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Medicine Nov 2005Rhabdomyolysis is a common and potentially lethal clinical syndrome that results from acute muscle fiber necrosis with leakage of muscle constituents into blood....
Rhabdomyolysis is a common and potentially lethal clinical syndrome that results from acute muscle fiber necrosis with leakage of muscle constituents into blood. Myoglobinuria is the most significant consequence, leading to acute renal failure (ARF) in 15%-33% of patients with rhabdomyolysis. Rhabdomyolysis occurs from inherited diseases, toxins, muscle compression or overexertion, or inflammatory processes, among other disorders. In some cases, no cause is found. We describe 475 patients from the Johns Hopkins Hospital inpatient records between January 1993 and December 2001 for the following discharge diagnosis codes: myoglobinuria, rhabdomyolysis, myopathy, toxic myopathy, malignant hyperthermia, neuroleptic malignant syndrome, and polymyositis. Of 1362 patients, 475 patients with an acute neuromuscular illness with serum creatine kinase (CK) more than 5 times the upper limit of normal (>975 IU/L) were included. Patients with recent myocardial infarction or stroke were excluded. The etiology was assigned by chart review. For all, the highest values of serum CK, serum creatinine and urine myoglobin, hemoglobin, and red blood cells were recorded. Forty-one patients had muscle biopsy within at least 2 months from the onset of rhabdomyolysis.Of the 475 patients, 151 were female and 324 were male (median age, 47 yr; range, 4-95 yr). Exogenous toxins were the most common cause of rhabdomyolysis, with illicit drugs, alcohol, and prescribed drugs responsible for 46%. Among the medical drugs, antipsychotics, statins, zidovudine, colchicine, selective serotonin reuptake inhibitors, and lithium were the most frequently involved. In 60% of all cases, multiple factors were present. In 11% of all cases, rhabdomyolysis was recurrent. Underlying myopathy or muscle metabolic defects were responsible for 10% of cases, in which there was a high percentage of recurrence, only 1 etiologic factor, and a low incidence of ARF. In 7%, no cause was found. ARF was present in 218 (46%) patients, and 16 died (3.4%). A linear correlation was found between CK and creatinine and between multiple factors and ARF, but there was no correlation between ARF and death or between multiple factors and death. Urine myoglobin detected by dipstick/ultrafiltration was positive in only 19%. Toxins are the most frequent cause of rhabdomyolysis, but in most cases more than 1 etiologic factor was present. Patients using illicit drugs or on prescribed polytherapy are at risk for rhabdomyolysis. The absence of urine myoglobin, by qualitative assay, does not exclude rhabdomyolysis. With appropriate care, death is rare.
Topics: Acute Disease; Adolescent; Adult; Aged; Aged, 80 and over; Alcoholism; Baltimore; Child; Child, Preschool; Drug Interactions; Female; Hospitalization; Humans; Illicit Drugs; Incidence; Male; Middle Aged; Muscle Fibers, Skeletal; Myoglobin; Necrosis; Polypharmacy; Rhabdomyolysis; Risk Assessment; Risk Factors
PubMed: 16267412
DOI: 10.1097/01.md.0000188565.48918.41 -
Critical Care (London, England) Apr 2005Rhabdomyolysis ranges from an asymptomatic illness with elevation in the creatine kinase level to a life-threatening condition associated with extreme elevations in... (Review)
Review
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 -
Tidsskrift For Den Norske Laegeforening... Jun 2019The soreness that commonly follows unaccustomed and strenuous exercise is unlikely to be due to inflammation of the muscles. However, the rarer and more serious... (Review)
Review
The soreness that commonly follows unaccustomed and strenuous exercise is unlikely to be due to inflammation of the muscles. However, the rarer and more serious exercise-induced rhabdomyolysis appears to have a different pathogenesis, with clinical signs including tissue inflammation and muscle cell death, as well as elevated creatine kinase and myoglobinuria. Soreness and rhabdomyolysis can both be caused by the same type of muscular activity.
Topics: Exercise; Humans; Inflammation; Muscle, Skeletal; Myalgia; Rhabdomyolysis
PubMed: 31238673
DOI: 10.4045/tidsskr.18.0727 -
Methods and Findings in Experimental... 2005Rhabdomyolysis is a condition caused by skeletal muscle injury and release of muscle cell contents into the circulation. It may result in myoglobinuria, the filtration... (Review)
Review
Rhabdomyolysis is a condition caused by skeletal muscle injury and release of muscle cell contents into the circulation. It may result in myoglobinuria, the filtration of myoglobin into the urine, and is often associated with acute renal failure (ARF). Rhabdomyolysis may complicate many disease states. In some, such as crush injury, muscle injury is obvious; in others, such as drug overdose, it may never be apparent. It may occur in the setting of an altered mental status, and even in the conscious patient, it may occur with minimal symptoms or physical findings. Therefore, diagnosis requires a high level of suspicion and appropriate sensitivity to abnormal laboratory values. Many insults can precipitate rhabdomyolysis and myoglobinuria. Disruption of the muscle cell membrane may result from a direct mechanical or toxic insult to the membrane or an inability to maintain ionic gradients across the membrane (as in ischemia or extreme exertion). This article reviews the etiology, pathogenesis, clinical features, complications, and management of rhabdomyolysis, particularly crush injuries in the setting of a major disaster.
Topics: Acute Kidney Injury; Humans; Rhabdomyolysis
PubMed: 15834458
DOI: 10.1358/mf.2005.27.1.875435 -
Orphanet Journal of Rare Diseases May 2015Rhabdomyolysis (RM) is a clinical emergency characterized by fulminant skeletal muscle damage and release of intracellular muscle components into the blood stream... (Review)
Review
Rhabdomyolysis (RM) is a clinical emergency characterized by fulminant skeletal muscle damage and release of intracellular muscle components into the blood stream leading to myoglobinuria and, in severe cases, acute renal failure. Apart from trauma, a wide range of causes have been reported including drug abuse and infections. Underlying genetic disorders are also a cause of RM and can often pose a diagnostic challenge, considering their marked heterogeneity and comparative rarity.In this paper we review the range of rare genetic defects known to be associated with RM. Each gene has been reviewed for the following: clinical phenotype, typical triggers for RM and recommended diagnostic approach. The purpose of this review is to highlight the most important features associated with specific genetic defects in order to aid the diagnosis of patients presenting with hereditary causes of recurrent RM.
Topics: Genetic Predisposition to Disease; Humans; Phenotype; Rhabdomyolysis
PubMed: 25929793
DOI: 10.1186/s13023-015-0264-3 -
Indian Journal of Pathology &... May 2022Metabolic myopathies are a diverse group of genetic disorders that result in impaired energy production. They are individually rare and several have received the 'orphan... (Review)
Review
Metabolic myopathies are a diverse group of genetic disorders that result in impaired energy production. They are individually rare and several have received the 'orphan disorder' status. However, collectively they constitute a relatively common group of disorders that affect not only the skeletal muscle but also the heart, liver, and brain among others. Mitochondrial disorders, with a frequency of 1/8000 population, are the commonest cause of metabolic myopathies. Three main groups that cause metabolic myopathy are glycogen storage disorders (GSD), fatty acid oxidation defects (FAOD), and mitochondrial myopathies. Clinically, patients present with varied ages at onset and neuromuscular features. While newborns and infants typically present with hypotonia and multisystem involvement chiefly affecting the liver, heart, kidney, and brain, patients with onset later in life present with exercise intolerance with or without progressive muscle weakness and myoglobinuria. In general, GSDs result in high-intensity exercise intolerance while, FAODs, and mitochondrial myopathies predominantly manifest during endurance-type activity, fasting, or metabolically stressful conditions. Evaluation of these patients comprises a meticulous clinical examination and a battery of investigations which includes- exercise stress testing, metabolic and biochemical screening, electrophysiological studies, neuro-imaging, muscle biopsy, and molecular genetics. Accurate and early detection of metabolic myopathies allows timely counseling to prevent metabolic crises and helps in therapeutic interventions. This review summarizes the clinical features, diagnostic tests, pathological features, treatment and presents an algorithm to diagnose these three main groups of disorders.
Topics: Algorithms; Heart; Humans; Infant, Newborn; Metabolism, Inborn Errors; Mitochondrial Myopathies; Muscular Diseases
PubMed: 35562160
DOI: 10.4103/ijpm.ijpm_1088_21 -
Movement Disorders Clinical Practice Oct 2020Movement disorders often emerge from the interplay of complex pathophysiological processes involving the kidneys and the nervous system. Tremor, myoclonus, ataxia,... (Review)
Review
Movement disorders often emerge from the interplay of complex pathophysiological processes involving the kidneys and the nervous system. Tremor, myoclonus, ataxia, chorea, and parkinsonism can occur in the context of renal dysfunction (azotemia and electrolyte abnormalities) or they can be part of complications of its management (dialysis and renal transplantation). On the other hand, myoglobinuria from rhabdomyolysis in status dystonicus and certain drugs used in the management of movement disorders can cause nephrotoxicity. Distinct from these well-recognized associations, it is important to appreciate that there are several inherited and acquired disorders in which movement abnormalities do not occur as a consequence of renal dysfunction or vice versa but are manifestations of common pathophysiological processes affecting the nervous system and the kidneys. These disorders are the emphasis of this review. Increasing awareness of these conditions among neurologists may help them to identify renal involvement earlier, take timely intervention by anticipating complications and focus on therapies targeting common mechanisms in addition to symptomatic management of movement disorders. Recognition of renal impairment in a patient with complex neurological presentation may narrow down the differentials and aid in reaching a definite diagnosis.
PubMed: 33043074
DOI: 10.1002/mdc3.13005