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Critical Care (London, England) Jun 2016Rhabdomyolysis is a clinical syndrome that comprises destruction of skeletal muscle with outflow of intracellular muscle content into the bloodstream. There is a great... (Review)
Review
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 -
Journal of Neurology Apr 2020Rhabdomyolysis (RML) is an interdisciplinary condition due to muscle cell injury followed by the release of cell components into circulation. Etiology of RML has a broad...
BACKGROUND
Rhabdomyolysis (RML) is an interdisciplinary condition due to muscle cell injury followed by the release of cell components into circulation. Etiology of RML has a broad range; a serious complication is acute kidney injury (AKI). Despite its high relevance, there is no established formal definition for RML.
OBJECTIVES
A systematic review, focusing on RML definition, providing a recommendation for clinicians.
METHOD
Systematic literature research in PubMed and Embase (1968-07/2018).
RESULTS
The database research presented 8136 articles in PubMed and 2151 in Embase. After screening, 614 papers were retained for statistical analysis. A retrospective study was the most used design (44%). A definition of RML was stated in 231 studies (37.6%), including a precise creatine kinase level (CK) cut-off most frequently (67.1%). In 53/231 (22.9%) studies the CK cut-off was > 5 × upper limit of normal (ULN), and in 64/231 (27.7%) studies > 1000 IU/L. Further components of definitions were elevated CK without specific thresholds, and clinical symptoms. Exclusion criteria referring to the definition of RML were established in 113 studies, including myocardial, renal, cerebral and neuromuscular characteristics.
CONCLUSION
At present, we recommend a clinical syndrome of acute muscle weakness, myalgia, and muscle swelling combined with a CK cut-off value of > 1000 IU/L/ or CK > 5 × ULN for the standard definition of a mild RML. Additionally measured myoglobinuria and AKI indicate a severe type of RML. Exclusion criteria as well as the chronological sequence need to be considered for a conclusive RML definition.
Topics: Acute Kidney Injury; Creatine Kinase; Humans; Muscle Weakness; Myalgia; Rhabdomyolysis; Syndrome
PubMed: 30617905
DOI: 10.1007/s00415-019-09185-4 -
Journal of Advanced Research Dec 2023Crush syndrome (CS) is a kind of traumatic and ischemic injury that seriously threatens life after prolonged compression. It is characterized by systemic inflammatory... (Review)
Review
BACKGROUND
Crush syndrome (CS) is a kind of traumatic and ischemic injury that seriously threatens life after prolonged compression. It is characterized by systemic inflammatory reaction, myoglobinuria, hyperkalemia and acute kidney injury (AKI). Especially AKI, it is the leading cause of death from CS. There are various cell death forms in AKI, among which ferroptosis is a typical form of cell death. However, the role of ferroptosis has not been fully revealed in CS-AKI.
AIM OF REVIEW
This review aimed to summarize the evidence of ferroptosis in CS-AKI and its related molecular mechanism, discuss the therapeutic significance of ferroptosis in CS-AKI, and open up new ideas for the treatment of CS-AKI.
KEY SCIENTIFIC CONCEPTS OF REVIEW
One of the main pathological manifestations of CS-AKI is renal tubular epithelial cell dysfunction and cell death, which has been attributed to massive deposition of myoglobin. Large amounts of myoglobin released from damaged muscle deposited in the renal tubules, impeding the normal renal tubules function and directly damaging the tubules with oxidative stress and elevated iron levels. Lipid peroxidation damage and iron overload are the distinguishing features of ferroptosis. Moreover, high levels of pro-inflammatory cytokines and damage-associated molecule pattern molecules (HMGB1, double-strand DNA, and macrophage extracellular trap) in renal tissue have been shown to promote ferroptosis. However, how ferroptosis occurs in CS-AKI and whether it can be a therapeutic target remains unclear. In our current work, we systematically reviewed the occurrence and underlying mechanism of ferroptosis in CS-AKI.
Topics: Humans; Acute Kidney Injury; Cell Death; Crush Syndrome; Ferroptosis; Myoglobin
PubMed: 36702249
DOI: 10.1016/j.jare.2023.01.016 -
JBI Database of Systematic Reviews and... Jun 2016Exertional rhabdomyolysis (ER) is the breakdown of skeletal muscle tissue following intense physical activity that results in impairment of the cell membrane, which... (Review)
Review
BACKGROUND
Exertional rhabdomyolysis (ER) is the breakdown of skeletal muscle tissue following intense physical activity that results in impairment of the cell membrane, which allows intracellular contents to be released into the bloodstream. Signs and symptoms include myalgia, myoglobinuria and increased creatine kinase (CK) levels. Athletes are vulnerable to this condition due to their increased level of physical activity. The severity and effects of this condition vary between individuals; however, all athletes are at risk of significant muscle damage, renal failure and perhaps death if not recognized and treated quickly. Effective methods for treatment and return to activity following this condition should be established.
OBJECTIVES
The objective of this review was to identify effective treatment methods associated with ER in athletes.
INCLUSION CRITERIA TYPES OF PARTICIPANTS
Adult and adolescent patients (15 years of age and older) in the athletic population who have been diagnosed with ER.
TYPES OF INTERVENTIONS
Fluid resuscitation/replacement or other treatment methods that aim to improve CK levels and decrease myoglobinuria and treat ER.
TYPES OF STUDIES
Due to the absence of randomized control trials, the quantitative component of the review considered descriptive studies, case series and individual case reports for inclusion.
PRIMARY OUTCOMES
CK and myoglobinuria levels.
SECONDARY OUTCOMES
length of hospital stay; length of time from diagnosis to premorbid levels of physical activity.
SEARCH STRATEGY
A comprehensive search of the following databases with no date limitation was conducted: CINAHL, PubMed, ProQuest, Embase, SPORTDiscus and Physical Education Index. Results were limited to those available in English.
METHODOLOGICAL QUALITY
Two independent reviewers evaluated the retrieved articles for methodological quality using the standardized critical appraisal instrument from the Joanna Briggs Institute Meta-Analysis of Statistics and Review Instruments.
DATA EXTRACTION
Data were extracted from the articles by two independent reviewers using the standardized Joanna Briggs Institute extraction tool.
DATA SYNTHESIS
Narrative and tabular synthesis.
RESULTS
Fourteen studies with a combined total of 53 participants were included. Aggressive intravenous (IV) fluid resuscitation was found to be the most commonly utilized treatment method for decreasing CK levels and resolving myoglobinuria. The addition of compounds within the IV fluid varied between studies.
CONCLUSION
Due to the types of included studies and variation in reported treatment methods and outcomes for ER among athletes, effectiveness of treatment could not be determined. The limited evidence available indicates that IV fluid replacement, specifically normal saline, is the most commonly reported treatment for decreasing CK levels and myoglobinuria following ER. It appears that normal saline may be combined with other compounds including sodium bicarbonate, sodium chloride or potassium chloride to achieve reduction of CK levels and myoglobinuria. Clinically, early IV fluid replacement appears to be delivered at a rate of approximately 400 ml/hour, with adjustments ranging between 200 and 1000 ml/hour, depending on severity and volume states. Hospitalization time varies, depending on severity of condition, and return to activity is widely inconsistent among the athletic population.
Topics: Adolescent; Adult; Athletes; Hospitalization; Humans; Length of Stay; Muscle, Skeletal; Rhabdomyolysis; Sports
PubMed: 27532656
DOI: 10.11124/JBISRIR-2016-001879 -
Journal of the Intensive Care Society May 2020Carnitine palmitoyltransferase 2 deficiency is an inherited metabolic disorder involving a deficiency in a mitochondrial enzyme necessary for long chain fatty acid... (Review)
Review
Carnitine palmitoyltransferase 2 deficiency is an inherited metabolic disorder involving a deficiency in a mitochondrial enzyme necessary for long chain fatty acid oxidation, and therefore decreased utilisation of fatty acids. The adult form of this condition leads to recurrent rhabdomyolysis triggered by exercise, fasting and infection. It is a very rare condition with only a few hundred reported cases worldwide. Here we present a case of severe rhabdomyolysis in the context of carnitine palmitoyltransferase 2 deficiency in which major organ involvement was avoided, and organ support was not needed. This prompted us to perform a systematic review of the existing case reports in the literature to ascertain the most frequent patterns of organ involvement and assess the outcomes that are seen in these patients. Our findings suggest that these patients most frequently develop isolated renal failure, often requiring renal replacement therapy; however, the outcomes following this are very good, supporting the early involvement of intensive care teams.
PubMed: 32489413
DOI: 10.1177/1751143719889766 -
Psychopharmacology Nov 2014The primary antipsychotic-induced creatine kinase elevation (i.e., not due to neuroleptic malignant syndrome, extrapyramidal symptoms, etc.) is a poorly studied... (Review)
Review
RATIONALE
The primary antipsychotic-induced creatine kinase elevation (i.e., not due to neuroleptic malignant syndrome, extrapyramidal symptoms, etc.) is a poorly studied condition.
OBJECTIVES
The aims of the present study were to provide an overview of published cases with antipsychotic-induced creatine kinase elevation and give recommendations for the clinical practice.
METHODS
PubMed and EMBASE were searched for eligible trials, case series, and case reports. We set a threshold at ten times the upper normal limit of the creatine kinase value in order to define an elevation as significant.
RESULTS
The prevalence of significant creatine kinase elevation ranged between 2 and 7%. We found a total of 42 eligible cases. Men were overrepresented in our sample (81%). Patients with myoglobinuria were more likely to be symptomatic (Fisher's exact test, p = 0.006), whereas neither myoglobinuria (Mann-Whitney test, p > 0.10) nor symptoms (Mann-Whitney test, p = 0.64) were related to the magnitude of the creatine kinase (CK) elevation. In the majority of the cases, the antipsychotic medication was discontinued (86%). Forced diuresis was given in 36% of the patients. Eighty-three percent of the patients had no further complications. Only one case was found with a de novo acute renal failure.
CONCLUSIONS
The discontinuation of the antipsychotic medication was a sufficient measure for the CK elevation to subside in the majority of the cases. Cases with myoglobinuria should eventually be treated more aggressively. Further recommendations for the clinical practice are presented.
Topics: Adult; Aged; Aged, 80 and over; Antipsychotic Agents; Creatine Kinase; Female; Humans; Male; Middle Aged
PubMed: 25319963
DOI: 10.1007/s00213-014-3764-2 -
The Cochrane Database of Systematic... Nov 2014Background McArdle disease (Glycogen Storage Disease type V) is caused by an absence of muscle phosphorylase leading to exercise intolerance,myoglobinuria rhabdomyolysis... (Meta-Analysis)
Meta-Analysis Review
Background McArdle disease (Glycogen Storage Disease type V) is caused by an absence of muscle phosphorylase leading to exercise intolerance,myoglobinuria rhabdomyolysis and acute renal failure. This is an update of a review first published in 2004.Objectives To review systematically the evidence from randomised controlled trials (RCTs) of pharmacological or nutritional treatments for improving exercise performance and quality of life in McArdle disease.Search methods We searched the Cochrane Neuromuscular Disease Group Specialized Register, CENTRAL, MEDLINE and EMBASE on 11 August 2014.Selection criteria We included RCTs (including cross-over studies) and quasi-RCTs. We included unblinded open trials and individual patient studies in the discussion. Interventions included any pharmacological agent or nutritional supplement. Primary outcome measures included any objective assessment of exercise endurance (for example aerobic capacity (VO2) max, walking speed, muscle force or power and fatigability). Secondary outcome measures included metabolic changes (such as reduced plasma creatine kinase and a reduction in the frequency of myoglobinuria), subjective measures (including quality of life scores and indices of disability) and serious adverse events.Data collection and analysis Three review authors checked the titles and abstracts identified by the search and reviewed the manuscripts. Two review authors independently assessed the risk of bias of relevant studies, with comments from a third author. Two authors extracted data onto a specially designed form.Main results We identified 31 studies, and 13 fulfilled the criteria for inclusion. We described trials that were not eligible for the review in the Discussion. The included studies involved a total of 85 participants, but the number in each individual trial was small; the largest treatment trial included 19 participants and the smallest study included only one participant. There was no benefit with: D-ribose,glucagon, verapamil, vitamin B6, branched chain amino acids, dantrolene sodium, and high-dose creatine. Minimal subjective benefit was found with low dose creatine and ramipril only for patients with a polymorphism known as the D/Dangiotens in converting enzyme(ACE) phenotype. A carbohydrate-rich diet resulted in better exercise performance compared with a protein-rich diet. Two studies of oral sucrose given at different times and in different amounts before exercise showed an improvement in exercise performance. Four studies reported adverse effects. Oral ribose caused diarrhoea and symptoms suggestive of hypoglycaemia including light-headedness and hunger. In one study, branched chain amino acids caused a deterioration of functional outcomes. Dantrolene was reported to cause a number of adverse effects including tiredness, somnolence, dizziness and muscle weakness. Low dose creatine (60 mg/kg/day) did not cause side-effects but high-dose creatine (150 mg/kg/day) worsened the symptoms of myalgia.Authors' conclusions Although there was low quality evidence of improvement in some parameters with creatine, oral sucrose, ramipril and a carbohydrate rich diet, none was sufficiently strong to indicate significant clinical benefit.
Topics: Creatine; Dietary Carbohydrates; Dietary Proteins; Dietary Supplements; Glycogen Storage Disease Type V; Humans; Physical Endurance; Ramipril; Randomized Controlled Trials as Topic; Sucrose
PubMed: 25391139
DOI: 10.1002/14651858.CD003458.pub5 -
The Cochrane Database of Systematic... Dec 2010McArdle disease (Glycogen Storage Disease type V) is caused by an absence of muscle phosphorylase leading to exercise intolerance, myoglobinuria rhabdomyolysis and acute... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
McArdle disease (Glycogen Storage Disease type V) is caused by an absence of muscle phosphorylase leading to exercise intolerance, myoglobinuria rhabdomyolysis and acute renal failure.
OBJECTIVES
To review systematically the evidence from randomized controlled trials of pharmacological or nutritional treatments for improving exercise performance and quality of life in McArdle disease.
SEARCH STRATEGY
We searched the Cochrane Neuromuscular Disease Group Specialised Register (17 May 2010), the Cochrane Central Register of Controlled Trials (Issue 2, 2010 in The Cochrane Library), MEDLINE (January 1966 to May 2010) and EMBASE (January 1980 to May 2010) using the search terms 'McArdle disease', 'Glycogen Storage Disease type V' and 'muscle phosphorylase deficiency'.
SELECTION CRITERIA
We included randomized controlled trials (including cross-over studies) and quasi-randomised trials. Unblinded open trials and individual patient studies were included in the discussion. Interventions included any pharmacological agent or nutritional supplement. Primary outcome measures included any objective assessment of exercise endurance (for example aerobic capacity (VO(2)) max, walking speed, muscle force or power and fatigability). Secondary outcome measures included metabolic changes (such as reduced plasma creatine kinase and a reduction in the frequency of myoglobinuria), subjective measures (including quality of life scores and indices of disability) and serious adverse events.
DATA COLLECTION AND ANALYSIS
Three review authors checked the titles and abstracts identified by the search and reviewed the manuscripts. In the first review two authors (RQ and RB) independently assessed methodological quality of relevant studies and extracted data onto a specially designed form. In this update methodological quality of data was assessed by RQ and AM with comments from BS.
MAIN RESULTS
We identified 31 studies,13 fulfilled the criteria for inclusion. Excluded trials are included in the Discussion. The largest treatment trial included 19 subjects. There was no benefit with: D-ribose, glucagon, verapamil, vitamin B(6), branched chain amino acids, dantrolene sodium, and high dose creatine. Minimal benefit was found with low dose creatine and ramipril only for patients with a polymorphism known as the D/D angiotensin converting enzyme (ACE) phenotype. A carbohydrate-rich diet resulted in better exercise performance compared with a protein-rich diet. Two studies of oral sucrose given at different times and in different amounts before exercise showed an improvement in exercise performance.
AUTHORS' CONCLUSIONS
Although there was low quality evidence of improvement in some parameters with creatine, oral sucrose, ramipril and a carbohydrate rich diet, none was sufficiently strong to indicate significant clinical benefit.
Topics: Creatine; Dietary Carbohydrates; Dietary Proteins; Dietary Supplements; Glycogen Storage Disease Type V; Humans; Randomized Controlled Trials as Topic
PubMed: 21154353
DOI: 10.1002/14651858.CD003458.pub4 -
The Cochrane Database of Systematic... Apr 2008McArdle disease (Glycogen Storage Disease type V) is caused by the absence of the glycolytic enzyme, muscle phosphorylase. People present with exercise-induced pain,... (Review)
Review
BACKGROUND
McArdle disease (Glycogen Storage Disease type V) is caused by the absence of the glycolytic enzyme, muscle phosphorylase. People present with exercise-induced pain, cramps, fatigue, and myoglobinuria, which can result in acute renal failure if it is severe.
OBJECTIVES
To systematically review the evidence from randomised controlled trials of pharmacological or nutritional treatments in improving exercise performance and quality of life in McArdle disease.
SEARCH STRATEGY
We updated the review by searching the Cochrane Neuromuscular Disease Group Trials Register (November 2007), MEDLINE (January 1966 to November 2007) and EMBASE (January 1980 to November 2007) using the search terms 'McArdle disease' and its synonym 'Glycogen Storage Disease type V'.
SELECTION CRITERIA
We included randomised controlled trials (including crossover studies) and quasi-randomised trials. Open trials and individual patient studies with no participant or observer blinding were included in the discussion. Types of interventions included any pharmacological agent or micronutrient or macronutrient supplementation. Primary outcome measures included any objective assessment of exercise endurance (for example aerobic capacity (VO(2)) max, walking speed, muscle force or power and improvement in fatiguability). Secondary outcome measures included metabolic changes (such as reduced plasma creatine kinase activity and a reduction in the frequency of myoglobinuria), subjective measures (including quality of life scores and indices of disability) and serious adverse events.
DATA COLLECTION AND ANALYSIS
Three review authors checked the titles and abstracts identified by the search and reviewed the manuscripts. Two review authors (RQ and RB) independently assessed methodological quality of the full text of potentially relevant studies and extracted data onto a specially designed form.
MAIN RESULTS
We reviewed 24 studies. Twelve trials fulfilled the criteria for inclusion, with two being first identified in this update. The 12 excluded trials are included in the discussion. The largest treatment trial included 19 cases. The other trials included fewer than 12 cases. As there were only single trials for a given intervention we were unable to undertake a meta-analysis.
AUTHORS' CONCLUSIONS
There is no evidence of significant benefit from any specific nutritional or pharmacological treatment in McArdle disease. In one small trial low dose creatine produced slight benefit but high dose creatine caused myalgia. Ingestion of oral sucrose immediately before exercise reduced perceived ratings of exertion and heart rate and improved exercise tolerance. This treatment will not influence sustained or unexpected exercise and may cause significant weight gain. A carbohydrate rich diet did benefit patients. Because of the rarity of McArdle disease, there is a need to develop international multicentre collaboration and standardised assessment protocols for future treatment trials.
Topics: Dietary Supplements; Glycogen Storage Disease Type V; Humans; Randomized Controlled Trials as Topic
PubMed: 18425888
DOI: 10.1002/14651858.CD003458.pub3 -
The Cochrane Database of Systematic... 2004McArdle's disease (Glycogen Storage Disease type V) is caused by the absence of the glycolytic enzyme, muscle phosphorylase. Patients present with exercise-induced pain,... (Review)
Review
BACKGROUND
McArdle's disease (Glycogen Storage Disease type V) is caused by the absence of the glycolytic enzyme, muscle phosphorylase. Patients present with exercise-induced pain, cramps, fatigue, myoglobinuria and acute renal failure, which can ensue if the myoglobinuria is severe.
OBJECTIVES
To systematically review the evidence from randomised controlled trials of pharmacological or nutritional treatments in improving exercise performance and quality of life in McArdle's disease.
SEARCH STRATEGY
We searched the Cochrane Neuromuscular Disease Group register (searched December 2001 and updated in December 2003), MEDLINE (January 1966 to December 2003) and EMBASE (January 1980 to December 2003) using the search term 'McArdle's disease and it's synonym 'Glycogen Storage Disease type V'.
SELECTION CRITERIA
We included randomised controlled trials (including crossover studies) and quasi-randomised trials. Open trials and individual patient studies with no patient or observer blinding were included in the discussion but not the review. Types of interventions included any pharmacological agent or micronutrient or macronutrient supplementation. Primary outcome measures included any objective assessment of exercise endurance (for example VO2 max, walking speed, muscle force/power and improvement in fatiguability). Secondary outcome measures included metabolic changes (such as reduced plasma creatine kinase activity and a reduction in the frequency of myoglobinuria); subjective measures (including quality of life scores and indices of disability); and serious adverse events.
DATA COLLECTION AND ANALYSIS
Two reviewers checked the titles and abstracts identified by the search, independently assessed methodological quality of the full text of potentially relevant studies and extracted data onto a specially designed form.
MAIN RESULTS
We reviewed 20 trials. Ten trials fulfilled the criteria for inclusion and ten trials were included in the discussion. The largest treatment trial included 19 cases, the other trials included fewer than 12 cases. As there were only single trials for a given intervention we were unable to undertake a meta-analysis.
REVIEWERS' CONCLUSIONS
It is not yet possible to recommend any specific treatment for McArdle's disease. Low dose creatine supplementation was shown to demonstrate a statistically significant benefit, albeit modest, in ischaemic exercise in a small number of patients. Ingestion of oral sucrose immediately prior to exercise reduces perceived ratings of exertion and heart rate and improves exercise tolerance. This treatment will not influence sustained or unexpected exercise and may cause significant weight gain. Because of the rarity of McArdle's disease, there is a need to develop multicentre collaboration and standardised assessment protocols for future treatment trials.
Topics: Dietary Supplements; Glycogen Storage Disease Type V; Humans; Randomized Controlled Trials as Topic
PubMed: 15266486
DOI: 10.1002/14651858.CD003458.pub2