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Rhabdomyolysis Clinical Presentation

  • Author: Eyal Muscal, MD, MS; Chief Editor: Lawrence K Jung, MD  more...
Updated: Jun 22, 2015


The classic triad of rhabdomyolysis comprises the following:

  • Myalgias
  • Generalized weakness
  • Darkened urine

In practice, however, the presentation of rhabdomyolysis varies considerably. The classic triad is actually seen in only about 50% of adult patients, and it may be even less common in children.[11] Additional nonspecific symptoms include fevers, nausea, and vomiting.

In most cases, the history reflects the inciting cause (eg, alcohol use and resultant unresponsiveness, agitation and illicit drug use, use of prescribed medications, or heatstroke).[59, 53, 39, 38] In children, infection and trauma are the most common causes.[6] Caregivers in contact with the patient before hospitalization may provide useful information about how the patient was found or what he or she had been doing most recently. Obtain information about prolonged immobilization from the patient (if possible) or an informant.

In some patients, the history is nonspecific and therefore is unreliable for diagnostic purposes.

Clinicians may need to investigate metabolic causes (eg, diabetic ketoacidosis and diabetes mellitus) and other nontraumatic causes (eg, congenital defects, viral infection, anesthesia use, physical exertion, and seizure disorder). Inflammatory myopathies of recent and acute onset may manifest as rhabdomyolysis.[11]


Physical Examination

The initial physical examination findings may be nonspecific (especially in pediatric populations).[6, 11]

Patients may have muscular pain and tenderness, decreased muscle strength, soft tissue swelling, and skin changes consistent with pressure necrosis. The most commonly involved muscle groups in adults include the calves and the lower back. Back, chest, and calf pain often mimics other common conditions such as deep vein thrombosis or angina.

On the whole, focal or diffuse skeletal muscle swelling is rare. In one series, only 5% of the patients presented with muscle edema. Tense and tender muscle compartments suggest compartment syndrome; peripheral pulses that are within reference range do not rule out compartment syndrome, because loss of distal pulses is a very late sign.

Hyperthermia, hypothermia, and electrical injuries are known to cause rhabdomyolysis and can often be detected upon physical examination. Examine for any crush injuries or deformities in long bones if orthopedic injures after trauma are suspected.

The presence of rhabdomyolysis should not be discounted if the patient lacks classic history, physical examination findings, or both. If evolving rhabdomyolysis is suspected based on the clinical scenario, an appropriate laboratory evaluation should be performed to diagnose muscle damage and organ dysfunction.[1]



Electrolyte abnormalities are prominent features of rhabdomyolysis. Hyperphosphatemia, hyperkalemia, hypocalcemia (early), hypercalcemia (late) hyperuricemia, and hypoalbuminemia have been described.[4, 14]

Hyperkalemia may be a result of both muscle injury and renal insufficiency or failure. This abnormality may cause life-threatening arrhythmias and should be immediately addressed.

Hypocalcemia is another common metabolic abnormality, resulting from deposition of calcium phosphate. It may also be due to a decreased level of 1,25-dihydroxycholecalciferol in patients with renal failure. Severe hypocalcemia may lead to cardiac arrhythmias, muscular contractions, and seizures. These events may further damage affected muscles. Late findings of hypercalcemia may be related of Ca leakage from damaged muscles and poor clearance if the case is complicated by kidney injury.

Hypoalbuminemia results from proteinuria and direct leakage of protein, whereas hyperuricemia is caused by direct damage to muscle and may contribute to renal tubular damage.

Compartment syndrome may be either a complication of or the inciting cause of rhabdomyolysis. If muscle injury has occurred, measure compartment pressures; if the pressure is higher than 30 mm Hg, fasciotomy is indicated.[1]

Acute kidney injury (AKI) occurs in 17-35% of adult patients[62] and in 5-42% in 2 pediatric case series.[6] Etiologies of AKI may be related to hypovolemia, vasoconstriction, and myoglobin toxicity.

AKI and disseminated intravascular coagulation (DIC, a late complication) are the most severe complications of rhabdomyolysis, often developing 12-72 hours after initial muscle damage. AKI may account for as many as 35% of adult cases. This figure may be as low as 5% in children.[6, 59] Rhabdomyolysis may account for 7-10% of acute kidney injuries in the United States.[3, 59]

Renal failure may also develop in patients treated with optimal measures. Mechanisms of renal injury are multifactorial and may include renal vasoconstriction, intraluminal myoglobin cast formation, and heme-protein cellular toxicity. Myoglobin and hemoglobin toxic effect on the glomerulus are enhanced by aciduria and hypovolemia.

Contributor Information and Disclosures

Eyal Muscal, MD, MS Assistant Professor, Section of Pediatric Immunology, Allergy, and Rheumatology, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital

Eyal Muscal, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American College of Rheumatology

Disclosure: Nothing to disclose.


Marietta Morales DeGuzman, MD Assistant Professor, Department of Pediatrics, Baylor College of Medicine; Consulting Staff, Section of Pediatric Rheumatology, Department of Pediatrics, Texas Children's Hospital, Ben Taub General Hospital

Marietta Morales DeGuzman, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Rheumatology, Texas Pediatric Society

Disclosure: Nothing to disclose.

Chief Editor

Lawrence K Jung, MD Chief, Division of Pediatric Rheumatology, Children's National Medical Center

Lawrence K Jung, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Rheumatology, Clinical Immunology Society, New York Academy of Sciences

Disclosure: Nothing to disclose.


Sandy Craig, MD, Residency Program Director, Carolinas Medical Center; Associate Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill School of Medicine

Sandy Craig, MD is a member of the following societies; Alpha Omega Alpha and the Society for Academic Emergency Medicine.

Disclosure: Nothing to disclose.

Herbert S Diamond, MD Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Lance W Kreplick, MD, FAAEM, MMM Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC

Lance W Kreplick, MD, FAAEM, MMM, is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives

Disclosure: Nothing to disclose.

Barry L Myones, MD Associate Professor, Departments of Pediatrics and Immunology, Pediatric Rheumatology Section, Baylor College of Medicine; Director of Research, Pediatric Rheumatology Center, Texas Children's Hospital

Barry L Myones, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American College of Rheumatology, American Heart Association, American Society for Microbiology, Clinical Immunology Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Tom Scaletta, MD Chair, Department of Emergency Medicine, Edward Hospital; Past-President, American Academy of Emergency Medicine

Tom Scaletta, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Binita R Shah, MD, FAAP, Professor of Clinical Pediatrics and Emergency Medicine, SUNY Health Sciences Center at Brooklyn; Director of Pediatric Emergency Medicine, Departments of Emergency Medicine and Pediatrics, Kings County Hospital Center

Binita R Shah, MD, FAAPis a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Renee Wilson, MD, Clinical Assistant Instructor, Department of Emergency Medicine, SUNY-Downstate and Kings County Hospital

Renee Wilson, MDis a member of the following medical societies: Society for Academic Emergency Medicine

Disclosure: Nothing to disclose

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Model of helical domains in myoglobin (protein linked to kidney damage in rhabdomyolysis).
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