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Airway complications after lung transplantation
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Airway complications after lung transplantation
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2016. | This topic last updated: Apr 29, 2016.

INTRODUCTION — During lung transplantation, the airway anastomosis is typically performed between the bronchus of the donor lung and that of the recipient. The airway anastomosis has traditionally been the most vulnerable site for operative complications of lung transplantation. Airway anastomotic complications include focal infection, bronchial necrosis and dehiscence, excess granulation tissue, tracheobronchomalacia, stenosis, and fistula formation.

The pathogenesis, diagnosis, treatment, and prevention of airway anastomotic complications of lung transplantation will be reviewed here. Other airway complications, such as bacterial and viral tracheobronchitis and bronchiolitis obliterans, and noninfectious problems related to lung transplantation are discussed separately. (See "Bacterial infections following lung transplantation" and "Chronic lung transplant rejection: Bronchiolitis obliterans" and "Noninfectious complications following lung transplantation".)

TYPES AND DEFINITION — Anastomotic airway complications after lung transplantation include those that typically develop within the first month (eg, anastomotic infection, necrosis, or dehiscence) and those that develop later (eg, excess granulation tissue, bronchomalacia, airway stenosis, bronchopleural fistula, bronchomediastinal fistula, or bronchovascular fistula) (table 1) [1].

Limited mucosal necrosis and sloughing at the anastomotic site are commonly observed during bronchoscopy in the first two to three weeks after transplant. These mild mucosal changes are not usually considered an "airway complication," if satisfactory healing occurs without intervention. Complications are considered significant when they necessitate an intervention such as debridement, dilatation, or stent placement.

INCIDENCE AND IMPACT — Reported incidences of airway anastomotic complications range from 2 to 33 percent, although most centers have rates in the range of 7 to 18 percent [1-3]. In a retrospective series of 232 lung transplants, 57 airway complications developed; the majority occurred in the first post-transplant year [2].

Although airway complications lead to increased costs, greater morbidity, and decreased quality of life, they are generally not associated with a substantial decrease in survival. In a series of 983 lung transplants, the hospital mortality of those with an airway complication was 10 versus 9.7 percent for those without an anastomotic complication [4].

PATHOGENESIS — The major reason for the high rate of complications at the bronchial anastomotic site is believed to be the loss of systemic blood supply to that site during transplantation. The normal bronchial blood supply is interrupted during the lung harvest procedure, leaving the bronchial vessels at the anastomotic site dependent on retrograde filling from the pulmonary arterial circulation through communications with pulmonary capillaries and precapillary anastomoses in the submucosal plexus [1,5,6].

Revascularization of the donor bronchus usually takes two to four weeks. This process may be more successful when the donor bronchus is shortened to within one to two cartilaginous rings of the take-off of the upper lobe bronchus [7]. While revascularization is occurring, the anastomotic site is subject to ischemic conditions and may develop varying degrees of necrosis and dehiscence. In some patients, the healing process of these areas of necrosis leads to development of granulation tissue and subsequent airway stenosis.

The surgical anastomotic technique may be a factor in the development of airway complications. The original technique of using an omentopexy (surrounding the anastomosis with a piece of omentum) was associated with a high rate of dehiscence [8]. Subsequent techniques have used a simple buttressing of the anastomosis with peribronchial tissues, which has decreased the rate of dehiscence [9,10].

An aspect of the anastomotic technique that remains controversial is telescoping the anastomosis by preferentially intussuscepting the recipient bronchus into that of the donor [1,2]. This technique may reduce early dehiscence, but may lead to increased rates of bronchial stenosis months later [1,11,12]. We typically use the end-to-end anastomotic technique and reserve the telescoping anastomotic technique for situations where there is a size discrepancy between the donor and recipient bronchi [1,2].

RISK FACTORS — Several factors are associated with an increased risk of anastomotic airway complications.

Severe reperfusion edema (primary graft dysfunction) [13]

Acute rejection within the first post-transplant year [14]

Pre and postoperative pulmonary infection [1,15]

Prolonged mechanical ventilation [16]

Single lung transplantation [17]

Colonization with Aspergillus fumigatus [15]

Preoperative Pseudomonas cepacia colonization [12]

Use of sirolimus prior to complete anastomotic healing [1]

Current doses of glucocorticoids used to suppress rejection are not felt to increase the risk of airway complications following lung transplantation, despite their adverse effects on wound healing in general.

AIRWAY SURVEILLANCE — We perform surveillance bronchoscopy with inspection of the anastomotic site at two weeks, six weeks, three months, and six months [12,17]. Bronchoscopy is also performed when symptoms suggest possible anastomotic complications.

SPECIFIC COMPLICATIONS — The clinical presentation of the airway anastomotic complications varies, depending on the specific complication. Most of the post-transplant bronchial complications can be treated successfully with non-surgical interventions, as described below.

Bronchial stenosis — Bronchial stenosis is the most common airway complication and often occurs in patients who have experienced anastomotic necrosis, dehiscence, or infection [1]. Bronchial stenosis usually manifests after the first posttransplant month, but sometimes not until years after lung transplantation [10].

Clinical features — Bronchial stenosis can be asymptomatic and diagnosed as an incidental finding during surveillance bronchoscopy, or it may present with dyspnea, wheezing, stridor, deteriorating pulmonary function tests, or postobstructive pneumonia. When presenting years after transplantation, the stenosis can cause progressive, often debilitating airflow obstruction. (See "Clinical presentation, diagnostic evaluation, and management of central airway obstruction in adults".)

Diagnostic evaluation — The diagnosis of bronchial stenosis is based upon bronchoscopic visualization. Computed tomography (CT), performed with multiplanar reconstruction of the bronchial tree or virtual bronchoscopy, is typically done to provide additional information regarding the exact location and length of the bronchial or anastomotic stenosis [18]. (See "Clinical presentation, diagnostic evaluation, and management of central airway obstruction in adults", section on 'Diagnostic evaluation and initial management'.)

Spirometry with flow-volume curves is used to assess the severity of airflow limitation. However, interpretation of spirometric results may be difficult in the setting of single lung transplantation for chronic obstructive pulmonary disease (COPD) as airflow obstruction may reflect the diseased native lung. Inspiratory and expiratory flow-volume curves help to distinguish between airflow obstruction caused by bronchial stenosis and that caused by bronchomalacia or bronchiolitis obliterans syndrome. Bronchial stenosis typically results in a pattern of fixed airflow limitation during both inspiration and expiration, while bronchomalacia has variable obstruction worse on expiration than inspiration (figure 1). (See "Flow-volume loops", section on 'Variable intrathoracic obstruction' and "Flow-volume loops", section on 'Mainstem bronchial obstruction' and "Physiologic changes following lung transplantation", section on 'Spirometry' and "Chronic lung transplant rejection: Bronchiolitis obliterans", section on 'Diagnosis'.)

Vanishing bronchus intermedius — Several cases have been reported of bronchial stenosis in the bronchus intermedius, distal to the anastomotic site [19]. This type of stenosis is known as the vanishing bronchus intermedius syndrome. The time of diagnosis is usually between two and six months posttransplant, but may be as late as 12 months posttransplant [19]. Ischemic injury is believed to be the inciting factor, as ischemic changes in this area are often visible on posttransplant bronchoscopy. However, acute cellular rejection may also contribute.

The diagnosis is typically made by fiberoptic bronchoscopy. Right middle and lower lobe collapse may be visible on chest radiography. A chest CT scan may be helpful to delineate the length of the obstruction. This type of bronchial stenosis is associated with a high mortality rate [1]. Management is similar to that for anastomotic stenosis, as described below, although it is difficult to keep a stent in the correct position without occlusion of the right upper lobe bronchus.

Management — Mild, asymptomatic bronchial stenosis (less than 50 percent of the bronchial diameter) can be managed conservatively with observation [20]. For more severe, symptomatic bronchial stenosis (usually greater than 50 percent of bronchial diameter), bronchoscopic dilation is the initial and preferred treatment [20,21]. Alternative measures for refractory stenosis include laser or cryosurgery, placement of an endobronchial stent, sleeve resection of the stenotic area, lobectomy, and retransplantation [22,23]. These choices are described further in the following paragraphs.

Endobronchial dilation – Endobronchial dilation is usually accomplished with a rigid or a flexible bronchoscope using balloon dilation [12,20,24-26]. In a series of 17 patients with moderate to severe bronchial stenosis after lung transplant, 14 patients were managed successfully with airway dilation via flexible or rigid bronchoscopy, while two required pneumonectomy and one retransplantation [20]. In the pediatric population, the balloon technique was found to be better for dilation, than using the rigid bronchoscope itself for dilation [12]. If stenosis recurs, dilation is usually repeated as this is often successful [20]. (See "Flexible bronchoscopy balloon dilation".)

Laser or electrosurgery – For patients whose stenosis is fibrotic and poorly responsive to balloon dilation, laser or electrosurgery may be used to create radial incisions in the stricture prior to balloon dilation [1,27]. Laser or cryotherapy may also be used to treat granulation tissue developing at the site [20]. (See "Clinical presentation, diagnostic evaluation, and management of central airway obstruction in adults", section on 'Diagnostic evaluation and initial management'.)

Endobronchial stents – The placement of endobronchial stents is reserved for cases of severe and refractory stenosis, as stents are associated with a high incidence of complications such as mucus impaction, granulation tissue formation, dislodgment, and migration [12,17,24,28,29]. (See "Airway stents", section on 'Complications'.)

Stent placement is often performed under general anesthesia, using rigid bronchoscopy, and may be combined with a dilation procedure to enable placement of the largest stent possible. Silicone stents are generally preferred over metallic stents because they are easily removable [30]. In a series of 27 lung transplant recipients, silicone stents were placed in 32 stenotic airway lesions [31]. Stents were left in place for a median of 6 months (range 1 to 22 months). Occasionally, inspissated secretions in the stents required bronchoscopic removal. Formation of granulation tissue at either end of the stent was common, but rarely required additional intervention and typically resolved after stent removal. Silicone stents are usually left in place until the airway appears healed.

Alternative stents, such as removable nitinol stents, are under investigation [32,33]. (See "Airway stents", section on 'Silicone stents' and "Airway stents", section on 'Metal stents'.)

Surgical intervention – When attempts at dilation and stenting fail, surgical strategies include sleeve resection, lobe resection, and also retransplantation [20,23,34]. (See "Lung transplantation: Procedure and postoperative management", section on 'Retransplantation'.)

Anastomotic infection — The bronchial anastomotic site is prone to infection by both bacterial and fungal organisms. This predisposition is probably related to immunosuppression, poor vascular supply, and impaired clearance of secretions [1]. Pseudomonas and Staphylococcus aureus are the most common bacterial infections. Aspergillus colonizes the airways of approximately 20 percent of lung transplant recipients in the immediate postoperative period and may become invasive in 3 to 6 percent [35,36]. Less common airway infections include Candida, Zygomycetes (mucormycosis), Scedosporium apiospermum, and Scedosporium prolificans [37,38]. The latter two can colonize suture material and infect the anastomosis from there [39]. (See "Fungal infections following lung transplantation", section on 'Other fungal infections'.)

Patients are often asymptomatic when anastomotic infection is detected at the time of surveillance bronchoscopy, although some patients have fever, cough, wheezing, and/or hemoptysis. Findings include airway erythema, pseudomembranes, ulcerations, and positive cultures of secretions. The diagnosis of invasive Aspergillus infection is based on the combination of endoscopic appearance and confirmation by histopathologic evidence of invasive Aspergillus and/or fungal culture. (See "Fungal infections following lung transplantation", section on 'Tracheobronchial aspergillosis'.)

Anastomotic infections appear to predispose to airway complications such as dehiscence, bronchomalacia, bronchial stenosis, and fistula formation. In one series, isolation of Aspergillus from respiratory secretions in the first 30 postoperative days was highly associated with subsequent bronchial complications [15].

Treatment of anastomotic infection includes bronchoscopic debridement of any devitalized tissue and specific antimicrobial therapy based on culture results. Aspergillus fumigatus infection is treated with a combination of systemic voriconazole and inhaled amphotericin. (See "Fungal infections following lung transplantation", section on 'Tracheobronchial aspergillosis'.)

Granulation tissue — Development of hyperplastic granulation tissue usually occurs within a few months of surgery [1]. The initial granulation reaction is thought to be caused by perioperative ischemia and repair. Infection, predominantly with Aspergillus, may exacerbate the growth of granulation tissue. (See "Fungal infections following lung transplantation", section on 'Tracheobronchial aspergillosis' and 'Anastomotic infection' above.)

Hyperplastic granulation tissue may be asymptomatic and detected on surveillance bronchoscopy or may result in dyspnea, cough, or postobstructive pneumonia [1]. Airflow limitation may be noted on spirometry in severe cases.

Continued observation is reasonable, if the amount of granulation tissue does not narrow the airway substantially and symptoms are minimal. However, when granulation tissue narrows the airway by 25 percent or more, the patient is symptomatic, and/or spirometry shows worsening airflow obstruction, the obstructing granulation tissue may be debrided via flexible bronchoscopy with laser or via rigid bronchoscopy (with forceps, cryotherapy, or laser) [1,16]. (See "Bronchoscopic cryotechniques in adults" and "Bronchoscopic laser in the management of airway disease in adults".)

Bronchial necrosis and dehiscence — Bronchial necrosis and dehiscence range from mild, focal mucosal sloughing to extensive bronchial wall necrosis that extends more than 2 cm from the anastomosis and may be associated with partial or complete separation of the anastomosis (table 1) [1]. Most patients have some degree of anastomotic site ischemic injury and necrosis in the days following transplantation. When anastomotic dehiscence occurs, it is usually in the first or second week after transplantation. Complete bronchial dehiscence is very rare and usually follows severe primary graft dysfunction or pneumonia in the early postoperative period.

Clinical features — Mild bronchial necrosis is asymptomatic. More severe necrosis and bronchial dehiscence may present with dyspnea, difficulty weaning from the ventilator, pneumomediastinum, subcutaneous emphysema, pneumothorax, and persistent air leak. Focal infection and peribronchial abscess may also occur. (See 'Fistulae' below.)

The plain chest radiograph is insensitive for detecting dehiscence; however, CT scanning can often identify dehiscence on the basis of bronchial wall defects and irregularities, mediastinal and subcutaneous air or fluid collections, pneumothorax, or poor allograft aeration [1,18].

Bronchial necrosis and dehiscence are usually identified during flexible fiberoptic bronchoscopy. At the time of bronchoscopy, the degree of necrosis, presence of unraveled sutures, and evidence of focal infection are assessed. Cultures of airway secretions are obtained, if indicated (table 1).

Management — Management of bronchial necrosis and dehiscence depends on the severity of necrosis and the presence of any associated complications.

If the necrosis involves the mucosa, but not the bronchial wall, and no air leak is detected (Grade II, (table 1)), conservative management with antibiotic treatment and surveillance may suffice [1]. Chest tube placement is optimized to facilitate full expansion of the transplanted lung.

For more extensive necrosis but without bronchial anastomotic dehiscence (Grade III, (table 1)), some experts suggest placement of an uncovered self-expanding metallic stent (eg, Ultraflex) during flexible fiberoptic bronchoscopy, which appears to facilitate healing by stimulating neoepithelialization [40-43]. These stents are usually removed after healing of the area of necrosis, which is usually about six to eight weeks [1]. However, our practice is to continue with conservative management rather than stent placement in order to avoid the risks associated with metallic stents.

Neither covered metallic stents nor silicone stents have been successful in the management of bronchial necrosis [40,42]. Silicone stents are generally avoided in this setting, as they do not promote neoepithelialization and the force required for silicone stent placement may enlarge the defect [42]. (See "Airway stents", section on 'Metal stents'.)

For patients with partial dehiscence, primary repair using application of fibrin glue or alpha-cyanoacrylate glue has been described in case reports, generally followed by placement of an uncovered metallic stent [42,44].

Failure of the above measures and complete dehiscence are associated with high morbidity and mortality. Open surgical repair for reanastomosis, pneumonectomy, or retransplantation may be considered based on factors such as the operability of the patient, anticipated response to pneumonectomy, and availability of a new lung for retransplantation [45,46].

Fistula formation between the bronchial anastomotic site and the pleura, mediastinum, or a vascular structure is a potential consequence of bronchial anastomotic necrosis. (See 'Fistulae' below.)

Tracheobronchomalacia — Tracheobronchomalacia is defined as a 50 percent or greater narrowing of the airway lumen during expiration; it is considered severe when the airway lumen is narrowed to 25 percent of its original area. The underlying cause is loss of integrity of the tracheal or bronchial cartilage, leading to collapsibility of the airway. Presumably, the cartilage is injured by peritransplant ischemia or infection. Tracheobronchomalacia may be seen in combination with an area of bronchial stenosis.

Signs and symptoms of tracheobronchomalacia overlap considerably with those of bronchial stenosis and include cough, dyspnea, difficulty clearing respiratory secretions, recurrent infections, wheeze, and stridor. Spirometric flow-volume loops typically show variable obstruction worse on expiration than inspiration (figure 1).

The diagnosis of tracheobronchomalacia may be suspected on the basis of clinical features and spirometric flow-volume loops, but must be confirmed bronchoscopically by visualization of airway collapse during expiration. Fiberoptic bronchoscopy is preferred over rigid bronchoscopy for optimal visualization of the dynamic reductions in airway diameter during spontaneous respiration. (See "Tracheomalacia and tracheobronchomalacia in adults", section on 'Diagnosis'.)

For patients with possible tracheobronchomalacia, inspiratory and expiratory CT views at different levels may be helpful to visualize the extent of the area of malacia, although this technique does not replace the need for bronchoscopy. (See "Tracheomalacia and tracheobronchomalacia in adults", section on 'Computed tomography'.)

Tracheobronchomalacia that is mild (eg, 50 to 75 percent airway collapse) and asymptomatic does not require immediate treatment, but should be observed for worsening. When symptomatic, patients can usually be managed with nocturnal noninvasive positive pressure ventilation. (See "Practical aspects of nocturnal noninvasive ventilation in neuromuscular and chest wall disease".)

When symptoms are not well-controlled with nocturnal noninvasive ventilation and 75 percent or greater occlusion of the airway due to airway collapse is observed during bronchoscopy, temporary stent(s) may be placed endoscopically [17,41]. In one small series of four patients with posttransplantation bronchomalacia, stent placement resulted in an 81 percent increase in forced expiratory volume in one second (FEV1) [17]. Rarely, surgical repair (tracheobronchoplasty) is needed [1]. (See "Tracheomalacia and tracheobronchomalacia in adults", section on 'Stenting'.)

Fistulae — Bronchopleural, bronchomediastinal, and bronchovascular fistulae have all been described in lung transplant recipients [1]. These complications are rare, but are associated with a high morbidity.

Clinical features — Signs of a bronchopleural fistula include a new or worsening pneumothorax, subcutaneous emphysema, respiratory distress, and hypotension [1,47,48]. Bronchomediastinal fistulae typically present with signs of mediastinal infection, such as fever, bacteremia, or a mediastinal abscess [1].

A chest CT scan will usually identify pleural or mediastinal air and can be useful in guiding aspiration or drainage of mediastinal fluid collections.

Bronchovascular fistulae may connect the bronchus with the pulmonary artery, pulmonary vein, aorta, or left atrium [1,49,50]. Patients may present with sepsis, hemoptysis, or air embolism. Risk factors for this complication include Aspergillus infection of the anastomotic site and the presence of a bronchial stent [1].

Management — The optimal management approach to bronchopleural, bronchomediastinal, and bronchovascular fistulae is not known, as these complications are rare. The following suggested approach is largely based on expert opinion and a few case reports.

Bronchopleural fistulae – Bronchopleural fistulae (BPF) are treated acutely with drainage of any pleural air or empyema fluid and initiation of antibiotic therapy [1]. Ventilator management of patients who have a BPF is discussed separately. (See "Management of bronchopleural fistula in patients on mechanical ventilation".)

For patients who have a small BPF (eg, 3 to 5 mm diameter) or are not candidates for surgical closure, endoscopic closure using fibrin glue may be effective [1,47,48,51].

Endoscopic glue closure is usually not effective for larger fistulae; these may require placement of a covered metallic stent or surgical flap closure and reinforcement, if the patient is able to tolerate a thoracotomy [51]. (See 'Management' above.)

Bronchomediastinal fistulae – Treatment of bronchomediastinal fistulae generally includes antimicrobial therapy and percutaneous drainage of any mediastinal fluid collections [1]. Depending on the extent of the mediastinal infection and the clinical stability of the patient, surgical debridement of the mediastinum may be indicated. Antimicrobial therapy should be broad initially and then narrowed when the sensitivities of the infecting organism are known. (See "Postoperative mediastinitis after cardiac surgery", section on 'Treatment'.)

Bronchovascular fistulae – Bronchovascular fistulae have a high mortality rate, due to their abrupt presentation with massive hemoptysis [1]. Successful management with lobectomy and pneumonectomy has been reported in individual cases [52,53].

PROGNOSIS — There is no significant difference in overall survival in comparison with patients in whom airway complications do not develop. Moreover, airway complication is NOT a risk factor for the development of chronic rejection [12].

PREVENTION — Attention to lung preservation, meticulous surgical technique and measures to prevent ischemia-reperfusion injury and acute rejection are important steps to prevent post-transplant airway complications. With careful management, the rate of major airway complications (dehiscence or stenosis requiring stenting) is usually less than 5 percent [54].

Bronchial anastomotic technique — Direct bronchial revascularization had been proposed by some centers in an effort to lower the incidence of airway complications [55,56]; however, there is no strong evidence to support this approach and it is not widely performed.

Prophylactic antibiotics — Most lung transplantation programs use antifungal prophylaxis starting within 24 hours of transplantation, as Aspergillus airway infection is associated with an increased risk of airway complications [15,57]. The optimal duration of antifungal prophylaxis is not known [1].

Delaying use of sirolimus — Sirolimus, a rapamycin derivative used to suppress transplant rejection, is associated with a markedly increased risk of airway complications when used in the first 90 days following lung transplantation. Most experts suggest delaying initiation of sirolimus until after the anastomosis is completely healed [1]. (See "Induction immunosuppression following lung transplantation".)

SUMMARY AND RECOMMENDATIONS

The airway anastomosis is a vulnerable site for operative complications following lung transplantation due to interruption of the bronchial artery blood supply in the transplantation process. Complications include focal infection, bronchial necrosis and dehiscence, excess granulation tissue, tracheobronchomalacia, stenosis, and fistula formation. (See 'Introduction' above.)

Bronchial stenosis may be asymptomatic and diagnosed during surveillance bronchoscopy, or it may present with dyspnea, wheezing, stridor, deteriorating pulmonary function tests, or postobstructive pneumonia. (See 'Bronchial stenosis' above.)

For patients with symptomatic anastomotic bronchial stenosis, we suggest initial dilation, rather than stent placement (Grade 1B). Balloon dilation may be performed via flexible or rigid bronchoscopy. Temporary stent placement is reserved for refractory stenosis, due to the relatively high complication rate associated with stents. (See 'Bronchial stenosis' above and "Airway stents".)

Anastomotic site infections are usually asymptomatic and diagnosed at the time of surveillance bronchoscopy. Pseudomonas and Staphylococcus aureus are the most common bacterial infections; Aspergillus infection is less common, but can lead to severe sequelae. (See 'Anastomotic infection' above and "Fungal infections following lung transplantation", section on 'Tracheobronchial aspergillosis'.)

Bronchial necrosis and dehiscence range from mild, focal mucosal sloughing to extensive bronchial wall necrosis, which may be associated with partial or complete separation of the anastomosis. (See 'Bronchial necrosis and dehiscence' above.)

The management of bronchial necrosis and dehiscence depends on the severity of necrosis and the presence of associated complications. For most patients with bronchial necrosis and dehiscence, we suggest conservative management with antibiotic treatment, maintenance of full expansion of the transplanted lung(s), and continued surveillance (Grade 2C). An alternative for patients with necrosis that extends beyond the mucosa is placement of an uncovered metallic stent with or without application of fibrin or cyanoacrylate glue. (See 'Management' above.)

Complete dehiscence of the anastomosis is associated with high morbidity and mortality. Open surgical repair for reanastomosis, pneumonectomy, or retransplantation may be considered based on factors such as the operability of the patient, anticipated response to pneumonectomy, and availability of a new lung for retransplantation. (See 'Management' above.)

Hyperplastic granulation tissue typically develops within a few months of transplantation. Symptomatic patients may have dyspnea, cough, or postobstructive pneumonia. When the granulation tissue narrows the airway by 25 percent or more, we suggest debridement via fiberoptic or rigid bronchoscopy (Grade 2C). Forceps, cryotherapy, or laser may be used to clear the granulation tissue. (See 'Granulation tissue' above.)

Tracheobronchomalacia is defined as a 50 percent or greater narrowing of the airway lumen during expiration, confirmed bronchoscopically. Asymptomatic airway collapse does not require treatment. For mild degrees of airway collapse (eg, 50 to 75 percent) associated with symptoms, we suggest supportive care with nocturnal noninvasive positive pressure ventilation, rather than stent placement (Grade 2B). When airway collapse is greater than 75 percent, nocturnal noninvasive positive pressure ventilation is less likely to be adequate to control symptoms. In these patients, we suggest placement of a temporary stent or surgical intervention (Grade 2C). (See 'Tracheobronchomalacia' above.)

Bronchopleural, bronchomediastinal, and bronchovascular fistulae are rare complications of lung transplantation. Treatment of bronchopleural fistulae includes acute drainage of pleural air or empyema fluid and antibiotic therapy, as fistulae are highly associated with anastomotic infection. Treatment of bronchomediastinal fistulae includes percutaneous drainage of any mediastinal abscess collection and antibiotic therapy. A variety of methods have been tried to close the bronchial orifice of fistulae including surgery, application of fibrin glue, and placement of a covered metallic stent. (See 'Fistulae' above.)

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