Stent Insertion for Severe Diffuse Excessive Dynamic Airway Collapse Caused by COPD

Published on 23/05/2015 by admin

Filed under Pulmolory and Respiratory

Last modified 23/05/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 3434 times

Chapter 14 Stent Insertion for Severe Diffuse Excessive Dynamic Airway Collapse Caused by COPD


This chapter emphasizes the following elements of the Four Box Approach: risk-benefit analysis and therapeutic alternatives; anesthesia and other perioperative care; and follow-up tests, visits, and procedures.

Case Description

The patient was a 64-year-old obese female with a body mass index (BMI) of 45, a 5-month history of progressive shortness of breath, and recent dyspnea at rest. Complaints included mucus production and inability to raise secretions. Recent hospitalization for pneumonia prompted treatment with systemic antibiotics. Comorbidities included obstructive sleep apnea (OSA) treated with 12 cm H2O of continuous positive airway pressure (CPAP), severe chronic obstructive pulmonary disease (COPD) requiring home oxygen (3 L via nasal cannula), recurrent bronchitis, usually treated in the ambulatory setting, diabetes, and gastroesophageal reflux disease (GERD). She lived in a nursing facility and had no close family members or friends. During the physical examination, the patient expressed her frustration that she was often ignored by nursing home staff. Bilateral diffuse rhonchi with early expiratory wheezing were noted on lung examination. Trace pedal edema was observed bilaterally. The arterial blood gas revealed pH of 7.46, PCO2 (partial pressure of carbon dioxide) of 38, and PO2 (partial pressure of oxygen) of 60 on 3 L of oxygen. Complete blood count showed a white blood cell (WBC) count of 18,000 and hemoglobin of 16.6. Chest radiograph showed bibasilar atelectasis, a right infrahilar infiltrate suggestive of pneumonia, and mild pulmonary vascular congestion. Echocardiography showed normal left and right ventricular function, but the right ventricular systolic pressure was calculated at 52 mm Hg. Chest computed tomography (CT) revealed bulging of the posterior membrane inside the airway lumen and 75% narrowing of the upper trachea associated with complete collapse of the lower trachea and mainstem bronchi during expiration, consistent with excessive dynamic airway collapse (EDAC) (Figure 14-1). Bronchoscopy confirmed CT findings (see video on (Video III.14.1image).

Case Resolution

Initial Evaluations

Physical Examination, Complementary Tests, and Functional Status Assessment

Dyspnea, recurrent pneumonia, and inability to raise secretions are nonspecific but common findings in patients with expiratory central airway collapse.1,2 Symptoms are usually refractory to conventional treatments such as corticosteroids and bronchodilators for suspected asthma and COPD.3 Occasionally, hypercarbic respiratory failure can occur. Once intubated, patients may be difficult to wean from mechanical ventilation.4,5 In nonintubated patients, spirometry often shows obstructive ventilatory impairment that is proportionate to the severity of the disease.6 The expiratory flow-volume loop (FVL) often reveals an airway collapse pattern* (Figure 14-2). Expiratory airway collapse is also seen during dynamic bronchoscopy,7 and in fact has been reported in up to 40% of patients with severe COPD.7,8

In our patient, a diagnosis of diffuse, severe expiratory central airway collapse was made bronchoscopically and on paired dynamic inspiratory-expiratory CT scanning. This was characterized by weakness of the posterior membranous wall, resulting in excessive bulging of the posterior membrane within the airway lumen and causing 100% airway narrowing in the mainstem bronchi and lower trachea (see Figure 14-1).2,9 No evidence of cartilaginous weakness was noted. Results from studies show that dynamic CT correlates well with bronchoscopy findings in patients with central airway collapse.10 CT scanning offers complementary information by revealing structures adjacent to the airway and by allowing quantitative measurements of the degree of airway narrowing before and after airway splinting procedures.11,12 No evidence of extrinsic compression was observed resulting from mediastinal masses or vascular structures (e.g., double aortic arch, aortic aneurysm); also, on expiratory images, no evidence of air trapping and mosaic attenuation suggested bronchiolitis. The patient’s severe limitation of physical activity at rest was consistent with functional impairment class IV based on World Health Organization (WHO) criteria.13 Other dyspnea or quality of life (QOL) instruments (St. George’s Respiratory Questionnaire [SGRQ], American Thoracic Society Dyspnea Scale [ATS], Baseline Dyspnea Index [BDI]/Transitional Dyspnea Index [TDI], Karnofsky Performance Scale [KPS], and 6-Minute Walk Test [6MWT]) have been studied in these patients to objectively determine response to interventions.14


This patient had no evidence of systolic or diastolic dysfunction on echocardiogram, but evidence revealed moderate pulmonary hypertension, which could result in hemodynamic instability during general anesthesia.15 She suffered from obesity and GERD, both of which increase the risk for aspiration of gastric contents during general anesthesia,16 which might be required for any form of bronchoscopic or surgical treatment of EDAC. Additionally, OSA raised concerns regarding difficult mask ventilation, difficult tracheal intubation, hypoxemia, postprocedure airway obstruction, cardiac arrhythmias, and myocardial infarction. The presence of both obesity and hypoventilation perioperatively has been shown to be associated with worse outcomes and higher mortality.17

Procedural Strategies


Treatment of severe diffuse EDAC includes minimally invasive or open surgical procedures.1,2 Some central airway narrowing during expiration is normal, however, and it has been suggested that airway splinting procedures should be considered only when excessive narrowing results in symptomatic airflow limitation.20 From both anatomic and physiologic perspectives, the boundary between normal and abnormal narrowing of the central airways is far from being established, and the exact degree of expiratory airway narrowing responsible for symptoms and requiring intervention remains unknown. For example, even an 80% reduction in tracheal lumen cross-section at the end of a “forced” expiration, when the flow in central airways physiologically nears zero, may well be within normal limits.* Some authors propose 30%21 and others 40%,22 but most investigators use 50% or greater reduction in airway caliber between inspiration and expiration to identify abnormal central airway collapse on dynamic CT or bronchoscopy.2325 Upon application of these criteria when a patient is asked to cough or perform a forced expiration, false positives may be noted; in one study, investigators reported that nearly 80% of normal people exceeded the diagnostic criteria of 50% or greater obstruction in the upper and/or lower trachea.26

Patients with concurrent COPD have reduced elastic recoil and peripheral airway obstruction. The expiratory airway collapse seen in the central airways thus represents normal physiology,20,27,28 because during flow-limited breathing, the central airways become severely compressed, particularly during forced expiration and cough. Both of these maneuvers are routinely used to detect this entity on dynamic imaging studies. The Starling resistor model shows that a pressure drop occurs across a very short length of airway, and that proximal airway resistance, downstream from the choke point, mouthward, should not affect airflow. Pressure catheter measurements demonstrate the flow-limiting choke point and lack of further pressure drop in airways between the mouth and the flow-limiting segment.29 Because the choke point in adult humans is often located at the level of the lobar bronchi, and is even more peripheral in patients with COPD,30 central airway collapsibility should not impede airflow.20,29

Patients with COPD and EDAC, however, may still improve their symptoms and functional status after central airway stabilization with stents or tracheoplasty despite lack of improvement in forced expiratory volume in 1 second (FEV1).31 By stabilizing and reducing central airway flow turbulence, in addition to improving secretion management and preventing excessive cough from chronic airway inflammation, these procedures might result in improved quality of life and dyspnea improvement with exertion caused by a reduction in hyperinflation.14,31 Our patient had severe (100%) collapse resulting in dyspnea at rest, inability to raise secretions, and recurrent pneumonia. These symptoms were not responding to optimal COPD treatment and CPAP for OSA. For these reasons, after taking into account the patient’s wishes, we elected to perform rigid bronchoscopy under general anesthesia to place an indwelling silicone stent that would splint open the lower trachea and mainstem bronchi. Our goal was to improve airway lumen patency to less than 50% collapse during exhalation, which, by convention, is currently considered within normal limits by most investigators.13

Expected Results

In the short term (up to 10 to 14 days), airway stabilization with silicone stents in patients with expiratory central airway collapse (malacia and EDAC) improves symptoms, quality of life, and functional status.4,14 In one study, quality of life and functional status scores improved in 70% of patients and dyspnea scores improved in 91% of patients after stent insertion.14 Stent-related complications included obstruction from mucus plugging and migration, and almost 10% of patients (5 of 52 patients) had complications related to the bronchoscopic procedure itself. Because the dynamic features of expiratory central airway collapse continuously alter the shape of the central airways, as well as the surface contact between a stent and the airway wall, stent-related complications may occur more frequently in dynamic forms of airway obstruction than in fixed benign obstruction or malignancy.4 In one study of 57 patients, 21 partial stent obstructions, 14 infections, and 10 stent migrations were noted.14 Although not life threatening, these stent-related adverse events required multiple repeat bronchoscopies.

Therapeutic Alternatives for Restoring Airway Patency

Other than silicone stent insertion, therapeutic alternatives for EDAC include noninvasive positive-pressure ventilation, metal stent insertion, and open surgical treatment.

Continuous positive airway pressure (CPAP): This patient was symptomatic despite already being on CPAP 12 cm H2O. Bronchoscopy on CPAP could have been performed to assess the optimal pressure needed to maintain patency of the central airways. This was not done however, because 24-hour continuous CPAP was not desirable (this patient’s symptoms were not only positional or presented only during sleep).32 CPAP decreases pulmonary resistance and can be used to restore and maintain airway patency, facilitate secretion drainage, and improve expiratory flow. Small studies showed that the addition of nasal CPAP improves spirometry values, sputum production, atelectasis, and exercise tolerance, but its long-term efficacy has not been clearly demonstrated.33,34

Metal stent insertion was used in the past for central airway collapse with variable success.9 Advantages include placement by flexible bronchoscopy, dynamic expansion, and preservation of airway mucociliary function with uncovered stents. In some studies, however, metal stents had to be removed because of stent failure or because of stent-related complications. Cases of stent fracture and fatal hemorrhage from perforation have prompted the Food and Drug Administration (FDA) to recommend against the use of metallic stents for histologically benign forms of airway obstruction.35

Membranous tracheoplasty

Buy Membership for Pulmolory and Respiratory Category to continue reading. Learn more here