Suprastomal lesions are often a result of cricothyroidotomy, high tracheostomy tube placement, or friction of the superior aspect of the tracheostomy tube with the anterior airway wall in patients with significant kyphosis.17,18 These lesions include subglottic stenosis, tracheal stenosis, and granulation tissue formation. We should also mention functional late complications such as functional voice changes and vocal cord dysfuntion.
Stomal lesions may result from fracture of the anterior tracheal wall following PDT. As a result, the anterior tracheal wall invaginates and protrudes into the tracheal lumen, resulting in a fixed obstruction.18,19 Risk factors for stomal stenosis include sepsis, stomal infection, hypotension, advanced age, male sex, steroids, oversized tube, excessive motion, prolonged placement, and disproportionate excision of the anterior tracheal ring. Granulation tissue can also develop at the superior border of the stoma and usually is suspected when there is difficulty exchanging the tracheostomy tube.
Finally, infrastomal complications include tracheal stenosis, tracheomalacia (TM), tracheoesophageal, and tracheoinnominate fistulas. Infrastomal lesions typically result from ischemia of the tracheal mucosa due to endotracheal tube cuff balloon pressure exceeding the perfusion pressure (>25 mm of water).20 Lesions caused by balloon expansion have decreased with the adoption of low-pressure, high-volume balloons.21 If ischemia is prolonged, it causes mucosal ulceration, followed by inflammation (chondritis) and necrosis in the mucosa and cartilage. This reaction stimulates the formation of a scar tissue, which obstructs the airways, resulting in circumferential stenosis.20 Risk factors for infrastomal lesions include female sex, older age, prolonged duration, and excessive endotracheal tube cuff pressures. Malacia may also complicate the stenotic segment. The mechanism of malacia formation is not fully understood, but may be related to concomitant chronic airway inflammation secondary to bacterial colonization or acid reflux.22 Common signs and symptoms that may indicate late complications are unexplained difficulty in weaning from the ventilator, dyspnea on exertion, cough, hemoptysis, stridor. Flow-volume loop and computed tomography (CT) scan with 3-dimensional reconstruction can be used as screening tools, 2 months after decannulation.
Tracheal stenosis describes a pathologic narrowing of tracheal lumen and can result from prolonged tracheostomy tube dependence. Tracheal stenosis is considered the most common late complication of tracheostomy tube placement. Some degree of tracheal stenosis is present in almost all patients with a tracheostomy tube, but only 3% to 12% of patients have clinically significant stenosis requiring intervention.23 Tracheal stenosis is typically seen at the level of the tracheostomy stoma or suprastomally, but below vocal cords20–24 (Fig. 2).
The pathogenesis of tracheal stenosis involves inflammation and the formation of granulation tissue. Trauma resulting from tracheostomy, mucosal ischemia due to excessive cuff pressures, persistent mucosal irritation stemming from the tip of tracheostomy tube, pooling of secretions, and gastroesophageal reflux disease are predisposing factors for development of ulceration and inflammation of cartilage, leading to the formation of granulation tissue. Subsequently, granulation tissue matures into a fibrous tissue layer covered with epithelium, leading to tracheal stenosis.20 Patients with tracheal stenosis are often asymptomatic until the size of trachea has reduced to <5 mm or 25% to 50% of the original diameter.24 Tracheal stenosis may be detected when the patient is still mechanically ventilated and can be clinically manifested as difficulty in weaning from the ventilator. Elevated peak airway pressures may be present for infrastomal stenosis. Dyspnea, stridor, and respiratory failure, may be present after decannulation. In addition, clinical manifestations of stenosis may present weeks to years after development, but typically are evident within 2 months following decannulation.20
Flexible bronchoscopy remains the gold standard to diagnose and characterize lesions of tracheal stenosis.25 Flexible bronchoscopy permits direct visual evaluation of the stenotic lesion. Airway lesions are described according to type, size, location, and degree of stenosis. Different types include A-shape (cartilage damage), simple, and complex stenosis. Size refers to the length in centimeters. Supraglottic, glottic, subglottic, and tracheal, are the locations. Distance from vocal cords, cricoid, and carina, are helpful. Degree of stenosis by quantifying percentage of obstructed lumen (grade I: <50%, grade II: 50% to 70%, grade III: 71% to 99%, and grade IV: 100%) (Fig. 2). Noninvasive testing such as pulmonary function testing is also sensitive in identifying fixed airway obstructions. Flow-volume loops permit localization and characterization of the obstruction. A stenosis outside the thoracic cage may show as blunting of the inspiratory limb of the flow-volume loop alone; and an intrathoracic obstruction would commonly show both inspiratory and expiratory blunting, resulting in a squared-off pattern. This method does not detect small changes in tracheal lumen in a diameter above 8 mm.26 In addition, CT scans with 3-dimensional reconstructions can predict the size and location of stenosis.
Stenotic lesions can be divided into simple (<1 cm, granulation tissue, web-like lesion, concentric lesion, no involvement of tracheal wall) and complex stenoses (>1 cm, scarring of trachea, presence of malacia). Correct classification of the stenotic lesion is essential in determining appropriate management. The initial approach to simple lesions is endoscopic. Recurrence of simple stenosis after multiple bronchoscopic treatments often requires surgical evaluation for definitive treatment. Complex lesions require a multidisciplinary approach often resulting in surgery (Fig. 3). Endoscopic dilatation can be performed in emergent cases or as a bridge to definitive surgical correction. The preferred surgical approach depends on involvement of the larynx and extent of tracheal involvement. Laryngotracheal reconstruction is performed when subglottic tracheal lesions involve the larynx, whereas tracheal resection and reconstruction is performed when complex lesions involve only the trachea.
TM is characterized as weakening of the tracheal wall leading to dynamic expiratory collapse and airway obstruction. TM is defined as >50% reduction in cross-section area of trachea during forced expiration.22 This complication is considered rare following tracheostomy placement. Ischemia from elevated tracheostomy tube cuff pressures, pooling of secretions around the cuff, and recurrent episodes of gastroesophageal reflux during mechanical ventilation may result in inflammation of the tracheal rings, also known as chondritis. Prolonged chondritis may lead to weakening of the tracheal rings that define the shape of the trachea. Such weakening can result in airway deformity, increased airway compliance, and hyperdynamic airway collapse during expiration. Unexplained difficulty in weaning from the ventilator along with repeated need for reintubation postdecannulation remain important clinical signs of TM after prolonged ventilation through a tracheostomy tube. Dyspnea on exertion, cough, recurrent pulmonary infections, difficult expectorating sputum, wheezing, hemoptysis, and syncope due to excessive coughing are common clinical symptoms of TM identified months to years after decannulation. Pulmonary function tests often reveal decreased peak expiratory flow along with notching and biphasic morphology on flow-volume loops. Dynamic expiratory chest CT reveals narrowing of airway lumen with expiratory maneuvers and is very sensitive for diagnosing TM (Fig. 4). Dynamic flexible bronchoscopy with expiratory maneuvers is the gold standard for diagnosing TM.27 Patients suffering from TM can be definitively treated with posterior membrane tracheoplasty or focal tracheal resection and reconstruction. Posterior membrane tracheoplasty may result in significant improvement in quality-of-life indicators, but not in physiological outcomes.28
Tracheoesophageal fistulas are rare complication following tracheostomy tube placement with an incidence of approximately 1%.20 This complication occurs secondary to increased tracheostomy tube cuff pressures and subsequent ischemia of the tracheal mucosa. Prolonged ischemia can lead to tracheal wall necrosis, ulceration, and perforation, with subsequent erosion into the esophagus. Other possible mechanisms include erosion of the posterior tracheal wall by the distal end of the tracheal tube when it impinges posteriorly. This complication is most commonly seen in patients with concomitant nasogastric tubes in place. Surgical correction is required with primary esophageal closure, interposition of viable tissue, and tracheal repair by tracheal or laryngotracheal resection with reconstruction in the presence of stenosis or a long tracheal defect.20 Patients who are not surgical candidates require a combination of tracheal stenting and esophageal stenting for palliative measures. Placement of the tracheal stent before placement of the esophageal stent is essential in this therapy, as the malleability of the esophagus can result in compression of the trachea due to excessive stent expansion.
Tracheoinnominate Artery Fistula (TIF)
TIFs are due to erosion into the innominate artery by the tracheostomy tube because of elevated pressure from the tracheostomy tube cuff or contact between the distal end of the tracheostomy tube and the innominate artery. Formation of a tracheoinnominate fistula following tracheostomy placement is a medical emergency. Innominate artery injury resulting in massive hemorrhage following tracheostomy is approximately 0.7%.20 Although less frequent, other vessels involved may be the common carotid artery, inferior thyroid artery, innominate vein, or the aortic arch. Risk factors for TIF include high tracheostomy tube cuff pressures, low tracheostomy insertion, and repetitive head movements resulting in repeated contact of the tracheostomy tube and the area over the innominate artery. Physicians identifying bleeding from the tracheostomy site or within the tracheostomy stoma 48 hours or later following tracheostomy should harbor a high suspicion for TIF. Management of possible sentinel bleeding should take place in the operating room using a rigid bronchoscope to examine the stoma and anterior wall with the tracheostomy tube removed. Equipment for prompt surgical intervention should be readily available. In case of a massive bleed, the rigid bronchoscope can be used to compress the innominate artery against the sternum, while providing adequate suction, oxygenation, and ventilation. Surgical treatment of TIF involves sternotomy with ligation of affected vessel, interposition of viable tissue, and tracheal wall repair.20,24
Tracheocutaneous Fistula (TCF)
TCFs are generated when cutaneous epithelium has healed into the tracheal epithelium. Risk factors include prolonged tracheostomy tube placement, steroid use, old age, and malnutrition. A TCF is present when the tracheostomy stoma fails to close 3 to 6 months following decannulation. Treatment includes cauterization and healing by secondary intervention, tract excision, and closure using a strap muscle flap.24
Tracheostomy tubes are devices that are increasingly being used in patients with chronic airway diseases. The placement of tracheostomy tubes facilities liberation from mechanical ventilation, increases the ability to mobilize patients with chronic respiratory failure, and reduces the dosage of sedation. Although these devices may be essential in facilitating recovery in chronic airway disease, they are not without risk for complication. Understanding the possible early and late complications of tracheostomy placement and identifying symptoms of such complications allow physicians to provide the optimal care for patients following tracheostomy.
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Keywords:Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
tracheostomy; tracheostomy complications; tracheal stenosis; tracheomalacia; bronchoscopy; interventional pulmonology