Excessive dynamic airway collapse: A condition behind the veil

Abstract

Excessive dynamic airway collapse (EDAC) is characterized by weakness in the posterior membranous wall of the airway, which results in more than 50% narrowing of the central airway lumen during expiration. EDAC differs from tracheobronchomalacia, which involves the weakening of the cartilage rather than the membranous wall. EDAC poses a diagnostic challenge due to overlapping symptoms with chronic obstructive pulmonary disease and asthma, including dyspnea, cough, and wheezing. The diagnosis of EDAC relies on dynamic airway imaging techniques, including bronchoscopy, dynamic computed tomography, dynamic magnetic resonance imaging, and endobronchial ultrasound, to assess airway collapse during expiration. Pulmonary function testing helps in ruling out obstructive lung disease. Treatment includes medical management of underlying comorbidities, pulmonary rehabilitation, and, in severe cases, bronchoscopy-guided stenting of the airway or tracheobronchoplasty. This mini-review discusses pathophysiology, diagnostic challenges, and evolving treatment strategies for EDAC, highlighting the need for increased clinical awareness and targeted therapies.

Key Words: Excessive dynamic airway collapse; Tracheobronchomalacia; Obstructive pulmonary disease; Pulmonary function test; Bronchoscopy; Dynamic computed tomography; Stenting; Tracheobronchoplasty

Core Tip: Excessive dynamic airway collapse (EDAC) is a less recognized condition with expiratory airflow limitations that is caused by laxity in the posterior membranous wall, leading to the excessive narrowing of the central airway lumen. The overlap of EDAC symptoms with chronic obstructive pulmonary disease and asthma often delays the accurate diagnosis. This mini-review discusses the role of dynamic imaging modalities in EDAC diagnosis and the different approaches in the management of EDAC, ranging from conservative treatments to surgical options like tracheobronchoplasty. Standardizing diagnostic criteria, tailoring management strategies, and increasing research are crucial in improving patient outcomes in EDAC.

INTRODUCTION

Excessive dynamic airway collapse (EDAC) is a clinical entity of the larger airways, which is characterized by laxity in its posterior membranous wall, leading to > 50% narrowing of the lumen during expiration[1,2]. EDAC also known as hyperdynamic airway collapse is often misdiagnosed as tracheobronchomalacia (TBM) which differs due to the collapse of the cartilaginous wall. These clinical entities are responsible for the narrowing of the central airways during expiration and are collectively known as expiratory central airway collapse (ECAC) or large airway collapse. Moreover, EDAC may also mimic obstructive respiratory diseases and can co-exist regardless of their disparities[1-5]. The majority of the patients with EDAC are asymptomatic. However, patients with > 75% of airway compromise usually develop symptoms resembling chronic respiratory diseases, making its diagnosis challenging[6,7].

During normal expiration, the posterior membranous wall of the central airways bulges inward to reduce the airway lumen by up to 50%, considered a dynamic airway collapse (DAC). This phenomenon is exaggerated in EDAC, which may worsen the symptoms depending on severity[2,8-10]. The bronchoscopy or dynamic computed tomography (CT) visualization of central airways during expiration: DAC, EDAC, and TBM can be observed from Figure 1[1,11].

Figure 1 The bronchoscopy or dynamic computed tomography visualization of central airways during expiration. A: It demonstrates the anatomical composition of the central airways which includes trachea and main bronchi. The posterior wall shows membranous portion while anterolateral wall represents the cartilaginous portion. The alteration in central airways during different phases of respiration are highlighted, where dynamic airway collapse can be appreciated in expiratory phase; B: It demonstrates different types of expiratory central airway collapse (ECAC), where defective membranous wall and cartilaginous wall result in the development of EDAC and different forms of tracheobronchomalacia. The arrows show diverse movement of airway lumen in varieties of ECAC. EDAC: Excessive dynamic airway collapse; TBM: Tracheobronchomalacia.

PREVALENCE

The history and prevalence of EDAC remain a mystery due to its diagnostic uncertainty in the old times. EDAC developed in 9.4%-20% of chronic obstructive pulmonary disease (COPD) patients while being barely symptomatic[12,13]. Similarly, 30.7% of asthmatic patients develop EDAC, with its higher prevalence concerned with older age, female gender, asthma severity, and asthmatics with thyroid dysfunction[14]. ECAC is prevalent among 40% of patients with obstructive airway disorders[15,16]. With recent advancements in the field of EDAC, factual data will ultimately be achieved soon. There are epidemiological limitations due to lack of standard definition, with no universally accepted cutoff value.

ETIOLOGY

Despite the disparities, two clinical entities of ECAC, i.e., EDAC and TBM, may have common risk factors. However, based on the etiology, EDAC develops secondarily due to congenital or acquired factors. It is commonly seen in patients with COPD and Asthma. Besides, any disease condition inducing chronic airway irritation and genetic disease like Mounier-Kuhn Syndrome also contributes to developing EDAC, as shown in Table 1[4,11,17].

Table 1 Etiological factors of excessive dynamic airway collapse.

Congenital/primary causes
Mounier-Kuhn Syndrome
Acquired/secondary causes
Irritant inhalation (smoking, air pollution)
Gastroesophageal reflux disease
Recurrent chest infections
Obstructive airway diseases (chronic obstructive pulmonary disease, asthma)
Drugs (corticosteroids, beta-agonists)
Others (obstructive sleep apnea, obesity)

Congenital causes

Mounier-Kuhn Syndrome: Mounier-Kuhn Syndrome is a rare clinical entity characterized by dilatation of the central airways due to its atrophy in smooth muscle and elastic tissue, leading to recurrent lower tract infections. Thus, also referred to as tracheobronchomegaly[18].

Acquired causes

The majority of EDAC cases are acquired owing to chronic airway inflammation. EDAC mainly develops in patients with COPD or Asthma.

Inhalation injury: Inhalational irritants such as smoke and chemical irritants can affect airways leading to chronic inflammation[19].

Gastroesophageal reflux disease: Gastroesophageal reflux disease (GERD) is a chronic gastrointestinal condition characterized by regurgitation of gastric contents into the esophagus[20]. A total of 45.3% of ECAC patients had GERD and had significant improvement in respiratory problems following the management of GERD[21].

Obstructive airway diseases: Obstructive airway diseases, mainly COPD and Asthma, can be characterized by expiratory airflow limitation either due to obstruction or narrowing. EDAC may be misdiagnosed as obstructive airflow disease due to its resemblance. Almost 9.4%-20% of COPD patients develop EDAC[11,12]. The prevalence of EDAC among asthmatic patients was 30.7%[14].

Drugs: Steroid-induced vasoconstriction reduces blood flow in the airway mucosa[22,23]. Persistent use of corticosteroids and beta-agonists in asthma and COPD leads to tracheobronchial smooth muscle atrophy and separation, ultimately advancing toward EDAC[7,24-26]. A prospective study may help establish the causality between EDAC and steroid use since this association may only be a manifestation of the severity of underlying COPD and asthma. Since steroids are prescribed in order to reduce inflammation in severe conditions, the association between EDAC and steroid use may be related to the severity of asthma or COPD rather than the effect of steroids as such[25,27].

Furthermore, EDAC is highly prevalent among the older population, female gender, asthmatic with thyroid dysfunction, and morbidly obese COPD patients[10,14,28]. Obstructive airway disease continues to be the leading cause of ECAC development among various etiological factors, as evidenced by prior studies.

PATHOPHYSIOLOGY

In a normal respiratory cycle, the posterior membranous wall of the tracheobronchial airway moves posteriorly during inspiration, increasing the luminal size while it protrudes inward to the lumen during expiration due to positive pleural pressure[2,4,29]. Up to 50% of narrowing of the lumen during expiration is considered unremarkable and called a DAC[2,8,10]. This phenomenon is maintained via resisting traction distributed by pars membranacea and smooth muscle contraction[29]. Typically, it can further progress during forced expiration and coughing, which is a major factor in clearing the secretions. Similarly, among the older population, the degree of central airway collapse may vary due to a reduction in elastic recoil of the lung[10]. However, whenever the narrowing surpasses 50% due to the posterior wall floppiness, the condition is known as EDAC[2,5,9]. In addition, patients with COPD are frequently on steroid, which can cause smooth muscle atrophy, reduced blood flow, and weakening of cartilaginous structures.

Expiratory flow limitation

A condition when expiratory airflow cannot increase despite forceful expiratory driving pressure is known as expiratory flow limitation (EFL). The concept of EFL can be represented by the hypothesis explaining equal pressure point (EPP) and choke point/flow limiting segment[7,30].

During the expiratory cycle, the driving pressure generated from the alveolar pressure (Palv) for a given lung volume is responsible for airflow. This driving force relies on total elastic recoil pressure (Pel) and pleural pressure (Ppl), i.e., Palv = Pel + Ppl. As the air flows from smaller airways to larger airways, the pressure declines until it equalizes with pleural pressure, i.e., Palv = Ppl. This is referred to as EPP, where EFL arises[7,31,32]. The point beyond EPP develops airway compression. In normal healthy individuals, EPP lies in the cartilaginous airway, which contributes to limited dynamic airway compression. In patients with chronic respiratory diseases like COPD, the EPP shifts to lower airways, i.e., non-cartilaginous airways, as shown in Figure 2. Thus, further advances in EDAC lead to severely compromised airways[1,7,10].

Figure 2 Schematic representation of expiratory flow limitation based on equal pressure point and wave speed theories, with dynamic airway collapse during normal expiration and with excessive dynamic airway collapse secondary to various causes. A: Dynamic airway collapses during normal expiration; B: Excessive dynamic airway collapses secondary to various causes. COPD: Chronic obstructive pulmonary disease; DAC: Dynamic airway collapse; EDAC: Excessive dynamic airway collapse; EPP: Equal pressure point; GERD: Gastroesophageal reflux disease; Palv: Alveolar pressure (Palv = Ppl + Pel); Patm: Atmospheric pressure; Pel: Total elastic recoil pressure; Pl: Intraluminal pressure; Ppl: Pleural pressure.

Additionally, wave speed theory contributes to EFL. This theory states that when the airflow velocity equals the speed of propagation of a pressure wave, the site is known as a choke point. This choke point corresponds with EPP, as shown in Figure 2[5,7,31].

The destruction of smooth muscle fibers, which form the posterior wall of the tracheobronchial tree, leads to excessive narrowing of the lumen during expiration, further developing into EDAC. Persistent use of medicines like corticosteroids has been shown to develop EDAC following smooth muscle atrophy[6,24,29,33].

The pathophysiology of EDAC in chronic airway diseases is summarized in Figure 3[1,7].

Figure 3  Flowchart showing the pathophysiology of excessive dynamic airway collapse in chronic airway diseases.

CLASSIFICATION

The classification of EDAC has a profound effect on determining appropriate treatment. FEMOS classification applied in EDAC comprises stratification factors, morphology, and origin of the disease, as demonstrated in Table 2. The World Health Organization has classified EDAC into different functional classes depending upon the functional impairment. Likewise, the extent and severity of the disease are assessed following bronchoscopy/dynamic CT[1,2].

Table 2 FEMOS classification of excessive dynamic airway collapse.

Components	Grade
	I (normal)	II (mild)	III (moderate)	IV (severe)
Functional class	Asymptomatic	Symptomatic on exertion	Symptomatic with regular activity	Symptomatic at rest
Extent	No abnormality	Focal	Multifocal	Diffuse
Morphology	Crescent
Origin	Idiopathic or secondary
Severity	0%-50% EAC	50%-75% EAC	75%-100% EAC	100% EAC with airway walls making contact

EAC: Esophageal adenocarcinoma.

CLINICAL FEATURES

EDAC, often asymptomatic, is diagnosed incidentally during bronchoscopy or dynamic CT scan. Most patients develop symptoms whenever airway compromise exceeds 75% during expiration. The patient usually develops dyspnea, refractory cough, often barking type, impaired mucociliary clearance, recurrent chest infection, and consequently respiratory failure. Wheezing is also common and presents immediately following forced vital capacity maneuvers such as exercise, Valsalva, postural changes, and forced exhalation/cough. Generally, EDAC diagnosis is quite complex due to its nonspecific clinical presentation and may mimic chronic conditions such as TBM, COPD, Asthma, GERD, and so on[2,4,9].

DIAGNOSIS

The majority of EDAC patients clinically resemble chronic respiratory diseases, often leading to misdiagnosis. EDAC diagnosis is often an incidental finding during bronchoscopy and CT scan performed for other indications. However, the patient can be evaluated based on the initial history, obstructive pulmonary diseases refractory to treatment, and suspicion following pulmonary function test. Diagnostic evaluation of EDAC predominantly revolves around bronchoscopy and dynamic CT scan[2,4,9,33,34]. Diagnostic testing used in EDAC is listed in Table 3.

Table 3 Diagnostic evaluation tools for excessive dynamic airway collapse.

Diagnostic evaluation tools
Pulmonary function testing
Bronchoscopy
Dynamic computed tomography scan
Dynamic magnetic resonance imaging
Endobronchial ultrasonography
Others: Vibration resonance imaging; pH or impedance probe testing

Pulmonary function testing

Spirometry predominantly helps to rule out obstructive or restrictive pulmonary diseases. Chronic respiratory disease can lead to EDAC or can accompany it regardless of its variance. A normal flow-volume loop graph on spirometry shows a distinct pattern of oval shape combined with triangular shape in the expiratory limb while oval shape in the inspiratory limb. A coved shape is obtained in the expiratory limb among obstructive lung diseases. Likewise, restrictive lung disease presents with a normal-shaped loop with an overall reduction in volume and size, as demonstrated in Figure 4[1,35,36]. The classic biphasic pattern can be visible in ECAC. However, the flow-volume loop graph can be normal in EDAC. Besides, it can help identify secondary factors responsible for EDAC, such as COPD[1,4,35-37].

Figure 4  Normal flow-volume loop with variable abnormal patterns.

Bronchoscopy

Bronchoscopy is the gold standard diagnostic measure of ECAC. Despite being utilized as a confirmatory diagnostic tool, it can be advantageous in evaluating extent, morphology, and severity, facilitating appropriate treatment plans for EDAC[4,34]. The advantages of bronchoscopy over other diagnostic tests are: (1) Direct visualization of the airway mucosa; (2) Can be performed in critically ill patients; (3) Avoidance of radiation exposure; and (4) Permits to assess responsiveness to noninvasive positive pressure ventilation as a treatment alternative[37-39]. It can be performed under conscious sedation at different postures (supine, erect, lateral decubitus) while implementing different respiratory maneuvers. A crescent configuration can be obtained in EDAC during bronchoscopy. On the other hand, different morphological types of TBM can be visualized, as shown in Figure 1[2,40].

Dynamic CT

Chest CT with dynamic expiratory imaging is as reliable as bronchoscopy for diagnosing EDAC. The asset of dynamic CT over bronchoscopy can be due to its non-invasive technique and scope in determining possible factors causing EDAC. Meanwhile, this test can be challenging in critically ill patients[2,37,41]. As per the protocol, a low-dose expiratory scan is performed to evaluate EDAC during forceful exhalation rather than regular thin-section chest CT. As a result, the extent, morphology, and severity of EDAC can be appreciated, as can bronchoscopy. The posterior membranous bulge within the airway lumen appears as the crescent structure with expiratory maneuvers among EDAC cases in dynamic CT, as demonstrated in Figure 1[42-44].

Dynamic magnetic resonance imaging

As dynamic magnetic resonance imaging (MRI) allows the assessment of the central airway dynamics, it can be utilized to diagnose EDAC. Contrary to CT scans, MRI could possess supremacy due to the absence of radiation exposure, higher resolution, and more specific soft tissue mass evaluation[1,42].

Endobronchial ultrasonography

Endobronchial ultrasound is applicable to assess various forms of central airway structure. The distinct hypo and hyper-echoic layers identical to the histological patterns of the airway wall can be demonstrated using EBUS[1,2,45].

Moreover, other diagnostic tools resembling ultrasonography, such as vibration resonance imaging, can also be utilized[1]. Besides, pH or impedance probe testing can be used to diagnose GERD, which can potentially aggravate EDAC[4].

MANAGEMENT

The treatment of EDAC relies predominantly on the patient’s symptoms. Moreover, the treatment protocol may vary depending on the etiology, severity, and extent of the airway collapse. However, no further workup is required for asymptomatic EDAC[2,9,34]. The treatment approach of symptomatic EDAC comprises medical management, minimally invasive interventional bronchoscopy, and surgical management, as summarized in the flowchart (Figure 5)[1,9,34,42].

Figure 5  Approach to management of excessive dynamic airway collapse.

Medical management

The primary treatment of symptomatic EDAC principally focuses on the medical management of underlying comorbid conditions, as mentioned in Table 1. EDAC often manifests with chronic cough, dyspnea, and inability to expectorate secretions, resulting in functional impairment. Thus, the management plan of EDAC requires disease-specific treatment, the use of mucolytics, bronchodilators, adjunct use of airway clearance devices such as flutter valves, high-frequency vest oscillation of the chest wall, and pulmonary rehabilitation[1,9,46].

In addition to the drug therapies, non-invasive positive pressure ventilation can be offered before applying invasive methods, which are generally retained for severe and refractory cases. It serves as a pneumatic stent, facilitating airway patency via secretion drainage and improvement of the expiratory flow. Moreover, there is improvement in dyspnea and quality of life. If the patient is unresponsive, the treatment approach escalates to interventional bronchoscopy[47-51].

Interventional bronchoscopy

Interventional bronchoscopy can be performed via the utilization of an airway stent for short intervals (2 weeks) to establish the potential benefit of the surgery[9,52]. Based on the wave speed theory of maximal EFL, stenting at the choke point (as shown in Figure 2) increases the cross-sectional area and supports the weakened airway wall[2,53]. Thus, considerable gains in EDAC were manifested, which included improvements in respiratory symptoms, quality of life, and functional status[54-56]. Patients who benefit from the stent trial can go for surgical intervention.

Approximately 60%-75% of patients undergoing stent trials experience symptomatic improvement and become eligible for surgical TBP. About 80% of candidates undergoing surgical TBP achieve improvement in symptoms, exercise tolerance, and quality of life[34,57,58]. Complications associated with stenting include infection, stent obstruction due to mucus plugging or granulation tissue growth, stent migration or fracture, hemoptysis, and airway perforation[59-61]. The early complication and late complication rates of self-expandable metallic stents (SEMS) are 7.3% and 23.9%, respectively. Early complications are defined as those occurring within 7 days, and late complications are defined as those developing after 7 days[62]. Careful evaluation and precise measurement of the airway, utilizing both dynamic bronchoscopy and CT scan, help minimize stent-related complications by enabling the selection of a suitable stent size and configuration[63].

SILICONE VS METAL STENTS

Previously, silicone Y stents were used for EDAC patients. Although silicone stents demonstrated symptomatic, functional, and quality of life improvements, high complication rates and the necessity for repeat bronchoscopy to maintain stent patency hinder their long-term use. Now, SEMS are frequently used during the stent trial phase in the EDAC patient. SEMS has the benefit of decreased mucus plugging. However, the drawbacks, such as the potential for excessive granulation tissue growth and higher costs, must still be considered before using SEMS[59,60,63]. SEMS costs around United States dollars (USD) 2500, whereas silicone stent costs around USD 700. The duration of hospital stay and the associated cost further increase when there is a necessity for SEMS replacement or removal due to complications, which is usually the case[60].

Surgical management

Surgical treatment comprising tracheobronchoplasty (TBP) is the definitive treatment for refractory and severe EDAC, responding positively to the stent trial. The ultimate goal of TBP is to strengthen and stabilize the posterior membranous wall of the central airways by applying sutures to polypropylene mesh, as shown in Figure 6[4,9,42,46,64]. TBP has improved respiratory symptoms, quality of life, and functional status. The airway is routinely assessed with dynamic CT following surgical intervention and compared with preoperative findings to determine the improvement in airway collapse. Further, routine surveillance[4] is performed to inspect recurrence and complications[44,52,65-67]. Robotic TBP is emerging as an effective alternative to the traditional open approach, with shorter intensive care unit and total hospital stays as well as comparable complication rates. However, further comparative studies are necessary to trace the long-term functional and quality of life outcomes[68].

Figure 6  Schematic representation showing plication of the posterior membranous wall with polypropylene mesh with the restoration of D-shaped airway during expiration.

NOVEL THERAPIES: BREAKTHROUGHS IN THE FIGHT AGAINST EDAC

Despite conventional treatment methods, novel therapies are applicable for managing EDAC, which include: (1) Laser TBP; (2) Argon plasma coagulation (APC); and (3) Customized three-dimensional (3D) stents. Due to its limited utilization, comprehensive upsides and downsides are yet to be determined. However, its potential can be employed to enhance EDAC management protocols.

Laser TBP

Laser TBP is an innovative approach where an endoscopic technique is applied to induce fibrosis of the posterior membranous wall, with successive reduction in airway collapse. It can be used for refractory cases unfit for traditional surgery[67-69].

APC

APC is predicted to be a valuable bronchoscopy approach to manage airway collapse by using thermal ablation, which produces desired fibrosis as appreciated by animal studies[34,70]. However, the implications of this in humans lack sufficient information on effectiveness and safety, mandating further research[71].

Customized 3D printed stents

3D-printed airway models enhance the precision of customized stents, ultimately leading to a better stent fit and improved cross-ventilation of the airways. Although 3D-printed stents play a crucial role in stent optimization, they do not significantly reduce stent-related complications, such as mucus secretions and stent migration[72].

Management approaches in the future might consider using biogenic stents and tracheobronchial replacement, too[4]. Biogenetic stents are absorbed within the body after a certain time. While tracheobronchial replacement is a surgical procedure performed to replace the damaged section of the trachea or bronchi with a substitute.

CONCLUSION

EDAC is an under-recognized clinical entity that causes airflow limitation with symptoms overlapping with other common respiratory conditions, such as COPD or asthma. The diagnosis of EDAC has been improved with dynamic imaging; however, challenges remain in standardizing diagnostic criteria and tailoring management strategies. A multidisciplinary approach involving pulmonologists, radiologists, and thoracic surgeons is essential for targeted treatment, ranging from conservative measures to surgical interventions. Further research is needed to validate non-invasive diagnostic tools, such as vibration response imaging, which can facilitate early and accurate diagnosis, particularly in patients who cannot tolerate invasive procedures. As novel therapeutic options, such as laser TBP and APC, emerge, ethical considerations must be carefully addressed through robust informed consent processes and by conducting experimental trials prioritizing patient safety and autonomy. With coordinated research and clinical efforts, EDAC can be better understood, diagnosed, and managed to improve patient outcomes.