies.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 people.11 However, it is likely an underestimate.

Rhabdomyolysis is more common in older adults (especially over age 60). There’s a higher incidence in men than women thought to be related to differences in muscle mass. The most frequently associated clinical conditions for rhabdomyolysis include trauma, immobilization, sepsis, vascular surgery and cardiac surgery.12 Additionally common external causes of rhabdomyolysis were exogenous toxins, including alcohol and illicit drugs and medical drugs.12 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 13-50% 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 overall mortality rate for rhabdomyolysis is 19.8%, with even higher mortality rates for those who develop sever AKI.4–6,16,19

Pathophysiology

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. With eventual reperfusion, leukocytes migrate into the damaged muscle and cause an inflammatory reaction with an increased number of cytokines, prostaglandins, and free radicals. This can cause further myolysis, necrosis of muscle fibers, and release of muscle breakdown products.

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

History/Symptoms

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, but muscle pain tends to be the most common presenting symptom of rhabdomyolysis. 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 Exertional rhabdomyolysis is also underdiagnosed, and athletes who have components of the classic triad, especially after strenuous events such as marathons or heavy weightlifting, should be screened for rhabdomyolysis.17

Specifically in pediatric rhabdomyolysis, common presenting symptoms may include fever and viral prodromes with muscle pain.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 each 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 secondarily appear. A high index of suspicion for these more severe sequalae of rhabdomyolysis is important in the initial presentation of the disease.

Functional assessment

With muscle weakness and pain, providers need 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 following4,5,16

  • 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 below 40,000 U/L on admission are unlikely to need renal replacement therapy.18 However, patients who initially present with CK levels greater than 5000U/L on admission often also have a concurrent AKI are more likely to progress to needing hemodialysis.18
  • Urinalysis or urine/serum levels of myoglobin: Myoglobin becomes elevated early during 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.5
  • 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 any impending liver failure. For electrolytes, hyperkalemia, hyperphosphatemia and calcium abnormalities are common. Hypocalcemia is often observed initially during intracellular calcium migration, followed by hypercalcemia when there is myolysis.
  • Complete blood count (CBC): A decrease in hemoglobin and platelets may be seen.
  • Prothrombin time (PT) and activated partial thromboplastin time (aPTT): Trended if clinical presentation is suggestive of DIC.
  • Lactate dehydrogenase (LDH): Elevated due to release from destroyed muscle cells.” 4,5,16

Supplemental assessment tools4,5,16

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. Wither hyperkalemia there may be peaked T waves, a prolonged PR interval, a wide QRS interval with or without conduction blocks, ventricular tachycardia, and asystole.
  • Muscle intracompartmental 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
  • Imaging is also becoming increasingly used to assess the extent of muscle and organ damage in rhabdomyolysis but is not necessary for clinical diagnosis. Magnetic resonance imaging (MRI) provides the best resolution of muscle and soft tissue injuries, and with rhabdomyolysis can help with precise assessment of both the spatial distribution and severity of muscle lesions, especially during fasciotomy considerations. There is a decreased signal on T1-weighted images and an increased signal on T2-weighted images and short-tau inversion recovery sequences.5 Computed tomography (CT) is a cheaper and faster imaging modality than MRI but is less preferred due to radiation exposure and lower resolution.
  • Electromyography may help to differentiate rhabdomyolysis from polymyositis. Acute denervation changes such as sharp waves and fibrillation potentials are usually not present in rhabdomyolysis, but 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.22 More recent studies have recommended using elevated NGAL to risk stratify patients who are at risk of AKI and AKI requiring dialysis.22
  • Patients with recurrent rhabdomyolysis or who develop it with minimal trauma or exertion should be considered for genetic testing and have a family history. Muscle biopsy and genetic testing help 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. 4-8% of patients with rhabdomyolysis ultimately need hemodialysis.19

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…etc.) 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

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.

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/acute13,23,24,26

  • Early, rather than late, intravenous fluid (IVF) replacement with crystalloids is recommended with the goal of normovolemia. There is no clear quality evidence on whether liberal or 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. Providers should take into consideration that normal saline’s chloride content and the potassium in lactated Ringer’s may worsen acidosis while balanced fluids may be inappropriate in hyperkalemic patients.5 An appropriate urine output goal for IVF resuscitation is 2–3 mL/kg/hr for most patients with rhabdomyolysis.4
  • 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. More recent systematic reviews show that there is no added benefit of adding bicarbonate to alkalinize urine and that mannitol should not be used to attempt to increase urine output due to significant risks of causing volume overload and hyperosmolarity.4 If bicarbonate is used, it should be promptly discontinued once pH reaches 7.5.4
  • 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

Subacute13,23,24,26

  • 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.

Chronic/stable13,23,24,26

  • Recurrent rhabdomyolysis has been described. Patient must be mindful of risks if performing strenuous activities. Patients with genetic myopathies can sometimes be treated with dietary changes and should have nutrition counseling.4
  • 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 caregivers 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.5,28 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.5,29

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

Rhabdomyolysis is also associated with COVID-19.31–33 In a scoping review of 117 individually reported cases of COVID-19 with rhabdomyolysis, the majority of the cases had at-least one non-COVID risk factor for developing rhabdomyolysis, and 28% of the cases resulted in death.33 This suggests that patients with COVID-19 should be monitored for developing concurrent rhabdomyolysis, and mortality is generally high. Caution should be taken when administering medications to COVID-19 patients that may increase rhabdomyolysis risk.33 This is an area of developing research.

Gaps in the Evidence-Based Knowledge

N/A

References

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  3. Torres PA, Helmstetter JA, Kaye AM, Kaye AD. Rhabdomyolysis: Pathogenesis, Diagnosis, and Treatment. The Ochsner Journal. 2015; 15(1):58–69.
  4. Sawhney, JS, Kasotakis, G, Goldenberg, A, Abramson, S, Dodgion, C, Patel, N, Khan, M, & Como, JJ. Management of rhabdomyolysis: A practice management guideline from the Eastern Association for the Surgery of Trauma. Am J Surg. 2022;224(1 Pt A),196-204. https://doi.org/10.1016/j.amjsurg.2021.11.022
  5. Yang, BF, Li, D, Liu, CL, Luo, Y, Shi, J, Guo, XQ, Fan, HJ, & Lv, Q. Advances in rhabdomyolysis: A review of pathogenesis, diagnosis, and treatment. Chin J Traumatol. 2025. https://doi.org/10.1016/j.cjtee.2024.10.005
  6. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis – An overview for clinicians. Critical Care. 2005;9(2):158-169. doi:10.1186/cc2978
  7. Quinlivan R, Jungbluth H. Myopathic causes of exercise intolerance with rhabdomyolysis. Developmental Medicine and Child Neurology. 2012;54(10):886-891. doi:10.1111/j.1469-8749.2012.04320.x
  8. Hohenegger M. Drug induced rhabdomyolysis. Current Opinion in Pharmacology. 2012;12(3):335-339. doi:10.1016/j.coph.2012.04.002
  9. Graves EJ, Gillum BS. Vital and Health Statistics From the CENTERS FOR DISEASE CONTROL AND PREVENTION / National Center for Health Statistics.; 1995.
  10. Paternostro C, Gopp L, Tomschik M, et al. Incidence and clinical spectrum of rhabdomyolysis in general neurology: a retrospective cohort study. Neuromuscular Disorders. 2021;31(12):1227-1234. doi:10.1016/j.nmd.2021.09.012
  11. Bolden BP, Isaacs DJ, Ahmed AE, Anderson SA. Epidemiology of Exertional Rhabdomyolysis in the United States: Analysis of NEISS Database 2000 to 2019. Phys Sportsmed. Published online 2021:1-8. doi:10.1080/00913847.2021.1956288
  12. Warren JD, Blumbergs PC, Thompson PD. Rhabdomyolysis: A review. Muscle and Nerve. 2002;25(3):332-347. doi:10.1002/mus.10053
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  14. Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: An evaluation of 475 hospitalized patients. Medicine. 2005;84(6):377-385. doi:10.1097/01.md.0000188565.48918.41
  15. Mannix R, Tan ML, Wright R, Baskin M. Acute pediatric rhabdomyolysis: Causes and rates of renal failure. Pediatrics. 2006;118(5):2119-2125. doi:10.1542/peds.2006-1352
  16. Torres PA, Helmstetter JA, Kaye AM, Kaye AD. Rhabdomyolysis: Pathogenesis, Diagnosis, and Treatment. 2015;
  17. Backer, HC, Richards, JT, Kienzle, A, Cunningham, J, & Braun, KF. Exertional Rhabdomyolysis in Athletes: Systematic Review and Current Perspectives. Clin J Sport Med. 2023;33(2):187-194. https://doi.org/10.1097/JSM.0000000000001082
  18. Michelsen J, Cordtz J, Liboriussen L, et al. Prevention of rhabdomyolysis-induced acute kidney injury – A DASAIM/DSIT clinical practice guideline. Acta Anaesthesiologica Scandinavica. 2019;63(5):576-586. doi:10.1111/aas.13308
  19. Yang, CW, Li, S, Dong, Y, Paliwal, N, & Wang, Y. Epidemiology and the Impact of Acute Kidney Injury on Outcomes in Patients with Rhabdomyolysis. J Clin Med. 2021;10(9). https://doi.org/10.3390/jcm10091950
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  26. Brown TP. Exertional rhabdomyolysis: early recognition is key. Phys Sportsmed. 2004;32(4):15-20. doi:10.3810/psm.2004.04.197
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  28. Xu Q, Tian M, Xia J, Zhu W, Yang L. Application of Ultrasonography in the Diagnosis of Rhabdomyolysis. Ultrasound in Medicine and Biology. 2021;47(12):3349-3355. doi:10.1016/j.ultrasmedbio.2021.08.012
  29. Kim JH, Kim YJ, Koh SH, et al. Rhabdomyolysis revisited: Detailed analysis of magnetic resonance imaging findings and their correlation with peripheral neuropathy. Medicine. 2018;97(33):e11848-e11848. doi:10.1097/MD.0000000000011848
  30. Carneiro A, Viana-Gomes D, Macedo-da-Silva J, et al. Risk factors and future directions for preventing and diagnosing exertional rhabdomyolysis. Neuromuscular Disorders. 2021;31(7):583-595. doi:10.1016/j.nmd.2021.04.007
  31. Mahmood UA, Mermis JD, Khan NM, el Atrouni W. Rhabdomyolysis With COVID-19. Infect Dis Clin Pract (Baltim Md). 2020;29(2):e129-e130. doi:10.1097/IPC.0000000000000968
  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. Preger, A., Wei, R., Berg, B., & Golomb, B. A. (2023). COVID-19-associated rhabdomyolysis: A scoping review. Int J Infect Dis, 136, 115-126. https://doi.org/10.1016/j.ijid.2023.09.002

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

Nova Hou, MD, Ziva Petrin, MD. Rhabdomyolysis. 6/16/2022

Author Disclosure

Nova Hou, MD
Nothing to Disclose

Ziva Petrin, MD
Nothing to Disclose