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Masseter Muscle Rigidity and Nondepolarizing Neuromuscular Blocking Agents

1997; Elsevier BV; Volume: 72; Issue: 4 Linguagem: Inglês

10.4065/72.4.329

1942-5546

Alison Albrecht, Denise J. Wedel, Gerald A. Gronert,

Ion channel regulation and function

Masseter muscle rigidity has been identified as a possible risk factor for malignant hyperthermia (MH) and is usually noted in children receiving intravenously administered succinylcholine chloride after mask induction with halothane. Nondepolarizing muscle relaxants are considered safe for persons susceptible to MH. In this article, we present a case of clinically recognized jaw rigidity in the absence of succinylcholine after administration of a nondepolarizing muscle relaxant that was reported to the Malignant Hyperthermia Association of the United States hot line. The patient had recurrent jaw rigidity during subsequent anesthesia when a different nondepolarizing muscle relaxant was given. The North American MH Registry was then reviewed for similar cases. Three cases of masseter muscle rigidity in the presence of nondepolarizing muscle relaxants were discovered. Two of the patients were not found to be susceptible to MH; however, the third patient had positive findings on muscle biopsy. These cases do not provide enough information to confirm the ability of nondepolarizing muscle relaxants to cause jaw rigidity in the absence of MH. Masseter muscle rigidity has been identified as a possible risk factor for malignant hyperthermia (MH) and is usually noted in children receiving intravenously administered succinylcholine chloride after mask induction with halothane. Nondepolarizing muscle relaxants are considered safe for persons susceptible to MH. In this article, we present a case of clinically recognized jaw rigidity in the absence of succinylcholine after administration of a nondepolarizing muscle relaxant that was reported to the Malignant Hyperthermia Association of the United States hot line. The patient had recurrent jaw rigidity during subsequent anesthesia when a different nondepolarizing muscle relaxant was given. The North American MH Registry was then reviewed for similar cases. Three cases of masseter muscle rigidity in the presence of nondepolarizing muscle relaxants were discovered. Two of the patients were not found to be susceptible to MH; however, the third patient had positive findings on muscle biopsy. These cases do not provide enough information to confirm the ability of nondepolarizing muscle relaxants to cause jaw rigidity in the absence of MH. Masseter muscle rigidity (MMR) has been previously described as part of the syndrome of malignant hyperthermia (MH). MMR most commonly occurs in the pédiatrie population after induction with halothane and succinylcholine chloride. When a case of MMR that occurred after administration of vecuronium bromide was reported to one of us (D.J.W.) on the Malignant Hyperthermia Association of the United States (MHAUS) hot line, the North American MH Registry (NAMHR) was searched for previously reported cases of MMR related to the administration of nondepolarizing neuromuscular blocking agents. At our request, the NAMHR was cross-referenced for cases that involved MMR and the administration of nondepolarizing muscle relaxants without the use of succinylcholine. Three such cases were identified, and the available information was forwarded to us after confidentiality of the patients was ensured. All four cases are subsequently described. MHAUS Case.—A 33-year-old woman, class 1 based on the American Society of Anesthesiologists (ASA) (weight, 61 kg), underwent diagnostic laparoscopy and hysteroscopy because of infertility. She had an 8-pack-year history of smoking and dysmenorrhea. The patient had previously undergone uncomplicated general anesthesia. She had no family history of anesthesia-related complications. A preoperative airway examination revealed no anatomic abnormalities. Routine monitoring included the use of a blood pressure cuff, precordial stethoscope, continuous electrocardiog-raphy, pulse oximetry, peripheral nerve stimulator, and temperature probe. After preoxygenation with 100% 02, midazolam, 2 mg, and fentanyl citrate, 100 g, were administered intravenously (IV). General anesthesia was induced with 250 mg of thiopental sodium IV and 3% desflurane. Vecuronium, 5 mg, was then administered IV to facilitate trachéal intubation. Once the nerve stimulator indicated loss of the train-of-four response, endotracheal intubation was attempted. The certified registered nurse anesthetist who administered vecuronium was unable to open the patient's mouth despite application of considerable force. Mask ventilation was unimpaired. A second dose of vecuronium, 4 mg, was administered IV. Finally, 30 mg of atracurium besylate was administered IV. No improvement in the degree of mouth opening occurred with any of these pharmacologie maneuvers, although the nerve stimulator continued to document neuromuscular blockade. At that point, the possibility of an atypical reaction to vecuronium or an MH episode was considered, and thus the MHAUS hot line was contacted. After a discussion with the hot line consultant, arterial blood gas (ABG), serum potassium (K+), and creatine kinase (CK) determinations were obtained. Results were as follows: pH, 7.35; partial arterial pressure of C02, 48 mm Hg; partial arterial pressure of 02,488 mm Hg; 02 saturation, 100%; base excess, 0.5; bicarbonate, 26 mEq/L (fraction of inspired oxygen, 100%); K+, 3.6 mEq/L; and CK, 132 U/L (normal, less than 199). End-tidal C02 (ETC02) was monitored by mass spectrometry; it reached a maximum of 36 mm Hg 1 hour after induction during mask ventilation. A variability in the ETC02 of 5 mm Hg was noted during anesthesia. Skin temperature was 36.7C on induction and decreased to 34.7C over a time frame of 1 hour. Because of concern that an MH trigger may have occurred, the surgical procedure was canceled, and the patient was allowed to recover from the anesthetic agent. Neuromuscular blockade was reversed with neostigmine, 5 mg, and glycopyrrolate, 1 mg IV. The patient was observed in the postanesthesia care unit and was later admitted to the hospital for overnight observation. No MH triggering was evident during the postoperative period. No further laboratory testing was performed. After the patient was informed of the intraoperative course of events, she was instructed to return the following week for the scheduled operation. The patient returned 5 days later. Midazolam, 2 mg, and fentanyl, 100 g, were administered IV for sedation. Bilateral superior laryngeal nerve blocks were performed with 0.5% lidocaine, 3.5 mL injected at each side. Two milliliters of 4% lidocaine was used for topical trachéal anesthesia; 1% lidocaine was used for topical oropharyngeal anesthesia. An endotracheal tube (internal diameter, 6.5 cm) was inserted under direct visualization of the vocal cords. Tube placement was confirmed, and general anesthesia was induced with thiopental sodium, 200 mg IV, and 3% desflurane in N20 and 02. The patient was given a trial dose of mivacurium chloride, 4 mg IV, to evaluate the response of the masseter muscle tone to this agent. Again, the patient had development of apparent MMR. Subsequently, mivacurium, 6 mg, was administered IV, with complete ablation of the train-of-four response to the peripheral nerve stimulator; however, no effect was noted on the degree of masseter muscle spasm. The surgical procedure was completed 10 minutes after the final dose of mivacurium. Neuromuscular blockade was reversed with atropine sulfate, 1 mg, and edrophonium chloride, 40 mg given IV. The MMR resolved as the patient recovered from anesthesia. Once the patient was responsive and alert and demonstrated purposeful movements, the trachea was extubated. She was transferred to the postanesthesia care unit and dismissed 1 hour after her arrival; no further sequelae occurred. NAMHR Cases. Case 1.—A 49-year-old woman, ASA class 3 (weight, 84 kg), was scheduled to undergo total abdominal hysterectomy, bilateral salpingo-oophorectomy, and bladder repair. The offspring of her mother's first cousin had MH. Additionally, this patient's maternal uncle died at the age of 12 during general anesthesia; however, MH was not directly implicated. Because of this death, the patient considered herself susceptible to MH. She had previously undergone general anesthesia for tonsillectomy and adenoidectomy at age 3 years as well as appendectomy at age 5 years without complication. The anesthetic agents used during these operations could not be specified. In preparation for anesthesia, the patient was given dantrolene sodium orally for several days preoperatively. Before induction of epidural anesthesia, the patient was given dantrolene, 60 mg IV. The epidural anesthetic was inadequate, and general anesthesia was induced with fentanyl, diazepam, thiopental sodium, and atracurium, 40 mg IV, as well as N20 in Or Despite an initial dose of 0.48 mg/kg of atracurium, mandibular range of motion was insufficient to allow endotracheal intubation. Mask ventilation was unimpaired. During the course of the anesthetic procedure, maximal ETC02 was 36 mm Hg, and her temperature increased 1C; thus, the patient had to be cooled with ice. No other treatment was instituted. Four years later, the patient required anesthesia for cholecystectomy, and she underwent concurrent muscle biopsy. General anesthesia was induced with propofol, fentanyl, N20 in 02, and vecuronium. MMR was not noted during the procedure. During direct laryngoscopy, however, the anesthesiologist noted some difficulty in visualizing the vocal cords relative to anterior positioning of the larynx and poor mouth opening. Caffeine halothane contracture testing of the muscle biopsy specimens was negative based on the North American MH protocol.1Larach MG (North American Malignant Hyperthermia Group). Standardization of the caffeine halothane muscle contracture test.AnesthAnalg. 1989; 69: 511-515Google Scholar Histologie findings and histochemistry of the muscle specimen were normal. Case 2.—An 11-year-old boy (weight, 38 kg) underwent a prolonged orthopedic procedure after induction of general anesthesia with thiopental sodium and atracurium IV to facilitate uneventful trachéal intubation and maintenance with isoflurane and N20 in 02. Three hours after the incision was made, tachycardia was noted. Isoflurane was discontinued, the breathing circuit changed, and the patient hyperventilated. ETC02 was noted to increase slightly and peak at 42 mm Hg during the course of several hours. After the development of tachycardia and the increase in temperature, MMR developed. The patient's temperature was noted to increase by less than 1 C during the entire procedure. Results of ABG analysis were within normal limits. Dantrolene, 80 mg, was given IV 50 minutes after the tachycardia was observed. Two years after this event, the patient underwent muscle biopsy. The CK level obtained concurrently was 2,165 U/L (normal, less than 250). Caffeine halothane contracture testing of the specimen was negative based on the North American MH protocol.1Larach MG (North American Malignant Hyperthermia Group). Standardization of the caffeine halothane muscle contracture test.AnesthAnalg. 1989; 69: 511-515Google Scholar Histologie findings and his-tochemistry of the sample were normal. Case 3.—A 22-year-old woman, ASA class 1 (weight, 49.5 kg), who was undergoing tonsillectomy and adenoid-ectomy had previously undergone two uneventful general anesthetic procedures. Anesthesia was induced with thio-pental sodium, midazolam, and fentanyl. Atracurium, 15 mg, was given IV to facilitate routine trachéal intubation. Anesthesia was maintained with isoflurane and N20 in 02. Ten minutes after induction, the surgeon attempted placement of an oral gag, which was unsuccessful due to severely decreased mandibular mobility. (The patient's generalized muscle tone was not described.) Atracurium, 5 mg, was given IV, and the level of anesthesia deepened by increasing the inspired isoflurane concentration. Mouth opening did not improve; the operation was canceled, the anesthesia was terminated, and the patient was allowed to recover. The masseter rigidity resolved spontaneously, and approximately 25 minutes later, trachéal extubation was uneventful. The patient's temperature did not change. Peak ETC02 was 39 mm Hg. Determinations of ABG analysis, K+, and CK were within normal limits. Six weeks later, the patient underwent muscle biopsy. The specimen was subjected to caffeine halothane contracture testing. During halothane contracture, one of the four strips demonstrated an increase in tone of 1.4 g; all others increased in tone by less than 0.5 g. This was interpreted as a positive halothane contracture test. Histologie findings and histochemistry were normal. Failure of mouth opening during general anesthesia does not commonly occur in the presence of neuromuscular blockade with nondepolarizing agents. The causes of this problem include inadequate depth of anesthesia, altered anatomic features of the soft tissue of the upper airway, dental abnormalities, tumor growth locally or in the central nervous system, foreign bodies in the oropharynx, structural abnormalities of the mandible or temporomandibular joint, primary masticatory muscle spasm, secondary masticatory spasm originating in the mesencephalic nucleus, and muscular rigidity due to MH after patient exposure to known triggering agents. The definition of MMR is subjective. In this article, MMR is considered an increased tone of the masseter muscle sufficient to impair mouth opening, a phenomenon that makes airway manipulation difficult or impossible. MMR has been identified as part of the syndrome of MH and has been reported to have a frequency as high as 1% in the pédiatrie population during coadministration of succinyl-choline and halothane.2Schwartz L Rockoff MA Koka BV Masseter spasm with anesthesia: incidence and implications.Anesthesiology. 1984; 61: 772-775Crossref PubMed Scopus (91) Google Scholar Rosenberg and Fletcher3Rosenberg H Fletcher JE Masseter muscle rigidity and malignant hyperthermia susceptibility.AnesthAnalg. 1986; 65: 161-164Google Scholar reported a 50% incidence of MH susceptibility in pédiatrie patients exhibiting MMR. Allen and Rosenberg4Allen GC Rosenberg H Malignant hyperthermia susceptibility in adult patients with masseter muscle rigidity.Can J Anaesth. 1990; 37: 31-35Crossref PubMed Scopus (24) Google Scholar found a 25% incidence of MH susceptibility in adult patients with a history of MMR and a 59% incidence in pédiatrie patients with MMR. All the patients in the reports by Schwartz and colleagues2Schwartz L Rockoff MA Koka BV Masseter spasm with anesthesia: incidence and implications.Anesthesiology. 1984; 61: 772-775Crossref PubMed Scopus (91) Google Scholar and Allen and Rosenberg4Allen GC Rosenberg H Malignant hyperthermia susceptibility in adult patients with masseter muscle rigidity.Can J Anaesth. 1990; 37: 31-35Crossref PubMed Scopus (24) Google Scholar received succinylcholine before the advent of MMR. Although MMR most commonly occurs after the use of succinylcholine in the presence of halothane, one case report described the occurrence of MMR without progression to MH after administration of pan-curonium bromide.5Polta TA Hanisch Jr, EC Nasser JG Ramsborg GC Roelofs RI Masseter spasm after pancuronium.Anesth Analg. 1980; 59: 509-511Crossref PubMed Scopus (18) Google Scholar Additionally, a case of diffuse muscle rigidity was described in a patient with Smith-Lemli-Opitz syndrome (developmental delay, microcephaly, elfin faciès, hypoplastic genitals, and syndactyly of the toes) who received vecuronium, and progression to fulminant MH occurred subsequently.6Petersen WC Crouch Jr, ER Anesthesia-induced rigidity, unrelated to succinylcholine, associated with Smith-Lemli-Opitz syndrome and malignant hyperthermia.Anesth Analg. 1995; 80: 606-608PubMed Google Scholar The occurrence of MMR with the use of other nondepolarizing neuromuscular blocking agents or with the isolated administration of potent inhalational anesthetics has not been described. Succinylcholine is known to produce MMR in the presence of complete neuromuscular blockade. Investigators have postulated that this phenomenon is related to the stimulation of the intramyocellular contractile system, independent of neuromuscular transmission.7Jantzen JP Eberle B Gaida BJ Hermes HJ Otto S Schafer M The effect of muscle relaxants on masseter tone: an experimental study in an MH-susceptible swine model.Anaesthesist. 1992; 41: 248-253PubMed Google Scholar This response may be a unique action of succinylcholine or may indicate a specific characteristic of the masseter muscle. No mechanism, however, has been postulated for the occurrence of MMR after administration of nondepolarizing agents. The MHAUS case is unusual in that MMR became clearly evident after the administration of vecuronium in a dose sufficient to result in complete neuromuscular blockade, as documented by the loss of train-of-four response on the nerve stimulator. This effect was also reproducible with the administration of mivacurium during subsequent anesthesia. MH can occur in the presence of potent inhalational anesthetics alone; however, no evidence shows that MMR occurs with the isolated administration of inhalational anesthetics, although generalized muscular rigidity may be noted. Moreover, assessment of ABG studies, K+, CK, heart rate, and temperature showed no evidence of an acute episode of MH occurring in this patient. Therefore, in this case, MMR seemed to occur in the presence of nondepolarizing muscle relaxants with no progression to MH. The cases of MMR from the NAMHR that occurred without use of succinylcholine are less consistent and may represent other problems. The first case from the NAMHR involved a patient with a family history of MH who had development of MMR after administration of an intubating dose of atracurium. Thus, multiple, prolonged intubation attempts were made. During a subsequent anesthetic procedure, difficult intubation was again noted relative to the anatomic structure of the airway. Likely, the difficulty with intubation during the first anesthetic procedure was related to these anatomic abnormalities. In the second case from the NAMHR, tachycardia during an orthopedic procedure resulted in a change in the anesthetic agent 3 hours after uneventful induction to reduce the use of triggering agents. This change in the depth of anesthesia may have resulted in the increase in masseter muscle tone. Although this patient did not have a positive caffeine halothane contracture test, his CK level was well above the normal limit; this fact may indicate that pathologic muscle contributed to the increased masseter tone. The third case from the NAMHR involved a patient who had masseter rigidity that was noted by the surgeon 10 minutes after atracurium was given during administration of isoflurane. Intubation had been successfully performed, a suggestion that the muscle rigidity may have been related to administration of isoflurane, a known MH trigger. On the basis of muscle biopsy, this patient was proved to be susceptible to MH. The NAMHR cases identified as MMR unrelated to use of succinylcholine are interesting but may indicate other problems. The available information was limited in terms of the timing of the intraoperative events and the timing and dose of medications. Additionally, these cases were complicated by anatomic and possible pathologic muscle conditions that we were unable to investigate further. The MHAUS case consisted of MMR associated with nondepolarizing muscle relaxants that was reproducible during subsequent anesthesia. This has been previously described during the administration of pancuronium.5Polta TA Hanisch Jr, EC Nasser JG Ramsborg GC Roelofs RI Masseter spasm after pancuronium.Anesth Analg. 1980; 59: 509-511Crossref PubMed Scopus (18) Google Scholar MMR associated with nondepolarizing muscle relaxants is rare and is unlikely to predict MH susceptibility, although data are insufficient to make definite recommendations. In the MHAUS case, the MMR did not resolve until the neuromus-cular blockade was reversed. Therefore, it is important to ensure that adequate mask ventilation is possible before these agents are administered because development of MMR may hinder the ability to perform direct laryngoscopy. We thank Henry Rosenberg, M.D., Jeff E. Fletcher, Ph.D., Harvey K. Rosenbaum, M.D., Steve Park, C.R.N.A., and Marilyn G. Larach, M.D., director of the NAMHR, for providing details on individual cases, and Julie M. Tuohy for secretarial assistance.