Expiratory central airway collapse

Defined by excessive airway collapse during expiration.

ECAC comprises two pathophysiologic entities: excessive dynamic airway collapse (EDAC), and trachiobronchomalacia (TBM).

common manifestations of the disease include dyspnea, chronic cough, and recurrent respiratory infections.

Dynamic flexible bronchoscopy is the diagnostic criterion standard with dynamic forced expiratory computerized tomography as helpful.

Excessive dynamic airway collapse (EDAC)

Refers to pathological collapse and narrowing of the airway lumen by >50%.

The etiology of ECAC is unknown: small airway obstruction, chronic inflammation, trauma, previous tracheostomy, relapsing polychondritis, other immune diseases, COPD, asthma, obesity, gastroesophageal reflux disease all have been linked to its development.

ECAC is an under diagnose disorder which can coexist with and mimic asthma, COPD, and bronchiectasis.

The use of inhaled corticosteroids, commonly used in  airway diseases may have some causative role.

Prevalence is unknown, although it is likely underdiagnosed: an overall prevalence of 13% has been suggested with an increase in 37% in those with COPD and other airway diseases.

Excessive dynamic airway collapse refers to an excessive forward displacement of the posterior membranous portion of the tracheal wall due to weakness and atrophy of the longitudinal elastic fibers.

It is suspected that large airway clapse is due to increased airway resistance, decreased lung elastic recall, and increased pleural pressure.

These factors, collectively, increase luminal airflow velocity and decrease pressure, creating a stress on luminal integrity and leading to smooth muscle fatigue, weakening of the smooth muscle tone, reduced elastic recoil, and greater narrowing lead to greater transmural pressure gradient resulting in ECAC.

The abnormal motion of the anterior lateral or cartilaginous portion of the trachobronchial  wall is termed TBM.

Collapse and narrowing of airway lumen is entirely due to the laxity of the posterior wall membrane with structurally intact airway cartilage.

It is pathophysiologically and morphologically distinct from tracheobronchomalacia.

The lung diseases most frequently associated with EDAC are the chronic obstructive pulmonary disease (COPD) and asthma.

The incidence of EDAC is 22% in patients with chronic obstructive pulmonary disease (COPD) and/or asthma.

The decrease in transmural pressure and the weakening of the posterior muscle membrane fosters the collapse of the airways during coughing and/or forced expiration.

A syndrome comprising two different pathophysiologic entities: excessive dynamic airway collapse (EDAC) and tracheobronchomalacia (TBM).

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.

EDAC is often asymptomatic and diagnosed incidentally.

It is pathophysiologically and morphologically distinct from tracheobronchomalacia.

Tracheobronchomalacia and EDAC are present in 4–23% of patients undergoing bronchoscopy for various indications.

The incidence of EDAC is 22% in patients with chronic obstructive pulmonary disease (COPD) and/or asthma.

Usually a 95% reduction is required to induce a symptomatology that requires therapy.

The severity criterion describes the degree of airway collapse (AC) during expiration.

During expiration, the posterior wall of the trachea and of the mainstem bronchi moves inward, reducing the lumen of the airways.

Smooth muscle tone normally keeps the airways open, preventing their collapse.

In most chronic respiratory diseases expiration becomes an active process required to overcome the loss of elasticity of the airways.

The pressure of the airways decreases as the air flow advances through the obstructed airways, generating a transmural pressure gradient that fosters EDAC.

Recurring cough, inflammation and the infections associated with chronic pulmonary diseases, further weaken the tone of the bronchial smooth muscle contributing to EDAC.

The decrease in transmural pressure and the weakening of the posterior muscle membrane causes the collapse of the airways during coughing and/or forced expiration.

Tracheobronchomalacia refers to a weakness of the anterior and/or lateral walls of the main airways caused by a softening of the cartilage.

Tracheobronchomalacia’s main difference from EDAC, because, when the anterior wall is most involved, its collapse causes a decrease in sagittal diameter, whereas a weakness of the lateral walls leads to a decrease in transverse diameter.

When both the lateral walls and the anterior wall are involved, we observe a concentric diameter reduction.

EDAC differs from TBM in that, in this pathology, lumen reduction is entirely due to the laxity and excessive invagination of the posterior wall.

The lung diseases most frequently associated with EDAC are the chronic obstructive pulmonary disease and asthma.

In most cases the symptoms of EDAC are ascribed to COPD and asthma, while the actual pathology is identified through a bronchoscopy or CT scan performed for other reasons.

It is characterized by dry cough, dyspnea, recurrent airways infections, difficult expectoration and respiratory failure.

A typical symptom is a wheezing that unresponsive to corticosteroid and bronchodilating therapy.

Can be responsible for the difficult weaning of patients from mechanical ventilation, because the endotracheal tube or the positive pressure of the air insufflated into the airways, reduces or prevents the invagination of the posterior tracheal wall.

The standard for EDAC diagnosis is bronchoscopy.

Pulmonary function testing has no diagnostic value and is not predictive of disease progress.

Bronchoscopy should be performed with a flexible instrument during spontaneous breathing with the patient conscious and alert, to follow instructions of deep breathing, forced expiration and coughing that increase the dynamic collapse of the airways.

The procedure is performed the with the patient laying supine, on the side, or seated, and the lumen of the airways is measured in the course of the various maneuvers and the observed anomaly is classified.

By measuring airway pressure proximal and distal to the narrow airway segment, the site of maximum obstruction and degree of narrowing can be physiologically assessed.

Bronchoscopy allows evaluating the therapeutic efficacy of positive pressure mechanical ventilation or of stenting.

High frequency endobronchial ultrasonography can identify the hypoechoic and hyperechoic layers that correlate with the histologic structures of the central airways.

CT scans can be used in the assessment as an alternative or complementary test to dynamic bronchoscopy, having a similar sensitivity.

Dynamic CT is often used in pre-operative assessment, to determine the degree, extension and nature of the narrowing.

The advantages of CT: lower invasiveness, the possibility to observe the structures surrounding the airways, which can be potentially responsible for the malacia and the characteristics of the lung tissue that contribute to the collapse.

Its disadvantages are the lack of information on the mucosa, the required high patient’s compliance and exposure to ionizing radiation.

In EDAC patient’s spirometry shows an obstructive syndrome, but gives no information as to the severity of the narrowing of the airways

Spirometry does not show the improvements that can follow therapeutic measures.

Airway collapse pattern is characterized by a decrease in flow rate from the peak flow to an inflection point less than 50% of peak flow rate.

Asymptomatic disease , regardless of the degree of airway collapse, should not be treated.

Functional impairment in excessive dynamic airway collapse may result from at least three causes: dyspnea, cough, and mucus retention.

Management includes disease specific treatment, and chest physiotherapy, mucolytic drugs, positive expiratory pressure to improve secretion management.

If conservative treatment fails and the patient is critically ill, stent insertion is performed.

If the patient is not critical ill, NIPPV application, can serve as a pneumatic stent.

It results from either cartilaginous weakening or redundancy of the posterior membranous wall.

Includes tracheobronchomalacia and excessive dynamic airway collapse.

Prevalence in people with respiratory problems ranges from 1-53%.

ECAC increasingly recognized in the adult population due to the use of CT scans of the chest, and especially noted in an association with cigarette smoking and COPD.

Small conducting airways less than 2 millimeters in diameter are the major site of resistance to airflow in COPD, collapse greater than 50% of the large central luminal area during exhalation has been hypothesized to cause additional airflow obstruction and respiratory morbidity.

Trachealbronchomalacia (TBM) is divided into cartilaginous or circumferential.

Cartilaginous TBM implies a weakness of the lateral cartilage wall and leads to splaying at the end of the tracheal cartilage, increasing the transverse diameter, decreasing the anterior posterior diameter.

TBM is a combined the anterior and lateral airway wall collapse usually related to inflammatory processes, such as relapsing polychondritis.

With forced expiration there is a anterior diameter narrowing of 50%, or so.

Diagnosis is often delayed due to the nonspecific clinical manifestations.

The lack of improvement from specific processes suggests the diagnosis: most common presentations include chronic bronchitis, chronic cough, dyspnea, and difficulty clearing secretions.

Chronic cough in these patients are paroxysmal, and described as seal like barking, and influenced by excessive vibration of the posterior tracheal wall against the anterior lateral borders of the tracheobronchial tree.

There is poor airway secretion clearance precipitated by the mechanical collapse and failure to expectorate retained airways equations which perpetuate chronic airway information and impaired mucociliary clearance.

Dyspnea may be due to air trapping and hyperinflation during forced expiration.

Patients may become deconditioned as there is limitation in their ability to exercise.

Pulmonary functions may reveal obstructive, 44%, or restrictive changes, 17.8%,  but are normal in 20% of patients with ECAC.

Dynamic flexible bronchoscopy is the most reliable test to confirm ECAC.

The patient purposely produces forced expiration as the bronchoscopist evaluates each segment of the central airways with your valuated as to the degree of collapsibility at the cricoid level, mid trachea, distal trachea, proximal left and proximal right mainstem bronchi and proximal bronchus intermedius.

ECAC disease severity is described as mild disease with collapse of 70 to 80%, moderate with collapse of 81 to 90%, and severe as  collapse of 91% or higher.

Treatment: commonly airway stents are placed to assess clinical improvement and to help identify patients that may benefit from surgery.

Stent trials are limited to 5 to 10 days due to complications of cough, mucous plugging, foreign body irritation and infection.

Up to 75% of patients in a stent trial exhibit an improvement and are considered for further surgical intervention.

Treatment for ECAC is determined by the severity of disease, the degree of collapse, and the severity of symptoms and comorbid conditions.

Optimal treatment for infections, airway disease, and the use of pulmonary hygiene measures are critical to care.

Intermittent or continuous bilevel positive airway pressure is part of management of mild to moderate disease.

Tracheobronchial or surgical central air stabilization by splinting is considered for patients with severe disease.

Tracheobronchial plasty is associated with 1% mortality,is associated with perioperatively adverse events in health of patients including respiratory failure or pneumonia.



One reply on “Expiratory central airway collapse”

can EDAC be caused by long time exposure to biproducts of combustion from homes, cars, plastics, metals etc fully engulfed?

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