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Excessive dynamic airway collapse for the internist: new nomenclature or different entity?
  1. Ankur Kalra1,
  2. Wissam Abouzgheib2,
  3. Mithil Gajera3,
  4. Chandrasekar Palaniswamy4,
  5. Nitin Puri3,
  6. Richard Phillip Dellinger3
  1. 1Division of Internal Medicine, Department of Medicine, Cooper University Hospital, UMDNJ-Robert Wood Johnson Medical School, Camden, New Jersey, USA
  2. 2Interventional Pulmonary, Sparks Health System, Fort Smith, Arkanas, USA
  3. 3Critical Care Medicine, Department of Medicine, Cooper University Hospital, UMDNJ-Robert Wood Johnson Medical School, Camden, New Jersey, USA
  4. 4Department of Medicine, New York Medical College, Westchester Medical Center, Valhalla, New York, USA
  1. Correspondence to Wissam Abouzgheib, Interventional Pulmonary, Fort Smith Lung Center, Sparks Health System, 1001 Towson Avenue, Fort Smith, Arkansas 72901, USA; wabouzgh{at}sparks.org

Abstract

Excessive dynamic airway collapse (EDAC) refers to abnormal and exaggerated bulging of the posterior wall within the airway lumen during exhalation. This condition is pathological if the reduced airway lumen is <50% of the normal. It is a relatively new disease entity that is recognised more easily now with the increased use of multi-detector row CT. EDAC is often asymptomatic and diagnosed incidentally. Although the term excessive dynamic airway collapse is often used interchangeably with tracheobronchomalacia, both entities represent morphologically and physiologically distinct processes. Considering the confusion between the two entities, the prevalence of stand-alone EDAC remains unclear. The prevalence of tracheobronchomalacia and EDAC depends upon the patient population, associated comorbidities and underlying aetiologies, diagnostic tools used and criteria used to define the airway collapse. This review defines EDAC and describes its pathophysiology, precipitating factors, associated symptoms and potential treatments.

  • Dynamic airway collapse
  • tracheobronchomalacia
  • DAC
  • TBM
  • adult intensive and critical care
  • respiratory medicine (see thoracic medicine)
  • bronchoscopy
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Introduction

Excessive dynamic airway collapse (EDAC) has recently been noted more often in the consultation notes of pulmonary specialists. It is also often mentioned, incidentally and interchangeably with tracheobronchomalacia (TBM), in CT scan and bronchoscopy reports. When symptomatic, EDAC may mimic symptoms of underlying pulmonary diseases, may delay response to therapy and may also worsen and complicate typical presentations of the underlying pulmonary comorbidities. General practitioners and specialists need to suspect and investigate EDAC when faced with ‘difficult to treat’ or ‘slow to respond’ patients with chronic lung diseases.

EDAC is a relatively common and new disease entity. It is pathophysiologically and morphologically distinct from TBM. It may exist in about one-fifth of patients with chronic airway diseases. It is often asymptomatic with a more benign course than TBM.

Dynamic airway collapse (DAC) of central airways occurs normally during expiration. The posterior tracheal and bronchial wall normally can approximate the anterior wall, reducing the airway lumen up to 50%.1 2 EDAC refers to abnormal and exaggerated bulging of the posterior wall within the airway lumen during exhalation.1 2 DAC is pathological or excessive (EDAC) if the reduced cross-sectional area is <50%. When severe, EDAC may worsen the symptoms of underlying conditions such as chronic obstructive airway disease. It may also lead to significant comorbidities such as difficulty in weaning from mechanical ventilation or need for long-term non-invasive mechanical ventilation. This review defines EDAC and describes its underlying pathophysiology and epidemiology. The article then distinguishes EDAC from TBM and describes its precipitating factors/co-morbidities, clinical presentation and associated symptoms, also in addition to covering its potential treatments and prognosis.

Definition

EDAC defines the pathological collapse and narrowing of the airway lumen by >50%, which is entirely due to the laxity of the posterior wall membrane with structurally intact airway cartilage.2

Prevalence

Considering the confusion between the two entities, the prevalence of stand-alone EDAC remains unclear. The prevalence of TBM and EDAC depends upon the patient population, associated comorbidities and underlying aetiologies, diagnostic tools used and criteria used to define the airway collapse. In a systematic review from Murgu et al,3 it appears that TBM and EDAC are present in 4–23% of patients undergoing bronchoscopy for various indications.

In a retrospective review, Park et al2 studied the prevalence of EDAC specifically. They found an incidence of 22% in patients with pre-procedural diagnosis of chronic obstructive pulmonary disease (COPD) and/or asthma.

With the increase in awareness about EDAC throughout the medical community and the routine use of multi-detector CT instead of single-detector CT scanners, the prevalence and detection of EDAC will probably increase. However, prospective trials to better define its true prevalence are still lacking.

Pathophysiology

During expiration, the posterior membrane of large- and moderate-size airways moves inward leading to narrowing of the airway lumen. Increased tension of the smooth muscle during forced expiration prevents exaggerated invagination and maintains the airway structure preventing excessive narrowing.4

In predisposing diseases or comorbidities such as chronic obstructive airway diseases, two main events may lead to EDAC. First, expiration becomes an active process, as more pressure is needed to overcome the resistance created by narrowed airways along with decreased elastic recoil. This area of narrowed or obstructed airway thus provides an area of stenosis resulting in an increased airflow along with a decrease in intraluminal pressure in accordance with the Bernoulli effect. This leads to an increased transmural pressure gradient favouring EDAC. Second, the smooth muscle tone of the posterior trachea is gradually weakened by recurrent cough, inflammation and infection also favouring EDAC.5 The decrease in transluminal pressure and weakening of the posterior smooth muscle membrane make the airways floppy or easily compressible and facilitate EDAC during cough or forced expiration. This effect occurs despite intact cartilaginous tracheal or airway rings, which are affected and softened in TBM (figure 1).

Distinction between EDAC and TBM (figure 2)

Although the term DAC is often used interchangeably with TBM, both entities represent morphologically and physiologically distinct processes. Both entities may affect diffusely all major airways or may selectively affect the trachea or major and lobar bronchi.

Figure 2

(A) Normal airway showing smooth muscle posterior membrane. (B) Excessive dynamic airway collapse showing ‘bowing’ of the posterior membrane and reduction of the cross-sectional airway diameter by <50%. (C) Sabre-sheath tracheobronchomalacia (TBM) affecting the lateral walls of the airway cartilage. (D) Crescent-shaped TBM affecting the anterior walls of the airway cartilage.

TBM is defined as weakness of the anterior and lateral airway walls primarily due to softening of the supporting cartilage. This represents the key difference from EDAC. When the anterior walls are mostly affected, the collapse leads to the narrowing of the sagittal airway diameter or crescent-shaped TBM. The lateral wall weakness affects the transverse airway diameter and causes transverse TBM. Bronchoscopic inspection of the trachea typically reveals abnormal cartilaginous structures.3

EDAC is different from TBM. In EDAC, the airway lumen narrowing is completely due to the laxity and exaggerated invagination of the posterior membranous portion of the airways with structurally intact cartilage.2 3

Clinical presentation and diagnosis

EDAC is usually asymptomatic and noted incidentally during routine bronchoscopy or CT obtained for other indications.

When symptoms occur, they are often attributed to and would be difficult to differentiate from underlying or associated conditions. When severe, EDAC can manifest as refractory cough, dyspnoea, inability to clear secretions, pneumonia or respiratory failure. Patients may be diagnosed months or years after failed treatment therapy for ‘refractory’ asthma, COPD or chronic cough.2 3

Wheezing also commonly occurs in these patients and, as anticipated, is refractory to treatment with corticosteroids and bronchodilators.2 3 6

EDAC can also manifest as difficulty in weaning from mechanical ventilation.7 The endotracheal tube and positive pressure ventilation overcome the tendency of the posterior membrane to invaginate during forced exhalation or cough. Typically, patients with significant EDAC have favourable weaning parameters especially if weaning trials are performed with pressure support and continuous positive airway pressure (CPAP). When extubated, these patients may develop recurrent respiratory failure needing re-intubation or non-invasive positive pressure ventilation.8 Diagnosing EDAC in these patients is a practical challenge. Bronchoscopy through an endotracheal tube or CT while on positive pressure ventilation would probably miss the diagnosis of EDAC. The endotracheal tube or the positive pressure ventilation acts as a pneumatic stent, keeping the tracheal lumen intact.

The gold standard test for diagnosing EDAC is bronchoscopy.8 Multi-detector CT of the chest is an important non-invasive diagnostic method.

During bronchoscopy, the most significant cough reflex occurs when the scope touches the vocal cords or the proximal part of the trachea. Therefore, the bronchoscopic diagnosis is typically made as soon as the scope enters the trachea. If bronchoscopy is performed to specifically evaluate for EDAC, we recommend performing it under ‘light’ or no sedation in order to elicit the cough reflex and optimise the patient's cooperation with deep breathing and forced exhalation. Taking still pictures and/or recording short video clips obviously helps determine and grade the degree of the collapse (figure 3).

Figure 3

(A) Inspiration and (B) forced expiration—localised excessive dynamic airway collapse of the right main bronchus.

Recent advances in technology have enabled cine viewing of the upper airways in a much less invasive manner. Dynamic CT of the chest using multi-detector CT scanners is a safe and accurate diagnosis method especially when bronchoscopy is contraindicated or deemed risky in patients with suspected EDAC (figure 4).9

Figure 4

Multi‐detector CT scans showing (A) inspiration and (B) forced expiration—localised excessive dynamic airway collapse of the right main bronchus.

Pulmonary function tests may exhibit salient features suggesting the presence of EDAC. These findings lack sensitivity and specificity as they may exist in TBM (figure 5).10–12

Figure 5

Airflow obstruction (A) without and (B) with notching of the expiratory limb.

  1. Diminished expiratory flow with typical notching in the flow–volume loop: the notch represents sudden diminution of flow at the beginning of expiration when the airway collapses. A small volume is rapidly exhaled followed by upward deflection in the curve and then continuation of exhalation.

  2. Biphasic flow–volume loop or flow oscillations (saw-tooth appearing loops).

Treatment

The treatment of EDAC depends upon the aetiology, the severity of symptoms and the extent of airway collapse. Medical management must be optimised prior to the consideration of minimally invasive or open surgical procedures. Endoscopic and surgical interventions should be absolutely reserved for severe and refractory situations leading to significant morbidities such as recurrent respiratory failure or inability to wean from mechanical ventilation. The lack of large randomised clinical trials weakens the strength of evidence for the different management and intervention techniques mentioned below.

Medical management

The treatment of underlying conditions must be obviously optimised prior to the targeted treatment of EDAC. This includes management of COPD and asthma in accordance with the standard of care practice guidelines as well as smoking cessation.

Non-invasive positive pressure ventilation has been effectively used to maintain airway patency. It acts as a pneumatic stent facilitating secretion drainage and improving expiratory flow.13 Ferguson and Benoist14 have reported improved spirometry, sputum production and clearance, atelectasis and exercise tolerance with the addition of nocturnal and intermittent day-time nasal CPAP of 10 cm H2O. Since the diagnosis of EDAC would not qualify for CPAP treatment under Medicare guidelines, screening for obstructive sleep apnoea in patients with documented EDAC should be performed.

Minimally invasive intervention

Airway stent insertion might result in symptomatic improvement. More than one stent may be needed as choke points, at times, migrate distal to the stent and limit airflow. Stent-related complications include migration, obstruction, infection, fracture and airway perforation. Murgu and Colt15 have reported that silicone stent insertions improve functional status immediately post-intervention in patients with EDAC but are associated with a high rate of stent-related adverse events and the need for repeat bronchoscopic interventions. Metal stents have also been used for the treatment of this condition and are less likely to migrate or cause obstruction as they preserve mucociliary clearance and aid in mucous clearance through dynamic compression during coughing. However, metallic stents should be avoided in accordance with the FDA public health notification, if the causes of central airway obstruction are benign.16

Surgery

Tracheostomy can be performed, as a long tracheostomy tube may be the surrogate for a stent to prevent collapse in the trachea. However, it may complicate EDAC by causing tracheomalacia and stomal site stenosis.17

Other proposed surgical techniques for EDAC include membranous tracheoplasty or strengthening of the posterior membrane using a polypropylene mesh that is incorporated into the membranous wall of trachea18; tying the posterior wall of the trachea with bone chips, fascia grafts and plastic prostheses; autologous costal cartilage grafts and tracheal suturing to dura mater grafts. These techniques are highly specialised and their comparative efficacy still needs to be determined.

Summary

EDAC is a new distinct entity, often asymptomatic, and most often diagnosed incidentally in patients with chronic obstructive airway diseases. When severe, it may worsen underlying conditions and respiratory failure. Therapeutic intervention is not required in the majority of affected patients. When needed, the treatment varies depending on the severity of symptoms, underlying aetiologies and the degree/extent of the airway collapse. Medical management should always be considered prior to bronchoscopic or surgical interventions.

Main messages

  • Dynamic airway collapse is distinct from tracheobronchomalacia

  • Common and may affect up to one-fifth of patients with chronic airway diseases

  • Often asymptomatic but may worsen symptoms of underlying diseases

  • Bronchoscopy and CT are gold standard diagnostic tests

Current research questions

  • What is the exact incidence of EDAC in all patients undergoing bronchoscopy for unrelated reasons?

  • What are the long-term effects of CPAP use on EDAC?

Key references

▶ Murgu SD, Colt HG. Tracheobronchomalacia and excessive dynamic airway collapse. Respirology 2006;11:388–406.

▶ Park JG, Edell ES. [Dynamic airway collapse. Different from tracheomalacia]. Rev Port Pneumol 2005;11:600–2.

▶ Carden KA, Boiselle PM, Waltz DA, et al. Tracheomalacia and tracheobronchomalacia in children and adults: an in-depth review. Chest 2005;127:984–1005.

▶ Ferguson GT, Benoist J. Nasal continuous positive airway pressure in the treatment of tracheobronchomalacia. Am Rev Respir Dis 1993;147:457–61.

▶ Murgu SD, Colt HG. Treatment of adult tracheobronchomalacia and excessive dynamic airway collapse: an update. Treat Respir Med 2006;5:103–15.

Self-assessment questions (true/false; answers after the references)

  1. Dynamic airway collapse is considered pathological if the reduced cross-sectional area is 50%.

  2. Dynamic airway collapse and tracheobronchomalacia are physiologically similar processes.

  3. Excessive dynamic airway collapse can manifest as difficulty in weaning from mechanical ventilation.

  4. The gold standard test for diagnosing excessive dynamic airway collapse is bronchoscopy.

  5. Endoscopic and surgical interventions are the cornerstone for the management of excessive dynamic airway collapse.

Answers

  1. False. Dynamic airway collapse is considered pathological if the reduced cross-sectional area is <50%.

  2. False. Dynamic airway collapse and tracheobronchomalacia are physiologically distinct processes.

  3. True. Excessive dynamic airway collapse can manifest as difficulty in weaning from mechanical ventilation.

  4. True. The gold standard test for diagnosing excessive dynamic airway collapse is bronchoscopy.

  5. False. Endoscopic and surgical interventions are reserved for severe and refractory situations leading to significant morbidities such as recurrent respiratory failure or inability to wean from mechanical ventilation.

References

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Footnotes

  • All the aforementioned authors had access to the data and a role in writing the manuscript.

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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