Posterior glottic laryngeal stenosis most commonly results from endotracheal intubation and less commonly from external trauma or from infection. Following extubation, the patient may have immediate or delayed onset of symptoms of airway obstruction. Often, as in bilateral vocal cord paralysis, voice symptoms are minimal. Indirect laryngoscopic examination usually establishes the diagnosis. Movement of the arytenoids is seen but is limited, and is reflected in poor mobility of the vocal cords. Direct laryngoscopic examination and palpation of the arytenoids for passive mobility confirms the diagnosis and rules out vocal cord paralysis from recurrent laryngeal nerve injury. With the establishment of stenosis, scarring and web formation occurs over the posterior cricoid lamina and may extend into one or both cricoarytenoid joints and into the interarytenoid muscle. Scar contracture in the posterior commissure causes medial fixation of the vocal processes of the arytenoid cartilages. When caused by endotracheal intubation, the initial injury is usually to the mucosa of the posterior cricoid lamina, vocal processes of the arytenoids, or both. Perichondritis may ensue, its location and severity determining the ultimate functional extent of scarring. When airway obstruction results, treatment is by laryngofissure, scar resection, grafting, and stenting. If bilateral cricoarytenoid joint fibrosis is discovered, arytenoidectomy, and in some cases laryngeal lumen augmentation, is invariably required to reestablish the airway, with probable detrimental effects on voice quality. Five of ten patients are presented to illustrate the etiology, pathogenesis, symptoms, management, and sequelae of this problem.
Vocal Cord Paralysis Following Endotracheal Intubation
