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Rhabdomyolysis Workup

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

Approach Considerations

Because patients may present without any obvious history or physical sign of rhabdomyolysis, clinicians must be aware of the potentially subtle presentation and keep the possibility of rhabdomyolysis in mind. In the evaluation of blunt trauma in children, it is vital to remain vigilant for signs of child abuse (nonaccidental injury). Consider rhabdomyolysis in cases of child abuse, drug-overdoses, heat-related events and pediatric orthopedic injuries.

Failure to consider this diagnosis could result in the most severe complication of rhabdomyolysis: pigment-associated renal inury. Rhabdomyolysis accounts for 5-25% of cases of acute kidney injury (AKI) in adult patients; rates in pediatric patients are unknown.


Laboratory Tests

Useful laboratory tests that should be ordered include the following:

  • Complete blood count (CBC), including hemoglobin, hematocrit, and platelets
  • Serum chemistries, including blood urea nitrogen (BUN), creatinine, glucose, calcium, potassium, phosphate, uric acid, and liver function tests (LFTs)
  • Prothrombin time (PT)
  • Activated partial thromboplastin time (aPTT) – Thromboplastin released from injured myocytes can cause disseminated intravascular coagulation (DIC)
  • Serum aldolase
  • Lactate dehydrogenase (LDH)

Hyperkalemia, an immediate threat to life in the hours immediately after injury, occurs in 10-40% of cases. Liberated potassium can cause life-threatening dysrhythmias and death. Hyperphosphatemia does not require specific therapy. Hypocalcemia occurs early in the course of rhabdomyolysis. Supplemental calcium is not recommended. Increased purine metabolism causes hyperuricemia. Specific therapy with uricosuric agents or allopurinol is not indicated.

The BUN-creatinine ratio may be decreased because of the conversion of liberated muscle creatine to creatinine. In an emergency department (ED)-based study of 97 adults with rhabdomyolysis, no patient presenting in an ED setting with an initial creatinine level of less than 1.7 mg/dL developed ARF.[63]

One series of 109 ED patients with rhabdomyolysis found that 50% had an elevated cardiac troponin I level. Of these, 58% were ultimately found (on the basis of electrocardiography [ECG] and echocardiography) to be true positives, 33% were false positives, and 9% were indeterminate.[64]

A study analyzed the specific features and mortality of patients with rhabdomyolysis and the relation between creatinine, creatinkinase and mortality. The study concluded that despite being a diagnostic marker for rhabdomyolysis, initials creatinkinase levels do not predict mortality. However, the authors added that creatinine initial levels are related to progression to acute renal injury and mortality at 30 days.[65]

Creatine kinase

The diagnosis of rhabdomyolysis can be confirmed using certain laboratory studies.[14] The most reliable and sensitive indicator of muscle injury is creatine kinase (CK). Assessing CK levels is most useful because of its ease of detection in serum and its presence in serum immediately after muscle injury.

CK levels rise within 12 hours of muscle injury, peak in 24-36 hours, and decrease at a rate of 30-40% per day.[66] The serum half-life of CK is approximately 36 hours. CK levels decline 3-5 days after resolution of muscle injury[14] ; failure of CK levels to decrease suggests ongoing muscle injury or development of a compartment syndrome. The peak CK level, especially when it is higher than 15,000 U/L, may be predictive of renal failure.[67]

Total CK elevation is a sensitive but nonspecific marker for rhabdomyolysis. CK levels 5 times the reference range suggest rhabdomyolysis, though CK levels in rhabdomyolysis are frequently as high as 100 times the reference range or even higher. Suspect early rhabdomyolysis in patients with serum CK levels in excess of 2-3 times the reference range and risk factors for rhabdomyolysis; initiate a full laboratory workup. Because the total CK may increase from the initial values, draw repeat total CK levels every 6-12 hours until a peak level is established.


Plasma myoglobin measurements are not reliable, because myoglobin has a half-life of 1-3 hours and is cleared from plasma within 6 hours. Myoglobin levels not measured at the right time may produce a false-negative result, though a positive result may help confirm the diagnosis. Urine myoglobin measurements are therefore preferable.

A urine myoglobin assay is helpful in patients with coexisting hematuria (confirmed with microscopic examination) when the presence of myoglobin is suspected. A urine dipstick test for blood that has positive findings in the absence of red blood cells (RBCS) suggests myoglobinuria. Myoglobinuria may be sporadic or resolve early in the course of rhabdomyolysis. Urine dipstick findings are positive in fewer than 50% of patients with rhabdomyolysis; thus, a normal test result does not rule out this condition.[68]


Radiography, CT, and MRI

Imaging studies generally play little role in the initial diagnosis of rhabdomyolysis. However, radiographs should be obtained when fractures are suspected. Computed tomography (CT) of the head may be necessary on a case-by-case basis when a patient with an altered sensorium is evaluated.[69] Patients with significant head trauma may require head CT. A head CT scan may also be obtained in patients with first-time seizure activity or prolonged seizures or in patients with neurologic deficits of unknown etiology.

Magnetic resonance imaging (MRI) may be useful in distinguishing various etiologies of myopathy. One study suggests that bacterial myositis, focal myositis, and idiopathic rhabdomyolysis show a characteristic gadolinium enhancement on MRI. Abscesses were found only in bacterial myositis. Polymyositis and dermatomyositis have a characteristic uniform distribution pattern with emphasis on the quadriceps muscles.

MRI is the imaging modality of choice for evaluating the distribution and extent of injury of affected muscles, especially when fasciotomy or involvement of deep compartments is considered.[70]


Other Tests

ECG should be performed early in the course of evaluation to evaluate for cardiac dysrhythmias related to hyperkalemia or hypocalcemia. ECG may reveal changes reflective of acute hyperkalemia, including peaked T waves, prolongation of the PR and QRS intervals, and loss of the P wave or the sine wave. Specific disease testing may be indicated to determine definitive causes during or after short-term management of rhabdomyolysis.

The compartment pressures should be measured in any patient with severe focal muscle tenderness and a firm muscle compartment. A fasciotomy may be needed if compartment pressures in excess of 25-30 mm Hg are sustained.[1]

Histology demonstrates necrotic muscle fibers in patients with rhabdomyolysis. A muscle biopsy may be required to demonstrate immunohistochemical features of necrosis only if underlying and often inherited muscle disease is a concern. Immunoblotting, immunofluorescence, and genetic studies may be necessary to find evidence of inflammatory conditions or dystrophinopathies.[14]

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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