Sugammadex and laryngospasm

Recent correspondence has questioned whether sugammadex caused or revealed laryngospasm during general anaesthesia 1-3. We have experienced a similar case during failed tracheal intubation for elective spinal surgery. The patient, who was not deemed to have a difficult airway pre-operatively, had a routine intravenous induction of general anaesthesia, with neuromuscular blockade provided by rocuronium 0.5 mg.kg−1. The consultant anaesthetist saw a Cormack and Lehane grade-3 view of the laryngeal aperture during direct laryngoscopy. Intubation was unsuccessful. A second attempt using an Airtraq videolaryngoscope (Prodol Meditec S.A., Vizcaya, Spain) also failed to achieve an appropriate view. Two consultant anaesthetists with a specialist interest in difficult airway anaesthesia were called for assistance. A further dose of rocuronium (0.5 mg.kg−1) was given. Two further attempts using videolaryngoscopy, with hand-mask ventilation between attempts allowing maintenance of anaesthesia, failed. The patient's lungs were ventilated via an i-gel™ (Intersurgical, Wokingham, UK), but secretions increased and ventilation became more difficult. Rather than attempt an airway exchange technique, neuromuscular blockade was reversed with sugammadex 16 mg.kg−1. Ventilation was achievable, but approximately a minute later, the patient's oxygen saturations fell to 80% and their lungs became significantly more difficult to ventilate. This improved with the application of PEEP, and lasted approximately 3 min before resolution. We postulate that this is due to the effect witnessed by Dr Macguire and Dr Dalton, of increased vocal cord tone following the use of sugammadex. In response to Dr Chrimes’ letter, we are confident that an adequate depth of anaesthesia was maintained throughout. Initially, the patient was ventilated with oxygen and sevofluorane, but after the second attempt at intubation, this was supplemented with a target controlled infusion of propofol, with single co-administered doses of midazolam and fentanyl. Although we did not use bispectral index monitoring, physiological parameters and the professional experience of three consultant anaesthetists suggested that inadequate depth of anaesthesia was not the reason for increased vocal cord tone following sugammadex. Whilst we accept that this is not conclusive evidence for the untoward action of sugammadex on the vocal cords, we cannot help but think it supports the argument that sugammadex appears to have caused laryngospasm. However, even if this were proven to be the case, it is difficult to know what would be done differently in the future. In all cases cited in the original editorial, and here, the hypoxaemic episode resolved without any adverse outcomes. Sugammadex offers rapid reversal of muscle paralysis in a ‘can't intubate, can't ventilate’ situation, and perhaps it is necessary in the future for one to be aware of this potential effect, instead of sidelining a useful agent.