Anesth Analg 2001;92:271-272
© 2001 International Anesthesia Research Society
CASE REPORTS
Severe Laryngospasm at Tracheal Extubation in a Patient with Superior Laryngeal Nerve Injury
Rosendo F. Mortero, MD*,
Zamira Orahovac, MD*,
Kentaro Tsueda, MD*, and
and Jeffrey M. Bumpous, MD
Departments of *Anesthesiology and Otolaryngology-Head and Neck Surgery, University of Louisville School of Medicine, Louisville, Kentucky
Address correspondence and reprint requests to Kentaro Tsueda, MD, Department of Anesthesiology, University of Louisville School of Medicine, Louisville, KY 40292. Address e-mail to rashep01 @gwise.louisville.edu.
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Abstract
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Implications: Episodes of severe laryngospasm at tracheal extubation, paroxysmal coughs with choking spells after thyroidectomy, and laryngoscopic findings of superior laryngeal nerve injury are consistent with episodic laryngospasm. Laryngeal hypersensitivity should be considered in patients exhibiting episodic symptoms of laryngeal obstruction and sensory abnormality after surgery.
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Introduction
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Episodic laryngospasm is often associated with occult gastroesophageal reflux disease (1,2). A recent report described six cases of hypersensitive laryngeal reflex developing a few weeks to 12 months after laryngeal nerve injury. Symptoms were paroxysms of coughing and stridor that progressed in some to brief episodes of complete airway obstruction (3), suggesting that laryngeal nerve injury may be an etiology in the syndrome of episodic laryngospasm. We report a severe laryngospasm at tracheal extubation in a patient with evidence of superior laryngeal nerve injury, presumably from thyroid lobectomy performed 5 yr earlier. The laryngospasm may have represented laryngeal hypersensitivity.
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Case Report
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A 54-yr-old woman, 173 cm tall and weighing 70.5 kg, underwent open reduction of a left foot fracture. She had had a hysterectomy, right thyroid lobectomy, and cholecystectomy 8, 5, and 4 yr before the current admission, respectively. After cholecystectomy, the anesthesiologist informed her that during emergence from anesthesia she had a "severe spasm" necessitating reintubation of the trachea, and suggested that she inform anesthesiologists in future operations. She had asthma for 20 yr; it was triggered recently by physical exertion and was characterized by a paroxysmal, persistent coughing and a choking sensation with stridor. Two recent episodes occurred during hiking and followed a dry and scratchy sensation of the throat. Neither episode responded to a bronchodilator. Rebreathing into a paper bag terminated the attacks. She had been aware of a subtle change in her voice for the past 5 yr. She denied smoking. Current medication included Atrovent TM (ipratropium bromide; Boehringer Ingelheim Pharmaceuticals, Inc, Ridgefield, CT) and hydrocodone. White blood cell count was 8.2 x 109 cells per liter. Chest roentgenogram was normal. Physical examination was normal. The patient requested general anesthesia.
Anesthesia was induced by propofol 200 mg IV and maintained by desflurane in a nitrous oxide-oxygen mixture and 200 µg of fentanyl. Tracheal intubation was facilitated by IV administration of succinylcholine. Rocuronium provided muscle relaxation. Her lungs were clear. Anesthesia time was 2 h 10 min. At the end of the operation, twitch response to train-of-four stimulation was normal. The patient reacted to the endotracheal tube and followed verbal commands. The bispectral index ranged from 91 to 93. At tracheal extubation, the patient developed laryngospasm. Oral airway and positive pressure ventilation established an airway with loud stridor. After several minutes of struggle, 40 mg propofol was given IV. Direct laryngoscopy showed clockwise rotation of the posterior commissure, with the right vocal cord at the intermediate position ( Fig. 1). There was no edema or inflammation of vocal cords. The trachea was reintubated. There was no expiratory wheezing. In the recovery room, the patient was awake and reacting to the endotracheal tube. The trachea was extubated without incident. The patient was scheduled for evaluation of laryngeal function but failed to keep her appointments.
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Figure 1. Direct laryngoscopic view of the larynx during tracheal reintubation after propofol 40 mg IV, showing a clockwise rotation of the posterior commissure.
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Discussion
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Severe laryngospasm at tracheal extubation, laryngoscopic findings, and changes in symptoms of asthma and phonation since thyroidectomy suggest that the observed laryngospasm may have been related to laryngeal nerve injury. The external division of the superior laryngeal nerve supplies motor innervation to the cricothyroid muscle on the contralateral side. Denervation of the cricothyroid muscle results in rotation of the posterior commissure toward, and shortening of the cord on, the inactive side because of unopposed contraction of the cricoarytenoid muscle (4). The deviation of the posterior commissure of the glottis away from the side of operation was consistent with injury to the superior laryngeal nerve on the operative side.
Stimulation of the superior laryngeal nerve produces low-threshold evoked potentials in adductor fibers of recurrent laryngeal nerve, and these potentials persist well beyond cessation of the stimulation (5,6). All patients reported by Wani and Woodson (3) had laryngeal nerve injuries. Blockade of internal division of the superior laryngeal nerve temporarily abolished laryngospasm. They suggested that laryngospasm in their patients may have been primarily a sensory problem resulting from aberrant sensory nerve repair, the process of regeneration, central sensitization in the glottic closure reflex arc, or a combination of these (3). A sensation of irritation in the throat was reported weeks before development of episodic laryngospasm (3). In our patient, however, the dry and scratchy sensation was associated with physical exertion and was felt shortly before onset of the laryngospasm. Hyperventilation induced by hiking may have activated laryngeal thermoreceptors, pressure receptors, or both (7). High carbon dioxide tension attenuates respiratory defensive reflexes in anesthetized patients (8). Suppression of glottic protective reflexes by rebreathing may have been a mechanism for the termination of the laryngospasm.
Paroxysmal airway obstruction was less frequent, phonatory change was subtle, and sensory symptoms were more brief in our patient than in those previously reported. Although neurophysiologic tests were not performed, these findings may be consistent with a milder form of the syndrome of laryngeal hypersensitivity. Superior laryngeal nerve block may be the only effective treatment (3). Laryngeal hypersensitivity should be considered in patients exhibiting episodic symptoms of laryngeal obstruction and sensory abnormality after surgery. Regional techniques may be appropriate. When general endotracheal anesthesia is required, opiate administration, awake extubation (9), topical anesthesia of larynx, superior laryngeal nerve block, or a combination of these may be useful in preventing laryngeal spasms.
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References
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Accepted for publication September 19, 2000.
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Abstract
Introduction
