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The Ulster Medical Journal May 2021Rhabdomyolysis (RML) is a pathological entity characterized by symptoms of myalgia, weakness and dark urine (which is often not present) resulting in respiratory failure... (Review)
Review
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 -
The Netherlands Journal of Medicine Oct 2009Rhabdomyolysis is a potentially life-threatening syndrome that can develop from a variety of causes; the classic findings of muscular aches, weakness and tea-coloured... (Review)
Review
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 -
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 -
Anaesthesia May 2021Malignant hyperthermia is defined in the International Classification of Diseases as a progressive life-threatening hyperthermic reaction occurring during general...
Malignant hyperthermia is defined in the International Classification of Diseases as a progressive life-threatening hyperthermic reaction occurring during general anaesthesia. Malignant hyperthermia has an underlying genetic basis, and genetically susceptible individuals are at risk of developing malignant hyperthermia if they are exposed to any of the potent inhalational anaesthetics or suxamethonium. It can also be described as a malignant hypermetabolic syndrome. There are no specific clinical features of malignant hyperthermia and the condition may prove fatal unless it is recognised in its early stages and treatment is promptly and aggressively implemented. The Association of Anaesthetists has previously produced crisis management guidelines intended to be displayed in all anaesthetic rooms as an aide memoire should a malignant hyperthermia reaction occur. The last iteration was produced in 2011 and since then there have been some developments requiring an update. In these guidelines we will provide background information that has been used in updating the crisis management recommendations but will also provide more detailed guidance on the clinical diagnosis of malignant hyperthermia. The scope of these guidelines is extended to include practical guidance for anaesthetists dealing with a case of suspected malignant hyperthermia once the acute reaction has been reversed. This includes information on care and monitoring during and after the event; appropriate equipment and resuscitative measures within the operating theatre and ICU; the importance of communication and teamwork; guidance on counselling of the patient and their family; and how to make a referral of the patient for confirmation of the diagnosis. We also review which patients presenting for surgery may be at increased risk of developing malignant hyperthermia under anaesthesia and what precautions should be taken during the peri-operative management of the patients.
Topics: Acidosis; Body Temperature; Calcium; Carbon Dioxide; Compartment Syndromes; Dantrolene; Disseminated Intravascular Coagulation; Heart Rate; Humans; Hyperkalemia; Malignant Hyperthermia; Muscle Relaxants, Central; Myoglobinuria; Pulmonary Ventilation; Risk Factors; Sodium Bicarbonate
PubMed: 33399225
DOI: 10.1111/anae.15317 -
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 -
Journal of the American Society of... Oct 2021Rhabdomyolysis, the destruction of skeletal muscle, is a significant cause of AKI and death in the context of natural disaster and armed conflict. Rhabdomyolysis may...
BACKGROUND
Rhabdomyolysis, the destruction of skeletal muscle, is a significant cause of AKI and death in the context of natural disaster and armed conflict. Rhabdomyolysis may also initiate CKD. Development of specific pharmacologic therapy is desirable because supportive care is nearly impossible in austere environments. Myoglobin, the principal cause of rhabdomyolysis-related AKI, undergoes megalin-mediated endocytosis in proximal tubule cells, a process that specifically injures these cells.
METHODS
To investigate whether megalin is protective in a mouse model of rhabdomyolysis-induced AKI, we used male C57BL/6 mice and mice (14-32 weeks old) with proximal tubule-specific deletion of megalin. We used a well-characterized rhabdomyolysis model, injection of 50% glycerol in normal saline preceded by water deprivation.
RESULTS
Inducible proximal tubule-specific deletion of megalin was highly protective in this mouse model of rhabdomyolysis-induced AKI. The megalin knockout mice demonstrated preserved GFR, reduced proximal tubule injury (as indicated by kidney injury molecule-1), and reduced renal apoptosis 24 hours after injury. These effects were accompanied by increased urinary myoglobin clearance. Unlike littermate controls, the megalin-deficient mice also did not develop progressive GFR decline and persistent new proteinuria. Administration of the pharmacologic megalin inhibitor cilastatin to wild-type mice recapitulated the renoprotective effects of megalin deletion. This cilastatin-mediated renoprotective effect was dependent on megalin. Cilastatin administration caused selective proteinuria and inhibition of tubular myoglobin uptake similar to that caused by megalin deletion.
CONCLUSIONS
We conclude that megalin plays a critical role in rhabdomyolysis-induced AKI, and megalin interference and inhibition ameliorate rhabdomyolysis-induced AKI. Further investigation of megalin inhibition may inform translational investigation of a novel potential therapy.
Topics: Acute Kidney Injury; Animals; Apoptosis; Blood Urea Nitrogen; Cilastatin; Disease Models, Animal; Endocytosis; Glomerular Filtration Rate; Kidney Tubules, Proximal; Low Density Lipoprotein Receptor-Related Protein-2; Male; Mice; Mice, Knockout; Myoglobin; Myoglobinuria; Protease Inhibitors; Rhabdomyolysis
PubMed: 34341182
DOI: 10.1681/ASN.2020030263