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Case Report

Masseter muscle rigidity after vecuronium

Jenkins, J. G.

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European Journal of Anaesthesiology: February 1999 - Volume 16 - Issue 2 - p 137-139

Abstract

Introduction

Masseter muscle rigidity after suxamethonium is well documented and, in many cases, has been a harbinger of malignant hyperthermia. There are only two previous case reports of masseter spasm or masseter muscle rigidity resulting from a non-depolarizing muscle relaxant [1,2]. I report a case in which laryngoscopy was impossible because of masseter rigidity following vecuronium.

Case report

A 42-year-old, 65 kg woman was admitted for total abdominal hysterectomy and bilateral salpingo-oophrectomy. As far as she was aware, her previous general anaesthetics had been uneventful, although she had always suffered from bad post-operative nausea and vomiting. She was taking norethisterone. Her past medical history was otherwise unremarkable. There was no family history of myotonia or malignant hyperthermia. No premedication was given. Anaesthesia was induced with propofol 200 mg and vecuronium 8 mg. The patient also received granisetron 1 mg, droperidol 2.5 mg, papaveretum 0.5 mL and tenoxicam 20 mg. The patient's lungs were ventilated with oxygen, nitrous oxide and 2% isoflurane. After 2 min, laryngoscopy was attempted but proved impossible because of spasm of the masseter muscles. Isoflurane was discontinued. Supramaximal peripheral nerve stimulation over the ulnar nerve showed complete suppression of neuromuscular transmission. The airway was secured by easy blind nasal intubation of the larynx. There was no evidence of muscle rigidity elsewhere. The pulse rate rose to 96 beats min−1 following intubation and then fell. The arterial oxygen saturation did not fall below 97%. The end-tidal carbon dioxide concentration was 5.7% after intubation, falling to 4.7% over the next 5 min.

Following transfer to the operating theatre, the patient's lungs were ventilated with oxygen and nitrous oxide, and 1% isoflurane was reintroduced. The electrocardiograph, blood pressure, arterial oxygen saturation, inspired oxygen and isoflurane concentrations, end-tidal carbon dioxide concentration and temperature were measured peroperatively. All these parameters remained within expected limits. Forty-five minutes after induction, there was evidence of spontaneous recovery on peripheral nerve stimulation and a further dose of vecuronium 1 mg was given to facilitate closure of the abdomen. Residual paralysis was reversed 60 min after induction using neostigmine 2.5 mg with glycopyrrolate 0.5 mg. The masseter muscle rigidity persisted throughout, resolving as the patient recovered from anaesthesia. Post-operatively, the patient had normal mouth opening.

Discussion

While the most sensitive indicator of potential malignant hyperthermia is an unanticipated increase in the end-tidal carbon dioxide concentration and the most specific sign of malignant hyperthermia is total body rigidity, other common signs are masseter rigidity, tachycardia and tachypneoa [3]. Masseter muscle rigidity is a sustained contracture of the jaw muscles, usually following suxamethonium, that may complicate airway management during anaesthesia. Masseter muscle rigidity following suxamethonium is commoner in children, the incidence being between 1 in 100 000 paediatric anaesthetics in the UK [4] and 1% of all children induced with halothane and then given suxamethonium in the USA [5]. About half the cases of masseter muscle rigidity are found to be malignant hyperthermia susceptible [4,6,7]. Clinical signs of malignant hyperthermia occur in about 10% of cases of masseter muscle rigidity. However, if generalized rigidity also occurs, then malignant hyperthemia is highly likely [3]. While masseter muscle rigidity usually occurs following concurrent administration of halothane and suxamethonium, it has also been reported following suxamethonium in the absence of a halogenated anaesthetic [8]. There is evidence that suxamethonium-induced masseter muscle rigidity is associated with a mutation in the adult muscle sodium channel α-subunit gene [9].

While all volatile anaesthetics can trigger malignant hyperthermia, no case of masseter muscle rigidity following the isolated use of inhalational anaesthesia has been reported. There are only two previous case reports of masseter muscle rigidity caused by a non-depolarizing muscle relaxant. In a case reported by Polka and colleagues, a 20-year-old, 70 kg man undergoing aortic valvulotomy developed masseter spasm after pancuronium [1]. Repeat exposure to pancuronium, later the same day, provoked the same response. On this second occasion, the authors were able to demonstrate a contracture response using electromyography. More recently, Albrecht and colleagues reported a case in which a 33-year-old, 61 kg woman scheduled to have a laparoscopy and hysteroscopy developed masseter muscle rigidity after vecuronium; the surgery was abandoned [2]. Five days later, the patient developed masseter muscle rigidity when given mivacurium. In both cases, the creatinine kinase was not raised. In each episode, the masseter muscle rigidity persisted throughout the anaesthetic.

Unexpected difficulty with mouth opening is not necessarily caused by masseter muscle rigidity. Temperomandibular joint disease, in particular anterior displacement of the temperomandibular disc, can cause the mouth to lock in the closed position [10]. Anatomical abnormalities or light anaesthesia may also reduce mouth opening.

It appears from the limited data available that non-depolarizing muscle relaxants can, very rarely, cause masseter muscle rigidity in adults. This masseter muscle rigidity may complicate airway management, but is unlikely to progress to generalized rigidity and malignant hyperthermia. The mechanism of masseter muscle rigidity after non-depolarizing muscle relaxants is unknown. Vecuronium, pancuronium and atracurium have been determined to be safe drugs for malignant hyperthermia patients, and the newer muscle relaxants mivacurium, rocuronium, pipercuronium and doxacurium are also considered safe [3]. Neither this nor the two previous case reports contradict that view.

References

1 Polka TA, Hanisch Jr EC, Nasser JG, Ramsborg GC, Roelofs RI. Masseter spasm after pancuronium. Anesth Analg 1980; 59: 509-511.
2 Albrecht A, Wedel DJ, Gronert GA. Masseter muscle rigidity and nondepolarizing neuromuscular blocking agents. Mayo Clin Proc 1997; 72: 329-332.
3 Malignant Hyperthermia Association of the United States. Managing malignant hyperthermia. Available from URL: http://gasnet.med.yale.edu/gta/mh/clinical_update.html.
4 Christian AS, Ellis FR, Halsall PJ. Is there a relationship between masseteric muscle spasm and malignant hyperpyrexia? Br J Anaesth 1989; 62: 540-544.
5 Schwartz L, Rockoff MA, Koka BV. Masseter spasm with anaesthesia: incidence and implications. Anesthesiology 1984; 61: 772-775.
6 Rosenberg H, Fletcher JE. Masseter muscle rigidity and malignant hyperthermia susceptibility. Anesth Analg 1986; 65, 161-164.
7 O'Flynn RP, Shutack JG, Rosenberg H, Fletcher JE. Masseter muscle rigidity and malignant hyperthermia susceptibility in pediatric patients. Anesthesiology 1994; 80: 1228-1233.
8 Marohn ML, Nagia AH. Masseter muscle rigidity after rapid-sequence induction of anesthesia. Anesthesiology 1992; 77: 205-207.
9 Vita GM, Olckers A, Jedlicka AE, George AL, Heiman-Patterson T, Rosenberg H, Fletcher JE, Levitt RC. Masseter muscle rigidity associated with glycine1306-to-alanine mutation in the adult muscle sodium channel α-subunit gene. Anesthesiology 1995; 82: 1097-1103.
10 Yemen TA. Are we obsessed with masseter rigidity? Temporomandibular joint disease mistakenly diagnosed as masseter muscle rigidity on two separate occasions in one patient. Anesth Analg 1993; 77: 848-850.
Keywords:

Non-depolarizing muscle relaxants; vecuronium; masseter muscle rigidity

© 1999 European Academy of Anaesthesiology