Review

Authors: F Y Khan

Rhabdomyolysis is a potentially life-threatening syndrome that can develop from a variety of causes; the classic findings of muscular aches, weakness and tea-coloured urine are non-specific and may not always be present. The diagnosis therefore rests upon the presence of a high level of suspicion of any abnormal laboratory values in the mind of the treating physician. An elevated plasma creatine kinase (CK) level is the most sensitive laboratory finding pertaining to muscle injury; whereas hyperkalaemia, acute renal failure and compartment syndrome represent the major life-threatening complications. The management of the condition includes prompt and aggressive fluid resuscitation, elimination of the causative agents and treatment and prevention of any complications that may ensue. The objective of this review is to describe the aetiological spectrum and pathophysiology of rhabdomyolysis, the clinical and biological consequences of this syndrome and to provide an appraisal of the current data available in order to facilitate the prevention, early diagnosis and prompt management of this condition.

Topics: Acute Kidney Injury; Arrhythmias, Cardiac; Compartment Syndromes; Creatine Kinase; Disseminated Intravascular Coagulation; Humans; Hypovolemia; Muscle Weakness; Muscles; Myoglobin; Myoglobinuria; Prognosis; Rhabdomyolysis; Risk Factors; Syndrome

PubMed: 19841484
DOI: No ID Found

Review

Authors: Ankur Gupta, Peter Thorson, Krishnam R Penmatsa...

Rhabdomyolysis (RML) is a pathological entity characterized by symptoms of myalgia, weakness and dark urine (which is often not present) resulting in respiratory failure and altered mental status. Laboratory testing for myoglobinuria is pathognomonic but so often not present during the time of testing that serum creatine kinase should always be sent when the diagnosis is suspected. Kidney injury from RML progresses through multiform pathways resulting in acute tubular necrosis. Early treatment (ideally<6 hoursfrom onset) is needed with volume expansion of all non-overloaded patients along with avoidance of nephrotoxins. There is insufficient data to recommend any specific fluid. The mortality rate ranges from 10% to up to 50% with severe AKI, so high index of suspicion and screening should be in care plan of seriously ill patients at risk for RML.

Topics: Acute Kidney Injury; Creatine Kinase; Humans; Mental Disorders; Myoglobinuria; Rhabdomyolysis

PubMed: 34276082
DOI: No ID Found

Review

Authors: Michał Tomaszewski, Karolina M Stępień, Joanna Tomaszewska...

Statins are considered to be safe, well tolerated and the most efficient drugs for the treatment of hypercholesterolemia, one of the main risk factor for atherosclerosis, and therefore they are frequently prescribed medications. The most severe adverse effect of statins is myotoxicity, in the form of myopathy, myalgia, myositis or rhabdomyolysis. Clinical trials commonly define statin toxicity as myalgia or muscle weakness with creatine kinase (CK) levels greater than 10 times the normal upper limit. Rhabdomyolysis is the most severe adverse effect of statins, which may result in acute renal failure, disseminated intravascular coagulation and death. The exact pathophysiology of statin-induced myopathy is not fully known. Multiple pathophysiological mechanisms may contribute to statin myotoxicity. This review focuses on a number of them. The prevention of statin-related myopathy involves using the lowest statin dose required to achieve therapeutic goals and avoiding polytherapy with drugs known to increase systemic exposure and myopathy risk. Currently, the only effective treatment of statin-induced myopathy is the discontinuation of statin use in patients affected by muscle aches, pains and elevated CK levels.

Topics: Animals; Creatine Kinase; Dose-Response Relationship, Drug; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Muscular Diseases; Myositis; Rhabdomyolysis

PubMed: 22001973
DOI: 10.1016/s1734-1140(11)70601-6

Authors: Jessica R Nance, Andrew L Mammen

Rhabdomyolysis is characterized by severe acute muscle injury resulting in muscle pain, weakness, and/or swelling with release of myofiber contents into the bloodstream. Symptoms develop over hours to days after an inciting factor and may be associated with dark pigmentation of the urine. Serum creatine kinase and urine myoglobin levels are markedly elevated. Clinical examination, history, laboratory studies, muscle biopsy, and genetic testing are useful tools for diagnosis of rhabdomyolysis, and they can help differentiate acquired from inherited causes of rhabdomyolysis. Acquired causes include substance abuse, medication or toxic exposures, electrolyte abnormalities, endocrine disturbances, and autoimmune myopathies. Inherited predisposition to rhabdomyolysis can occur with disorders of glycogen metabolism, fatty acid β-oxidation, and mitochondrial oxidative phosphorylation. Less common inherited causes of rhabdomyolysis include structural myopathies, channelopathies, and sickle-cell disease. This review focuses on the differentiation of acquired and inherited causes of rhabdomyolysis and proposes a practical diagnostic algorithm. Muscle Nerve 51: 793-810, 2015.

Topics: Humans; Lactic Acid; Muscles; Rhabdomyolysis

PubMed: 25678154
DOI: 10.1002/mus.24606

Review

Authors: Luis O Chavez, Monica Leon, Sharon Einav...

BACKGROUND

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 review was to summarize the current state of knowledge regarding the epidemiologic data, definition, and management of rhabdomyolysis.

METHODS

A systematic search was conducted using the keywords "rhabdomyolysis" and "crush syndrome" covering all articles from January 2006 to December 2015 in three databases (MEDLINE, SCOPUS, and ScienceDirect). The search was divided into two steps: first, all articles that included data regarding definition, pathophysiology, and diagnosis were identified, excluding only case reports; then articles of original research with humans that reported epidemiological data (e.g., risk factors, common etiologies, and mortality) or treatment of rhabdomyolysis were identified. Information was summarized and organized based on these topics.

RESULTS

The search generated 5632 articles. After screening titles and abstracts, 164 articles were retrieved and read: 56 articles met the final inclusion criteria; 23 were reviews (narrative or systematic); 16 were original articles containing epidemiological data; and six contained treatment specifications for patients with rhabdomyolysis.

CONCLUSION

Most studies defined rhabdomyolysis based on creatine kinase values five times above the upper limit of normal. Etiologies differ among the adult and pediatric populations and no randomized controlled trials have been done to compare intravenous fluid therapy alone versus intravenous fluid therapy with bicarbonate and/or mannitol.

Topics: Acute Kidney Injury; Crush Injuries; Fluid Therapy; Humans; Ischemia; Muscle, Skeletal; Muscular Diseases; Physical Exertion; Rhabdomyolysis; Risk Factors

PubMed: 27301374
DOI: 10.1186/s13054-016-1314-5

Authors: Jean-Louis Montastruc

Rhabdomyolysis is a serious adverse drug reaction of statins. There are few studies comparing the risk of rhabdomyolysis between the different statins. Using the WHO pharmacovigilance database, VigiBase®, we compared the risk of rhabdomyolysis reporting of seven statins (atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin and simvastatin, with cerivastatin excluded). All reports of rhabdomyolysis in VigiBase® in adults with statins until 31 December 2022 were included. Results are expressed as reporting odds ratio (ROR, 95% CI). Among 10 657 reports with rhabdomyolysis with statins, simvastatin was the highest risk statin in comparison with others: ROR = 2.20 (2.11-2.29). The risk was higher in men, older than 74 years and in cases of drug interactions.

Topics: Male; Adult; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Pharmacovigilance; Simvastatin; Atorvastatin; Rhabdomyolysis

PubMed: 37186323
DOI: 10.1111/bcp.15757

Review

Authors: Tiffany Hoang, Regina A E Dowdy

Muscular dystrophy encompasses a group of genetic conditions with progressive muscle damage and weakness. Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are X-linked recessive disorders that affect the production of the protein dystrophin. Emery-Dreifuss muscular dystrophy (EDMD) is typically an X-linked-recessive disorder involving the gene that codes for emerin. Facioscapulohumeral muscular dystrophy and oculopharyngeal muscular dystrophy (OPMD) are both autosomal dominant disorders. Although commonly mistaken as a condition in which patients are susceptible to malignant hyperthermia with volatile inhalational anesthetics, muscular dystrophy is more closely associated with rhabdomyolysis. Providers developing an anesthetic plan for dental patients with muscular dystrophy must take into consideration the patient's baseline cardiac and pulmonary function as well as the potential for abnormalities. Nondepolarizing neuromuscular blocker use is safe but likely to result in prolonged skeletal muscle relaxation. Succinylcholine and volatile anesthetics are generally contraindicated due to the risks of rhabdomyolysis and hyperkalemia with subsequent ventricular fibrillation, cardiac arrest, and death if left untreated. In-depth understanding of the more commonly encountered forms of muscular dystrophy is vital to providing safe and effective ambulatory anesthesia care for patients undergoing dental treatment outside the traditional hospital operating room setting.

Topics: Humans; Muscular Dystrophies; Anesthesia, Dental; Muscular Dystrophy, Duchenne; Rhabdomyolysis; Dental Care for Chronically Ill

PubMed: 39503119
DOI: 10.2344/673191

Review

Authors: Nadezda Petejova, Arnost Martinek

Rhabdomyolysis, a clinical syndrome caused by damage to skeletal muscle and release of its breakdown products into the circulation, can be followed by acute kidney injury (AKI) as a severe complication. The belief that the AKI is triggered by myoglobin as the toxin responsible appears to be oversimplified. Better knowledge of the pathophysiology of rhabdomyolysis and following AKI could widen treatment options, leading to preservation of the kidney: the decision to initiate renal replacement therapy in clinical practice should not be made on the basis of the myoglobin or creatine phosphokinase serum concentrations.

Topics: Acute Kidney Injury; Humans; Renal Replacement Therapy; Rhabdomyolysis

PubMed: 25043142
DOI: 10.1186/cc13897

Review

Authors: Ana L Huerta-Alardín, Joseph Varon, Paul E Marik...

Rhabdomyolysis ranges from an asymptomatic illness with elevation in the creatine kinase level to a life-threatening condition associated with extreme elevations in creatine kinase, electrolyte imbalances, acute renal failure and disseminated intravascular coagulation. Muscular trauma is the most common cause of rhabdomyolysis. Less common causes include muscle enzyme deficiencies, electrolyte abnormalities, infectious causes, drugs, toxins and endocrinopathies. Weakness, myalgia and tea-colored urine are the main clinical manifestations. The most sensitive laboratory finding of muscle injury is an elevated plasma creatine kinase level. The management of patients with rhabdomyolysis includes early vigorous hydration.

Topics: Acute Kidney Injury; Antioxidants; Creatine Kinase; Crush Syndrome; Disseminated Intravascular Coagulation; Diuresis; Fluid Therapy; Free Radical Scavengers; Humans; Myoglobinuria; Renal Dialysis; Retrospective Studies; Rhabdomyolysis; Risk Factors

PubMed: 15774072
DOI: 10.1186/cc2978

Authors: Yan Lu, Javier A Neyra

Topics: Humans; Rhabdomyolysis; Acute Kidney Injury

PubMed: 37934632
DOI: 10.2215/CJN.0000000000000372