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Table of Contents
Year : 2011  |  Volume : 27  |  Issue : 3  |  Page : 380-382

Rocuronium and sugammadex: An alternative to succinylcholine for electro convulsive therapy in patients with suspected neuroleptic malignant syndrome

Department of Anaesthesia, Consultant, Letterkenny General Hospital, Letterkenny, Ireland

Date of Web Publication11-Aug-2011

Correspondence Address:
Karthik G Ramamoorthy
23, Fox Hills, Letterkenny Ireland, Letterkenny
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-9185.83687

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We report a case of presumptive neuroleptic malignant syndrome requiring muscle relaxation for electro-convulsive therapy. short acting muscle relaxation without the use of succinylcholine was achieved using rocvronivm reversed with the novel reversal agent sugammadex. We suggest that this combination is a safe and effective alternative to succinylcholine in such cases.

Keywords: Neuroleptic malignant syndrome, electro convulsive therapy, succinyl choline, rocuronium, sugammadex

How to cite this article:
Ramamoorthy KG, Downey H, Hawthorne P. Rocuronium and sugammadex: An alternative to succinylcholine for electro convulsive therapy in patients with suspected neuroleptic malignant syndrome. J Anaesthesiol Clin Pharmacol 2011;27:380-2

How to cite this URL:
Ramamoorthy KG, Downey H, Hawthorne P. Rocuronium and sugammadex: An alternative to succinylcholine for electro convulsive therapy in patients with suspected neuroleptic malignant syndrome. J Anaesthesiol Clin Pharmacol [serial online] 2011 [cited 2020 Jan 27];27:380-2. Available from:

   Introduction Top

Since 1938, when the use of electro convulsive therapy (ECT) was first described in the literature, it has played a major role in psychiatric medicine. [1] Also, since its introduction in the 1950's, succinylcholine has remained the most common muscle relaxant used to modify the motor effects of ECT. A coincidental association between neuroleptic malignant syndrome (NMS) and malignant hyperthermia (MH) may render succinylcholine unsafe in some patients undergoing ECT. There is conflicting evidence for this in the literature. [2],[3]

   Case Report Top

A 69-year-old woman, of weight 50 kg, was admitted to the psychiatric service requiring anesthesia for ECT to treat severe depression. She presented with a presumptive diagnosis of NMS, Parkinson's disease, rheumatoid arthritis, celiac disease, and hypertension. Current medications included dantrolene, bromocriptine, amlodipine, thiamine, and calcium. She was found to be non-verbal, rigid, and posturing. She had an edentulous airway, with Mallampatti score of II, and had limited neck movement. Magnetic resonance imaging (MRI) showed moderate degenerative changes at C3/4 vertebrae and a normal odontoid peg. A review of other systems was unremarkable. Her heart rate was 80/min, blood pressure was 130/86 mm Hg, and temperature was 36.5°C.

All ECT procedures were performed in the operating theatre with standard monitoring. ECT was administered using Thymatron System IV (SOMATICS Lake Bluff, IL, USA), with bitemporal electrode placement. Induction of anesthesia was accomplished with propofol 80 mg and rocuronium 50 mg (1 mg/kg).The patient was hyperventilated by face mask with 100% O 2 through a vapor-free Datex-Ohmeda anesthesia machine. Three minutes after the administration of rocuronium and deep blockade confirmed with a neuromuscular monitor (Life -Tech model ms IV; Mini Stim), ECT was performed. The treatment produced a satisfactory motor and electroencephalogram (EEG) seizure. The mean EEG endpoint of seizure was 26.5 sec. Muscle relaxation with rocuronium was satisfactory in preventing violent muscle contraction. Sugammadex 800 mg (16 mg/ kg) was administered after ECT approximately 5 min after the administration of rocuronium. Recovery of train of four (TOF) ratio to 0.9 was within 2 min and the time to first spontaneous breath was within 3 min from the administration of sugammadex. HR, BP, and temperature were measured before anesthesia induction, pre-seizure, post-seizure, and every minute for 10 min thereafter, and remained stable throughout the procedure. Rocuronium and sugammadex were employed in all subsequent ECTs and found to be an excellent and safe alternative to succinylcholine in this patient.

   Discussion Top

Neuroleptic malignant syndrome is a relatively rare but potentially fatal complication of the use of neuroleptic drugs. [4] NMS has been associated with all dopamine blocking drugs such as antipsychotics (phenothiazines, butyrophenones, thioxanthenes, benzamides, and recent drugs such as clozapine and risperidone) [5] and antiemetics (metoclopramide, prochlorperazine, promethazine, and droperidol). [5] Abrupt withdrawal of dopaminergic drugs may also produce an NMS-like condition.

NMS pathophysiology is complex and probably involves an interplay between multiple central and systemic pathways and neurotransmitters. Dopamine blockade in the hypothalamus is believed to contribute to thermoregulatory failure, and blockade in the nigrostriatal system may contribute to muscle rigidity and hypermetabolism. The loss of dopaminergic input to the anterior cingulate-medial orbitofrontal circuit and the lateral orbitofrontal circuit likely contributes to changes in the mental status and catatonic features seen in NMS. [6] These medications in susceptible individuals block dopamine, thereby triggering NMS. NMS typically develops over a period of 24-78 hours following antipsychotic initiation, although the condition can occur at any time during treatment.

Diagnosis of NMS is based on clinical criteria. The presence of all three major or two major and four minor manifestations indicates a high probability of NMS. [7] [Table 1]
Table 1: Clinical criteria for diagnosis of NMS[7]

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NMS is a self-limiting condition once the offending agent has been discontinued. General symptomatic treatment such as hydration, nutrition, reduction of fever, and treatment of secondary complications (hypoxia, acidosis, renal failure) are essential. [8] Specific treatments include lorazepam, dantrolene, bromocriptine, and amantadine. [8] ECT itself also appears to be rapidly effective. [9]

Muscle relaxants are often administered during ECT to prevent myalgia and more serious musculoskeletal complications. [10] Succinylcholine remains the most commonly used muscle relaxant, [11] but is not recommended in patients with a history of susceptibility to MH, NMS, catatonic schizophrenia or organophosphate poisoning. [12],[13] There are clinical reports describing the use of other muscle relaxants in this high-risk group of patients.

Mivacurium is the drug most often administered as an alternative to succinylcholine during ECT. [3] However, a dose-finding study reported that only a full intubating dose of mivacurium (0.2 mg/kg) was associated with effective muscle relaxation during ECT. [14] At least two clinical studies have demonstrated that at higher doses, it causes clinically significant histamine release and hypotension. [11],[15] Atracurium has been used as an alternative, but a dose of 0.5 mg/kg required more time to achieve a satisfactory TOF ratio and recovery. [16],[17] Rapacuronium at doses of 0.6-0.8 mg/kg provided effective muscle relaxation for ECT and was readily reversible with edrophonium and atropine. Frequent occurrence of bronchospasm led to its withdrawal from the market, [18],[19] so it is no longer a viable alternative.

We submit that the combination of rocuronium and sugammadex offers a serious alternative to succinylcholine in patients with neuroleptic malignant syndrome for ECT.

   References Top

1.Khan A, Mirolo MH, Hughes D, Bierut L. Electroconvulsive therapy. Psychiatr Clin North Am 1993;16:497-513.  Back to cited text no. 1
2.Devanand DP, Sackeim HA, Finck AD. Modified ECT using succinylcholine after remission of Neuroleptic malignant syndrome. Convuls Ther 1987;3:284-90.  Back to cited text no. 2
3.Kelly D, Bruell SJ. Neuroleptic malignant syndrome and mivacurium: A safe alternative to succinyl choline? Can J Anaesth 1994;41:845-9.  Back to cited text no. 3
4.Caroff SN, Mann SC. Neuroleptic malignant syndrome. Med Clin North Am. 1993;77:185-202  Back to cited text no. 4
5.Keck PE Jr, Pope HG Jr, McElroy SL. Declining frequency of neuroleptic malignant syndrome in a hospital population. Am J Psychiatry. 1991;148:880-882.  Back to cited text no. 5
6.Mann SC, Caroff SN, Fricchione G, Campbell EC. Central dopamine hypoactivity and the pathogenesis of neuroleptic malignant syndrome. Psychiatr Ann 2000;30:363-74.  Back to cited text no. 6
7.Levenson JL. Neuroleptic malignant syndrome. Am J Psychiatry 1985;142:1137-45.  Back to cited text no. 7
8.Rosenberg MR, Green M. Neuroleptic malignant syndrome: Review of response to therapy. Arch Intern Med 1989;149:1927-31.  Back to cited text no. 8
9.Hermesh H, Aizenberg D, Weizman A. A successful electroconvulsive treatment of neuroleptic malignant syndrome. Acta Psychiatr Scand 1987;75:237-9.  Back to cited text no. 9
10.Nott MR, Watts JS. A fractured hip during electro-convulsive therapy. Eur J Anaesthesiol 1999;16:265-7.  Back to cited text no. 10
11.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.  Back to cited text no. 11
12.Cooper RC, Baumann PL, McDonald WM. An unexpected hyperkalemic response to succinylcholine during electroconvulsive therapy for catatonic schizophrenia. Anesthesiology 1999;91:574-5.  Back to cited text no. 12
13.Jaksa RJ, Palahniuk RJ. Attempted organophosphate suicide: A unique cause of prolonged paralysis during electroconvulsive therapy. Anesth Analg 1995;80:832-3.  Back to cited text no. 13
14.Cheam EW, Critchley LA, Chui PT, Yap JC, Ha VW. Low- dose mivacurium is less effective than succinylcholine in electroconvulsive therapy. Can J Anaesth 1999;46:49-51.  Back to cited text no. 14
15.Gitlin MC, Jahr JS, Margolis MA, McCain J. Is mivacurium chloride effective in electroconvulsive therapy? A report of four cases, including a patient with myasthenia gravis. Anesth Analg 1993;77:392-4.  Back to cited text no. 15
16.Lui PW, Ma JY, Chan KK. Modification of tonic-clonic convulsions by atracurium in multiple-monitored electroconvulsive therapy. J Clin Anesth 1993;5:16-21.  Back to cited text no. 16
17.Hickey DR, O'Connor JP, Donati F. Comparison of atracurium and succinylcholine for electroconvulsive therapy in a patient with atypical plasma cholinesterase. Can J Anaesth 1987;34:280-3.  Back to cited text no. 17
18.Kadar AG, Kramer BA, Barth MC, White PF. Rapacuronium: An alternative to succinylcholine for electroconvulsive therapy. Anesth Analg 2001;92:1171-2.  Back to cited text no. 18
19.White PF. Rapacuronium: Why did it fail as a replacement for succinylcholine? Br J Anaesth 2002;88:163-5.  Back to cited text no. 19


  [Table 1]

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2 Prolonged neuromuscular block with succinylcholine after ultrashort anaesthesia - Do we need alternatives? [Verlängerte neuromuskuläre blockade durch succinylcholin nach ultrakurznarkose: Sind alternativen notwendig?]
Mangen, J. and Ghezel-Ahmadi, V. and Beck, G.
Anasthesiologie und Intensivmedizin. 2013; 54(5): 254-257


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