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Supraglottoplasty for airway obstruction.

A 54-year-old man presented to the office with a 40-year history of voice problems. He had been diagnosed with "vocal polyps" when he was a teenager, and he was treated with his first surgical excision. Since then, he had undergone a series of surgeries for polyp removal. Pathology specimens and reports of these procedures were not available. During the last of those procedures, which had been performed approximately 6 years prior to his latest presentation, a tracheotomy had been performed in order to secure the airway after extensive resection.

On examination, the patient's voice was moderately breathy and hoarse. He denied dysphagia and dyspnea with the tracheotomy tube in place, although he did complain of frequent coughing and bleeding from the tracheotomy site. His medical history included obesity and chronic obstructive pulmonary disease, which was not responsive to continuous positive airway pressure (CPAP) therapy. He had been taking intensive anti-reflux therapy. He did not smoke cigarettes or drink alcohol, and the remainder of his medical history was noncontributory. He was extremely anxious to be decannulated.

Initial strobovideolaryngoscopy found no significant abnormality of the supraglottic and glottic structures except for vocal fold scarring, which was presumably the result of his previous surgery. Operative tracheoscopy and bronchoscopy revealed the presence of granulation tissue, which was resected from the area of the tracheotomy. No supraglottic abnormality was noted. The tracheotomy tube was left in place, but a comprehensive pulmonary and sleep evaluation for possible decannulation was requested.

Over the next 2 years, the patient followed an aggressive weight loss plan with close pulmonary follow-up in order to work toward decannulation. Sleep studies continued to show intolerance to capping trials and a high apnea-hypopnea index. Strobovideolaryngoscopy revealed a patent airway, but it also showed an excessive amount of collapsing supraglottic tissue that had not been present initially (figure 1). The collapsing tissue led to airway obstruction. Staged surgery was scheduled in the hope of preparing his upper airway for decannulation.

Operative laryngoscopy revealed a remarkable amount of redundant, prolapsing soft tissue emanating from both ventricular folds and from the posterior portion of the larynx. The interarytenoid tissue covered the glottis all the way to the anterior commissure. Supraglottoplasty and laryngoplasty were performed with a C[O.sub.2] laser, including excision of redundant supraglottic tissue on one side and of the posterior laryngeal mucosa, was performed. The tracheotomy tube was left in place.

Postoperatively, the patient's laryngeal patency improved. Seven months later, supraglottoplasty was performed on the contralateral side, and the obstruction at the laryngeal level resolved (figure 2). Although the patient's laryngeal condition was sufficiently improved to allow for decannulation, the pulmonologist has not yet approved decannulation for pulmonary reasons.

The collapse of supraglottic tissue necessitating supraglottic laryngoplasty has been described primarily in children with laryngomalacia. Supraglottic mucosal redundancy in conjunction with adult obstructive sleep apnea/hypopnea syndrome (OSAHS) has been described in only a few case reports during the past 15 years. (1,2) For example, Rodriguez Adrados et al described the case of a 48-year-old woman with obstructive sleep apnea that did not respond to either CPAP or bilevel positive airway pressure. (1) The patient was noted to have massive arytenoid mucosal hyperplasia. Her airway symptoms resolved after endoscopic laser excision of the excessive mucosa.

We believe that a high index of suspicion should be maintained for supraglottic and glottic pathology in cases of OSAHS that are refractive to aggressive treatment with positive airway pressure and optimal medical management, especially when limited oropharyngeal redundancy is noted. Supraglottoplasty may be helpful in a patient with tracheotomy-dependent OSAHS that is causally related to or aggravated by supraglottic obstruction.


(1.) Rodriguez Adrados F, Esteban Ortega F, Pefla Grinan F. Massive hyperplasia of the arytenoid mucosa with sleep apnea and stridor. Endoscopic resection by C[O.sub.2] laser [in Spanish]. Acta Otorrinolaringol Esp 1999;50(8):664-6.

(2.) Purser S, Irving L, Marry D. Redundant supraglottic mucosa in association with obstructive sleep apnea. Laryngoscope 1994; 104(1 Pt 1):114-16.

Nausheen Jamal, MD; Farhard Chowdhury, DO; Reena Gupta, MD; Robert T. Sataloff, MD, DMA, FACS

From the Department of Head and Neck Surgery, David Geffen School of Medicine, University of California, Los Angeles (Dr. Jamal); ENT and Allergy Associates, Woodbridge, N.J. (Dr. Chowdhury); the Osborne Head and Neck Institute, Los Angeles (Dr. Gupta); and the Department of Otolaryngology-Head and Neck Surgery, Drexel University College of Medicine, Philadelphia (Dr. Sataloff).
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Author:Jamal, Nausheen; Chowdhury, Farhard; Gupta, Reena; Sataloff, Robert T.
Publication:Ear, Nose and Throat Journal
Article Type:Case study
Date:Jun 1, 2013
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