Egyptian Journal of Bronchology

Vol 1, No 1, Dec., 2007

REVIEW ARTICLE
EXPIRATORY CENTRAL AIRWAY COLLAPSE: A CONCISE REVIEW
By
Septimiu D. Murgu, Henri G. Colt
Pulmonary and Critical Care Medicine, Department of Medicine, University of California School of Medicine, Irvine,
CA.

Expiratory central airway collapse is a clinical syndrome characterized by airflow limitation due to
excessive narrowing of the central airways during exhalation. The syndrome consists of two entities,
tracheobronchomalacia and excessive dynamic airway collapse, which are different in terms of
morphology, physiology, etiology and structure. Treatment alternatives, which include conservative
medical management, interventional bronchoscopic procedures and open surgery, should be individualized
based on functional status, extent of disease and severity of airway collapse.

DEFINITIONS central airways.

Expiratory central airway collapse (ECAC) refers
to airflow limitation due to excessive narrowing of During normal exhalation, increased pleural
the central airway lumen during exhalation. This pressure promotes a small degree of dynamic
process has been described in the literature as airway collapse (DAC) that can reduce the cross
tracheobronchial collapse,(1) expiratory sectional area of the airway lumen by a maximum
tracheobronchial collapse, expiratory of 40%.(6) DAC is a physiologic process
tracheobronchial stenosis,(2) tracheobronchial characterized by invagination of the posterior
dyskinesia, tracheobronchomalacia and dynamic
(3) membrane of the tracheobronchial tree.
airway collapse.(4,5) Although, these
terms suggest a dynamic central airway Excessive dynamic airway collapse (EDAC), on the
obstruction, they do not distinguish between a other hand, refers to abnormal and exaggerated
process that involves the cartilaginous rings and bulging of the posterior membrane within the
one that involves the membranous part of the airway lumen during exhalation. This might cause
a reduction in cross sectional area of 50 % or

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more.(7) It may not be responsible for airflow develop expiratory flow limitation and respiratory
limitation since it may just represent a failure.
consequence of the increased intrathoracic
pressure and decreased intraluminal pressure MORPHOLOGY
often seen in patients with significant obstructive
Both computed tomography and bronchoscopy
ventilatory disorders such as asthma and COPD.(8)
can be used to diagnose ECAC and determine the
Tracheobronchomalacia (TBM) refers to softening configuration of airway lumen during
of the airway cartilaginous structures. As a result, exhalation.(10,14) There is good correlation between
the trachea and main bronchi lose their stiffness. the two tests and they are complementary rather
Airflow limitation is probably caused by the way than competitive.(15) Paired inspiratory –expiratory
the airway walls come closer together, especially CT scanning reveals the airway collapse during
during exhalation. expiration, and accurately determines the degree
of airway narrowing as well as assesses the
CLINICAL PRESENTATION adjacent pulmonary parenchyma and vasculature,
thus aiding in determining the etiology of the
The excessive reduction of the airway lumen airway collapse.(16) The test is associated, however,
during exhalation may be asymptomatic and with radiation exposure, and requires patient
detected during routine bronchoscopy or cooperation which may be difficult in the critically
computed tomography obtained for other ill or dyspneic patient.
reasons.(9) Expiratory Central Airway Collapse can
also present as a disease state characterized by
Dynamic flexible bronchoscopy, on the other
refractory cough, dyspnea, inability to clear
hand, can be performed at the bedside with
secretions, pneumonia and respiratory failure.(10)
minimal sedation. The patient is moved through
These signs and symptoms are nonspecific and
body positions (supine, erect, lateral decubitus)
similar to those of patients with chronic lung
and asked to perform several respiratory
disease. In fact, many patients are diagnosed
maneuvers (deep inspiration, expiration, cough) in
months or years after being treated for
order to assess the degree of airway collapse and
“refractory” asthma or COPD.(11) The cough in
extent of airway abnormality, as well as to identify
patients with ECAC has been described as a
associated lesions such as mucosal edema, stenosis
characteristic, seal-like barking, presumably
or secretions.(17)
because of expiratory collapse and vibration of the
floppy airway walls. Wheezing is common and
usually occurs early during a forced vital capacity Dynamic CT and bronchoscopy demonstrate that
maneuver because it is caused by large airway EDAC has a crescent configuration because of the
collapse. In severe cases, both TBM and EDAC can bulging of the posterior membrane within the
cause respiratory failure requiring mechanical lumen in the presence of intact cartilaginous
ventilation.(12) Occasionally, ECAC is diagnosed as structures. TBM, on the other hand, has three
a cause for inability to wean off the mechanical morphologic types.(10) When the lateral airway
ventilation.(13) In these patients, ECAC may not be walls are weakened, the configuration during
easily appreciated because the endotracheal tube exhalation is that of a saber sheath. When the
(ETT) partially stents the trachea and prevents the anterior wall is weakened, the airway lumen takes
expiratory collapse. Furthermore, positive- the shape of a crescent. If the anterior and lateral
pressure ventilation keeps the airway lumen open cartilaginous walls are involved, the morphology
acting as a pneumatic stent. Once the positive is circumferential. This is usually seen in patients
pressure or the ETT is removed, the patient may with relapsing polychondritis and may be
accompanied by mucosal edema (Fig. 1).

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 Fig 1A. Normal tracheal lumen during inspiration. B. During exhalation there is a certain degree
of dynamic airway collapse (DAC) that reduces the cross sectional area (CSA) by a maximum of
40%. C. A reduction of CSA by 50 % or more defines excessive dynamic airway collapse (EDAC)
which is caused by bulging of the posterior membrane within the airway lumen during exhalation
in the presence of intact cartilaginous structures. D. In tracheobronchomalacia (TBM), if the
anterior wall is weakened, the airway lumen takes the shape of a crescent. E. When the lateral
walls are weakened, the configuration during exhalation is that of a saber sheath. F. If both
anterior and lateral cartilaginous walls are involved, the type of TBM is called the
circumferential type, and is associated with significant edema and seen mainly in relapsing
polychondritis.

Fig 2A. Schematic diagrams of the thorax and airways. The pressure in the alveoli (Palv) is the
sum of total elastic recoil pressure (Pst) and pleural pressure (Ppl): Palv = Ppl + Pst; B. During
exhalation, alveolar pressure rises above athmospheric (Pm) to cause air to flow from alveoli to
the mouth. Since the pressure at the mouth is zero (athmospheric) and P alv > 0, the intraluminal
pressure (PL) at some point has to equal the Ppl; this point is called equal pressure point (EPP)
which divides the airway into an upstream and a downstream segment; EPP is not fixed, but
migrates from extrathoracic airways into the small airways as the lung volume decreases and Ppl
increases during expiration; C. When the compliance of the airways is increased as in expiratory
central airway collapse (ECAC), increased airway compressibility causes the EPP to become fixed
at a point closer to the thoracic outlet.

EJB, Vol 1, No 1, Dec., 2007 89

 PHYSIOLOGY intrathoracic airways (Fig. 2B). At some point in
DAC and Equal Pressure Point Theory: Airways the airways, therefore, pressure inside and outside
within the lung are surrounded by alveoli. The will be equal and, from that point downstream,
pressure in these alveoli is the sum total of elastic only the elastic recoil pressure will driving airflow
recoil pressure and pleural pressure (Fig. 2A). (Fig. 2B). This point is called the equal pressure
During inspiration, pleural pressure is negative point (EPP). It has been shown that, during the
relative to atmospheric pressure and so is alveolar forced vital capacity maneuver, EPP is in the
pressure in order to cause air to flow from the extrathoracic airways (e.g., cervical trachea) at
atmosphere into the alveoli. Hence, the pressure high lung volumes but, as lung volume declines,
acting on the outside of airways causes them to the EPP moves within the thorax progressively
enlarge and causes diminished resistance to towards and into the small airways.
airflow. During quiet expiration, pleural pressure
remains negative but alveolar pressure rises above EDAC
atmospheric pressure so that air flows from the In obstructive ventilatory dysfunction (i.e. COPD,
alveoli to the atmosphere. In contrast to what asthma), small airways are already narrowed by
occurs during inspiration, extramural airway disease. Airway resistance rises dramatically as
pressure is positive and the airways tend to these are suddenly compressed to very small
become smaller as the resistance to flow increases. diameters. In COPD, decreased elastic recoil at all
The large, central airways are, somewhat protected lung volumes (emphysema) and inflammatory
from dynamic compression and collapse by the narrowing of small airways (bronchitis) usually
presence of cartilaginous rings. These rings encase coexist. In the presence of emphysema, elastic
the large airway circumferentially, except tissue is decreased. Airways are compressed and
posteriorly in an area occupied by the may collapse during exhalation and especially
membranous structures. During expiration, this during a forced vital capacity maneuver. Airway
area bows slightly inwards causing DAC (Fig. 1). collapse can also be seen in bronchitis and possibly
This tendency increases during forced exhalation in asthma when obstruction is severe and occurs
or cough when pleural and alveolar pressures rise primarily in small airways. An “airway collapse”
considerably. pattern on flow volume loop is seen in 40% of
patients with chronic airflow obstruction.(18) This
The degree of large airway narrowing (DAC) consists of a sudden decrease the peak expiratory
which occurs during exhalation is moderated by flow, defined as a drop of 50% within 10 % of
the degree of external airway support. The major forced volume capacity
external support of airways is the elastic tissue of (Fig. 3A). Results from density dependence of flow
the alveoli which encloses the intraparenchymal studies using heliox showed that for patients with
airways. As large airways narrow they tend to COPD with this flow volume loop pattern, the
pull the lung parenchyma inwards. To the extent flow limiting segments (choke points) are
that intact elastic tissue is normal, airway collapse peripheral [18] and not central as might be
is opposed and airway narrowing is limited. expected when large airway collapse is identified
During expiration, driving alveolar pressure is on bronchoscopy or CT. Recent evidence suggests
completely dissipated along airway walls, that in bronchoscopically-documented EDAC,
reaching atmospheric pressure just outside the lips central airway collapse is not closely related to
or nose. Because elastic recoil is greatest at total airflow obstruction, and expiratory flow limitation
lung capacity and least at residual volume, at rest often occurs in peripheral airways without
alveolar pressure becomes progressively central airway collapse.(19) Localizing the choke
dependent upon only pleural pressure as lung points to central or peripheral airways, therefore,
volume decreases. However, pleural pressure acts becomes important in such patients, because if
directly not only upon alveoli but also upon the obstruction is located in the peripheral

90 Egyptian Journal of Bronchology

intrapulmonary airways, these patients might not performed to stiffen the central
improve after stent insertion or tracheoplasty, airways.

Fig 3. Flow volume loop patterns in patients with expiratory central airway collapse. A. Low
maximal flow and airway collapse pattern: maximal flow is reached quickly followed by a
sudden large fall in flow (defined as 50% drop within 10% of forced vital capacity) although only
a small volume is exhaled. There is subsequently a phase in which flow rate falls very little during
the remainder of expiration resulting in a long plateau. B. Flow oscillations or saw–tooth
appearance is defined as a reproducible sequence of alternating decelerations and accelerations of
flow. This pattern is considered a nonspecific indicator of upper airway dysfunction because it
can also be seen in patients with obstructive sleep apnea, structural or functional disorders of the
larynx, neuromuscular diseases, Parkinson disease, pedunculated tumors of the upper airway and
upper airway burns.

TBM and wave speed theory: Mechanisms been described in the wave speed theory of flow
responsible for expiratory airflow limitation are limitation which implies that maximum expiratory
not limited, however, to lung elastic recoil flow is dependent on airway compliance.(20)
pressure, lung volume, and location of the EPP. Increasing large airway compliance increases
Also implicated in this process is the density of the airway resistance and decreases maximum
gas flowing through the airways, the airway expiratory flow, which could contribute to the
compressibility and smooth muscle tone at the airway obstruction associated with TBM because
compressibility point described earlier, the overall flow velocity reaches the speed of wave
geometry and mechanical properties of the propagation at the choke point, closely related to
tracheobronchial tree, the area through which EPP, which is now located further downstream
airflow occurs, convective acceleration loss towards the airway opening in the central airways
(Bernoulli effect), and the frictional pressure loss (Fig. 2C).
during expiration. Interaction of these factors has
Therefore, it appears that from a physiologic
standpoint, the two forms of ECAC are different.
Patients with EDAC may have partially reversible

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small airway obstruction which may respond to standing extrinsic compression that eventually
bronchodilator treatment, while patients with weakens the cartilaginous rings as seen in thyroid
TBM have centrally located choke points such that goiter(25) or postpneumonectomy syndrome.(26)
bronchodilators may actually worsen airway EDAC, on the other hand, is commonly seen in
obstruction because of increased airway COPD and asthma but can also be caused by
compliance and smooth muscle relaxation.(21) chronic irritation of the airways or atrophy of
elastic fibers as seen in congenital
Pulmonary Function Tests: Pulmonary function tracheobronchomegaly.(27)
tests in ECAC might show diminished expiratory
flow, the airway collapse pattern described above STRUCTURE
on flow-volume loop (FV loop), dynamic airway Histological evidence of structural differences in
compression (calculated as Slow Vital Capacity TBM and EDAC is scarce and usually based on
minus Forced Vital Capacity) or flow case reports or small case series.(10) It is unclear
oscillations(10) (Fig. 3B). Such flow oscillations or whether these histopathologic changes are
saw–tooth appearance, defined as a reproducible primary or simply end-products of injury from
sequence of alternating decelerations and other disorders. In tracheomalacia, the tracheal
accelerations of flow are however, considered a cartilage-to-soft tissue ratio is sometimes as low as
nonspecific indicator of upper airway 2:1, while normally it is approximately 4.5:1. In
dysfunction.(22) TBM due to relapsing polychondritis, an extensive
inflammatory component of the tracheobronchial
Recent evidence suggests that expiratory central cartilage showing empty lacunae (empty spaces
airway collapse is not correlated with the degree within the cartilage) and a mixed population of
of obstruction as assessed by FEV1, and that inflammatory cells has been described.(28) In
ECAC could be found irrespective of the degree of patients with described EDAC, atrophy of
expiratory flow limitation during quiet longitudinal elastic fibers as well as flaccid and
breathing.(19) Thus, significant expiratory central dilated membranous portion of the airway in the
airway collapse cannot be assumed in patients absence of cartilaginous abnormalities has been
with obstructive airway disease, and symptomatic noted.(4)
ECAC may exist without significant airflow
obstruction as assessed by FEV1. Other Endobronchial ultrasound (EBUS) shows
physiologic variables such as markers of dynamic differences in airway structural composition in
hyperinflation (e.g. inspiratory capacity) or normal airways as well as in airway disease
density dependence of flow may better identify caused by tuberculosis,(29) compression from
and predict which patients with symptomatic vascular rings,(30) cancer invasion(31) or relapsing
ECAC will benefit from central airway splinting polychondritis.(32) EBUS shows distinct hypo and
using airway stents or surgical membranous hyper-echoic layers corresponding to the laminar
tracheoplasty. histological structures of the airway wall(33) (Fig.
4A). Recently, it has been reported that the EBUS
ETIOLOGY findings in DAC, EDAC and TBM are different.(34)
Both TBM and EDAC can be idiopathic or In DAC, there are no cartilaginous abnormalities
secondary. While both forms of expiratory central noticed and the posterior membrane is of normal
airway collapse may have common risk factors, thickness (Fig. 4B). In EDAC caused by COPD,
their etiologies are usually different Table 1. TBM EBUS images reveal intact cartilage of normal
is often a consequence of pressure necrosis from thickness while the posterior membrane is thinner
indwelling tracheostomy or endotracheal tubes,(23) than normal (Fig 4B). In TBM caused by chronic
chronic inflammatory states of the airways such as inflammation from indwelling tracheostomy, the
relapsing polychondritis,(24) or caused by long EBUS image reveals thickened and destroyed

92 Egyptian Journal of Bronchology

cartilage, thickening of the submucosa overlying while the posterior membrane is normal (Fig. 4B).
the cartilaginous rings and increased thickness of If confirmed in larger studies, these findings
the submucosa in the posterior membrane, while would support the hypothesis that the two forms
in TBM from relapsing polychondritis EBUS of ECAC are distinct not only morphologically,
revealed that the cartilage is thickened and physiologically and etiologically but also
destroyed, the submucosa is thickened as well, structurally.

Fig 4A. Endobronchial ultrasound (EBUS) reveals hypo- and hyper-echoic layers (left
panel) which correlate with the histological structural layers of the central airways
(right panel). B. EBUS findings in various forms of expiratory central airway collapse.
In tracheobronchomalacia (TBM) from relapsing polychondritis, the cartilage is thick
and the posterior membrane is normal; in TBM from chronic inflammation due to
indwelling tracheostomy tube, the cartilage is thick but also the posterior membrane is
thick; in excessive dynamic airway collapse (EDAC) the cartilage is normal but the
posterior membrane is thin; in dynamic airway collapse (DAC), both the cartilage and
the posterior membrane are of normal thickness. Photos are courtesy of Prof. Noriaki
Kurimoto, St. Marianna University School of Medicine, Kawasaki, Japan.

TREATMENT these patients, we have recently proposed a

Treatment alternatives for patients with expiratory multidimensional classification system that
central airway collapse should depend on the incorporates all of the elements needed to identify
severity of symptoms, the degree and extent of and compare patients with various forms of
airway collapse, and the underlying cause.(35) Very expiratory central airway collapse.(36) This
few studies, however, addressed the treatment of classification system, referred to as FEMOS,
these conditions, and because of a lack of addresses Functional status, Extent of
universally accepted definitions and classification, abnormalities noted, Morphology of the
study results cannot be generalized. abnormality, Origin (or etiology) of the
abnormality, and Severity of the disease process
Table 2. FEMOS can be used during the diagnostic
In order to facilitate a comprehensive approach to

EJB, Vol 1, No 1, Dec., 2007 93

approach to patients with ECAC, as well as to Interventional Bronchoscopy: The goal of
objectively compare findings after therapeutic bronchoscopic interventions is to prevent airway
interventions. The common language offered by collapse responsible for airflow limitation and
this multidimensional classification system, can symptoms. Because it maybe difficult to determine
help clinicians and researchers to answer existing the specific contribution of ECAC to a patient’s
questions regarding patient functional impairment, a comprehensive
selection and outcomes for various therapeutic pretreatment evaluation should be performed
interventions. especially to distinguish symptoms from those
related to underlying airflow
Conservative medical management: Treatment of obstruction from asthma or COPD. This may
the underlying condition should be optimized include density dependence studies using heliox
before considering invasive therapies. This is (HeO2) to determine the choke point location.
possible however, only in the absence of Physiologic studies showed that the predominant
respiratory distress or critical airway narrowing sites of airflow limitations (choke points) in
and impending respiratory failure in which case, asthmatics can be defined by comparing
the airway has to be urgently stabilized. For stable maximum expiratory flow volume (MEFV) curves
patients, it is logical that drug therapy be after the inhalation of air and after the inhalation
attempted whenever possible before proceeding to of HeO2 (80%-20%).(18) HeO2 is lighter than air,
more aggressive interventions. This is particularly modifies gas density, and subsequently improves
the case in patients with relapsing polychondritis, the flow in the central airways.
for whom non-steroidal anti-inflammatory drugs HeO2 should not change flow in patients with
or high-dose corticosteroids and various peripheral choke points because small airway flow
immunosuppressants are warranted. is mainly determined by gas viscosity rather than
Although these drugs are often effective in density. A reduced density dependence of flow,
treating chondritis, they do not stop the therefore, will favor predominantly
late loss of cartilaginous support and may not peripheral choke points, whereas increased
influence survival.(24) In patients with underlying density dependence (∆V E max> 20%) will be
asthma or COPD, treatment should obviously be consistent with choke points localized
in accordance to published guidelines. As in the large airways.(18) The predictive value of
mentioned previously, a dramatic fall in peak flow these tests, however, has not been tested in
may occur in response to central airway smooth patients with ECAC or any other forms
muscle relaxation after bronchodilator of central airway obstruction and will require
administration. (37) validation before implementation in clinical
practice.
Noninvasive positive pressure ventilation acts as
a pneumatic stent and can be used in selected From a practical standpoint, a therapeutic trial of
cases to maintain airway patency, facilitate airway stent insertion might result in symptomatic
secretion clearance, and improve expiratory flow. improvement (Fig. 5).(14,35) If objective measures of
Small case series support the addition improvement are also documented
of nocturnal and intermittent daytime nasal using dynamic CT or bronchoscopy and the
continuous positive airway pressure (10 cm H2 O) multidimensional FEMOS classification, for
to improve spirometry, sputum instance, then the stent can be left in
production, atelectasis, and exercise place or a decision should be taken regarding a
tolerance.(38) surgical correction by membranous
tracheoplasty.

94 Egyptian Journal of Bronchology

 Fig 5. Airway lumen during bronchoscopy before and after stent insertion in a patient with severe idiopathic
excessive dynamic airway collapse (EDAC) A. Distal trachea and mainstem bronchi during rigid
bronchoscopy before stent insertion: EDAC is characterized by exaggerated bulging of the posterior
membrane within the airway lumen. B. Distal trachea and mainstem bronchi during rigid bronchoscopy
show complete restoration of the airway lumen after three silicone stents were inserted (one in the lower
trachea and two in the mainstem bronchi).

It is difficult, however, to draw conclusions about bronchoscopy usually occurred within the first
the efficacy of airway stents pertaining only to four weeks after stent insertion. This supports a
ECAC. More than one stent may be required if the practice of early surveillance bronchoscopy, close
symptoms persist, presumably because choke clinical follow-up and immediate bronchoscopy in
points may migrate distal to the stent and limit case of clinical deterioration.
airflow.(39) If symptoms do not improve, stent
removal is warranted to avoid stent-related Various results from metal stent insertion for
complications, including migration, obstruction by patients with central airway obstruction including
mucus or granulation tissue, infection, fracture, malacia have been reported.(35) Metal stents are
and airway perforation. less likely to migrate or to cause obstruction by
mucus plugging because they may preserve
Silicone stents require rigid bronchoscopy for mucociliary clearance if uncovered and are
placement, but have excellent force compression capable of a certain degree of dynamic
characteristics and are easily removable in case of compression during coughing to facilitate mucus
complications. Using FEMOS system pre and post clearance. In one case series addressing the role of
operatively, we have recently reported that metal stents in 4 patients with tracheomalacia,
silicone stent insertion improves functional status however, stents had to be removed because of
immediately post intervention in patients with failure and complications.(42) Metal stents are more
expiratory central airway collapse, but is difficult to remove, tend to cause recurrent
associated with a high rate of stent-related adverse stenosis and are predisposed to fracture and
effects and need for repeat bronchoscopic collapse especially in a dynamic process such as
interventions.(40) A high rate of complications is ECAC. In accordance with an FDA warning
also reported by others,(41) and is likely explained regarding fatalities and stent-related adverse
by the dynamic features and frequently inflamed events, metal stents should probably be avoided in
airway mucosa associated with expiratory central patients with benign causes of central airway
airway collapse. In our study, stent-related obstruction.(43)
adverse events requiring emergent flexible or rigid

EJB, Vol 1, No 1, Dec., 2007 95

Bronchoscopists have also attempted to strengthen more normal C shape from their flattened pattern.
the posterior membrane in order to prevent ECAC. This is done by reinforcing the posterior
The injection of sclerosing agents into membrane with a polypropylene mesh which
pericartilaginous tissues resulted in significant becomes permanently incorporated into the
peritracheal fibrosis compared with controls.(44) membranous wall through. Wright et al recently
Nd:YAG laser therapy has been used to tighten the published their 10 year experience during which
airway wall by creating a fibrotic reaction of the 14 consecutive membranous wall tracheoplasties
posterior membrane.(45) This technique may be were performed.(49) There were no postoperative
hazardous because the posterior wall is only 3-5 deaths and the most frequent morbidity was
mm thick and, to our knowledge, no experimental retention of secretions during the immediate
studies have confirmed feasibility. Although postoperative period in 7 of the 14 patients. All
preliminary results in a few patients suggest patients felt subjective improvement early after
improvement in symptoms, ventilatory function surgery. Among ten patients followed long-term, 6
and bronchoscopic aspects, long term outcomes were subjectively judged to have an excellent
have not been reported. result, 2 were good, and 2 were judged as failures.
This procedure is also limited to specialized
SURGERY centers and has been only offered to a small group
of patients judged to be ideal surgical candidates.
The goal of open surgical procedures is to remove
or bypass the abnormal airway segment for focal Other methods of surgical airway splinting
disease or to splint the airway by externally include tying the posterior wall of the trachea with
stiffening the airway walls in the setting of bone chips, fascia grafts or plastic prostheses,
multifocal or diffuse ECAC. performing autologous coastal cartilage grafts and
suturing the trachea to dura mater grafts.(10)
A tracheostomy tube may stent the collapsed Surgical placement of external tracheal stents has
airway and allows ventilatory support when been advocated for severe cases of malacia.(50) The
needed.(46) Tracheostomy, however, should not be results of these techniques are encouraging, but
considered a first line treatment in elective cases their application and efficacy remain to be
because it can be complicated by secondary determined before being widely recommended.
tracheomalacia and stenosis at the stoma site(47)
and may exacerbate airway collapse because it SUMMARY
bypasses the physiologic function of the glottis
(the glottis assures positive transmural pressure Excessive central airway collapse consists of two
which keeps the airway lumen patent). distinct entities, TBM and EDAC, which may be
seen separately, but also together. Morphologic
Tracheal resection with end-to-end anastomis has differences are noted by bronchoscopic and
been proposed for focal tracheomalacia. Outcomes radiologic imaging. Available evidence suggests
are good in 93% of patients, and mortality is about that these two entities have different etiologies and
2 % in experienced centers specialized in tracheal pathophysiology. A multidimensional
surgery.(48) classification system to objectively assess and
compare patients with ECAC may assist
researchers and clinicians in answering existing
Airway splinting via membranous tracheoplasty questions regarding patient selection for various
has been used to consolidate and reshape the therapeutic interventions.
airway wall. Outcomes are favorable in
uncontrolled studies.(49) This technique involves
restoring the proper anatomic configuration of the
airway so that cartilage rings are brought into a

96 Egyptian Journal of Bronchology

 Table 1. Risk factors and etiologies for the two forms of expiratory central airway collapse.
Potential risk factor Underlying disease or process Form
Pressure necrosis Tracheostomy and ETT with inflatable cuff TBM
Unrecognized tracheobronchial fracture Closed chest trauma TBM

Chronic irritation of the airways Smoking EDAC

Air pollution EDAC
Chronic tracheostomy or endotracheal tubes TBM
Impairment of blood supply Tracheostomy and ETT with inflatable cuff TBM
Post lung transplantation TBM
Inflammation Relapsing polychondritis TBM
Chronic, recurrent infections TBM
COPD and asthma EDAC
Destruction of the cartilage: Malignancy Lung cancer, thyroid cancer TBM
Iatrogenic Endobronchial electrosurgery TBM
Mechanical factors Post lung transplantation TBM
Post thyroid surgery TBM
Postpneumenectomy syndrome TBM
Long standing extrinsic compression Mediastinal goiter TBM
Tumors (carcinoma, teratoma, lymphoma, neuroblastoma) TBM
Vascular anomalies (innominate artery, aortic arch ring, pulmonary artery
sling, aberrant R subclavian ) TBM
Cysts (thymic cyst, bronchogenic cyst, lymphatic malformation) TBM
Cardiac (enlarged L atrium, enlarged pulmonary arteries or veins) TBM
Continuous cycling pressures on the Chronic ventilation through uncuffed tracheostomy tubes TBM
airway wall
Atrophy of the elastic fibers
Congenital Mounier Kuhn syndrome EDAC
Acquired COPD EDAC
TBM: tracheobronchomalacia; EDAC: excessive dynamic airway collapse; ETT: endotracheal tube; COPD: chronic obstructive pulmonary
disease.

Table 2. FEMOS classification for patients with expiratory central airway collapse.
Criteria Description
Functional class Normal 1; Mild 2; Moderate 3; Severe 4
Extent Normal 1; Focal 2; Multifocal 3; Diffuse 4
Morphology EDAC (Crescent)
TBM (Crescent; Saber-sheath; Circumferential)
Origin Idiopathic; Secondary
Severity Normal 1; Mild 2; Moderate 3; Severe 4

Functional class refers to the degree of functional impairment as assessed by World Health Organization: 1-no
limitation of usual physical activity; ordinary physical activity does not cause symptoms; 2-mild limitation of physical
activity; there is no discomfort at rest, but normal physical activity causes increased symptoms; 3-marked limitation of
physical activity; there is no discomfort at rest, but less than ordinary activity causes increased symptoms; 4-unable to

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perform any physical activity at rest; symptoms may be present at rest, and symptoms are increased by almost any
physical activity.
Extent defines the region of the tracheobronchial wall affected as documented by bronchoscopy/ computed
tomography: 1-Normal: there is no airway abnormality; 2-Focal: abnormality is present in one main or lobar bronchus
or one tracheal region (upper, mid- or lower); 3-Multifocal: abnormality is present in two contiguous or at least two
noncontiguous regions; 4-Diffuse: abnormality is present in more than two contiguous regions.

Morphology describes the shape of the airway lumen which is reduced during expiration and respiratory movements
as assessed by bronchoscopy/computed tomography: EDAC: reduction in the antero-posterior diameter caused by
excessive bulging of the posterior membrane in the absence of cartilaginous abnormalities resulting in a crescent shape
airway lumen configuration. TBM: reduction in the airway lumen due to weakness of the cartilaginous structures:
Saber-sheath: refers to reduction in the transversal (coronal) diameter; Crescent type: refers to reduction in the antero-
posterior (sagittal) diameter; Circumferential: refers to reduction in both transversal and anteroposterior diameters.

Origin describes the underlying mechanism responsible for the abnormality; idiopathic: no underlying etiology is
identified; secondary: may be due to known underlying processes.

Severity describes the degree of the airway collapse during expiration as documented by bronchoscopy/ computed
tomography: 1-Normal: Expiratory collapse of less than 50%; 2-Mild: Expiratory airway collapse of 50-75%; 3-
Moderate: Expiratory airway collapse of 75-100%; 4-Severe: Expiratory airway collapse of 100%; the airway walls
make contact.

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