Did sugammadex cause, or reveal, laryngospasm?

Abstract

I wonder whether the laryngospasm described in McGuire and Dalton's case report was not caused by sugammadex, but rather by instrumenting the airway at an insufficient depth of anaesthesia 1? From the description of the technique provided, it appears that the Bailey manoeuvre was performed at a maintenance anaesthesia depth of 0.7 MAC. I frequently use the Bailey manoeuvre, and preciptiating laryngospasm by undertaking it at this plane of anaesthesia would not be surprising in a patient with normal muscle tone. The presence of deep neuromuscular blockade does not alter the airway stimulation produced by this manoeuvre, it merely conceals the motor consequences of this stimulation until normal muscle tone has been restored by reversal with sugammadex, allowing the efferent nerve impulses to cross the neuromuscular junction and cause adduction of the vocal cords. It would be reasonable to expect an identical response if normal muscle tone were restored using neostigmine reversal. The issue here seems to stem from an understandable misinterpretation of the Difficult Airway Society's guidelines for extubation 2, which state that ‘either deep anaesthesia or neuromuscular blockade is essential’ to avoid airway stimulation during the Bailey manouevre, when neuromuscular blockade should, in fact, be considered an adjunct rather than an alternative to deep anaesthesia. Without deep anaesthesia, the afferent limb of the reflex arc that results in laryngospasm will still be produced and will be revealed upon return of normal muscle tone. The depth of anaesthesia required to prevent stimulation of laryngeal reflexes at extubation is similar to that required to safely place a supraglottic airway device (SAD) at induction, and is likely to exceed the depth of anaesthesia achieved using 0.7 MAC of volatile agent. My practice is to administer a bolus of propofol before performing the Bailey manoeuvre, spray the vocal cords with 10% lidocaine and optimally position the patient for re-intubation in case placement of the SAD is unsuccessful. I do not remove the tracheal tube until the SAD is correctly positioned, and do not perform the Bailey manouevre in patients who would not otherwise have been suitable for use of an SAD. Inflating the lungs before deflating the tracheal tube cuff, and confirming exhaled gas is being vented via the laryngeal lumen of the SAD, provides further reassurance (if not a guarantee) that the SAD is positioned correctly and will function as a patient airway once the tracheal tube is removed. In short, placing an SAD at the end of a case as part of the Bailey manoeuvre requires the same conditions, preparation and considerations as would be required to place it de novo at induction of anaesthesia.