Clinical Review & Education

Clinical Problem Solving | ENDOSCOPY

Bilateral Vocal Fold Immobility Kelli A. Quercetti, DO; Amanda Hu, MD, FRCSC

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Figure. Intraoperative images. A, Image from flexible laryngoscopy revealing bilateral vocal fold immobility. B, The airway was exposed with a Dedo laryngoscope, and a Hunsaker tube was used for jet ventilation. C, The posterior scar band was successfully lysed after a metal suction was bent to the appropriate angle to act as a sheath for the carbon dioxide laser fiber.

A man in his 50s was injured in a motor vehicle crash and was intubated at the scene. On day 10 of intubation, he underwent a tracheotomy. He was successfully decannulated 8 months later. The patient then presented 1 year later with complaints of hoarseness since intubation. He felt short of breath at the end of sentences. He had undergone a neurosurgical procedure after the motor vehicle crash and was notified by the anesthesiologist that he was a difficult intubation. On physical examination, he had a rough, hoarse voice without any stridor. His oral cavity revealed a Mallampati classification IV. Flexible laryngoscopy revealed bilateral vocal fold immobility (Figure, A). Results of a computed tomographic scan of his neck

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were unremarkable. Findings from a laryngeal electromyography were normal. The patient subsequently underwent a microdirect laryngoscopy with jet ventilation for diagnostic and therapeutic purposes. On first attempt of intubation, the Hunsaker tube got stuck in the posterior glottis. The attending otolaryngologist then exposed the airway with a Dedo laryngoscope and intubated the patient (Figure, B). An interarytenoid adhesion with a posterior opening was visualized. Palpation of the cricoarytenoid joints demonstrated that the joints were mobile. There was no evidence of subglottic or tracheal stenosis. What is your diagnosis?

(Reprinted) JAMA Otolaryngology–Head & Neck Surgery February 2015 Volume 141, Number 2

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Clinical Review & Education Clinical Problem Solving

Diagnosis Posterior glottis stenosis (PGS), type I Bogdasarian

Discussion Posterior glottis stenosis is a complex diagnosis that has evolved over the past century. Prior to World War II, the most common etiology was infection; however, this was replaced by external laryngeal trauma, caustic ingestion, and inhalation injury with the introduction of effective antibiotics.1,2 After the poliomyelitis epidemic and the proliferation of mechanical ventilation, prolonged intubation is now the most common cause.1,2 The posterior glottis is an intricate anatomical site comprised of the posterior one-third of the vocal folds, posterior commissure, interarytenoid muscles, cricoid lamina, cricoarytenoid joints, and arytenoids.1 The overlaying mucosa is composed of respiratory epithelium.1 Unlike the squamous mucosa of the anterior glottis, this respiratory epithelium is more susceptible to trauma.1 Risks factors for PGS include duration of intubation; trauma during intubation; larger tube sizes; multiple extubations and reintubations; movement of the endotracheal tube (ETT); infection; medical conditions, such as diabetes mellitus; nasogastric tube placement; gastroesophageal reflux disease; and chemical irritation.1,3,4 Despite this long list, the duration of intubation is the most important factor.4 Although there have been many advances in ETT design, the incidence of laryngeal damage has not changed. The reported incidence of PGS is as high as 12% to 14% after 10 days of intubation.1,5 It is the curved shape of the ETT that allows for it to rest against the posterior glottis.3 Pressure from the ETT causes ischemia and ulceration. This leads to disruption of the perichondrium, microabscesses of the cartilages, fibrous replacement of the tissues, and scar formation of the cricoarytenoid joint complexes.2 Bogdasarian and Olson6 classified PGS into 4 types based on the tissue depth of the injury.2,7 Type I PGS (PGS-I) involves scarring between the vocal processes with an interarytenoid synechia and a patent opening posteriorly. Type II PGS progresses to involve the ARTICLE INFORMATION

REFERENCES

Author Affiliations: Department of Otolaryngology–Head and Neck Surgery, Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania (Quercetti); Department of Otolaryngology–Head and Neck Surgery, Drexel University College of Medicine, Philadelphia, Pennsylvania (Hu).

1. Hoasjoe DK, Franklin SW, Aarstad RF, Day TA, Stucker FJ. Posterior glottic stenosis mechanism and surgical management. Laryngoscope. 1997;107 (5):675-679.

Corresponding Author: Amanda Hu, MD, FRCSC, Department of Otolaryngology–Head and Neck Surgery, Drexel University College of Medicine, 219 N Broad St, 10th Floor, Philadelphia, PA 19102 ([email protected]). Section Editor: Albert L. Merati, MD. Published Online: December 11, 2014. doi:10.1001/jamaoto.2014.3192. Conflict of Interest Disclosures: None reported.

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interarytenoid space without a posterior opening. Progressive involvement between the inferior surface of the arytenoid cartilage and the superior surface of the cricoid cartilage unilaterally leads to type III PGS and bilaterally to type IV PGS.2,7 Presenting signs and symptoms of PGS are fairly nonspecific and include hoarseness, dyspnea, and difficulty on extubation.1 Our patient had bilateral vocal fold immobility on flexible laryngoscopy. It was unclear whether this was a result of neurologic injury or a structural deformity. Laryngeal electromyography allowed for this differentiation.1 There is no standardized treatment regimen for PGS owing to the diversity of this diagnosis. Most of the literature focuses on types II to IV, which require more detailed surgical approaches.1,4,8,9 Meyer and Wolf2 reported on the surgical outcomes from the largest known series of PSG-I cases.2 In this retrospective review of 13 cases, all patients underwent endoscopic surgical intervention. This study concluded that patients with PSG-I had excellent prognosis for decannulation, but a significant proportion can have persistent dysphonia. The carbon dioxide laser has been proven to be a safe and successful operative technique for treatment of PGS.8 For the patient described herein, an endoscopic carbon dioxide laser lysis of the interarytenoid adhesion was performed. Initially, the laser fiber hand piece did not accommodate for the curved angle necessary to reach the posterior adhesion. Finally, a metal suction was bent to the appropriate angle to act as a sheath for the laser fiber, and the posterior scar band was successfully lysed (Figure, C). Patients with PSG-I have good outcomes with simple endoscopic carbon dioxide laser lysis because there is preservation of the posterior mucosa and no deep involvement of the posterior interarytenoid tissues. At the patient’s 1-week postoperative visit, he reported improvement in his voice and resolution of his shortness of breath. Diagnostic flexible laryngoscopy showed greatly improved vocal fold mobility. Laryngeal examination findings have remained stable for the past 2 years.

2. Meyer TK, Wolf J. Lysis of interarytenoid synechia (type I posterior glottic stenosis): vocal fold mobility and airway results. Laryngoscope. 2011;121(10):2165-2171. 3. Lundy DS, Casiano RR, Shatz D, Reisberg M, Xue JW. Laryngeal injuries after short- versus long-term intubation. J Voice. 1998;12(3):360-365. 4. Hawkins DB. Glottic and subglottic stenosis from endotracheal intubation. Laryngoscope. 1977;87(3): 339-346.

6. Bogdasarian RS, Olson NR. Posterior glottic laryngeal stenosis. Otolaryngol Head Neck Surg (1979). 1980;88(6):765-772. 7. Rovó L, Venczel K, Torkos A, Majoros V, Sztanó B, Jóri J. Endoscopic arytenoid lateropexy for isolated posterior glottic stenosis. Laryngoscope. 2008;118 (9):1550-1555. 8. Riffat F, Palme CE, Veivers D. Endoscopic treatment of glottic stenosis: a report on the safety and efficacy of CO2 laser. J Laryngol Otol. 2012;126 (5):503-505. 9. Lorenz RR. Adult laryngotracheal stenosis: etiology and surgical management. Curr Opin Otolaryngol Head Neck Surg. 2003;11(6):467-472.

5. Whited RE. A prospective study of laryngotracheal sequelae in long-term intubation. Laryngoscope. 1984;94(3):367-377.

JAMA Otolaryngology–Head & Neck Surgery February 2015 Volume 141, Number 2 (Reprinted)

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Bilateral vocal fold immobility.

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