LARYNGEAL AND TRACHEAL STENOSIS
The unique anatomy and delicate tissues of the larynx and trachea predispose these sites to scarring and stenosis in response to injury. Some of the more common causes include prolonged endotracheal intubation, long-term tracheostomy, bacterial or viral infection, systemic inﬂammatory conditions, neoplasia, and trauma. In many cases, the stenosis is a relatively late sequela of the initial pathologic process and may not be recognized until it progresses to the point of symptomatic airway compromise (stridor or dyspnea) or impaired laryngeal function (hoarseness).
Laryngeal stenosis may occur at any level within the larynx. Supraglottic and glottic stenosis are usually a result of external trauma or prolonged intubation but are also seen with caustic ingestions, inhalation burns, and postsurgical scarring. Subglottic stenosis is the most common form of laryngeal stenosis. Prolonged endotracheal intubation can damage the thin inner perichondrium of the cricoid cartilage, leading to circumferential scarring and cicatrix formation. Long- term tracheostomy tubes can also cause subglottic stenosis as a result of superior migration of the tube and ensuing destruction of the cricoid ring. Other common causes of subglottic stenosis include laryngopharyngeal reﬂux, Wegener granulomatosis, and a congenital form seen in young children. When a speciﬁc cause cannot be identiﬁed, the term idiopathic subglottic stenosis (ISS) is used. It is likely that many cases of ISS are caused, at least in part, by unrecognized laryngopharyngeal reﬂux or autoimmune disorders.
Tracheal stenosis is a potentially devastating sequelae of prolonged endotracheal intubation and tracheostomy in patients with respiratory failure requiring cuffed tubes for mechanical ventilation. In the anterior and lateral tracheal walls, the vertical blood vessels that course between the mucosa and the cartilage rings may be readily compressed by a distending cuff or balloon. Decreased blood supply leads to perichondritis, avascular necrosis, and fragmentation of the tracheal cartilage. The resultant stricture often has a triangular conﬁguration on transverse section because of anterior weakening of the cartilaginous arch with lateral wall collapse. Posteriorly, the membranous trachea is more pliable, and the vascular supply is less likely to be compressed. Thus, in about 50% of cases of postintubation or post- tracheostomy balloon stenosis, the posterior tracheal wall is spared.
The characteristics and extent of tracheal stenosis can be demonstrated radiographically with traditional tomography in the frontal and lateral projections or with computed tomography (CT) images in the coronal and sagittal planes. The stenotic segment may be narrow and weblike, involving only one tracheal ring, or it may be longer, involving two to ﬁve tracheal rings with tapering margins. If the affected segment is thin or pliable, obstruction may only occur with inspiration or expiration (tracheomalacia), depending on whether the affected segment is extrathoracic (neck) or intrathoracic (thorax), respectively. Tracheomalacia may result in greater functional impairment than is apparent radiographically. If dynamic collapse is suspected, ﬂow- volume loops demonstrating reduced inspiratory or expiratory ﬂow or ﬁberoptic bronchoscopy demonstrating inspiratory or expiratory collapse may be useful diagnostic tools. In some cases, multiple stenoses may occur, especially after the use of tubes of different lengths or tubes with double cuffs.
Postintubation and posttracheostomy balloon steno- sis remains a serious problem despite the advent of low-pressure cuffs and increased vigilance in the clinical care setting. It has been recommended that the cuff be deﬂated at intervals to avoid an excessively prolonged compression of the tracheal mucosa. The problem with this method is that the cuff may not empty completely, and if it is reinﬂated with the minimal ﬁxed volume of air recommended for ﬁlling, overinﬂation may occur. Proper cuff pressures are best achieved by inﬂating under auscultatory control until there is no leakage of air with positive-pressure ventilation. If stenosis develops despite these measures, surgery in the form of endoscopic laser incision and dilatation or tracheal resection with anastomosis may be necessary.