Tracheal stenosis is a relatively uncommon problem that has a variety of etiologies. It frequently has an insidious onset, and the early signs and symptoms may be disregarded or mistaken for a variety of other disorders. Shortness of breath on exertion, which may progress to dyspnea at rest, a brassy cough, recurrent pneumonitis, wheezing, stridor, and cyanosis may all be a part of the clinical presentation. because many of these symptoms, especially dyspnea on exertion and wheezing, can be easily attributed to other respiratory disorders such as chronic bronchitis and asthma, the patient's past medical history becomes particularly important.
A previous history of endotracheal intubation or tracheotomy should not be taken lightly during the evaluation of a patient with upper airway symptomatology. Only awareness of the possibility that tracheal stenosis might exist will lead to its early recognition.
When stenosis is suspected, a variety of methods exist that may be used for evaluation. In addition to standard chest radiographs, simple tracheal radiographs should be obtained first. These include anteroposterior filtered tracheal views and lateral soft tissue views of the neck. In some instances, tracheal tomograms can provide additional information. Tracheal fluoroscopy may occasionally be helpful for identifying areas of malacia that can be present along with stenosis. In general, CT scans are not as helpful in the evaluation of tracheal strictures, since they provide only axial views. MRI, on the other hand, can be extremely useful in assessing the length and width of the stenotic region with coronal and sagittal views.
Endoscopy is critically important not only for evaluation of the tracheal but also for evaluation of the larynx. Laryngoscopy should be performed prior to undertaking a definitive procedure to detect the presence of glottic or subglottic stenosis or to detect the presence of vocal cord dysfunction. Likewise, rigid bronchoscopy is essential for evaluating stenotic lesions in the trachea. The length and width of the stricture and the degree of tracheal inflammation should be assessed, and areas of malacia and granulation tissue should be identified. In addition, if granulation tissue alone is causing stenosis, endoscopic removal may be the only treatment necessary. Flexible bronchoscopy under topical anesthesia should be avoided since secretions, edema, and the bronchoscope itself can precipitate sudden, complete airway obstruction. Also, accurate tracheal measurements with the flexible bronchoscope are virtually impossible to make.
Flow volume loops are not particularly helpful for making the initial diagnosis of tracheal stenosis but can be useful for monitoring possible recurrent stenosis after endoscopic or surgical procedures.
There are multiple causes of benign tracheal stenosis, the most common being traumatic. however, if there is no prior history of tracheal trauma, the etiology of the stenosis may be obscure and difficult to determine, necessitating a systematic approach to make the diagnosis. Exclusive of trauma, the differential diagnosis of tracheal stenosis can be subdivided into four categories: congenital, neoplastic, infectious, and inflammatory. Congenital tracheal stenosis is really quite rare and is often the result of posterior fusion of the tracheal rings, thereby forming complete rings. Other causes of congenital stenosis include vascular rings and other congenital cardiovascular anomalies such as an anomalous subclavian artery.
Primary benign tumors of the trachea such as chondromas, fibromas, squamous papillomas, hemangiomas, and granular cell tumors are also unusual causes of stenosis. In addition, extrinsic compression of the trachea can occur by thyroid neoplasms and goiters.
A number of infections of the bronchopulmonary tree can lead to tracheal stenosis. Fungal infections such as histoplasmosis and blastomycosis should always be considered when the etiology of the stenosis is unclear. Serologic testing and histopathologic examination can be helpful in this regard. Other infectious causes of tracheal stenosis include rhinoscleroma, tuberculosis, syphilis, and diphtheria.
Noninfectious, inflammatory causes of tracheal stenosis include sclerosing mediastinitis, primary amyloidosis, and sarcoidosis. Wegener's granulomatosis and relapsing polychondritis can also cause tracheal stenosis, but they are almost always seen in combination with other, more classic hallmarks of these diseases.
By far, most cases of benign tracheal stenosis are the result of tracheal trauma, the majority of which are secondary to endotracheal intubation. Prior to the advent of compliant, high-volume, low-pressure cuffs, the incidence of tracheal stenosis following intubation was as high as 20%. By 1981, some studies were reporting incidences as low as 1%. There are two principal types of strictures that occur after intubation: strictures at the site of the endotracheal tube cuff, which is the most common location of postintubation stenosis, and those that occur at the site of a tracheotomy stoma.
High-pressure cuffs, or low-pressure cuffs that have been converted to high-volume high-pressure cuffs by overinflation, produce a circumferential pressure injury in the trachea. Since the mean capillary pressure in the tracheal mucosa is approximately 20 mm Hg, obstruction of blood flow to the trachea will occur when the cuff pressures exceed this pressure. This in turn leads to inflammation and erosion of the mucosa and can progress to necrosis, with ultimate destruction of the tracheal architecture. Cuff strictures can occur after as little as 36 hours of intubation and usually become symptomatic within an average of five weeks after extubation.
Stomal structures usually occur in patients who have required mechanical ventilation. Although this injury may be the result of the particular surgical technique used, improper suspension of ventilator equipment, causing leverage of the tracheotomy tube against the stoma, appears to be the most significant factor leading to stomal stenosis. Invasive tracheal infection and duration of intubation play a role in all types of postintubation tracheal stenosis.
The methods available for treating postintubation stenosis fall into two categories: endoscopic and open surgical methods. Endoscopic modalities should at least be attempted prior to undertaking one of the more aggressive surgical techniques.
Endoscopic dilation alone as the sole treatment of functional tracheal stenosis is not successful on a long-term basis and should be used as a temporizing measure prior to definitive therapy. Restenosis will usually develop within days to weeks. The most important application of dilatation is in the emergent treatment of tracheal strictures by establishing an airway and thereby allowing for a thorough evaluation of the patient on a more elective basis. Dilatation is accomplished with filiform dilators or with graduated rigid bronchoscopes. One must always be aware of the risk of tracheal rupture or total airway obstruction by blood or edema. Postdilatation edema can be minimized with racemic epinephrine and steroids.
Laser vaporization of tracheal strictures has been employed with variable success and, as with dilatation, is only a temporary measure in most cases. Several different types of laser techniques have been described, and either the carbon dioxide or the Nd:YAG laser can be used with equal efficacy. Regardless of the laser technique used, it should only be used in select circumstances. Poor results are guaranteed when there is circumferential scarring, the stenosis is greater than one centimeter in vertical dimension, there has been loss of cartilage, tracheomalacia is present, or when there is a history of tracheal infection secondary to a tracheotomy.
The use of stents after dilatation, while not curative, can be used to manage a tracheal stricture indefinitely. Montgomery T-tubes for upper tracheal lesions, long-armed T-tubes for low stenoses, and occasionally bifurcated T-Y tubes for stenoses that involve the carina, are reasonably well tolerated. Likewise, tracheotomy tubes can be used for the lifelong management of tracheal stenoses. These options should always be kept in mind, especially for the patient with multiple medical problems.
Finally, when endoscopic management fails, tracheal resection with end-to-end anastomosis is indicated and is considered the treatment of choice for most cases of benign tracheal stenosis. It is now widely accepted that up to 70% of the trachea, depending on the patient's age and of the factors, can be safely resected. A combined approach with both otolaryngologists and thoracic surgeons may be needed for the more extensive resections. Prosthetic material should be used for tracheal reconstruction, and cutaneous, muscle, and other soft tissue flaps are also almost never needed.
The majority of tracheal resections can be performed through a cervical or a cervicomediastinal approach. A high posterolateral thoracotomy, with or without a cervical incision, is rarely necessary. The most common complication of a tracheal resection is the development of granulation tissue at the suture line. This complication can be minimized by using absorbable sutures and by placing the knots on the outside of the trachea. Restenosis can also occur and is usually the result of excessive tension on the anastomosis. It can also be secondary to excessive circumferential dissection of the trachea, destroying its laterally-based blood supply. Less often, restenosis may result from incomplete resection of the involved trachea. The recurrent laryngeal nerves are also at risk for injury, and erosion of the innominate artery can occur if it is not protected from the anastomotic site by pleural or muscle interposition flaps.
Because tension on the anastomosis should be avoided at all costs, several methods have been devised to reduce such tension. Neck flexion yields the greatest degree of tracheal mobilization, often up to 6 cm. Complete anterior and posterior mobilization of the trachea can yield 1.5 cm of additional length. If these maneuvers are not sufficient, laryngeal release can then be performed. Suprahyoid laryngeal release is preferred (2 cm), since the incidence of dysphagia after infrahyoid release is unacceptably high. Mobilization of the right hilum and inferior pulmonary ligament (1.5 cm), intrapericardial dissection of the pulmonary artery and vein (1 cm), and division and reimplantation of the left mainstem bronchus (2.5 cm) are rarely ever necessary.
A 13-year-old white female, in otherwise good physical health, took an intentional overdose of amitriptyline and required intubation and mechanical ventilation for 72 hours. Although she initially recovered uneventfully and was discharged to home, she experienced progressive dyspnea on exertion over the ensuing four weeks. She subsequently developed stridor, wheezing, and fevers to 102° and was admitted to an outlying hospital with a provisional diagnosis of pneumonia. A chest radiograph taken on admission showed a left lingular infiltrate, and arterial blood gases on room air revealed a pO2 of 58 and a pCO2 of 43. Intravenous antibiotics and aminophylline were begun. After further review of her chest radiograph, a short segment of tracheal stenosis at the level of the sixth and seventh cervical vertebrae was noted. She was started on intravenous methylprednisolone, and a CT scan of her neck was performed, confirming the diagnosis of tracheal stenosis. She was then transferred to The Methodist Hospital for further therapy.
After arrival, she was continued on antibiotic and corticosteroid therapy. An MRI scan of her neck demonstrated a two centimeter length of tracheal stenosis at the level of C6 and C7, at which point the airway narrowed to approximately five millimeters in diameter. Rigid bronchoscopy was performed, revealing marked circumferential stenosis of the tracheal lumen at the second and third tracheal rings. The stenotic region was vaporized with the carbon dioxide laser and dilated to 12.0mm. Postoperatively, she did well, with no further stridor or respiratory compromise. One week later, bronchoscopy was repeated, and the involved area remained patent with only minimal residual stenosis. She was discharged home but required readmission three weeks later for a progressive cough, dyspnea on exertion, and intermittent stridor with cyanosis. Tracheal resection with a suprahyoid laryngeal release was then performed, with resection of tracheal rings two through five. Circumferential stenosis was found, with a tracheal lumen of 6.0mm. Histologic examination of the resected trachea demonstrated squamous metaplasia of the mucosa with chronic inflammation, granulation tissue, and fibrosis. She was extubated on postoperative day one, and her neck was maintained in flexion with a suture tethering her chin to her chest. This suture was removed on postoperative day eight, and she was discharged. Flexible laryngoscopy performed prior to discharge revealed normal vocal cord function bilaterally and a widely patent tracheal anastomosis. On follow-up examination six weeks postoperatively, she was doing well without respiratory compromise.
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