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).

Figure 8–2 Diagrams of principal postintubation tracheal lesions. A, Cuff stenosis from the cuff of an endotracheal tube. B, Cuff stenosis from the cuff of a tracheostomy tube, usually lower in the trachea than that from an endotracheal tube. Stoma stenosis also occurs at the site of the tracheostomy itself. Malacia may occur either at the level of the cuff or in the segment between the stoma and the cuff stenosis. C, Cuff stenosis at the site of a high tracheostomy stoma, which has eroded into the lower margin of the cricoid cartilage. In older patients, this may erode back further into the subglottic larynx, producing a laryngotracheal stenosis. D, Tracheoesophageal fistula (TEF) produced by pressure of the cuff against the membranous wall, often abetted by an indwelling, firm, nasogastric tube. E, One type of tracheoinnominate fistula (TIF), the result of a high-pressure cuff erosion. The more common type, but also rare, is that seen with a low-placed tracheostomy stoma, which rests against the innominate artery itself. Not shown here are the lesions that occur in the larynx as the result of endotracheal tubes.

(From Grillo HC. Surgical management of postintubation tracheal injuries. J Thorac Cardiovasc Surg 1979;78:860.)

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 or tracheostomy tube cuffs. The radial pressure exerted from the cuff causes circumferential pressure necrosis, which results in cicatricial scaring stenosis (Fig. 8-3).^7,8 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 as well as in those with previous tracheostomy. The development of the large-volume, low-pressure cuff for tracheostomy and endotracheal tubes for ventilation has greatly lowered the incidence of cuff stenoses. However, overinflation of these cuffs can result in local airway damage and subsequent scar formation, and it contributes to the continued incidence of these lesions. Stenosis in the subglottic region may occur as a result of prolonged intubation with endotracheal tubes, after cricothyroidotomy, or after high placement of a tracheostomy where the tube erodes through the cricoid cartilage.⁹

Figure 8–3 Cuff-level stenosis. The stenosis here is circumferential and the remaining lumen round.

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 instigating large stoma may 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 may extend into the subglottic larynx if the previous tracheostomy was placed inappropriately high in the trachea.

Figure 8–4 Tracheostomy stomal site stenosis. The characteristic A-shaped lumen is evident and results from a primarily anterior and lateral cicatricial process.

Prolonged endotracheal intubation combined with a nasogastric tube may lead to a tracheoesophageal fistula (Fig. 8-5). This results from pressure necrosis generated by a ventilating cuff in the trachea and a prolonged 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 may 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 may arise either from a tracheostomy tube placed too low in the trachea or from an innominate artery lying high at the sternal notch.

Figure 8–5 Endoscopic view of tracheoesophageal fistula.

Idiopathic Laryngotracheal Stenosis

Rarely, a patient presents with 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. An overwhelming majority of these patients are female, and they typically present with signs and symptoms of upper airway obstruction. This process is confined intrinsically to the wall of the airway and the immediately surrounding connective tissue.

It is impossible to predict the future course of the disease. When airway obstruction becomes severe and does not respond for sufficiently long intervals to dilation, 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.^10,11

Tracheobronchomalacia

Airway malacia may be a consequence of a postintubation injury. However, in patients with chronic obstructive pulmonary disease, malacia may develop in the lower trachea, main bronchi, and sometimes the more distal bronchi, even in the absence of prior intubation.¹² 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 present with dyspnea, cough, and secretion retention. It is possible to surgically address the deformity 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, none with complete success. These have included fascia lata, pericardium, lyophilized bone, polytetrafluoroethylene, and rigid plastic splints. We currently use sheets of polypropylene mesh to plicate the membranous wall as described by Rainer and colleagues.¹³

Tracheal Tumors

Primary tracheal tumors are rare, with an estimated incidence of 2.7 cases per million per year.¹⁴ Approximately two thirds of primary tracheal tumors are either squamous cell carcinomas (SCCs) or adenoid cystic carcinomas (ACCs). These two types occur with equal frequency. The remaining third of the tumors are widely distributed in a heterogeneous group of tumors, both malignant and benign. Secondary tumors that involve the trachea include carcinomas of the larynx, thyroid, lung, and esophagus. Rarely, tumors may metastasize to the submucosa of the trachea or to the mediastinum, with secondary invasion of the trachea.

Squamous cell carcinomas may be either exophytic (Fig. 8-6) or ulcerative. The tumor can metastasize to the regional lymph nodes, and, in its more aggressive and late forms, it invades mediastinal structures. In general, its progress appears to be relatively rapid in comparison with that of adenoid cystic carcinoma. A number of these patients develop synchronous or metachronous second SCC primary cancers of the lung or oropharynx. Squamous cell carcinoma occurs predominantly in men who are cigarette smokers.¹⁵

Figure 8–6 An exophytic squamous cell carcinoma of the trachea.

ACC often has a very prolonged course of clinical symptoms, sometimes extending for years. After resection, many years may pass before a recurrence is noted. It may extend submucosally over long distances in the airways, and also along perineural tissue. It can spread to regional lymph nodes, although this is less characteristic than in SCC. Although it may invade the thyroid or the muscular coats of the esophagus by contiguity, ACC that has not been surgically interfered with frequently displaces mediastinal structures before actually invading them. Metastases to the lungs, bone, and other organs can occur. These may grow very slowly over a period of many years and remain asymptomatic until they become quite large. In contrast to patients with tracheal SCC, the male-to-female ratio of ACC is essentially equal, and any smoking history of these patients appears to be incidental.¹⁵

The third group of primary tracheal tumors is composed of a multitude of tumor types and varying degrees of malignancy, including both epithelial and mesenchymal neoplasms. The list includes pleomorphic adenomas, leiomyomas, chondromas, carcinoid tumors, mucoepidermoid tumors, and sarcomas.

Secondary neoplasms may involve the trachea through direct extension. Thyroid carcinomas typically invade the trachea at the second and third rings, where the thyroid isthmus is adherent to the trachea (Fig. 8-7).¹⁶ More commonly, invasion is seen after thyroidectomy for carcinoma, when the surgeon was aware of shaving off the tumor from the trachea. In such cases, concurrent or early resection of the involved trachea should be considered. Both bronchogenic and esophageal carcinomas can erode into the trachea from local extension.

Figure 8–7 Bronchoscopic view of a papillary thyroid carcinoma with tracheal invasion.