JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (3)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Werawatganon, T.
Right arrow Articles by Punyatavorn, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Werawatganon, T.
Right arrow Articles by Punyatavorn, S.
Related Collections
Right arrow Airway
Right arrow Pharmacology

Anesth Analg 2004;98:1676-1679
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000112313.67414.53


ANESTHETIC PHARMACOLOGY

Muscular Injury After Succinylcholine and Electroconvulsive Therapy

Thewarug Werawatganon, MD, Oranuch Kyokong, MD, MSc, Somrat Charuluxananan, MD, MSc, and Sahadol Punyatavorn, MD

From the Department of Anesthesiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand

Address correspondence and reprint requests to Thewarug Werawatganon, Department of Anesthesiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand 10330. Address email to thewarug{at}hotmail.com


    Abstract
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Both succinylcholine and seizures cause muscular injury during electroconvulsive therapy. We compared the muscular damage in two groups of patients. The psychiatric patient group received succinylcholine for electroconvulsive therapy. The surgical patient group received succinylcholine for endotracheal intubation. Serum myoglobin was measured as a marker for muscular injury and myalgic symptoms were also recorded. Serum myoglobin increased from baseline in both groups at 5 and 20 min. The surgical patients, however, had a higher myoglobin level than the psychiatric patients at 5 and 20 min after the administration of succinylcholine (P < 0.001). The median (range) of myoglobin concentration at 20 min in psychiatric patients was 32.6 (23.1–60.1) ng/mL, compared with 61.2 (31.6–1687.0) ng/mL in surgical patients. The incidence of myalgia was not different between the two groups. In conclusion, we unexpectedly conclude that the psychiatric patients who received electroconvulsive therapy had less effect of muscular damage associated with succinylcholine than the surgical patients did.

IMPLICATIONS: Both succinylcholine and electroconvulsive therapy cause muscular injury. However, we unexpectedly found that psychiatric patients who received succinylcholine and electroconvulsive therapy had less muscular damage than surgical patients who received succinylcholine for intubation. Therefore, appropriate use of succinylcholine can attenuate the muscular damaging effect from the therapy.


    Introduction
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Succinylcholine has been used to attenuate the severity of motor convulsion in the body and to minimize injury from electroconvulsive therapy (ECT) (1). However, succinylcholine is associated with muscular injury and increased muscle enzymes (2,3). Serum myoglobin levels have been found to increase in a dose-related manner after succinylcholine administration (4).

There have been reports of muscle pain after ECT, both with and without succinylcholine (5–7). Some patients suffer from severe myalgia, which interferes with their normal daily activity. They do not move because of muscle pain, like catatonic patients. Seizures can cause direct muscular injury and increase serum muscle enzymes (8). There has been no investigation focusing on the muscular injury and myoglobin increases from ECT. Does succinylcholine combined with ECT cause more muscular injury than succinylcholine alone? It is not known whether convulsions or succinylcholine plays the most important role in muscular injury during the therapy. The objective of this study was to assess the muscle damaging effect from ECT by comparing myoglobin levels in psychiatric patients who received succinylcholine and ECT with those of surgical patients who received succinylcholine without electroconvulsive stimulation.


    Methods
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
The Ethics Committee of the Faculty of Medicine, Chulalongkorn University approved this study protocol. We used a match paired cohort study design. The first group consisted of psychiatric patients who were scheduled to receive ECT. Those in the control group were surgical patients who were scheduled to receive operations that required succinylcholine for endotracheal intubation (Table 1). The case and the control were matched by sex, age, weight, and height. All patients were older than 20 yr of age. The patients or their responsible relatives gave their informed consent for the study. The exclusion criteria were a history of systemic diseases or neuromuscular problems or receiving medications that might interact with the effect of succinylcholine or serum myoglobin.


View this table:
[in this window]
[in a new window]
 
Table 1. Patients and Type of Operation
 
The primary outcome measurement was myoglobin concentration at 20 min after succinylcholine injection. From previous study, the standard deviation (SD) of myoglobin concentrations was 102.4 ng/mL (9). We set the minimal difference in means to be detected at 0.6 SD, which was 60 ng/mL. By allowing type I error at 0.05 with 80% power, the sample size for match paired study should be 25 patients per group.

Thiopental 4–5 mg/kg was given IV for induction of anesthesia. Then 1.0 mg/kg of succinylcholine was injected IV after the patients were unconscious. After full relaxation, psychiatric patients received electrical stimulation for convulsion by MECTA SR (MECTRA Corporation, Portland, OR). A responsible psychiatrist determined the proper stimulus for each patient. In case of multiple electroconvulsive therapies or failure to induce seizure, additional electrical stimulus could be given at the psychiatrist’s discretion. Supplemental doses of thiopental or succinylcholine were allowed when needed.

The surgical patients, who received the same medication in the same manner, received endotracheal intubation instead of ECT. Then anesthesia was maintained with isoflurane, nitrous oxide, and nondepolarizing muscle relaxant. The preparation for surgery, such as positioning and cleaning, was allowed, but the main surgical procedure was started after the last blood sampling.

Venous blood samples were collected before induction of anesthesia and at 1, 5, and 20 min after the administration of succinylcholine. Serum from these samples was centrifuged, separated, and stored for analysis of myoglobin by the electrochemiluminesent technique (Elecsys Myoglobin STAT; Roche Diagnostics GmbH, Mannheim, Germany). The measurement was sensitive up to 3000 ng/mL and had lower limit of quantification at 21 ng/mL. The normal range, 2.5th–97.5th percentiles, in healthy men was 28–72 ng/mL, which was slightly higher than the normal range in women.

After 1 and 24 h from the procedure, the patients were questioned about the presence and severity of myalgia, which was graded as nil (absence of pain), mild (muscle stiffness or pain requiring no treatment), moderate (muscle stiffness and pain complained of by the patient spontaneously, requiring analgesia), or severe (incapacitating generalized muscle stiffness or pain, interfering with daily activity).

The data analysis was performed at the end of the study using SPSS version 9.0 software for Windows (SPSS, Chicago, IL). The assumption of normal distribution was checked with a scatter plot, histogram, and Shapiro-Wilk test. If the assumption was rejected, a nonparametric test would be done to compare the difference of serum myoglobin between the two groups after succinylcholine administration. The level of statistical significance was set at P < 0.05.


    Results
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
There were 25 psychiatric patients and 25 surgical patients recruited into the study. The characteristics of the patients in both groups were comparable (Table 2). The average dose of thiopental in surgical patients was more than in psychiatric patients. The myoglobin level data had many outliers and their distribution was not normal (Shapiro-Wilk test; P = 0.01); therefore, nonparametric statistics were used. The myoglobin level in both groups significantly increased from baseline at 5 and 20 min after succinylcholine administration. When we compared the level between the groups (Table 3), the surgical patients had a higher myoglobin level than the psychiatric patients at 5 min and 20 min after succinylcholine administration (Wilcoxon’s signed-ranks test; P < 0.001). There were 4 patients in each group who had myalgia, but their symptoms were mild and required no analgesic medication. No other serious adverse effects, such as acute rhabdomyolytic renal failure or malignant hyperthermia, were found.


View this table:
[in this window]
[in a new window]
 
Table 2. Demographic Data of the Psychiatric ECT Group Compared with Surgical, Non-ECT Group
 

View this table:
[in this window]
[in a new window]
 
Table 3. Myoglobin Level in the Serum of the Patients in Both Groups (ng/mL)
 
The study patients received ECT 10 times (median), ranging from 2 to 253 times. The antipsychotic medications taken by the patients consisted of major tranquilizers, benzodiazepines, and antidepressants. No patient took medications known to interact with the effect of succinylcholine or serum myoglobin according to the exclusion criteria.


    Discussion
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Succinylcholine depolarizes muscles before paralysis. Some patients had an abnormal response and showed symptoms and signs of muscular injury, such as myalgia and increased muscle enzymes in their serum (10). In this study, we compared the muscular injury from succinylcholine in the ECT patients and in the surgical patients, and the myoglobin level increased in both groups. The results from the surgical patients were comparable to that of previous reports (2,3,11).

However, there was an unexpected finding that, for some reason, the psychiatric patients who received both succinylcholine and ECT had a lower level of serum myoglobin than the surgical patients who received succinylcholine without ECT. The blood sampling in the surgical patients was performed before the surgical operation that might have caused some degree of muscular injury. The differences in the surgical group were endotracheal intubation, isoflurane, nitrous oxide, a nondepolarizing muscle relaxant, and preparation for the surgery such as positioning and cleaning of the operative site. After endotracheal intubation, the surgical patients required some anesthetics to maintain anesthetic depth before surgery. Some patients could have had high serum myoglobin from an abnormal response to succinylcholine in the presence of volatile anesthetics (12,13). There are studies showing that IV or volatile anesthetics given before succinylcholine may affect myoglobin concentrations (11), but whether these effects occur if the anesthetics are given after is less clear (14). Therefore we chose to use inhaled anesthetics that we commonly continue for the entire surgical procedure.

However, the different factors in the ECT group were the antipsychotic medications and the experience of repeated exposure to succinylcholine. The psychiatric patients had received ECT many times. It was unclear whether the repeated exposure to succinylcholine attenuated the effect of the muscular damaging effects of succinylcholine. Hence, further investigations are required.

Serum myoglobin was measured as a marker for muscular injury because it responds more rapidly than other chemical changes and has been cited in most studies. As a biochemical marker of skeletal muscle damage, serum myoglobin concentration at 20 min after suxamethonium administration correlated well with the serum creatine kinase at 24 h after operation (3). Serum potassium was not measured because it increased in the case of hemolysis when the serum was not properly separated and might have confused the results (4).

Myalgia was a common clinical outcome; other serious sequelae of muscular injury, such as acute renal failure, were extremely rare. The overall incidence of myalgia in our study was 16%, which was quite small compared with other studies (15,16). It was surprising that there were no episodes of severe myalgia. The postoperative analgesic drugs in surgical patients might have lessened the incidence and severity of these results, but this would not explain all the results.

The recommended dose of succinylcholine for ECT is between 0.5 and 1.0 mg/kg (17,18). Murali et al. (19) had shown that 1 mg/kg of succinylcholine was more effective than 0.5 mg/kg in modifying peripheral convulsion. Succinylcholine 1 mg/kg was also suitable for endotracheal intubation in a surgical patient; therefore we gave this amount of succinylcholine to each patient in both groups.

A limitation of this study was that we could not take blood samples from the patients who received only succinylcholine without other interventions because there was no justified clinical situation. We did not study the patients who received only electrical stimulation without succinylcholine because of ethical concerns. Another limitation was that the investigator who took the blood samples and the investigator who collected the data about the muscle pain could not be blinded. However, this did not affect the laboratory results.

In conclusion, when motor convulsions were properly attenuated, succinylcholine and ECT did not cause more muscular injury in psychiatric patients than in surgical patients to whom succinylcholine was administered for endotracheal intubation. Further studies are required to explain the smaller change in myoglobin concentration in the patients having both succinylcholine and ECT.


    Acknowledgments
 
Supported, in part, by the Ratchadapiseksompotch Fund, Faculty of Medicine, Chulalongkorn University.


    References
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Fink M. Optimizing ECT. Encephale 1994; 20: 297–302.[Web of Science][Medline]
  2. Laurence AS. Biochemical changes following suxamethonium: serum myoglobin, potassium and creatinine kinase changes before commencement of surgery. Anaesthesia 1985; 40: 854–9.[Web of Science][Medline]
  3. Laurence AS. Myalgia and biochemical changes following intermittent suxamethonium administration: effects of alcuronium, lignocaine, midazolam and suxamethonium pretreatments on serum myoglobin, creatinine kinase and myalgia. Anaesthesia 1987; 42: 503–10.[Web of Science][Medline]
  4. McLoughlin C, Leslie K, Caldwell JE. Influence of dose on suxamethonium-induced muscle damage. Br J Anaesth 1994; 73: 194–8.[Abstract/Free Full Text]
  5. Delilkan AE. Electroconvulsive therapy no-relaxant anaesthesia. Br J Anaesth 1969; 41: 884–9.[Abstract/Free Full Text]
  6. Cheam EW, Critchley LA, Chui PT, et al. Low dose mivacurium is less effective than succinylcholine in electroconvulsive therapy. Can J Anaesth 1999; 46: 49–51.[Web of Science][Medline]
  7. Amornyotin S, Santawat U, Rachatamukayanant P, et al. Can lidocaine reduce succinylcholine induced postoperative myalgia? J Med Assoc Thai 2002; 85 (Suppl 3): S969–74.[Medline]
  8. Nielsen HV, Garsdal P, Hansen PB, et al. Transient impairment of renal function and myoglobin turnover after generalised seizures. Lancet 1987; 2: 104–5.[Medline]
  9. Hernandez-Palazon J, Tortosa JA, Garcia-Palenciano C, et al. Pretreatment with rocuronium prevents fasciculations and blood biochemical changes after suxamethonium administration Br J Anaesth, 1999: 139.
  10. Wong SF, Chung F. Succinylcholine-associated postoperative myalgia. Anaesthesia 2000; 55: 144–52.[Web of Science][Medline]
  11. Noguchi I, Sankawa H, Andou M. The effect of ketamine or thiamylal on succinylcholine-induced myoglobinemia under halothane anesthesia in adults. Anesth Analg 1995; 81: 1015–8.[Abstract]
  12. Broekema AA, Boersma GA, Hennis PJ. A case of malignant hyperthermia? Anaesthesia 1991; 46: 942–5.[Web of Science][Medline]
  13. Sekino N, Hiroki K, Namatame R et al. Effect of induction methods of pediatric anesthesia on serum myoglobin [in Japanese]. Masui 1990; 39: 284–92.[Medline]
  14. Plotz J, Braun J. Effect of selected anesthetics on serum myoglobin levels after administration of succinylcholine: comparison of halothane, enflurane and isoflurane with thiopental in adults [in German]. Anaesthesist 1987; 36: 352–5.[Web of Science][Medline]
  15. Kararmaz A, Kaya S, Turhanoglu S, Ozyilmaz MA. Effects of high-dose propofol on succinylcholine-induced fasciculations and myalgia. Acta Anaesthesiol Scand 2003; 47: 180–4.[Web of Science][Medline]
  16. Schreiber JU, Mencke T, Biedler A, et al. Postoperative myalgia after succinylcholine: no evidence for an inflammatory origin. Anesth Analg 2003; 96: 1640–4.[Abstract/Free Full Text]
  17. Fredman B, Smith I, d’Etienne J, White PF. Use of muscle relaxants for electroconvulsive therapy: how much is enough? Anesth Analg 1994; 78: 195–6.
  18. Konarzewski WH, Milosavljevic D, Robinson M, et al. Suxamethonium dosage in electroconvulsive therapy. Anaesthesia 1988; 43: 474–6.[Web of Science][Medline]
  19. Murali N, Saravanan ES, Ramesh VJ, et al. An intrasubject comparison of two doses of succinylcholine in modified electroconvulsive therapy. Anesth Analg 1999; 89: 1301–4.[Abstract/Free Full Text]
Accepted for publication November 24, 2003.




This article has been cited by other articles:


Home page
Anesth. Analg.Home page
R. Miller
Will Succinylcholine Ever Disappear?
Anesth. Analg., June 1, 2004; 98(6): 1674 - 1675.
[Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (3)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Werawatganon, T.
Right arrow Articles by Punyatavorn, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Werawatganon, T.
Right arrow Articles by Punyatavorn, S.
Related Collections
Right arrow Airway
Right arrow Pharmacology


Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2004 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press