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Succinylcholine has long been the neuromuscular blockade agent of choice for the emergency physician for rapid sequence intubation because of its rapid onset and relatively brief duration of action. However, it has many known life-threatening side effects and contraindications including allergy, histamine release, dysrhythmias, hyperkalaemia, and malignant hyperthermia.1 It has also been known to cause significant masseter spasm in children when used in conjunction with volatile anaesthetics such as halothane.2–5 In adults, succinylcholine can also produce transient masseter spasm that resolves when fasciculation stops. This potentially deadly side effect has been noted in other specialties but the incidence in adults is unknown.6,7 The generally agreed upon treatment is to stop the anaesthetic and reschedule the procedure at a later date with different agents and evaluation for malignant hyperthermia.4 However, in the emergency department that management option is not available to the emergency physician. Knowledge of the potential side effects of this commonly used medication is paramount to successful airway management.
We present a case of succinylcholine induced masseter spasm in the emergency department requiring surgical cricothyroidotomy for airway control. We believe that this is the only reported case of masseter spasm resulting in a failed airway requiring surgical cricothyroidotomy during rapid sequence intubation.
The patient was a 56 year old man brought in by ambulance for altered mental status and hypotension. His vital signs in the field were: blood pressure 97/58 mm Hg; heart rate 135; respiratory rate 19; and SAo2 98% on 100% oxygen. Finger stick whole blood glucose was normal. The ambulance team reported that the patient’s apartment was covered with bloody vomitus and melaena, and the patient was noted in the field to be covered in what appeared to be old blood and stool. He presented complaining only of irritation at the site of his recently inserted percutaneous endoscopic gastrostomy (PEG) tube and vomiting. He was awake and alert but slow to respond.
His past medical history was significant only for squamous cell carcinoma of the head and neck of unknown staging. The PEG tube had been inserted for feeding just two weeks before he was brought to our emergency department. He stated that his only medications were “nausea medications” and he had no known drug allergies. He was an ex-smoker and regularly consumed large quantities of alcohol. He had had the last drink three days prior to arrival.
Normal values, Brooke Army Medical Center Laboratory
Blood urea nitrogen: 4.8–20 mg/dl
Creatinine: 0.7–1.3 mg/dl
Sodium: 138–146 mmol/l
Potassium: 3.5–5.1 mmol/l
Chloride: 99–109 mmol/l
CO2: 21–32 mmol/l
Glucose: 65–105 mg/dl
Lactate: 0–1.8 mmol/l
Arterial blood gases
Pco2: 35–45 mmHg
Po2: 80–100 mmHg
HCO3: 22–26 mEq/l
O2 saturation: 95–98%
His physical exam was significant for hypotension (98/59 mm Hg) and tachycardia at 135 beats per minute, and he had a rectal temperature of 39.7 °C (103.4 °F). He appeared much older than his stated age of 56 years. His exam was remarkable for dried blood in the posterior pharynx, he had a Mallampati class II airway with three fingers width mandibular opening, and his trachea was in the midline. His lungs demonstrated scattered rhonchi; his PEG tube was excoriated and leaked haeme positive brown fluid but otherwise showed no signs of infection. His abdomen was not tender and there were no peritoneal signs. Rectal exam demonstrated obvious melaena with mixed blood. His extremities were cool, and his skin was covered in old blood and stool but there were no rashes or petechiae. His neurological exam was non-focal.
We placed the patient on oxygen by non-rebreathing mask, inserted two large bore intravenous catheters, and administered 3 l of normal saline by 1 l boluses. Urinary output was monitored by inserting a Foley catheter. The patient was placed on a cardiac monitor, which showed sinus tachycardia. He was typed and crossed for four units of packed red blood cells. He was given ceftriaxone 2 g intravenously. His electrocardiogram (ECG) showed only sinus tachycardia and a portable chest x ray was negative for infiltrates. Laboratory studies revealed sodium 125 mmol/l, potassium 2.6 mmol/l, chloride 78 mmol/l, CO2 25 mmol/l, creatinine 1.3 mg/dl, and glucose 124 mg/dl (see box for normal values). His complete blood count showed leucocytosis at 20.4 million white cells with left shift and haematocrit 37%. Urinalysis showed only trace ketones. Lactate was >12 mmol/l. Cardiac enzymes and a head computed tomography (CT) scan were negative. A lumbar puncture was performed and was negative.
The patient had required occasional doses of midazolam 2 mg intravenously for facilitation of studies and procedures. Although he would occasionally become agitated, his mental status never deteriorated and his vital signs normalised after resuscitation and one unit of packed red blood cells.
Approximately four and a half hours into his resuscitation the patient began having difficulty maintaining his airway with sonorous respirations and became unrousable. An arterial blood gas (ABG) at that time was: pH 7.228; Pco2 96 mm Hg; Po2 317 mm Hg; HCO3 8.7 mEq/l and O2 saturation 99%. The patient was prepped for intubation by placing into the sniffing position, suction was made ready, and bag and mask with end tidal CO2 detector was ready for use. As the patient had normal external anatomy with a Mallampati class II airway with three fingers width mandibular opening he was deemed to be a safe candidate for rapid sequence intubation. Etomidate 20 mg and succinylcholine 100 mg were administered through the intravenous catheter. Cricoid pressure was maintained throughout the procedure. Fasciculations were noted, and flaccid paralysis was noticed approximately 30 seconds after administration of succinylcholine. The mouth could not be opened and the masseter muscles appeared to be in spasm. The teeth were clenched together and movement of the mandible was not possible. An additional 100 mg of succinylcholine without atropine was administered without effect on the spasm. The on-call anaesthesia service was notified, and the patient was ventilated by bag and mask without difficulty. The attending anaesthesiologist and senior resident arrived within minutes and attempted to insert a nasotracheal airway with fibreoptic visualisation but were unable to see the patient’s vocal cords. Anticipating a potential failed airway, the patient’s anterior neck was prepped with Betadine for a cricothyroidotomy. The patient eventually became difficult to ventilate, and his oxygen saturation dropped to 82% and could not be brought back up. Flaccid paralysis of the extremities was noted throughout the procedure. A failed airway was declared and a surgical airway was deemed necessary. No additional anaesthetic medications were administered. However, the entire time course was less than 10 minutes and the etomidate originally administered should have been sufficient for anaesthesia and amnesia.
A 2 cm vertical incision was made over the cricothyroid membrane with a number 10 blade scalpel. The membrane was visualised and horizontally incised with the scalpel. The membrane space was dilated with haemostats and an attempt at passing a 5.0 mm endotracheal tube was made but the tube would not pass. A second attempt with a 5.0 mm endotracheal tube was made, and it successfully passed into the trachea. A colorimetric end tidal CO2 detector showed yellow colour change with six breaths from the bag with a subsequent rise in his pulse oximetry to the mid-90s. Bilateral breath sounds were auscultated in four lung fields. At this time midazolam 5 mg was administered intravenously. Five minutes after the completion of the cricothyroidotomy, the attending anaesthesiologist was able to place a 7.0 mm nasotracheal airway. The 5.0 mm endotracheal tube was removed from the cricothyroidotomy site as the 7.0 mm tube allowed easier ventilation and the site was closed with sutures.
The patient was transferred to the medical intensive care unit and was extubated four days later. He eventually required reintubation with awake nasotracheal intubation for respiratory distress. He died 14 days while in intensive care. Autopsy demonstrated a large 3×4 cm gastric ulcer that had eroded into a submucosal artery.
Rapid sequence intubation has been shown to be successful and safe when used in the emergency department for airway control. Dufour examined the charts of 219 patients who underwent rapid sequence intubation and only one patient had a fatal outcome unrelated to the intubation and 32 patients had mild complications.8 Sakles and colleagues evaluated the charts of 610 intubations in the emergency department and rapid sequence intubation was used in 84%.9 Of those intubated with rapid sequence intubation, 99% were successfully intubated with one adverse outcome of hyperkalaemic cardiac arrest. The use of neuromuscular blocking agents has been shown to increase both the safety and success rate of rapid sequence intubation.10
Masseter spasm has been implicated as an early indicator of susceptibility to malignant hyperthermia. Other markers for malignant hyperthermia include hyperpyrexia, increased end tidal CO2, generalised rigidity, autonomic instability, and rhabdomyolysis. The exact incidence of patients who develop masseter spasm and actually go on to develop malignant hyperthermia is unknown. An incidence as high as 50% has been reported in children, but some authors believe that this may be due to overreporting.3,11 The incidence of malignant hyperthermia is unknown in adults with masseter spasm, although isolated masseter spasm is not pathognomonic for malignant hyperthermia.12 Although not given to our patient, the treatment for malignant hyperthermia is dantrolene 1 mg/kg administered intravenously. This may be repeated until symptoms resolve or a maximum dose of 10 mg/kg is reached.
Did malignant hyperthermia cause our patient’s masseter spasm? We do not think so. The patient did not develop generalised rigidity, nor did he develop increased end tidal CO2 based on repeat blood gases. His creatinine phosphokinase never rose above 100 IU/l and he did not develop myoglobinuria. A repeat rectal temperature approximately 30 minutes after masseter spasm was 38 °C (100.4 °F). It has been recommended that patients who develop masseter spasm undergo muscle biopsy for evaluation of potential susceptibility to malignant hyperthermia. We did not take a muscle biopsy from our patient, however, his family was extensively questioned and there was no family history of anaesthetic reactions. His grown children were advised to have biopsies done to determine if they were susceptible to malignant hyperthermia.
Many lessons can be learned from this case report. First and foremost, succinylcholine has many adverse effects that must be anticipated. Secondly, a patient’s external anatomy should not be entirely relied upon as an indicator of the ease of intubation as many other factors such as medication side effects can contribute to a failed airway. Finally, dantrolene administration should be considered if masseter spasm is encountered after succinylcholine as this may signal the development of malignant hyperthermia.
Succinylcholine is the neuromuscular blocking agent of choice in rapid sequence intubation due to its rapid onset of action and relatively rapid return of muscle tone.13 Emergency physicians need to be aware of the significant adverse side effects of succinylcholine and must be prepared to deal with them, including the potential for masseter spasm and malignant hyperthermia.
Competing interests: none declared
Consent was obtained from the patient’s wife.