Tracheal Lesions

Postintubation Injuries

Iatrogenic injuries resulting from tracheal intubation have long been the most common lesion afflicting the airway. Postintubation injuries include granulomas, strictures, malacia, and tracheoesophageal and tracheoinnominate fistulas ( Fig. 8-2 ).

Postintubation tracheal stenosis represents the most common iatrogenic injury of the trachea. It occurs after intubation and develops principally at the level of the endotracheal tube (ETT) or tracheostomy tube cuffs. The radial pressure exerted from the cuff causes circumferential pressure necrosis, which results in cicatricial scaring stenosis ( Fig. 8-3 ). The route of entry of the ventilatory tube does not affect the occurrence of cuff injury, only its level. These lesions are seen in patients who have had only oral endotracheal intubation and in those with previous tracheostomy. The development of the large-volume, low-pressure cuff for tracheostomy and ETTs for ventilation has greatly lowered the incidence of cuff-related stenoses. However, overinflation of these cuffs can still result in local airway damage and subsequent scar formation, and it contributes to the continued incidence of these lesions. Stenosis in the subglottic region can occur because of prolonged intubation with ETTs, after cricothyroidotomy, or after high placement of a tracheostomy where the neck of the tube erodes through the cricoid cartilage.

Stomal stenosis results from the gradual enlargement of a tracheal stoma and its eventual healing by contraction. This pulls the sides of the defect together, distorting the tracheal lumen to a triangular configuration, with the base of the triangle located posteriorly and consisting of the uninjured membranous wall ( Fig. 8-4 ). The large stoma can result from overzealous excision of anterior tracheal cartilage at the time of the initial tracheostomy, from erosive infection around the margins of the stoma, or, most commonly, from erosion resulting from leverage by equipment attached to the tracheostomy tube during ventilation. The stenotic process can extend into the subglottic larynx if the previous tracheostomy was placed inappropriately high in the trachea.

Prolonged endotracheal intubation combined with a nasogastric tube can lead to a tracheoesophageal fistula ( Fig. 8-5 ). This fistula results from pressure necrosis generated by a ventilating cuff in the trachea and a nasogastric feeding tube in the esophagus. Consequently, these fistulas occur in the shared location between the membranous tracheal wall and the anterior wall of the esophagus. Anterior injuries of the trachea can lead to the `development of a tracheoinnominate artery fistula. These most often result from direct erosion of the inner elbow of the tracheostomy tube in an inferiorly placed stoma, and they can arise either from a tracheostomy tube placed too low in the trachea or from an innominate artery lying high, near the sternal notch.

Idiopathic Laryngotracheal Stenosis

Rarely, a patient has stenosis of the airway without history of trauma, infection, inhalation injury, or airway intubation. Idiopathic laryngotracheal stenosis is a diagnosis of exclusion, characterized by an inflammatory cicatricial stenosis at the level of the subglottic larynx, cricoid, and upper trachea. Causes such as gastroesophageal reflux with silent aspiration, Wegener granulomatosis, and connective tissue disorders must be excluded. As part of the routine preoperative workup, all patients undergo serologic screening (antinuclear antibody [ANA], antineutrophil cytoplasmic antibody [ANCA]) for these conditions. Over 95% of patients with idiopathic laryngotracheal stenosis are female between the third and fifth decade of life, and they typically exhibit signs and symptoms of upper airway obstruction. Pharyngeal and laryngeal anatomy and vocal cord function are usually normal, whereas the inflammatory process leading to luminal narrowing is confined intrinsically to the wall of the airway and the immediately surrounding connective tissue of a short (<2.5 cm) segment at the level of the cricoid cartilage.

The biggest clinical challenge in the surgical management of idiopathic laryngotracheal stenosis lies in the unpredictability and variability of the future clinical course. When airway obstruction becomes severe and dilation does not provide sustained relief of symptoms, surgery may be entertained, with, however, the clear caveat that the disease may progress. Most patients are best treated with definitive laryngotracheal resection and primary reconstruction. Timing of resection and reconstruction is central and must be done when inflammation is minimal. Bridging the time to definitive operation may require repeated bronchoscopic dilation. We prefer dilation to be performed in the operating room with rigid bronchoscopes starting with pediatric sizes increasing to adult bronchoscopes.

Tracheobronchomalacia

Airway malacia may be a consequence of a postintubation injury; however, in patients with chronic obstructive pulmonary disease, malacia can develop in the lower trachea, main bronchi, and sometimes the more distal bronchi, even in the absence of prior intubation. When the patient attempts a deep expiration or a cough, the membranous wall approximates to the anterior, softened cartilaginous wall, causing nearly total obstruction. Subsequently, the posterior membranous wall elongates and becomes redundant. Afflicted patients may have dyspnea, cough, and secretion retention. It is possible to address the deformity surgically by pulling the ends of the cartilages toward one another posteriorly, restoring a more circular shape to the airway. The redundant membranous wall must be tacked to a posterior splinting material to prevent it from falling forward into the lumen. Various materials have been used for splinting, but none with complete success. These have included fascia lata, pericardium, lyophilized bone, polytetrafluoroethylene, and rigid plastic splints. Biomesh and cryopreserved aortic allografts can be useful biologic alternatives to synthetic tissues, especially when tissue quality or comorbidities are a factor, and airway erosion is of concern. To obtain maximum long-term relief, we currently use sheets of nonabsorbable polypropylene mesh to plicate the membranous wall as described by Rainer and colleagues.