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Exertional Rhabdomyolysis: Physiological Response Or Manifestation of an Underlying Myopathy?

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Exertional Rhabdomyolysis: Physiological Response Or Manifestation of an Underlying Myopathy? Open Access Review BMJ Open Sport Exerc Med: first published as 10.1136/bmjsem-2016-000151 on 7 September 2016. Downloaded from Exertional rhabdomyolysis: physiological response or manifestation of an underlying myopathy? Renata S Scalco,1 Marc Snoeck,2 Ros Quinlivan,1 Susan Treves,3,4 Pascal Laforét,5 Heinz Jungbluth,6,7,8 Nicol C Voermans9 To cite: Scalco RS, ABSTRACT What are the new findings Snoeck M, Quinlivan R, et al. Exertional rhabdomyolysis is characterised by muscle Exertional rhabdomyolysis: breakdown associated with strenuous exercise or ▪ physiological response or Exertional rhabdomyolysis (ERM) may be the normal exercise under extreme circumstances. Key manifestation of an first manifestation of a genetic muscle disease underlying myopathy? features are severe muscle pain and sudden transient that lowers the exercise threshold for developing BMJ Open Sport Exerc Med elevation of serum creatine kinase (CK) levels with or muscle breakdown. 2016;2:e000151. without associated myoglobinuria. Mild cases may ▪ Consider a genetic cause of the ERM in case of doi:10.1136/bmjsem-2016- remain unnoticed or undiagnosed. Exertional recurrent episodes; high creatine kinase (CK) 000151 rhabdomyolysis is well described among athletes and levels (>50×upper limit of normal) or persisting military personnel, but may occur in anybody exposed hyperCKaemia; absence of unaccustomed exer- ▸ Prepublication history for to unaccustomed exercise. In contrast, exertional cise; absence of (recreational or medical) drugs; this paper is available online. rhabdomyolysis may be the first manifestation of a or a positive family history of rhabdomyolysis or To view these files please genetic muscle disease that lowers the exercise other exertional symptoms. Protected by copyright. visit the journal online threshold for developing muscle breakdown. Repeated ▪ Type 1 ryanodine receptor (RYR1) mutations (http://dx.doi.org/10.1136/ episodes of exertional rhabdomyolysis should raise the have been recently recognised to account for a bmjsem-2016-000151). suspicion of such an underlying disorder, in particular substantial proportion of patients presenting with in individuals in whom the severity of the ERM. rhabdomyolysis episodes exceeds the expected ▪ Participants with a genetic predisposition to HJ and NCV shared senior response to the exercise performed. The present review ERM need specific guidance when they recom- authorship. aims to provide a practical guideline for the acute mence exercise and sporting activities. management and postepisode counselling of patients with exertional rhabdomyolysis, with a particular Accepted 1 August 2016 emphasis on when to suspect an underlying genetic variety of physicians, in particular to general disorder. The pathophysiology and its clinical features practitioners and physicians working in are reviewed, emphasising four main stepwise sports medicine, emergency and internal approaches: (1) the clinical significance of an acute episode, (2) risks of renal impairment, (3) clinical medicine, neurology and the neuromuscular fi http://bmjopensem.bmj.com/ indicators of an underlying genetic disorders and (4) eld, and for the military. As a result of the when and how to recommence sport activity following diversity of medical personnel having to deal an acute episode of rhabdomyolysis. Genetic with ERM, most physicians will have experi- backgrounds that appear to be associated with both ence with some but not necessarily all enhanced athletic performance and increased aspects of this important condition. rhabdomyolysis risk are briefly reviewed. ERM results in the entry of skeletal muscle contents, in particular CK and myoglobin, into the systemic circulation. In most cases, INTRODUCTION the condition has a mild course charac- Exertional rhabdomyolysis (ERM) is the terised by postexertional myalgia with general term for muscle breakdown asso- mild-to-moderate CK increases, mild pigmen- on September 29, 2021 by guest. ciated with strenuous exercise and is well turia, and will often not even come to described among athletes and military per- medical attention. However, in a minority of sonnel. Although there is no universally patients the clinical course can be severe, fi fi For numbered affiliations see accepted de nition, ERM is often de ned as resulting in marked hyperCKaemia, compart- end of article. a clinical syndrome associated with severe ment syndrome, acute renal injury, dissemi- muscle pain, sudden elevation (and subse- nated intravascular coagulation, cardiac Correspondence to quent fall) of serum creatine kinase (CK) arrhythmias secondary to electrolyte imbal- Dr Renata Scalco; r.scalco@ levels with or without myoglobinuria. ances, and even cardiac arrest if left ucl.ac.uk Individuals experiencing ERM present to a untreated. The annual rhabdomyolysis Scalco RS, et al. BMJ Open Sport Exerc Med 2016;2:e000151. doi:10.1136/bmjsem-2016-000151 1 Open Access BMJ Open Sport Exerc Med: first published as 10.1136/bmjsem-2016-000151 on 7 September 2016. Downloaded from prevalence has been reported as 26 000 cases in the disorders on when and how to recommence exercise USA, with 47% meeting the diagnostic criteria of ERM.1 and sporting activities. In other studies, a lower percentage of ERM has been We will first discuss the pathophysiology of ERM and suggested,2 a discrepancy which reflects differences in its typical clinical features, and provide examples of the cohorts studied. typical physiological ERM. Next, we will propose a struc- ERM most often represents a ‘physiological’ response tured approach to patients with ERM, based on the fol- to extreme physical exercise or to normal exercise under lowing four key questions: (1) is the ERM clinically extreme circumstances. In contrast, ERM might also be significant, requiring hospital admission and intravenous the first manifestation of a genetic muscle disease, which fluids administration? (2) What is the risk of developing lowers the exercise threshold for developing muscle acute renal failure (ARF)? (3) Is the ERM the (first) breakdown. A genetic cause should always be considered manifestation of a genetic disorder? And (4) when and in individuals with repeated episodes of ERM and in how to restart exercise and sporting activities? We expect those in whom the severity of rhabdomyolysis exceeds that such an approach will be of benefit for a wide the expected response to the exercise performed. range of physicians facing this severe and challenging The recognition of a patient with an underlying condition in different medical settings. genetic disorder is essential for acute management as well as (and most importantly) for counselling after- wards. First, in type 1 ryanodine receptor (RYR1)-related WHAT IS ERM? cases of ERM,3 the specific RyR1 antagonist dantrolene Background could be administered to limit further muscle break- In muscle tissue, the process of neuronal signal transduc- down and CK increases and more severe, potentially life- tion leading to muscle contraction is called excitation- threatening downstream medical complications. Patients contraction coupling (ECC). During ECC, presynaptic with RYR1-related ERM will have a higher recurrence acetylcholine release induces postsynaptic depolarisation risk and will have to be specifically advised with regard of the sarcolemma, resulting in activation of the voltage- to subsequent sporting activities. The same patients are gated L-type calcium channels (also known as dihydro- also at increased risk of malignant hyperthermia suscep- pyridine receptors (DHPRs)). Unlike in cardiac muscle, Protected by copyright. tibility (MHS), a pharmacogenetic response to volatile it is not this calcium influx itself but rather the direct anaesthetics and/or the depolarising muscle relaxant interaction between DHPRs and RyR1s that causes the succinylcholine, with important consequences for opening of RyR1 Ca2+ channels, leading to a rapid affected individuals but possibly also for their relatives release of Ca2+ from the intracellular sarcoplasmic reticu- carrying the same RYR1 variants. Furthermore, certain lum (SR) stores. The increased myoplasmic Ca2+ (from genetic myopathies carrying an increased rhabdomyoly- about 10-7 to 10-5 M) induces the effective interaction sis risk may also be associated with cardiac or other sys- between thick and thin filaments by binding to troponin temic symptoms that will have to be screened for. Finally, C, and this ultimately leads to muscle contraction. After certain medications may be relatively contraindicated contraction, calcium needs to be restored. This happens and exercise advice should be individually adapted in through active transport facilitated by the Ca2+ATPase, case of an underlying genetic cause. an active process that on the molecular level takes 105 The present review therefore aims to provide a prac- times longer than does RyR1-induced calcium release 2 tical guideline for the acute management and postepi- but is compensated for by the large number of Ca http://bmjopensem.bmj.com/ sode counselling of patients with ERM. The vast majority +-ATPases on the surface of the SR membrane.10 of the relevant literature until now has focused either on Irrespective of its cause(s), the pathophysiological the physiological circumstances of ERM (particularly in events in rhabdomyolysis follow a common pathway. publications with an emphasis on sports or military Normally, ion pumps and channels in the sarcolemma medicine),45on general causes of rhabdomyolysis,6 or maintain a low intracellular
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