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Use of ketorolac in the prevention of suxamethonium myalgia
Abstract
We have evaluated the effect of ketorolac in the prevention of suxamethonium myalgia. Sixty ASA I patients who presented for extraction of wisdom teeth as day cases were allocated randomly to one of three equal groups. Patients received either 0.9% saline (placebo), atracurium 0.05 mg kg-1 i.v. or ketorolac 10 mg i.v., 3 min before induction of anaesthesia. Follow-up postal questionnaires (97% response rate) at 48 h showed no reduction in the incidence of myalgia after ketorolac pretreatment compared with saline. The use of atracurium reduced the incidence of myalgia by 60% (P < 0.001) and the severity of fasciculations (P < 0.001). There was no difference in the severity of fasciculations between the saline and ketorolac groups. Intubating conditions were comparable in the three groups.
... Fasciculations and postoperative myalgia are well-known disadvantages of succinylcholine. Many attempts have been made to control these undesired effects caused by succinylcholine, which include pretreatment with nondepolarizing muscle relaxants, [1] lignocaine, [2] calcium gluconate, [3] nonsteroidal antiinflammatory drugs (NSAIDs), [4,5] diazepam, [6] etc., with variable results. Induction of anesthesia with magnesium sulfate and thiopentone has been tried for this purpose also. ...
... Unfortunately, its use is associated with muscular fasciculations and postoperative myalgia. Pretreatment with various drugs such as rocuronium, [1] atracurium, [2] lignocaine, [2] calcium, [3] ketorolac, [4] diclofenac sodium, [5] diazepam, [6] magnesium sulfate, [7] thiopentone sodium, [8] small dose of succinylcholine (self-taming), [9] d-tubocurare, [10] and pancuronium, [11] vecuronium [12] have been tried to reduce these side effects. Intravenous induction agents, thiopentone and propofol, modify succinylcholineinduced side effects. ...
Magnesium sulfate and propofol have been found to be effective against succinylcholine-induced fasciculations and myalgia, respectively, in separate studies. A prospective randomized double blind controlled study was designed to assess the effect of a combination of magnesium sulfate with propofol for induction of anesthesia on succinylcholine-induced fasciculations and myalgia.
Randomly selected 60 adult patients scheduled for elective surgery under general anesthesia were allocated to one of the two equal groups by draw of lots. The patients of MG Group were pretreated with magnesium sulfate 40 mg/kg body weight in 10 ml volume, while patients of NS group were given isotonic saline 0.9% in the same volume (10 ml) intravenously slowly over a period of 10 min. Anesthesia was induced with fentanyl 1.5 mcg/kg and propofol 2 mg/kg, followed by administration of succinylcholine 2 mg/kg intravenously. Muscle fasciculations were observed and graded as nil, mild, moderate, or severe. Postoperative myalgia was assessed after 24 h of surgery and graded as nil, mild, moderate, or severe. Observations were made in double blind manner.
Demographic data of both groups were comparable (P > 0.05). Muscle fasciculations occurred in 50% patients of MG group versus in 100% patients of NS group with a significant difference (P < 0.001). After 24 h of surgery, no patient of MG group and 30% patients of NS group had myalgia with a significant difference (P < 0.002).
Magnesium sulfate 40 mg/kg intravenously may be used with propofol for induction of anesthesia to control succinylcholine-induced fasciculations and myalgia.
... Therefore, Many attempts have been made to avoid these undesirable effects, which include pretreatment with rocuronium [3], atracurium [4], lignocaine [4], calcium [5], ketorolac [6], diclofenac sodium [7], diazepam [8], Magnesium (Mg) sulfate [9], thiopentone sodium [10], d-tubocurare and vecuronium [9]. ...
Introduction: Succinylcholine induced fasciculation, myalgia
and hyperkalemia are common complications in surgical
procedures. Magnesium (Mg) sulfate is proposed to
reduce the negative effects caused by succinylcholine.
Aim: we aimed to assess the effects of different doses of
Mg sulfate on muscle fasciculation, myalgia, hyperkalemia
and hemodynamic responses due to intubation by succinylcholine.
Patients and methods: This randomized clinical trial was
conducted on 60 patients, scheduled for elective surgeries
under general anesthesia, allocated into three groups; 20
patients each. In group 1; the patients received intravenous
(I.V.) Mg sulfate 20 mg/kg. In group 2; the patient received
I.V. Mg sulfate 30 mg/kg and in group 3; the patients received
40 mg/kg I.V. Mg sulfate, over 10 minutes before induction.
Patients were monitored for occurrence of fasciculation,
myalgia or hyperkalemia.
Results: Of the sixty patients, 53.3% were males and
46.7% were females, their mean age was 41.1±10 years. The
incidence of fasciculation was 80%, 55% and 30% in groups
1, 2 and 3, respectively. The highest incidence of myalgia
occurred in group 1 (25% of patients), while just 15% and
10% of groups 2 and 3 developed myalgia. The three groups
showed significant fall in the heart rate and blood pressure
immediately after induction of anesthesia (P<0.05). After
one minute of induction, there was significant increase in
blood hemodynamic measures, patients in group 1 showed
the highest rise. The dose of Mg sulfate had significant positive
correlation with the serum Mg level (r = 0.887, P< 0.05)
and significant negative correlation with the serum Potassium
level after injection of Mg sulfate (r = - 0.512, P< 0.05).
Conclusion: Intravenous Mg sulfate in dose of 40 mg/
kg was the most effective dose in reducing succinylcholine
induced fasciculation, attenuation of the haemodynamic
responses after intubation, and attenuating the increase in
serum K associated with Succinylcholine administration.
... However, according to some proposed mechanisms, sustained muscle contractions cause increased calcium ion concentration in cytoplasm of muscle cells and cause degradation of cell membrane phospholipid resulting in increased release of free fatty acids and free radicals. [3] Many attempts have been made to avoid these undesirable effects, which include pretreatment with rocuronium [4], atracurium [5], lignocaine [5], calcium [6], ketorolac, diclofenac sodium [6], diazepam, magnesium sulphate [7], thiopentone sodium [8], d-tubocurare and vecuronium [9]. It was noticed that many studies have not been carried out in this sub region on trials in attempt to reduce the complications associated with Suxamethonium which is the common readily available short acting muscle relaxants available. ...
... POM is revealed as source of distress to patients than surgical site wound for its unpleasant consequences to patients' quality of life (delayshospital admission period, expose to unplanned expenses, prolongs time to return to daily activity and influence individual's productivity) [17,18]. The incidence of POM also varies among IV induction agents (minimal among propofol [19,20]) and interventional studies reported that its incidence was minimized by pretreatment of atracurium [21], rocuronium [22], vecuronium [23] diclofenac [24], ketorolac [25],phenytoin [26], lidocaine [27], benzodiazepines [28], calcium gluconate [29] and magnesium sulfate [30]. ...
Background: Suxamethonium induced fasciculation (SIF) and post-operative myalgia (POM) is one the side effects occurred
following administration of suxamethonium.
Objective: The present study aimed to assess the incidence and severity of SIF and POM, and their association with different
IV induction agents among adult patients underwent elective surgery at Jimma medical center (JMC).
Methods: Prospective cohort study design was employed among a sampled 140 patients whoinduced by four IV induction
agents (propofol, thiopentone, ketamine and ketofol) where in each group 35 patients were equally distributed. SIF and POM
were assessed by separated structured grading and scoring toolsintraoperatively and post-operatively (respectively) after exposing patients toalready mentioned four induction agents. Data was entered into Epidata version 4.3.1 and finally exported to
SPSS version 20 for further analysis. Cross tabulation/chi square and binary logistic regression were applied to determine their
association. P-value < 0.05 was declared as statistically significant.
Results: The incidence of SIF was 94.3% and differs among induction agents (non-statistically significant difference) (propofol 32(22.9%), thiopentone 34(24.3%), ketamine 33(23.6%) and ketofol 33(23.6%) (P-value=0.204). The incidence of POM
was 29.3% and highest among ketamine group 15(10.7%) and also varies among groups (propofol 6(4.3%), thiopentone
and ketofol (each10(7.1%)) (P-value=0.255). The likelihood of POM occurrence was more likely among patients induced by
ketamine [OR 1.8(0.7-5.1), p=0.215)] and thiopentone [OR 1.1(0.3-2.8), p=0.999)] but less likely among patients induced by
propofol [OR 0.5(0.1-1.6), p=0.259)] by taking patients induced by ketofol as reference. The likelihood of SIF occurrence was
also varies among IV induction agent(about two fold among thiopentone groups [OR 2.1(1.2-23), p=0.563]), but not showed
statistically significant difference among groups.
Conclusion and Recommendation: Even though, the incidence of both SIF and POM were profound and no statistically
significant safe IV inductions that mitigate this adverse effect(fasciculation and POM) following administration of suxamethonium, other option of muscle relaxant was warranted.
... POM is revealed as source of distress to patients than surgical site wound for its unpleasant consequences to patients' quality of life (delayshospital admission period, expose to unplanned expenses, prolongs time to return to daily activity and influence individual's productivity) [17,18]. The incidence of POM also varies among IV induction agents (minimal among propofol [19,20]) and interventional studies reported that its incidence was minimized by pretreatment of atracurium [21], rocuronium [22], vecuronium [23] diclofenac [24], ketorolac [25],phenytoin [26], lidocaine [27], benzodiazepines [28], calcium gluconate [29] and magnesium sulfate [30]. ...
... Our study showed results conflicting with the above reports as diclofenac failed to reduce the incidence of pain compared to the control group. is result however is in agreement with that of another study where ketorolac was used as the pretreatment drug (4) and no reduction in the incidence myalgia was observed. ...
after approval by the institutional ethical committee. 120 in-patients were selected for the study using purposive sampling after obtaining consent. Inclusion criteria Ÿ Adult ASA I and II physical status of either sex Ÿ Age between 18 and 50 years Ÿ Weight-40 to 65 kg Ÿ Posted for elective minor surgeries Exclusion criteria Ÿ Major surgeries Ÿ Pregnant and lactating women Ÿ Neuromuscular disorders Ÿ Emergency surgical procedures Ÿ Age below 18 years or above 50 years Ÿ Patient refusal Ÿ True allergy to lidocaine and diclofenac All patients were subjected to pre anaesthetic evaluation on the day prior to surgery. Routine pre-operative investigations were done. All patients were kept nil per oral for 8 hours with pre medication of Tab Ranitidine 150 mg orally 12 hours before surgery. Patients were divided into three groups of 40 each, based on random number generated by computer software and pretreatment was given accordingly. In the operating room, baseline SpO2, heart rate and ECG were recorded. Intravenous access was secured. Inj. fentanyl 2 µg/kg IV was given 5 minutes before induction of anaesthesia. Patients were pre-oxygenated and induced with 5 mg/kg IV thiopentone sodium followed by 1.5 mg/kg of succinycholine given IV. Tracheal intubation was performed once the fasciculations reached the toes. Anaesthesia was maintained with nitrous oxide 66% in oxygen and isofluorane 0.6%. Loading dose of 0.1 mg/kg vecuronium was given IV followed by maintenance dose of 0.02 mg/kg every 20 minutes IV. Neuromuscular blockade was reversed with IV neostigmine 0.05 mg/kg and 0.01 mg/kg IV glycopyrrolate at the end of the procedure. Standardized post operative care was given to all the participants. Pain related to the surgical procedure was treated with IV pethidine in a dose of 1mg/kg. Severity and intensity of post operative myalgia was assessed by the investigator with a standardized questionnaire 1hour, 24 hours and 48 hours after surgery.
... 6 Use of different pretreatment modalities including benzodiazepines, nondepolarizing neuromuscular blockers, local anesthetics, chlorpromazine, phenytoin, ketorolac, Vitamin E derivatives, pretreatment with rocuronium and remifentanil have been tried to reduce the severity of succinylcholine-induced myalgia. [7][8][9][10][11][12][13][14] The surgical procedure serves as noxious stimulus, results in initial sensitization and establishment of altered processing of afferent input to central nervous system (CNS), following Background: Succinylcholine is a drug of choice for rapid induction of anesthesia but produces postoperative myalgia. Preemptive analgesia is intended to decrease perception of pain before exposure to painful stimuli. ...
Background:
Succinylcholine is a drug of choice for rapid induction of anesthesia but produces postoperative myalgia. Preemptive analgesia is intended to decrease perception of pain before exposure to painful stimuli. Pregabalin and gabapentin, analogs of the inhibitory neurotransmitter gamma aminobutyric acid, are effective in several models of neuropathic pain, incisional, inflammatory, and formalin-induced injury. However, the data available on their preemptive analgesic efficacy in succinylcholine myalgia are sparse. This study was designed to compare the preemptive analgesic efficacy and safety of pregabalin and gabapentin.
Materials and methods:
This randomized clinical trial included 120 surgical patients of either sex, between 18 and 70 years, and of American Society of Anesthesiologists-I/II grade. Patients were randomly allocated to control and test groups; received respective treatments 30 min before induction of anesthesia. Myalgia and pain scores were recorded using the myalgia scale and visual analog/facial rating scale at awakening at 6, 12, 18, and 24 h, respectively. Postoperative analgesic requirement over 24 h was recorded. Data were analyzed using OpenEpi (Andrew G. Dean and Kevin M. Sullivan, Atlanta, GA, USA) statistical softwares.
Results:
Significantly lower pain scores were observed in the pregabalin group at 6, 12, and 24 h, and in gabapentin group at 24 h as compared to control and placebo (P < 0.05). They were however found to be equianalgesic when compared to each other (P > 0.05). Pregabalin-treated patients were more comfortable throughout with significantly less postoperative myalgia and analgesic requirement (P < 0.05).
Conclusions:
Results strongly suggest the preemptive analgesic efficacy of a single oral dose of pregabalin and gabapentin over diclofenac in postoperative myalgia and pain management. However, on the basis of safety profile, pregabalin may be preferred over gabapentin in succinylcholine-induced myalgia.
... 1 The pathophysiology of fasciculations is unclear, but it may be induced by axonal depolarisation caused by connection between succinylcholine and presynaptic and cholinergic nicotinic receptors. 2 Many attempts have been made to avoid these undesirable effects, which include pretreatment with rocuronium, 3 atracurium, 4 lignocaine, 4 calcium, 5 ketorolac, 6 diclofenac sodium, 7 diazepam, 8 magnesium sulphate, 9 thiopentone sodium, 10 d-tubocurare 11 and vecuronium. 12 Intravenous induction agents, thiopentone and propofol, modify succinylcholine-induced side effects. ...
... Diferentes modalidades de pré-tratamento foram experimentadas para reduzir a incidência e gravidade da fasciculação e mialgia, incluindo a pré-curarização com uma dose pequena de relaxante muscular não despolarizante, 3 uso de lidocaína pré-succinilcolina, 4 gluconato de cálcio, 5 sulfato de magnésio, 6 medicamentos anti-inflamatórios não esteroides (AINEs), 7 dexmedetomidina, 8 benzodiazepínicos, 4 remifentanil, 9 fenitoína 10 ou cetorolaco. 11 A eficácia de cada um é variável. ...
A succinilcolina é comumente usada para atingir um bloqueio neuromuscular profundo, de início rápido e de curta duração.
... Pre-treatment with diclofenac [1] , ketorolac [2] , calcium [3] , diazepam [4] , lignocaine [5] , magnesium [6] , small dose of succinylcholine as self-taming [7] , atracurium [ etc. have been tried to reduce or prevent succinylcholine induced fasciculations and myalgia but, none of them were thoroughly successful. The most effective method is pretreatment with a small dose of non-depolarizing agent but it is associated with blurred vision, diplopia, and difficulty in breathing and higher dose of succinylcholine to obtain optimal intubating condition which leads to a longer recovery and apnoea period. ...
Background: Succinylcholine induced fasciculations and myalgia may be a source of greater distress to the patient than the surgical pain. Aims & Objective: This study was designed to see if propofol offered any protection against succinylcholine induced fasciculations and myalgia compared with thiopentone sodium. Material and Methods: This prospective, randomized study was conducted in a teaching and tertiary care hospital. The study included 99 adult patients scheduled to undergo general anaesthesia for elective surgery. The patients were allocated randomly and equally into Group P1, P2 and T. Anaesthesia was induced in group P1 with propofol 2.5 mg/kg, group P2 with propofol 3.5 mg/kg and group T with thiopentone sodium 5 mg/kg. Tracheal intubation was facilitated by administration of intravenous succinylcholine 2 mg/kg. Incidence and severity of fasciculations were recorded. Anaesthesia was maintained with 50% Nitrous oxide in oxygen, Isoflurane and Vecuronium bromide. At the end of surgery, neuromuscular blockage is reversed and patients were extubated. All the patients were assessed at 6, 12 and 24 hours postoperatively to evaluate the incidence and severity of myalgia. Anova test was applied for quantitative data and Chi-square test for qualitative data. P value < 0.05 was taken as significant. Results: The demographic data of patients of the three groups were comparable. The total incidence of fasciculations were 25(75.76%), 16(48.48%) and 26(78.79%) in group P1, P2 and T respectively (p<0.001). Total score of fasciculations was 44(44.44%), 22(22.22%) and 53(53.54%) in group P1, P2 and T respectively. The severity of fasciculations was reduced more in group P2 than group P1 and T (p=0.0006). The total incidence of myalgia were 19(57.57%), 10(30.3%) and 23(69.7%) in group P1, P2 and T respectively (p<0.001). Total score of myalgia was 35(35.35), 18(18.18) and 45 (45.45) in group P1, P2 and T respectively. The severity of myalgia was reduced more in group P2 than group P1 and T (p<0.001). There was no correlation between fasciculations and myalgia in the present study (Pearson’s r correlation, r = - 0.139). Conclusion: Propofol 3.5 mg/kg in comparison with propofol 2.5 mg/kg and thiopentone sodium 5 mg/kg is effective in reducing the incidence and severity of succinylcholine induced fasciculations and myalgia.
... This includes precurarization with a small dose of non-depolarizing muscle relaxant, 3 pre succinylcholine use of lidocaine, 4 calcium gluconate, 5 magnesium sulphate, 6 nonsteroidal anti-inflammatory drugs (NSAIDs), 7 dexmedetomidine, 8 benzodiazepines, 4 remifentanil, 9 phenytoin 10 or ketorolac. 11 The efficacy of each is variable. ...
Succinylcholine is commonly used to achieve profound neuromuscular blockade of rapid onset and short duration.Objective
The present study compared the efficacy of pregabalin for prevention of succinylcholine-induced fasciculation and myalgia.DesignProspective, randomized, placebo controlled, double blinded study.Materials and methodsPatients of both genders undergoing elective spine surgery were randomly assigned to two groups. Patients in Group P (pregabalin group) received 150 mg of pregabalin orally 1 h prior to induction of anesthesia with sips of water and patients in Group C (control group) received placebo. Anesthesia was induced with fentanyl 1.5 mcg/kg, propofol 1.5–2.0 mg/kg followed by succinylcholine 1.5 mg/kg. The intensity of fasciculations was assessed by an observer blinded to the group allotment of the patient on a 4-point scale. A blinded observer recorded postoperative myalgia grade after 24 h of surgery. Patients were provided patient-controlled analgesia with fentanyl for postoperative pain relief.ResultsDemographic data of both groups were comparable (p > 0.05). The incidence of muscle fasciculation's was not significant between two groups (p = 0.707), while more patients in group C had moderate to severe fasciculation's compared to group P (p = 0.028). The incidence and severity of myalgia were significantly lower in group P (p < 0.05).Conclusion
Pregabalin 150 mg prevents succinylcholine-induced fasciculations and myalgia and also decreases the fentanyl consumption in elective sine surgery.
... [3,4] The exact underlying mechanism of succinylcholine-induced myalgia is not known, thus, different pre-treatment modalities have been attempted to reduce the incidence and severity of succinylcholine-induced myalgia. Non-depolarizing neuromuscular blockers, [3] lignocaine, [5] chlorpromazine, [6] benzodiazepines, [4] phenytoin, [7] ketorolac, [8] diclofenac, [9] vitamin C [10] and vitamin E [6] derivatives, remifentanil, [11] gabapentin [12] and magnesium sulphate, [13] have all been tried with variable success. Pregabalin, like gabapentin, is shown to be effective in several models of neuropathic pain, incisional injury, inflammatory injury and formalininduced injury. ...
Context:
Succinylcholine a depolarizing muscle relaxant with rapid onset, predictable course and short duration of action is associated with myalgia.
Aim:
The aim of this study is to evaluate the efficacy of pregabalin, gabapentin and diclofenac on the incidence and severity of succinylcholine-induced myalgia.
Settings and design:
Tertiary Care Teaching Hospital.
Materials and methods:
A total of 120 patients undergoing laparoscopic cholecystectomy were randomly assigned into three groups: Pregabalin group received 150 mg of pregabalin, gabapentin group received 600 mg of gabapentin and diclofenac group received 100 mg of diclofenac sodium orally 2 h prior to surgery. Anesthesia was induced with fentanyl 3 μg/kg, propofol 2-2.5 mg/kg and succinylcholine 1.5 mg/kg and was maintained with oxygen with sevoflurane in the air and intermittent vecuronium bromide. A blinded observer recorded post-operative pain scores on visual analog scale at different time intervals and myalgia at 24 h. Post-operative pain relief was provided with fentanyl based patient-controlled analgesia. Fentanyl consumption in 24 h was recorded as a primary outcome.
Statistical analysis:
Patients' characteristics and total fentanyl consumption were compared using one-way ANOVA followed by post-hoc test. Pain score was compared amongst the groups using Kruskal Wallis test.
Results:
The myalgia occurred in 15, 14 and 13 patients in pregabalin, gabapentin and diclofenac sodium group respectively (P > 0.85). Patients in diclofenac group had significantly higher fentanyl consumption (674.85 ± 115.58 μg) compared with pregabalin group (601.87 ± 129.57 μg) (95% confidence interval [CI] = 34.8-120.7) and gabapentin group (612.29 ± 105.12 μg) (95% CI = 14.9-170.5). However, there was no significant difference in fentanyl consumption between pregabalin and gabapentin groups (95% CI = -34.8-120.7). There was a significant difference in visual analog score at time points 12, 18 and 24 h among the study groups.
Conclusion:
Pre-treatment with pregabalin, gabapentin and diclofenac had equal efficacy in reducing the incidence and severity of succinylcholine-induced myalgia. However, pre-treatment with pregabalin and gabapentin decreased post-operative pain scores and fentanyl consumption.
... However, there are debates about inflammatory origin of succinylcholine induced myalgia 15,16 , and several authors considered anti inflammatory mechanism for NSAIDs in lessening POM 11,12,17 .There may be parallels between the calcium influx seen after succinylcholine and that observed in experimentally induced muscle damage. Lipo-oxygenase products are mediators of calcium induced intracellular enzyme efflux from skeletal muscle, whereas cyclo-oxygenase products may mediate myalgia. ...
Succinylcholine-induced myalgia is a minor but frequent complication. Its incidence and severity is different according to the studied population. The aim of this study was evaluation of the diclofenac patch effect on postoperative succinylcholine-related myalgia in cesarean section.
The study was a prospective randomized double blind, placebo-controlled trial. One hundred twenty six participants undergoing elective cesarean section (previous cesarean section) were randomized in two equal groups (63 participants in each): the diclofenac patch (containing 180 mg of diclofenac epolamine salt) and the placebo. Surgery was performed following rapid sequence induction of general anesthesia. All patients were paralyzed for intubation by succinylcholine (1.5 mg/kg). Data on baseline characteristics, fasciculation, postoperative myalgia (at 12, 24 and 48 hours after operation), the need to analgesic agents, and adverse effects of diclofenac patch were collected.
The basic characteristics were comparable between the two groups. The severity of fasciculation did not significantly vary between two groups. In diclofenac group, the incidences of myalgia at 12, 24 and 48 hours after operation were 23.8%, 19.1%, and 12.7% respectively versus incidences of 52.4%, 47.6%, and 44.4% respectively in placebo group. The incidence and severity of myalgia were significantly lower in patients receiving diclofenac through three evaluation periods (all p values less than 0.01). No participants left the study because of the complications.
Diclofenac patch is effective and safe in the prevention of postoperative succinylcholine induced myalgia after cesarean section.
... A signi®cant reduction in postoperative myalgia was noted with aspirin 600 mg given 1 h before operation [65]. However, results from studies designed to evaluate the effectiveness of NSAIDs in reducing postoperative myalgia have been inconclusive [37,66]. ...
The 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.
Corrigendum
Corrigendum to: The Effect of Pregabalin on the Prevention
of Succinylcholine-Induced Fasciculation and Myalgia. Journal
of PeriAnesthesia Nursing, 2020;35(3):255−259
Shahryar Sane, MD, PhDa
, Mir Moussa Aghdashi, MD, PhDa
, Behzad Kazemi Haki, BSca
,
Behzad Gholamveisi, MScb
, Mina Rajabzadeh, MDc
, Parang Golabi, BScd
a Department of Anesthesiology, Urmia Imam Khomeini Hospital, Urmia University of Medical Science, Urmia, Iran
b Department of Operating Room, Faculty of Nursing and Midwifery, Kurdistan University of Medical Sciences, Sanandaj, Iran
c Department of Medicine, Urmia University of Medical Science, Urmia, Iran
d Department of Anesthesiology, Mahabad Imam Khomeini Hospital, Urmia University of Medical Science, Mahabad, Iran
“The Effect of Pregabalin on the Prevention of Succinylcholine-Induced Fasciculation and Myalgia”, published in the June 2020 issue [2020;35
(3):255-259], contains errors in matching data for Table 2 and Figure 2. In addition, the myalgia severity data were missing, and the following
text should be added to the Results section:
“In the placebo group, 14 patients (28%) had no myalgia, 20 patients (40%) had muscle stiffness and pain related to one region, and 13
patients (26%) had muscle stiffness and pain that is spontaneously expressed by the patient and may require an analgesic, and 2 patients (4%)
had diffuse muscle pain with unbearable discomfort. Myalgia severity in the pregabalin group was lower than the placebo group, 23 patients
(46%) had no myalgia, 21 patients (42%) had muscle stiffness and pain related to one region, and 6 patients (6%) had muscle stiffness and pain
that is spontaneously expressed by the patient and may require an analgesic, and no patient had diffuse muscle pain with unbearable discom-
fort. A t test showed a significant difference in the severity of myalgia between the two groups (P = .012).”
The corrected versions of Table 2 and Figure 2 appear below. The authors apologize for any inconvenience that the errors may have caused.
Table 2
Comparison of Pain Scores at 6, 12, 18, 24 Hours After Surgery in the Two Groups
Variable PG = 50 P = 50 P Value
6 h 1.05 § 1.31 5.98 § 1.02 .01
12 h 3.44 § 1.58 5.14 § 1.30 .007
18 h 2.43 § 1.62 5.98 § 1.02 .02
24 h 5.22 § 1.47 3.24 § 1.80 .03
P, placebo group; PG, pregabalin group. The mean pain score in 6, 12, and 18 hours
after surgery in the PG (pregabalin group) was significantly lower than the P (placebo
group). In 24 hours after surgery, the PG group’s pain score was higher than the P
group, possibly caused by one of the side effects of pregabalin (eg, headache).
DOI of original article: http://dx.doi.org/10.1016/j.jopan.2019.11.005.
https://doi.org/10.1016/j.jopan.2021.04.009
1089-9472/© 2021 American Society of PeriAnesthesia Nurses. Published by Elsevier Inc. All rights reserved.
https://www.jopan.org/article/S1089-9472(21)00084-8/fulltext
Succinylcholine, a depolarizing muscle relaxant possesses a unique property of rapid onset and short duration of action, but is accompanied by side effects such as fasciculation and myalgia. The aim of this study was to investigate the prophylactic effect of intravenous lignocaine on the incidence and severity of succinylcholine-induced postoperative myalgia. This was a randomized controlled double blind study conducted at National Institute of ENT Dhaka, during September to December 2017. Eighty adult patients of American Society of Anesthesiologists status I and II of both sexes for elective surgery under general anesthesia were randomly allocated into two equal groups, lignocaine group and normal saline group. The patients of lignocaine group were pretreated with lignocaine 1.5 mg/kg body weight in 5 ml volume, while patients of normal saline group were given isotonic saline 0.9% in the same volume (5 ml) intravenously. Thereafter, anesthesia was induced in all patients, by injecting 1.5 mg/kg of fentanyl and 2 mg/kg of propofol intravenously. Following the loss of eyelid reflex, 1.5 mg/kg of succinylcholine was injected intravenously as a muscle relaxant and then the patients were intubated. The incidence and severity of myalgia were assessed by a blinded observer 24 hours after surgery. In terms of demographic data, the results of this study showed that there is no significant difference between patients in both groups (P>0.05). Overall, the incidence and severity of succinylcholine-induced myalgia in lignocaine group was significantly less, when compared with normal saline group (P<0.05). Pretreatment with intravenous lignocaine is effective in prevention of postoperative succinylcholine induced myalgia. Faridpur Med. Coll. J. Jan 2019;14(1): 13-15
Purpose:
This study evaluates the effect of pregabalin on fasciculation and myalgia after using succinylcholine.
Design:
This randomized double-blind prospective study was conducted among 100 patients aged 20 to 60 years old.
Methods:
Pregabalin (300 mg) and placebo (in capsule form) were placed in similar containers. The results were analyzed by SPSS 23 software, and statistical analysis consisted of χ2 test and t test, and a P value less than .05 was considered significant.
Findings:
The mean pain score in the group receiving pregabalin was lower than the placebo group. According to the χ2 test, there was a significant difference between the two groups in the frequency of fasciculation (P = .003). Mean fasciculation severity in the pregabalin group was lower than placebo group. According to t test, there was a significant difference in the mean fasciculation severity between the two groups (P = .002).
Conclusions:
This study showed that 300 mg of pregabalin was effective in reducing postoperative fasciculation and myalgia in patients treated with succinylcholine.
Background: Succinylcholine a depolarizing muscle relaxant with rapid onset, predictable course and short duration of action is associated with myalgia. Objectives: To assess the efficacy of intramuscular injection of diclofenac sodium in preventing succinylcholine-induced myalgia. Materials and Methods: Eighty healthy adults scheduled for elective surgery under general anesthesia were enrolledin a double-blind study and randomly allocated into two groups of forty patients. Patients in Group I (diclofenacgroup) were pretreated with inj. diclofenac 75 mg deep intramuscularly into gluteal region one hour prior to induction of anesthesia, while patients in Group II (saline group) received an equivalent volume of saline inj. in same site. Anesthesia was induced in both groups with fentanyl 1.5 mcg/kg, propofol 2.0 mg/kg and succinylcholine1.5 mg/kg. Postoperative myalgia was assessed 24 hours after induction and graded as nil, mild, moderate, or severe. Results:The demographic data for both groups were comparable (p > 0.05). Postoperative myalgia was recorded at 24 hours after induction in diclofenac group with twelve (30%) patients and 24 (60%) patients in normal saline (control) group respectively (p < 0.05). Conclusion: Prophylactic use of intramuscular injection of diclofenac is effective in the prevention of postoperative myalgia KYAMC Journal Vol. 10, No.-1, April 2019, Page 35-38
Objective: We investigated the efficacy of precurarization in preventing succinylcholine-induced postoperative myalgia (POM) and the correlation between fasciculations and POM. Method. This study included 48 patients (ASA I) scheduled for elective minor surgery. The patients were randomized to receive vecuronium 0.01 mg kg-1, cisatracurium 0.02 mg kg-1 or saline, 3 minutes prior to 1.5 mg kg-1 of succinylcholine. Standard general anesthetic technique by thiopental, fentanyl and isoflurane was used for all the patients. The intensities of fasciculations and POM were assessed using four point scales. Results: Fasciculations were observed less frequently in the vecuronium and cisatracurium groups compared with the saline group (p< 0.05). There were no differences among the groups with respect to the incidence and severity of POM. There was no correlation between the incidences and intensities of fasciculations and POM. Conclusion: Precurarization did not effect the incidence and severity of succinylcholine-induced POM and there is no correlation between succinylcholine-induced fasciculations and POM.
The Side Effects of Drugs Annuals form a series of volumes in which the adverse effects of drugs and adverse reactions to them are surveyed. The series supplements the contents of Meyler's Side Effects of Drugs: the International Encyclopedia of Adverse Drug Reactions and Interactions. This review of the 2011 publications on neuromuscular blocking agents and skeletal muscle relaxants covers the depolarizing neuromuscular blocking agent suxamethonium (succinylcholine), the non-depolarizing neuromuscular blocking agent rocuronium, the rocuronium-reversing agent sugammadex, and several skeletal muscle relaxants (baclofen, botulinum toxins, cyclobenzaprine, dantrolene sodium, tetrabenazine, and tizanidine). It includes a special review on the management of rocuronium-induced anaphylaxis with sugammadex.
Background:
Succinylcholine is used for rapid-sequence induction of anesthesia. Fasciculations and myalgia are adverse effects. The pretreatment modalities prevent or minimize its adverse effects.
Aims:
The present study is designed to evaluate the efficacy of gabapentin on the incidence of fasciculation and succinylcholine-induced myalgia.
Settings and design:
The study was conducted at a tertiary care teaching hospital in a randomized, double-blinded, placebo-controlled manner.
Materials and methods:
Patients of both genders undergoing laparoscopic cholecystectomy were randomly assigned to two groups. Patients in Group I (Gabapentin group) received 600 mg of gabapentin orally 2 h prior to surgery and patients in Group II (placebo group) received matching placebo. Anesthesia was induced with fentanyl 3 μg/kg, thiopentone 3-5 mg/kg and succinylcholine 1.5 mg/kg. All patients were observed and graded for fasciculations by a blinded observer and patients were intubated. Anesthesia was maintained with oxygen in air, sevoflurane and intermittent vecuronium bromide. After completion of surgery, neuromuscular blockade was reversed. A blinded observer recorded myalgia grade at 24 h. Patients were provided patient-controlled analgesia with fentanyl for postoperative pain relief.
Statistical analysis:
Demographic data, fasciculation grade, fentanyl consumption, and myalgia grade were compared using student t test and test of proportions.
Results:
The study included 76 American Society of Anesthesiologists' Grade I or II patients of either gender undergoing laparoscopic cholecystectomy. But only 70 patients completed the study. Results demonstrated that the prophylactic use of gabapentin significantly decreases the incidence and the severity of myalgia (20/35 vs. 11/35) (P<0.05) and decreases fentanyl consumption significantly in the study group (620+164 μg vs. 989+238 μg) (P<0.05) without any effects on the incidence and severity of fasciculations.
Conclusions:
Prophylactic use of gabapentin 600 mg in laparoscopic cholecystectomy decreases the incidence and severity of myalgia and fentanyl consumption.
The present visual and electromyographic study was designed to evaluate muscle fasciculations caused by succinylcholine in adults pretreated with either remifentanil 1.5 microg/kg or saline.
The effect of remifentanil on succinylcholine-induced muscle fasciculations was studied using a double-blind method in 40 adults. After i.v. pretreatment with either remifentanil 1.5 microg/kg (remifentanil group, n = 20) or an equivalent volume of i.v. saline (saline group, n = 20), patients were anaesthetized with a 2.0 mg/kg of i.v. propofol followed by i.v. succinylcholine 1.0 mg/kg. Intensity and duration of muscle fasciculation following i.v. succinylcholine administration were recorded. Electromyography (EMG) was used to quantify the extent of muscle fasciculation following i.v. succinylcholine injection. Myalgia was evaluated 24 hours after induction time. Serum potassium levels were measured five minutes after i.v. succinylcholine administration and creatine kinase (CK) levels 24 hours after induction time.
Compared to saline treated controls, remifentanil decreased the intensity of muscle fasciculations caused by i.v. succinylcholine [fasciculation severity scores (grade 0 to 3) were 2/1/12/5 and 3/13/4/0 (patients numbers) in the saline group and the remifentanil group, respectively, p < 0.001]. The mean (SD) maximum amplitude of muscle action potential (MAP) by EMG was smaller in the remifentanil group [283.0 (74.4) microV] than in the saline group [1480.4 (161.3) microV] (p = 0.003). Postoperative serum CK levels were lower in the remifentanil group (p < 0.001). Postoperative myalgia was not different between the two groups.
Remifentanil 1.5 microg/kg attenuated intensity of muscle fasciculations by succinylcholine.
Unlabelled:
A common side effect associated with succinylcholine is postoperative myalgia. The pathogenesis of this myalgia is still unclear; inflammation has been suggested but without convincing evidence. We designed the present study to investigate whether an inflammatory reaction contributes to this myalgia. The incidence and severity of succinylcholine-associated myalgia was determined in 64 patients pretreated with saline or dexamethasone before succinylcholine (n = 32 for each). Incidence and severity of myalgia did not differ significantly between the two groups: 15 patients in the dexamethasone group complained of myalgia compared with 18 patients in the saline group, and severe myalgia was reported by five patients and three patients, respectively (not significant). At 48 h after surgery, 12 patients in both groups still suffered from myalgia (not significant). In addition, interleukin-6 (IL-6) as an early marker of inflammation was assessed in a subgroup of 10 patients pretreated with saline. We found an increase of IL-6 for only three patients, but only one patient reported myalgia; no relationship between myalgia and the increase of IL-6 was found. In conclusion, there is no evidence for an inflammatory origin of succinylcholine-associated myalgia.
Implications:
Administration of dexamethasone before succinylcholine was not effective in decreasing the incidence or the severity of succinylcholine-induced postoperative myalgia. Furthermore, there was no significant relationship between postoperative myalgia and time course of interleukin-6 concentrations, a marker of inflammation. Pretreatment with dexamethasone is not justified to prevent postoperative myalgia after succinylcholine.
This article reviews the pharmacologic treatment options available for myofascial pain conditions.
Fifty-two randomized trials (5,318 patients) were included in this meta-analysis. In controls, the incidence of fasciculation was 95%, and the incidence of myalgia at 24 h was 50%. Nondepolarizing muscle relaxants, lidocaine, or magnesium prevented fasciculation (number needed to treat, 1.2-2.5). Best prevention of myalgia was with nonsteroidal antiinflammatory drugs (number needed to treat, 2.5) and with rocuronium or lidocaine (number needed to treat, 3). There was a dose-dependent risk of blurred vision, diplopia, voice disorders, and difficulty in breathing and swallowing (number needed to harm, < 3.5) with muscle relaxants. There was evidence of less myalgia with 1.5 mg/kg succinylcholine (compared with 1 mg/kg). Opioids had no impact. Succinylcholine-induced fasciculation may best be prevented with muscle relaxants, lidocaine, or magnesium. Myalgia may best be prevented with muscle relaxants, lidocaine, or nonsteroidal antiinflammatory drugs. The risk of potentially serious adverse events with muscle relaxants is not negligible. Data that allow for a risk-benefit assessment are lacking for other drugs.
Data from several studies implicate that pre-treatment with non-selective cyclooxygenase inhibitors such as aspirin or diclofenac may decrease the incidence of postoperative succinycholine-related myalgia. We tested the influence of a preoperatively administered selective cyclooxygenase 2 inhibitor, parecoxib, on postoperative myalgia.
After Ethics Committee approval, 68 patients were randomized into two groups (n = 34 each). Group 1 received parecoxib 40 mg intravenously 3 min before induction of anaesthesia, and Group 2 received saline (in a double-blinded manner). Incidence and severity of myalgia was evaluated systematically with a standardized questionnaire 24, 48 and 72 h after anaesthesia. We also the assessed the number of patients who felt limited in their activity due to myalgia.
Seven patients in the parecoxib-treated group complained of myalgia compared with 11 in the control group (not significant). No significant difference in the severity of myalgia or in the limitation of patients activity was found between the groups.
Intravenous parecoxib 40 mg, when administered before induction of anaesthesia, did not reduce incidence and severity of postoperative myalgia and did not improve activity in those who suffered from myalgia.
The role of arachidonic acid metabolism in the efflux of intracellular enzymes from damaged skeletal muscle has been examined in vitro using inhibitors of cyclo-oxygenase and lipoxygenase enzymes. Damage to skeletal muscle induced by either calcium ionophore A23187 (25 microM) or dinitrophenol (1 mM) caused an increase in the efflux of prostaglandins E2 and F2 alpha together with a large efflux of intracellular creatine kinase. Use of a cyclo-oxygenase inhibitor completely prevented the efflux of prostaglandins, but had no effect on creatine kinase efflux. However, several agents having the ability to inhibit lipoxygenase enzymes dramatically reduced creatine kinase efflux following damage. These data suggest that a product or products of lipoxygenase enzymes may be mediators of the changes in plasma membrane integrity which permit efflux of intracellular enzymes as a consequence of skeletal muscle damage.
Treatment of isolated rat skeletal muscles with the Ca2+ ionophores, A23187 or ionomycin, increased overall protein degradation 45-140%. Removal of extracellular Ca2+ reduced overall proteolysis and most of the stimulation by A23187. Treatment of the muscles with the sulfhydryl inhibitor, mersalyl, completely inactivated the Ca2+-activated protease without altering overall protein breakdown or the stimulation by A23187. This agent did not inhibit the lysosomal protease, cathepsin B, in the muscle; however, leupeptin and Ep-475, which inhibit this enzyme in intact cells, decreased the stimulation of proteolysis by Ca2+. Thus, this effect does not require the Ca2+-activated enzyme, but seems to involve lysosomal proteases. Prostaglandin E2 (PGE2) and its precursor arachidonic acid, were previously shown to stimulate protein degradation in rat muscle through an effect on lysosomal function. We tested whether the enhancement of muscle proteolysis by Ca2+ ionophores may result from increased synthesis of PGE2. A23187 increased release of PGE2 and PGF2 alpha by the muscles 3-4-fold. High extracellular potassium also markedly promotes muscle proteolysis, apparently by increasing intracellular Ca2+, and this treatment also stimulates prostaglandin production. Indomethacin and aspirin, which inhibit the cyclooxygenase, and mepacrine, which inhibits the Ca2+-activated phospholipase A2, markedly reduced the increase in prostaglandin production. These agents also reduced the enhancement of protein degradation by Ca2+ or high K+. Thus, Ca2+ appears to promote protein breakdown by stimulating synthesis of PGE2, which in turn activates the lysosomal apparatus.
We have studied the effects of preoperative administration of diclofenac on suxamethonium-induced myalgia, plasma met-enkephalin-like
activity (ELA), prostaglandin E2-like activity (PGE2-LA), leukotriene C4-like activity (LTC4-LA), and histamine-like activity (H-LA). Thirty-four ASA I patients undergoing elective ophthalmic surgery were allocated
randomly to two groups to receive either saline placebo or diclofenac 75 mg i.m. 20 min before operation, in a double-blind
design. Anaesthesia was induced with thiopentone 5–7 mg kg−1 followed by suxamethonium 1.5mg kg−1 and maintained with 67% nitrous oxide and halothane in oxygen. Plasma PGE2-LA, LTC4-LA, H-LA and E-LA were measured before premedication, 1 min after the administration of suxamethonium and 24 h after operation.
Muscle fasciculations, intubation conditions and postoperative myalgia were graded numerically. Postoperative myalgia in the
diclofenac group was significantly (P<0.05) less (47.1 %) than in the control group (76.5%). Postsuxamethonium and 24-h concentrations of plasma PGE2-LA and LTC4 were also significantly (P<0.05) greater than baseline in the control group. Plasma H-LA was increased in both groups after suxamethonium and this increase
was significant (P<0.05) in the control group. We conclude that diclofenac reduces significantly the incidence and intensity of suxamethonium-induced
myalgia.
Postoperative muscle pains occurred in 16% of 25 patients given 10 mg diazepam IV 5 minutes prior to succinylcholine. Postoperative muscle pains occurred in 60% of 25 patients not given diazepam before succinylcholine. The difference is statistically significant. Diazepam reduced the severity and duration of postoperative muscle pains, as well as their frequency.
Diazepam in a dose of 0.05 mg/kg was studied to determine its effect on a subsequently administered dose of 1 mg/kg of succinylcholine. This dose of diazepam prior to succinylcholine (1) significantly diminished the incidence of postoperative muscle pain; (2) decreased the usual increase in serum potassium; (3) did not prevent the rise in creatine phosphokinase; (4) reduced the incidence of muscle fasciculation; and (5) did not affect the magnitude or duration of the succinylcholine neuromuscular block. It was concluded that diazepam had several advantages over d-tubocurarine in the prevention of succinylcholine-induced muscle pain.
Ketorolac is a new chiral nonsteroidal anti-inflammatory drug (NSAID) which is marketed for analgesia as the racemate. The drug is administered as the water soluble tromethamine salt and is available in tablets or as an intramuscular injection. The absorption of ketorolac is rapid, Cmax being attained between 20 to 60 min. Its oral bioavailability is estimated to range from 80 to 100%. The drug is extensively bound (>99%) to plasma proteins and has a volume of distribution (0.1 to 0.3 L/kg) comparable with those of other NSAIDs. Only small concentrations of ketorolac are detectable in umbilical vein blood after administration to women in labour. The elimination half-life is between 4 and 6h and is moderate in comparison with other NSAIDs. The area under the plasma concentration-time curve of ketorolac is proportional to the dose after intramuscular administration of therapeutic doses to young healthy volunteers.
Ketorolac is extensively metabolised through glucuronidation and oxidation; little if any drug is eliminated unchanged. Most of the dose of ketorolac is recovered in the urine as conjugated drug. Although ketorolac is excreted into the breast milk, the amount of drug transferred comprises only a small fraction of the maternal exposure. Little stereoselectivity was present in the pharmacokinetics of ketorolac in a healthy volunteer receiving single intravenous or oral doses. The elderly exhibit reduced clearance of the drug. Renal insufficiency appears to cause an accumulation of ketorolac in plasma, although hepatic disease may not affect the pharmacokinetics.
The incidence of muscle pains and changes in serum concentrations of potassium, calcium and creatine kinase following suxamethonium were investigated after no pretreatment or pretreatment with intravenous tubocurarine 0.05 mg.kg-1, intravenous chlorpromazine 0.1 mg.kg-1, alphatocopherol (vitamin E) 600 mg in three divided doses orally, aspirin 600 mg orally or intravenous calcium chloride 5 mg.kg-1 in groups of 20 patients each. The incidence of myalgia was reduced significantly by tubocurarine, chlorpromazine and alphatocopherol. However, the increase in creatine kinase was attenuated only in the groups of patients who received tubocurarine and chlorpromazine. The changes in serum potassium and calcium concentrations were within acceptable limits. The intubating conditions were not as good in the patients who received tubocurarine as in the other groups. Effectiveness of chlorpromazine in preventing both the myalgia and the biochemical changes suggests the involvement of phospholipases in the pathogenesis of suxamethonium-induced muscle damage.
Meta-analysis is a term used to describe statistical methods for evaluating a series of research reports; this analysis transcends the limitations that may be inherent in each of the individual studies summarized. Forty-five research reports of clinical trials for the prevention of myalgias after succinylcholine were assembled. Four classes of preventive drugs (nondepolarizing muscle relaxants, benzodiazepines, succinylcholine in "self-taming" doses, and local anesthetics) were reported in detail sufficient to allow for inclusion in a meta-analysis of clinical efficacy. Each study was summarized by determining the difference in the incidence of myalgias on the first postoperative day between treatment and control groups. A random-effects variance components approach was used. Seven meta-analyses were performed (atracurium, d-tubocurarine, gallamine, pancuronium, diazepam, succinylcholine in self-taming doses, and lidocaine). For each meta-analysis there was statistically significant heterogeneity among studies. Atracurium, d-tubocurarine, gallamine, pancuronium, diazepam, and lidocaine all significantly decreased the frequency of myalgias by about 30%. Succinylcholine in self-taming doses alone was not efficacious.
The occurrence, location, and severity of muscle pain were determined when vecuronium was used in lieu of succinylcholine during outpatient laparoscopy. Postoperative muscle pain, in 11 body parts, was assessed by a linear analogue scale questionnaire that was completed by each patient on the evening of surgery and for the next three mornings. All patients had general endotracheal anesthesia with nitrous oxide, thiopental, and fentanyl. Succinylcholine 1.5 mg/kg (3-4 min after 3 mg of d-tubocurarine) was given to 14 patients for tracheal intubation and then by infusion for additional muscle relaxation. Another 14 patients received vecuronium 50 micrograms/kg iv as the only muscle relaxant used; all of these patients had residual neuromuscular blockade antagonized with glycopyrrolate 7 micrograms/kg and edrophonium 0.5 mg/kg iv. Both groups were similar in age, weight, length of procedure, time to discharge, and amount of thiopental and fentanyl used (P greater than 0.05). No difference was noted in either group with respect to the severity of pain by body part over time. Mean total body pain scores were generated for each group at all four intervals as an alternate type of analysis. No statistical significance was demonstrated by a Student's t test in any group at any interval sampled. The authors failed to demonstrate that the substitution of vecuronium for succinylcholine lowers the incidence of myalgia when used in outpatient diagnostic laparoscopy. They refrain from concluding that vecuronium contributes to postanesthetic myalgia, but feel justified in stating that the avoidance of succinylcholine did not lower the severity or occurrence of muscle pains after laparoscopy when vecuronium was used in its place.
We compared the incidence of postoperative myalgia (POM) and fasciculations when atracurium (ATR) or d-tubocurarine (DTC) was given prior to succinylcholine (SDC) for tracheal intubation in 44 ASA class I or II outpatient females undergoing laparoscopy. The subjects were assigned to one of three groups: group 1 received 0.025 mg/kg ATR; group 2 received 0.05 mg/kg DTC; and group 3 received saline (NS), all in a double-blind manner. Thiopental was administered 1 min and 45 sec after pretreatment in doses adequate to allow control of ventilation. Three minutes after pretreatment, SDC 1.5 mg/kg was given, and fasciculations were recorded on a scale of 0-3. All patients were questioned 1 and 3 days postoperatively about POM, using a scale of 0-3. Fasciculations occurred in 79% of patients given saline, in 46% of those receiving ATR, and in 12% of those given DTC. Eighty-five percent of ATR patients were free of POM on postoperative day 1. The corresponding figures for DTC and NS were 59% and 43%, respectively. Only the difference between ATR and NS achieved statistical significance. On the third postoperative day, POM was rare and there were no significant differences among the groups. We conclude that DTC is a better defasciculant than ATR. DTC was, however, not significantly better than NS in the prevention of POM. The findings suggest that ATR may be the drug choice for the prevention of POM.
The hypothesis that prostaglandin inhibitors might reduce the incidence and severity of suxamethonium-induced myalgia was
investigated using lysine acetyl salicylate (LAS) 13 mg kg−1 i.v. 3 min before the administration of suxamethonium in 20 patients. A comparison was made with atracurium 0.09 mg kg−1 (and placebo) in a double-blind prospective randomized trial. LAS and atracurium were effective in reducing the incidence
and severity of post-suxamethonium myalgia and the increases in serum potassium concentration. There were no appreciable changes
in serum calcium, sodium, chloride, phosphate, magnesium, creatinine, creatine phosphokinase concentrations or plasmacholinesterase
activity. Atracurium caused a delay in the onset of action and a decrease in the intensity of suxamethonium-induced neuromuscular
block. It is concluded that LAS pretreatment might have a place in suitable patients in the prevention of suxamethonium-induced
myalgia and increases in serum potassium concentration.
This study compares the action of inhibitors of the eicosanoid cascade on calcium-induced myofilament damage in cardiac muscle of the perfused frog heart and incubated frog ventricle slices, and in skeletal muscle of incubated mammalian diaphragm and isolated and saponin-skinned amphibian pectoris cutaneous muscle. Mepacrine (10(-5) M) and indomethacin (3 x 10(-6) M) protected completely against myofilament damage induced by entry of calcium in the 'calcium-paradox' in frog heart. However, inhibition of phospholipase A2 (PLA2) (with chlorpromazine, 2 x 10(-4) M, or mepacrine, 10(-5) M, 5 x 10(-5) M), of cyclo-oxygenase enzymes (with indomethacin, 3 x 10(-6) M to 10(-5) M or BW755C, 3.8 x 10(-4) M), or of lipoxygenase enzymes (with BW755C, 3.8 x 10(-4) M or nordihydroguaiaretic acid, 2 x 10(-6) M or 5 x 10(-6) M) all failed in intact cardiac or skeletal muscle cells to prevent the myofilament damage that is rapidly triggered by 10(-2) M caffeine, 6 x 10(-6) M ruthenium red, 10(-4) M DNP or 5 micrograms ml-1 A23187. These agents also failed completely to protect against myofilament damage in saponin-skinned amphibian skeletal muscle when [Ca]i was raised to 8 x 10(-6) M. Thus, inhibition of PLA2 does not protect the myofilament apparatus against calcium released intracellularly, and it is suggested that mepacrine and indomethacin can block entry of calcium in the calcium-paradox in the amphibian heart. Chlorpromazine (2 x 10(-4) M) and mepacrine (10(-3) M) at zero [Ca] caused severe myofilament damage in skinned muscle, possibly due to an effect on membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
Eighty-four fit, unpremedicated patients who presented for routine surgery and received a standard anaesthetic technique were allocated randomly to three equal groups. Group 1 received tubocurarine 0.05 mg/kg before induction of anaesthesia. Group 2 received soluble aspirin 600 mg orally one hour before surgery, while Group 3 received no pretreatment. Aspirin prophylaxis produced a significant reduction in the incidence of subsequent suxamethonium-induced myalgia and the improvement was similar to that achieved with tubocurarine pretreatment. Pre-operative oral administration of aspirin effectively reduces muscle pains and avoids many of the complications associated with pretreatment with non-depolarising agents.
Muscle fasciculations and pain following the administration of suxamethonium were assessed in a group of patients who performed
a series of stretch exercises approximately 1 h before operation. Comparison was made with a group who received suxamethonium
but no pretreatment. Fasciculations were significantly reduced in the exercised group, and the incidence of muscle pain decreased
from 52% in the untreated group to 12% in the exercised group. A significant relationship was shown between the severity of
visible fasciculations and muscle pain.
One hundred gynaecological patients for laparoscopy divided into five groups were studied to determine the effects of a number of pretreatments on serum myoglobin, creatinine kinase and myalgia following intermittent suxamethonium administration. One group acted as controls, while the other groups were given intravenous pretreatments of alcuronium 2 mg, midazolam 0.15 mg/kg, lignocaine 1.5 mg/kg and suxamethonium 7 mg. Serum myoglobin was determined by radio-immunoassay. The mean increases in the control group were 167 micrograms/litre myoglobin at 20 minutes and 196 IU creatinine kinase at 24 hours; 13 out of 20 patients responded with a marked increase of serum myoglobin at 20 minutes and of creatinine kinase at 24 hours. Only alcuronium pretreatment prevented myoglobin increase at 20 minutes, abolished creatinine kinase increase at 24 hours and reduced 24-hour myalgia. The other pretreatments slightly reduced myoglobin increase at 20 minutes and 24-hour creatinine kinase but did not reduce myalgia. Only one patient in the whole study had markedly elevated serum myoglobin at 24 hours. We conclude that only non-depolarising relaxant pretreatment is effective in the reduction of some of the adverse effects of suxamethonium administration.
In fit unpremedicated patients undergoing minor operations and who were ambulant on the afternoon of the operations, pretreatment with magnesium sulphate given intravenously did not reduce the incidence of suxamethonium induced myalgia below that in a similar series who received no prophylactic therapy. The injection of magnesium in conscious patients is followed by unpleasant side effects.
The frequency of post-suxamethonium pain after pretreatment with small doses of non-depolarizing neuromuscular blocking agents
was studied in 299 patients. Gallamine 10 and 20 mg, tubocurarine 5 mg and pancuronium 1 mg were equally effective when a
2-min interval was allowed between their injection and suxamethonium administration. Fazadinium was ineffective and caused
difficulty with intubation. No evidence supporting the concept that dosage should be related to patient's weight was found.
Inpatients suffered from post-suxamethonium pain as much as did outpatients.
The role of calcium-activated degenerative processes in the efflux of enzyme from experimentally damaged mouse muscle has been studied using an isolated mouse soleus muscle preparation. Inhibition of mitochondrial activity with dinitrophenol or sodium cyanide was found to cause a large efflux of enzyme. This was largely prevented by withdrawal of the extracellular calcium suggesting that mitochondrial calcium overload does not play a major role in the damage leading to enzyme efflux.
Treatment of the muscles with a variety of protease inhibitors had no effect on the enzyme efflux from muscles following exhaustive contractile activity indicating that activation of protease activity is not a major factor in the damaging process. Certain inhibitors of phospholipase-A activity (i.e. dibucaine, chlorpromazine and mepacrine) have been found to significantly reduce the enzyme efflux following treatment of the muscles with dinitrophenol, although other phospholipase inhibitors were without effect.
It is suggested that the changes in muscle membrane permeability leading to enzyme efflux following experimental muscle damage are probably the result of calcium-mediated activation of phospholipase A leading to changes in membrane phospholipid metabolism.
Isolated, intact frog muscles bathed in control saline release creatine kinase (CK) and lactate dehydrogenase (LDH) at constant rates for several hours. The basal rates of release from "toe" muscles (CK 0.087%/min; LDH 0.105%/min) were one order of magnitude greater than those from semitendinosus muscles. This is attributed to differences in muscle mass and geometry, and to the smaller diameter of toe muscle fibers. Enzyme release rates were not affected by Na-free or Cl-free solutions, whereas LDH release rate doubled during exposure to Ca-free (EGTA-containing) saline or in the presence of isosmotic solutions containing 120 mM KCl or potassium propionate. Following mechanical injury or detergent treatment (Brij 58), the enzyme release rates into Ca-free medium reached peak values 4 and 16 times (toe muscle), and 16 and 20-30 times (semitendinosus), respectively, the control rates. The greater effect of detergent treatment is ascribed to a larger area of sarcolemmal damage plus possible changes in the state of the enzymes in the sarcoplasm.
A technique of induction of anaesthesia using lignocaine throat spray before injection of suxamethonium is described. The
frequency and severity of suxamethonium-induced muscle pains were significantly reduced compared with a control group who
received the same anaesthetic without lignocaine.