Rhabdomyolysis

Common Name(s)

Rhabdomyolysis

Rhabdomyolysis is the breakdown of muscle and the release of muscle cell contents into the bloodstream. Rhabdomyolysis can be caused by genetic or environmental factors. Environmental factors that may cause rhabdomyolysis include crushing trauma, long surgeries, extreme temperatures, or severe muscle strain such as after a marathon or other athletic event. Other causes include severe dehydration, infection, drug use, and seizures. Genetic disorders such as those causing a reduction in muscle enzymes may also lead to rhabdomyolysis. The risk of rhabdomyolysis may be reduced by proper hydration after workout or injury.

Affected individuals may notice dark red or brown urine due to the excretion of muscle breakdown products. Other symptoms of rhabdomyolysis include vomiting, confusion, muscle aches, weakness, low blood pressure, and a rapid heart rate. In severe cases, complications such as permanent kidney damage may occur.

While some individuals may experience the symptoms described above, milder cases are often asymptomatic and later discovered on blood tests. Medications may be used to regulate urine output, and fluid may be given to restore electrolyte levels and prevent shock and kidney damage. Dialysis may be required to remove muscle breakdown products from the blood in individuals with poor kidney function. If you or your child has been diagnosed with rhabdomyolysis, talk to your doctor about the most current treatment options.

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Advocacy and Support Organizations

 

Condition Specific Organizations

Following organizations serve the condition "Rhabdomyolysis" for support, advocacy or research.

There are currently no organizations listed in Disease InfoSearch that support this condition. Create a listing.

 

 

General Support Organizations

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Scientific Literature

Articles from the PubMed Database

Research articles describe the outcome of a single study. They are the published results of original research.
The terms "Rhabdomyolysis" returned 501 free, full-text research articles on human participants. First 3 results:

Severe hypokalemic paralysis and rhabdomyolysis occurring after binge eating in a young bodybuilder: Case report.
 

Author(s): Tae Won Lee, Eunjin Bae, Kyungo Hwang, Ha Nee Chang, Hee Jung Park, Dae-Hong Jeon, Hyun Seop Cho, Se-Ho Chang, Dong Jun Park

Journal: Medicine (Baltimore). 2017 Oct;96(40):e8251.

 

Severe hypokalemia can be a potentially life-threatening disorder and is associated with variable degrees of skeletal muscle weakness.

Last Updated: 31 Dec 1969

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Febrile rhabdomyolysis of unknown origin in refugees coming from West Africa through the Mediterranean to Calabria, Italy.
 

Author(s): Alfredo Vallone, Roberto Marino, Sandro Vento

Journal: Int. J. Infect. Dis.. 2017 10;63():99-100.

 

Last Updated: 31 Dec 1969

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Dynamic changes in Bach1 expression in the kidney of rhabdomyolysis-associated acute kidney injury.
 

Author(s): Masakazu Yamaoka, Hiroko Shimizu, Toru Takahashi, Emiko Omori, Hiroshi Morimatsu

Journal:

 

Free heme, a pro-oxidant released from myoglobin, is thought to contribute to the pathogenesis of rhabdomyolysis-associated acute kidney injury (RM-AKI), because renal overexpression of heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, confers protection against ...

Last Updated: 31 Dec 1969

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Reviews from the PubMed Database

Review articles summarize what is currently known about a disease. They discuss research previously published by others.
The terms "Rhabdomyolysis" returned 48 free, full-text review articles on human participants. First 3 results:

Fatal endocarditis with methicilin-sensible Staphylococcus aureus and major complications: rhabdomyolysis, pericarditis, and intracerebral hematoma: A case report and review of the literature.
 

Author(s): Anca Meda Georgescu, Leonard Azamfirei, Krisztina Szalman, Edit Szekely

Journal: Medicine (Baltimore). 2016 Oct;95(41):e5125.

 

Over the last decades Staphylococcus aureus (SA) has become the dominant etiology of native valve infective endocarditis, with the community-acquired methicillin-sensible Staphylococcus aureus (CA-MSSA) strains being the prevailing type.

Last Updated: 31 Dec 1969

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Serotonin Syndrome Induced by Combined Use of Mirtazapine and Olanzapine Complicated with Rhabdomyolysis, Acute Renal Failure, and Acute Pulmonary Edema-A Case Report.
 

Author(s): Chi-Shun Wu, Show-Hwa Tong, Cheung-Ter Ong, Sheng-Feng Sung

Journal: Acta Neurol Taiwan. 2015 Dec;24(4):117-21.

 

Serotonin syndrome is a potentially life-threatening complication of serotonergic agents. Although mirtazapine is a relatively safe antidepressant and has a comparatively low incidence of side effects, it still could induce serotonin syndrome.

Last Updated: 31 Dec 1969

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Beyond muscle destruction: a systematic review of rhabdomyolysis for clinical practice.
 

Author(s): Luis O Chavez, Monica Leon, Sharon Einav, Joseph Varon

Journal:

 

Rhabdomyolysis is a clinical syndrome that comprises destruction of skeletal muscle with outflow of intracellular muscle content into the bloodstream. There is a great heterogeneity in the literature regarding definition, epidemiology, and treatment. The aim of this systematic literature ...

Last Updated: 31 Dec 1969

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Clinical Trial Information This information is provided by ClinicalTrials.gov

Evaluate the Muscle Protection Effect of Sevoflurane Sedation in Vascular Surgery
 

Status: Recruiting

Condition Summary: Vascular Surgery

 

Last Updated: 10 Jul 2017

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Fatty Acid Oxidation Defects and Insulin Sensitivity
 

Status: Recruiting

Condition Summary: Very Long-chain Acyl-CoA Dehydrogenase Deficiency; Trifunctional Protein Deficiency; Long-chain 3-hydroxyacyl-CoA Dehydrogenase Deficiency; Medium-chain Acyl-CoA Dehydrogenase Deficiency; Normal Volunteers

 

Last Updated: 26 Sep 2016

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Fat and Sugar Metabolism During Exercise in Patients With Metabolic Myopathy
 

Status: Recruiting

Condition Summary: Metabolism, Inborn Errors; Lipid Metabolism, Inborn Errors; Carbohydrate Metabolism, Inborn Errors; Long-Chain 3-Hydroxyacyl-CoA Dehydrogenase Deficiency; Glycogenin-1 Deficiency (Glycogen Storage Disease Type XV); Carnitine Palmitoyl Transferase 2 Deficiency; VLCAD Deficiency; Medium-chain Acyl-CoA Dehydrogenase Deficiency; Multiple Acyl-CoA Dehydrogenase Deficiency; Carnitine Transporter Deficiency; Neutral Lipid Storage Disease; Glycogen Storage Disease Type II; Glycogen Storage Disease Type III; Glycogen Storage Disease Type IV; Glycogen Storage Disease Type V; Muscle Phosphofructokinase Deficiency; Phosphoglucomutase 1 Deficiency; Phosphoglycerate Mutase Deficiency; Phosphoglycerate Kinase Deficiency; Phosphorylase Kinase Deficiency; Beta Enolase Deficiency; Lactate Dehydrogenase Deficiency; Glycogen Synthase Deficiency

 

Last Updated: 31 Aug 2017

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