Effect of Stretch Exercises on Suxamethonium Induced Fasciculations and Myalgia

Magee, D. A.; Robinson, Richard

doi:10.1093/bja/59.5.596

Cited by 12 publications

(5 citation statements)

References 22 publications

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“…If it is assumed that postoperative myalgia is caused by damage to muscles after fasciculations, stretching exercises may reduce postoperative myalgia. Stretching exercises have been shown to reduce significantly the incidence of both fasciculations and postoperative muscle pains [40]. The muscle stretch receptors are progressively desensitised as the receptor potential adapts under conditions of prolonged slow stretch.…”

Section: Methods Used To Reduce Myalgiamentioning

confidence: 99%

“…With a reduction in the rate of gamma efferent discharge from the muscle spindles, the excitability of alpha motor neurones is modified. It has been suggested that this may increase the threshold for motor units, thus altering the action of succinylcholine [40, 41]. It is unfortunate that no further studies are available to substantiate the results of the original work, since stretching exercises cost nothing and are safe.…”

Section: Methods Used To Reduce Myalgiamentioning

confidence: 99%

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Succinylcholine‐associated postoperative myalgia

Wong

Chung

2000

Anaesthesia

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SummaryThe subject of postoperative myalgia associated with the use of succinylcholine is reviewed. We discuss the mechanisms of succinylcholine-induced myalgia and the techniques available to prevent and treat the myalgia. In situations where patients are at risk of developing myalgia and succinylcholine is the neuromuscular blocker of choice, the use of a combination of techniques may prove to be a useful strategy.

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Section: Methods Used To Reduce Myalgiamentioning

confidence: 99%

Section: Methods Used To Reduce Myalgiamentioning

confidence: 99%

Succinylcholine‐associated postoperative myalgia

Wong

Chung

2000

Anaesthesia

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“…pancuronium, vecuronium, pipecuronium and rocuronium) are generally free of the troublesome side effects associated with non‐steroidal neuromuscular relaxants (e.g. histamine release (Basta et al , 1983) and malignant hyperthermia (Magee et al , 1987)).…”

Section: Introductionmentioning

confidence: 99%

Interaction of neuromuscular blocking drugs with recombinant human m1–m5 muscarinic receptors expressed in Chinese hamster ovary cells

Cembala

Sherwin

Tidmarsh

et al. 1998

British J Pharmacology

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1 Neuromuscular blocking drugs (NMBD's) are known to produce cardiovascular side e ects manifesting as brady/tachycardias. In this study we have examined the interaction of a range of steroidal NMBD's with recombinant human m1 ± m5 muscarinic receptors expressed in Chinese hamster ovary cells. Our main hypothesis is that NMBD's may interact with m2 (cardiac) muscarinic receptors. 2 All binding studies were performed with cell membranes prepared from CHO m1 ± m5 cells in 1 ml volumes of 20 mM HEPES, 1 mM MgCl 2 at pH 7.4 for 1 h. Muscarinic receptors were labelled with [ 3 H]-NMS and displacement studies were performed with pancuronium, vecuronium, pipecuronium, rocuronium and gallamine. In addition a range of muscarinic receptor subtype selective reference compounds were included. In order to determine the nature of any interaction the e ects of pancuronium, rocuronium and vecuronium on methacholine inhibition of forskolin stimulated cyclic AMP formation in CHO m2 cells was examined. Cyclic AMP formation was assessed in whole cells using a radioreceptor assay. All data are mean+s.e.mean (n55). 50 ) by pirenzepine in CHO m1 membranes (7.97+0.04), methoctramine in CHO m2 membranes (8.55+0.1), 4-diphenylacetoxy-Nmethyl piperidine methiodide (4-DAMP) in CHO m3 membranes (9.38+0.03), tropicamide in CHO m4 membranes (6.98+0.01). 4-DAMP, pirenzepine, tropicamide and methoctramine displaced [ 3 H]NMS in CHO m5 membranes with pK 50 values of 9.20+0.14, 6.59+0.04, 6.89+0.05 and 7.22+0.01 respectively. These data con®rm homogenous subtype expression in CHO m1 ± m5 cells. 5 [ 3 H]NMS binding was displaced dose-dependently (pK 50 ) by pancuronium (m1, 6.43+0.12; m2, 7.68+0.02; m3, 6.53+0.06; m4, 6.56+0.03; m5, 5.79+0.10), vecuronium (m1, 6.14+0.04; m2, 6.90+0.05; m3, 6.17+0.04; m4, 7.31+0.02; m5, 6.20+0.07), pipecuronium (m1, 6.34+0.11; m2, 6.58+0.03; m3, 5.94+0.01; m4, 6.60+0.06; m5, 4.80+0.03), rocuronium (m1, 5.42+0.01; m2, 5.40+0.02; m3, 4.34+0.02; m4, 5.02+0.04; m5, 5.10+0.03) and gallamine (m1, 6.83+0.05; m2, 7.67+0.04; m3, 6.06+0.06; m4, 6.20+0.03; m5, 5.34+0.03). 6 Cyclic AMP formation was inhibited dose dependently by methacholine in CHO m2 cells pEC 50 for control and pancuronium (300 nM) treated cells were 6.18+0.34 and 3.57+0.36 respectively. Methacholine dose-response curves in the absence and presence of rocuronium (1 mM) and vecuronium (1 mM) did not di er signi®cantly. Pancuronium, vecuronium and rocuronium did not inhibit cyclic AMP formation alone indicating no agonist activity. 7 With the exception of rocuronium there was a signi®cant interaction with m2 muscarinic receptors with all NMBD's at clinically achievable concentrations suggesting that the brady/tachycardias associated with these agents may result from an interaction with cardiac muscarinic receptors. Furthermore pancuronium at clinically achievable concentrations antagonised methacholine inhibition of cyclic AMP formation in CHO m2 cells further suggesting that the tachycardia produced by this agent results from muscarinic antagonism. The mech...

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“…Pre-treatment with a small dose of a non-depolarizing neuromuscular blocking agent prior to the administration of succinylcholine, remains the most commonly employed method, dating back to a 1957 report of the use of gallamine [7]. Other methods including stretching exercises and supplementation of vitamin C, have been reported to be effective [22,23]. Since it has been postulated that calcium influx enhances the intensity of muscle fiber contractions, inducing spindle damage and subsequent pain, pre-treatment with medications such as dantrolene which interfere with intracellular calcium release have been reported to be effective [24].…”

Section: Discussionmentioning

confidence: 99%

Succinylcholine-Induced Postoperative Myalgia: Etiology and Prevention

et al. 2018

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Succinylcholine is a neuromuscular blocking agent frequently used to facilitate endotracheal intubation during general anesthesia. It is usually preferred due to its rapid onset of action and short duration of action. However, the effectiveness of this drug is limited by certain adverse effects, one of which is postoperative myalgia. Although generally considered a minor adverse effect, the myalgia may be severe and interfere with return to normal activities of daily life. We present an 18-year-old with a history of ulcerative colitis who presented for anesthetic care during liver biopsy. Due to comorbidities including obesity, succinylcholine was chosen to provide rapid neuromuscular blockade and facilitate endotracheal intubation. Postoperatively, the patient complained of bilateral calf pain. The etiology of muscle pain related to succinylcholine is discussed and potential strategies to reduce its incidence reviewed.

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Effect of Stretch Exercises on Suxamethonium Induced Fasciculations and Myalgia

Cited by 12 publications

References 22 publications

Succinylcholine‐associated postoperative myalgia

Succinylcholine‐associated postoperative myalgia

Interaction of neuromuscular blocking drugs with recombinant human m1–m5 muscarinic receptors expressed in Chinese hamster ovary cells

Succinylcholine-Induced Postoperative Myalgia: Etiology and Prevention

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