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67
Clinical Brief
Ventilatory Management of Severe Tracheal Stenosis
Rakesh Lodha, Lokesh Guglani, S.C. Sharma
1
and S.K. Kabra
Departments of Pediatrics and
1
Otorhinolaryngology, AIIMS, New Delhi
ABSTRACT. We present here a 4 year old child with severe tracheal stenosis and respiratory failure. The patient was not
responding to conventional ventilation settings and had significant hypercarbia. The difficulty in mechanical ventilation was
handled successfully with specific ventilatory strategy: use of low respiratory rate, long inspiratory time and normal inspiratory
time : expiratory time ratio. Thereafter the child was managed surgically and the stenosis was corrected. The child was
discharged after a Montgomery T-tube placement. [Indian J Pediatr 2006; 73 (5) : 441-444]
E-mail: rakesh_lodha@hotmail.com
Key words : Tracheal stenosis; Hypercarbia; Montgomery T-tube placement
Laryngotracheal stenosis is a congenital or acquired
narrowing of the airway that may affect the glottis,
subglottis or trachea. It causes severe symptoms and
should be suspected in children less than 1 year of age
with either multiple episodes of croup or croup which
fails to respond to medical management or requires
endotracheal intubation.
1
The term subglottic stenosis was
previously used as the subglottic region is the most
common site of airway stenosis, mostly secondary to
prolonged endotracheal intubation. The onset may be
acute or it may develop over a period of time and a
thorough assessment, radiologic and endoscopic
evaluation may be necessary to guide further therapy and
management. We present a case of acquired tracheal
stenosis that required prolonged ventilatory support with
adaptations for the obstructive pathology and discuss the
implications for ventilation of a child with upper airway
obstruction.
CASE REPORT
A 4-year-old boy presented with history of intermittent
high grade fever and cough without expectoration of 3
months’ duration. After 5 days of onset of fever, he
developed noisy breathing and progressively increasing
respiratory distress. There was no history of cyanosis,
wheezing episodes or any history of foreign body
aspiration. There was no history of contact with
tuberculosis and no past history of any significant illness.
The respiratory distress and the intensity of noisy
breathing increased gradually over 3 months and were
Correspondence and Reprint requests : Dr. Rakesh Lodha,
Department of Pediatrics, AIIMS, New Delhi-110029.
Indian Journal of Pediatrics, Volume 73—May, 2006
now also persisting during sleep. There was no history
suggestive of diphtheria and the child was immunized for
age.
On presentation, the child had marked respiratory
distress, was sitting up bending forward and had marked
suprasternal recessions and severe biphasic stridor. He
had a respiratory rate of 48/minute, and had good
volume pulses with no cyanosis and SpO
2
of 99% on
facemask oxygen. Chest examination showed
hyperinflation of the chest wall with symmetrical
movements of both sides of the chest wall, centrally
placed trachea on palpation and equally resonant
percussion note on both sides. Chest auscultation revealed
equal air entry on both sides and conducted breath
sounds. Examination of cardiovascular and other body
systems was unremarkable. Initial arterial blood gas
analysis showed a pCO
2
of 48.6 mm Hg and PaO
2
of 198.4
mm Hg with pH of 7.391.
At presentation the possibility of severe upper airway
obstruction was kept and radiographs of soft tissue of
neck (lateral view) did not show any evidence of
epiglottitis or narrowing of the cervical portion of the
trachea. Chest X ray showed bilateral hyperinflated lung
fields with no lung parenchymal abnormalities and
normal cardiothoracic ratio (48%). However, over the next
few hours child showed progressive deterioration with
rising pCO
2
values up to 80 mm Hg and had to be
intubated for respiratory support and was therefore
transferred to the Pediatric Intensive Care Unit (PICU) for
further management.
On arrival to the PICU he was ventilated with Siemens
Servo 300 ventilator on SIMV (volume controlled) mode
with initial conventional settings but did not show
adequate chest rise and had progressive CO
2
accumulation (values up to 150 mm Hg) on blood gas
analysis. The initial settings were: rate 30/min, tidal
volume 80 ml, Ti 0.7 seconds, I:E ratio of 1:2 and positive
441
68
Rakesh Lodha
et al
end expiratory pressure of 4 cm H
2
O. On increasing the
tidal volume alone, there was no further improvement in
PaCO
2
levels assessed after 1 hour. The peak pressure
requirement was 38 cm H
2
O. On bagging with self-
inflating bag, high resistance was felt and adequate chest
rise could be achieved only if long inspiratory time was
used. Subsequently the settings were modified in keeping
with the requirements so that the ventilator now had low
rates (10/min) and a prolonged inspiratory time (Ti) of
1.8 seconds, an I:E ratio of 1:2 and PEEP of 5 cm H
2
O.
With these settings, he maintained oxygenation and
showed improvement in PaCO
2
levels. The peak pressure
requirement also fell to 23 cm H
2
O. The rationale for these
settings is discussed below.
Subsequently, a fibreoptic bronchoscopy was done
through the endotracheal tube in the PICU after initial
stabilization and it showed severe narrowing at the distal
end of the trachea just above the carina. A diagnosis of
supracarinal tracheal stenosis was established and the
child underwent endoscopic balloon dilatation of trachea
under general anaesthesia the next morning.
TABLE 1. Case-series of Tracheal Stenosis
Intraoperatively, the stenotic area showed some
granulation tissue with inflamed mucosa and loss of
tracheal rings, and from this a biopsy specimen was
obtained and dilatation was done with Fogarty’s
Catheter. An endotracheal tube of 4.5 Fr size was inserted
under bronchoscopic guidance with tip extending beyond
the stenotic segment and lying above the carina. He was
subsequently continued on ventilatory support for the
next 10 days with gradual weaning. A diagnosis of
tubercular tracheal stenosis was considered and
antitubercular therapy was started but subsequent work
up did not reveal any evidence of tubercular infection.
However, there was satisfactory clinical response as the
fever subsided and tracheal granulations on repeat
examination were absent. The biopsy form the lesion
showed mild non-specific inflammatory changes with no
granulomas.
A repeat fibreoptic bronchoscopy done 8 days after the
dilatation procedure in the PICU showed no significant
stenosis but persistence of inflamed mucosa. He was then
weaned off ventilatory support but endotracheal tube was
Series No. Etiology Techniques used Outcome
(1) Kumar P et al
7
n = 17 External vascular compression=9,
Post transplant strictures=4
Malignant masses=2
Postintubation =2
Airway Stenting with self-
expanding metal stents in 10
cases, silicone stents in 7.
47% alive on follow up, 6/8
ventilator dependent
extubated
(2) Anton-Pacheco JL et al
8
n = 13 All cases Congenital;
Mild – 4
Moderate – 6,
Severe – 3
Costal cartilage tracheoplasty
(CCT)=5,
Tracheal resection = 3,
Slide tracheoplasty=2,
Endoscopic dilation=3
Laser Resection=1
Overall mortality 23%, 3
early deaths-all after CCT
(3) Dunham ME et al
9
N= 23 Congenital complete tracheal
rings producing long segment
stenosis of trachea
Pericardial Patch Tracheoplasty 83% survival at mean follow
up of 4.5 years
(4) Har-El G et al
10
N= 19 Post-intubation or tracheotomy
in 80%
Circumferential tracheal
resection with end-to-end
anastomosis
Anastomosis success rate of
94.7%
(5) Loeff DS et al
11
N= 22 Vascular rings/slings in 50% Localized-dilatation,
tracheostomy, and resection
with end-to-end anastomosis,
Funnel shaped defects-
tracheal reconstruction with
grafts
Overall mortality rate 77%
(6) Weber TR et al
12
N= 62 Acquired Tracheal Stenosis
(4 weeks to 14 years age)
Endotracheal intubation-44
Caustic aspiration-6
Recurrent infection-5
Bronchoscopic perf-4
Gastric aspiration-3
Site of airway stenosis
Subglottic/upper – 47
Midportion-8
Distal/Carinal-7
Individualized treatment:
Balloon dilatation-20,
Bronchoscopic electrocoagu-
lation resection- 44, Steroid
injection-48, T tube stent-8,
Resection anastomosis-12,
Cricoid split-3, and
Rib cartilage graft-12.
7(11%) died of unrelated
causes. 44 of 55 patients
(80%) are without
tracheostomy.
442 Indian Journal of Pediatrics, Volume 73—May, 2006
69
Ventilatory Management of Severe Tracheal Stenosis
left in situ as it was bypassing the stenosed segment. He
had recurrence of respiratory distress, which required
resumption of ventilatory support and he then underwent
repeat dilatation after 20 days of admission, which
showed collapse and re-stenosis of trachea, which could
be easily dilated. Tracheostomy and Montgomery T tube
insertion was done for maintaining long-term patency of
the airway. He was discharged from the hospital 2
months after admission and is on regular follow up
DISCUSSION
The importance of appropriate ventilatory management
of severe proximal airway obstruction is highlighted by
this case and it is important to understand the rationale
for the ventilatory settings described above. The trachea
and the upper airway although considered to be relatively
rigid conducting airways, do show some changes in
caliber during the normal respiratory cycle. There is
expansion of the intrathoracic airways along with the
expanding lungs while the extrathoracic airway
diminishes in caliber due to their intraluminal pressure
being lower than atmospheric pressure. The reverse of
this process occurs during expiration. If intrathoracic
trachea is soft (tracheomalacia), the narrowing will
accentuate during expiration due to positive intrathoracic
pressure. The flow in these large airways is usually
turbulent due to the high flow rates and this turbulence
increases in the presence of an obstruction in the airway.
This turbulence further increases the airway resistance.
The mechanics of critical tracheal stenosis is such that
it would severely compromise delivery of gases beyond
the obstruction and it would not allow adequate
emptying out of the lungs as well. Other obstructive
upper airway anomalies like subglottic stenosis could be
overcome by use of tracheostomy, which would bypass
the site of stenosis, but in more distal lesions of the trachea
(as in this case, just above the carina) ventilatory
management is more challenging.
With conventional ventilator settings in the patient
with severe tracheal stenosis, there would be inadequate
delivery of gases beyond the site of obstruction and there
would be a build up of pressure proximal to it. In this
scenario, there would be progressive CO
2
retention and
inadequate lung expansion. Also because of inadequate
emptying of the lungs during expiration due to limited
airflow across the site of stenosis, there would be a
progressive air-trapping and subsequent decrease in
cardiac output. Increasing the airway pressures or
frequency alone will not help overcome these effects of
the obstruction. Increase in the airway pressure may
increase the risk of barotraumas. In order to ensure
adequate delivery of gases beyond the obstruction, it is
necessary to prolong the inspiratory time (Ti) so that
adequate lung expansion can be achieved. In view of the
markedly increased resistance the time constant will also
be increased justifying the need for high Ti. For this, the
frequency of breaths would have to be kept at low values
in order to allow adequate time for expiration also and at
the same time avoid progressive gas trapping (auto-
PEEP). It is unlikely that use of CPAP alone would have
lead to adequate delivery of volumes across such severe
tracheal stenosis.
There have been reports of use of percutaneous
transtracheal jet ventilation for cases with tracheal stenosis
and other forms of airway obstruction in the more
proximal airways.
2
For patients undergoing surgical
repair of the tracheal lesions, extracorporeal membrane
oxygenation has also been used.
3
In animal models of
tracheal stenosis, a comparison of conventional
ventilation versus transtracheal jet ventilation showed
that although there were no significant differences in
PaCO
2
but mean peak airway pressure values, both at the
distal portion of stenosis and at the proximal portion,
decreased more significantly during jet ventilation than
during conventional mechanical ventilation.
4
Overall the
mean arterial pressure, mean pulmonary arterial pressure,
central venous pressure, and cardiac output did not
change significantly between conventional mechanical
ventilation and jet ventilation with the stenosis.
Pulmonary Artery Occlusion Pressure (PAOP) increased
significantly more during conventional mechanical
ventilation than during jet ventilation in animal models
with stenosis.
During ventilation, the use of flow-volume loops
would demonstrate plateaus in both inspiratory and
expiratory limbs due to the limitation in both phases
caused by the obstruction. Miller and Hyatt
5
showed that
in patients with fixed airway obstruction, the FEV1
diminishes progressively as the resistance increases but
the FVC may remain unchanged, suggesting that the flow
rates will be reduced and the ratio of maximal expiratory
and inspiratory flow at 50% of vital capacity (MEF
50
/
MIF
50
) may approach unity (0.9 to 1).
Another contentious issue was the underlying cause of
tracheal stenosis in this child since the duration of
symptoms was 3 months and he had no respiratory
symptoms prior to this illness. Initial impression of
granulation tissue being visible on bronchoscopy directed
towards a diagnosis of tuberculosis but the work up was
negative and the biopsy from the lesion was inconclusive.
However, the tracheal inflammation could be due to a
tubercular lymph node in the mediastinum. Despite no
objective evidence of tuberculosis, response to
antitubercular therapy supports the diagnosis of
tuberculosis. A possibility of acquired tracheal stenosis
secondary to an initial episode of bacterial tracheitis was
considered.
The most common cause of acquired laryngotracheal
stenosis is prolonged endotracheal intubation, accounting
for 90% cases. Other acquired causes include
postinfectious scarring, autoimmune disorders
(Wegener’s granulomatosis, sarcoidosis), inhalation
Indian Journal of Pediatrics, Volume 73—May, 2006 443
70
Rakesh Lodha
et al
injuries, blunt trauma to the neck, previous tracheostomy
or cricothyrotomy, and gastroesophageal reflux.
6
Prior to
the advent of antibiotics, scarring from infections like
diphtheria and syphilis were usually a common cause of
stenosis. In the trachea, the narrowing may be extrinsic or
intrinsic, and diffuse or localized. Among the extrinsic
lesions, disorders of the thyroid gland and great vessels
are the most common while the intrinsic ones may be due
to infectious, granulomatous, neoplastic, traumatic,
immunologic and post-inflammatory conditions.
There are several case series of laryngotracheal stenosis
in children, with majority of reports being that of surgical
repair techniques (Table 1). The ventilatory management
of these patients has not been highlighted but it does pose
problems in the perioperative and post-operative period.
There have been reports where unstable children with
critical stenoses requiring high airway pressures for
ventilation and still having CO
2
retention, have required
initiation of extracorporeal support, which was followed
by diagnostic endoscopy and then finally definitive
surgical repair.
3
But these facilities may not exist at all
institutions and initial optimal ventilatory support in such
sick children may be crucial before they can be shifted to
centers where surgical repair can be done. Therefore, it is
only with a understanding of the mechanics of tracheal
stenosis and its optimal ventilatory management that we
can ensure adequate treatment and outcome for these
patients by surgical or non-surgical (e.g. balloon
dilatation) means.
In conclusion, this case demonstrates the importance of
appropriate ventilatory management of airway
obstruction caused by tracheal stenosis and highlights the
fact that critical stenosis of trachea may be ventilated with
low rates and high inspiratory times. Management of
tracheal stenosis in children is complex and requires the
teamwork of specialists involved in emergency
management, intensive care and otorhinolaryngology.
REFERENCES
1. Lesperance MM, Zalzal GH. Assessment and management of
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2. Spoerel WE, Narayanan PS, Singh NP. Transtracheal
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3. Walker LK, Wetzel RC, Haller JA. Extracorporeal membrane
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4. Shinozaki M, Sueyoshi A, Morinaga T, Tsuda H, Muteki T.
Effect of conventional mechanical ventilation and jet
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5. Miller RD, Hyatt RE. Obstructing lesions of the larynx and
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Indian Journal of Pediatrics, Volume 73—May, 2006 444
