Laryngospasm is the reflex spasmodic adduction of the vocal cords leading to partial or complete airway obstruction. It is a serious and potentially life-threatening complication of anesthesia, which can lead to hypoxia, ischemic end-organ injury, negative pressure pulmonary edema, and death. Risk factors include increased airway irritability and irritation from asthma, gastroesophageal reflux disease, smoking, and pungent inhaled volatile anesthetics, such as desflurane or isoflurane.1 There is a higher incidence in the pediatric population and in shared airway surgery. Conventional management includes the application of positive end-expiratory pressure, jaw thrust, the removal of any offending stimuli, the deepening of anesthesia, or the administration of muscle relaxants as a last resort. The incidence of laryngospasm is estimated at <1% in the adult and pediatric population.2 The incidence of recurrent laryngospasm and laryngospasm in a fully conscious postoperative patient is unknown.
In this case report, we describe the novel use of nebulized lidocaine to treat postoperative laryngospasm, which was refractory to conventional medical management in a middle-aged woman who had undergone thoracic surgery.
Written consent was obtained from the patient for this case report.
A 51-year-old Caucasian woman presented for an urgent video-assisted thoracoscopic surgery for drainage of a right-sided empyema. Before hospitalization, she was healthy and did not take any regular medication. She had no allergies and was a nonsmoker. She was 63 kg and 155 cm tall, giving her a body mass index of 26.2.
Anesthesia was induced and maintained with a propofol target-controlled infusion using the Marsh model (8 μg/mL for induction and 3 μg/mL subsequently) and remifentanil infusion 0.5 μg·kg−1·minute−1 to target a bispectral index of 40–60. Thirty milligrams of rocuronium was given to facilitate tracheal intubation. A grade 1 Cormack–Lehane view was obtained at laryngoscopy, and a 35-French left-sided double-lumen endotracheal tube (ETT) was sited without incident and secured at 24 cm at her lips. The position of the double-lumen tube was confirmed with a fiberoptic scope, and lung isolation was satisfactory.
During the 50-minute procedure, she received IV diclofenac 75 mg, diamorphine 5 mg, ondansetron 4 mg, dexamethasone 8 mg, and just >1 L of Hartmann’s solution.
Before awakening, train-of-four stimulation revealed 4 strong twitches with no visually appreciable fade. Her trachea and upper airways were suctioned, and as the propofol infusion was discontinued, 200 mg of sugammadex was given to reverse any potential residual neuromuscular blockade. The double-lumen tube was removed when she was able to obey commands, and the remifentanil infusion was stopped at this point. She promptly experienced laryngospasm, which persisted despite a firm jaw thrust with 40–60 cm of positive end-expiratory pressure applied through a tight-fitting facemask. The propofol infusion was recommenced, after which the laryngospasm subsided. As she was now unconscious and apneic, a size 4 supraglottic airway I-Gel (Intersurgical, Wokingham, Berkshire, United Kingdom) was carefully inserted to facilitate a gradual awakening in the postoperative recovery ward with weaning of the propofol infusion.
Shortly after arriving in the postoperative recovery ward, she again experienced laryngospasm with marked stridor. The airway was removed and positive end-expiratory pressure applied through the facemask. After a few minutes, the laryngospasm abated. At this point, the patient was able to obey commands, including hand squeezing and head nodding.
Approximately 20 minutes later, she complained that she had a painful dry throat, which felt very tight. An oxygen-driven saline and salbutamol nebulizer was started but had no appreciable effect. Her oxygen saturations dropped to 85% despite her being on 8 L of oxygen. She was fully awake and indicated that her throat felt very tight and that breathing was difficult. Her voice was hoarse and soft with marked stridor. Partial laryngospasm was diagnosed and positive end-expiratory pressure at 40–60 cm H2O applied through a facemask for 5 minutes. With the application of positive end-expiratory pressure, her oxygen saturations increased to 94%, but as soon as the mask was removed, they decreased to 85%. She again indicated that her throat felt very tight. At this point, we decided to nebulize 200 mg lidocaine (10 mL of 2% lidocaine), which is half the dose of lidocaine the authors would nebulize to provide surface anesthesia to the upper airway before awake fiberoptic intubation (10 mL of 4% lidocaine). We reasoned that, because 400 mg of lidocaine afforded adequate relaxation to allow the unhindered passage of an ETT through the vocal cords, 200 mg might be sufficient to reduce their reactivity without causing a temporary palsy.
Within 10 minutes of starting the lidocaine nebulizer, she felt “a lot better”; her voice returned to normal pitch and volume and she stated that the tightness in her throat had disappeared. She said that her throat was not as painful as it was before the nebulizer. Her oxygen saturations were 97% on 5 L of oxygen. The nebulized lidocaine was well tolerated throughout, with no adverse effects.
A portable chest x-ray was ordered to exclude other differentials, like negative-pressure pulmonary edema. Apart from demonstrating a poor inspiratory film, her chest x-ray was unremarkable. Before discharge to the ward an hour later, the patient stated that she felt “fine,” her oxygen saturations were 99% on 5 L of oxygen, and there were no signs that the laryngospasm had returned.
When reviewed the next day, she no longer required oxygen therapy. When asked about her immediate postoperative experience, she said that while she was fully awake in the postoperative recovery ward and able to move all 4 limbs, she felt as though she was suffocating, and it “felt like someone was strangling” her. She reported that this sensation passed shortly after the nebulized lidocaine was given.
Lidocaine is a versatile drug with numerous uses. Apart from its conventional indication as a sodium channel blocker in local, regional, and neuraxial anesthesia, it has also been given IV as an antitussive for ophthalmic surgery,3 a minimum alveolar concentration-sparing agent in human and veterinary anesthesia,4 as an analgesic for acute pain, an antiarrhythmic for ventricular arrhythmias, and as a cardioplegic for cardiac surgery5 or fetocide.6 It is also applied topically as a plaster for neuropathic pain or a cream preceding IV cannulation in the young or needle-phobic and nebulized before awake airway instrumentation or for intractable cough.7 Alkalinized lidocaine has even been instilled in the cuffs of ETTs to reduce the incidence of postoperative sore throat.8
Intraoperative IV lidocaine and the topical application of lidocaine to the vocal cords are known to minimize postoperative laryngospasm in children,9 but their effects on adults are less well studied. A plausible explanation is that nebulized lidocaine decreases upper airway reactivity by a local anesthetic effect. In a study with adult volunteers, Hall et al10 noted that nebulized lidocaine reduced the irritant effect that a dilute inhaled ammonia vapor had on upper airway reflexes.
To date, there is only one other known case report of postoperative laryngospasm, which was successfully treated with nebulized lidocaine,11 but it is unclear if the authors also used conventional measures first.
Our patient had none of the risk factors for increased airway irritability—she did not smoke and did not suffer from asthma, gastroesophageal reflux disease, obstructive sleep apnea, or an upper respiratory tract infection. In addition, the use of an intraoperative remifentanil and propofol infusion and the careful suctioning of secretions before awakening would have minimized postoperative laryngospasm. However, the 35-French double-lumen ETT inserted to facilitate 1-lung anesthesia may have irritated the vocal cords.
The patient had repeated episodes of laryngospasm and, when awake, was able to complain of symptoms suggestive of laryngospasm. The following day, she was able to describe how she felt while suffering from it and how her symptoms abated after the administration of nebulized lidocaine.
Although lidocaine has a half-life of 100 minutes, it effectively terminated her laryngospasm, whereas the intermittent boluses of propofol only offered transient relief, with laryngospasm recurring with the return of consciousness. While neuromuscular blocking drugs would effectively relieve the sustained adduction of the vocal cords, they would neither be indicated nor appreciated by the awake patient.
As anesthesiologists, we are accustomed to treating laryngospasm in unconscious patients but not in conscious ones. Perhaps nebulized lidocaine might be a useful tool in the anesthetic armamentarium for the management of these patients. E
Name: Zhihao Oon, FFPMRCA, FRCA, MBBS, BSc(Hons).
Contribution: This author helped care for the patient, review the literature, and prepare, write, and revise the manuscript.
Name: Chiew-Bing Ha, MBBS, BSc(Hons).
Contribution: This author helped review the literature, and prepare, write, and revise the manuscript.
Name: Marcin Sicinski, DESA, PhD, MD.
Contribution: This author helped prepare and revise the manuscript.
This manuscript was handled by: BobbieJean Sweitzer, MD, FACP.
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