2009

drtbalu

Dr. T. Balasubramanian

[CERVICAL TRACHEAL
STENOSIS AND ITS
MANAGEMENT]
T
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Cervical tracheal stenosis and

its management

By

Dr. T. Balasubramanian M.S. D.L.O.

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Definition: Subglottis is defined as the area extending from the lower surface of true vocal
cords to the lower surface of cricoid cartilage. In adults this area measures about 10mm inferior
to anterior commissure and 5mm inferior to posterior commissure.

Subglottic stenosis could be congenital / acquired.

Commonly occurs in adults. The incidence of subglottic stenosis was rare in the early parts of
20th century. After 1960 its incidence dramatically increased in the neo natal population due
to increased survival of low birth weight infants and increased use of intubation in air way
management of these infants.

Management of laryngotracheal stenosis is a really challenging problem faced by a Head &

Neck surgeon.

Now a days a multidisciplinary approach has been resorted to in managing these patients.

Differences between infantile & adult larynx:

1. At birth the infant's larynx is about 1/3 the size of adult larynx.
2. Proportionally speaking infantile larynx is larger than the adult in comparison with the
whole air way.
3. In infantile larynx the vocal process of arytenoid takes up about 1/2 the length of vocal
cord while in adult it forms only a quarter of the length of vocal cord.
4. The narrowest portion of the upper airway is the vocal cord level in adults and
subglottic region in an infant.
5. In an infant a subglottic diameter of 4mm is considered to be the lower limit of normal.
6. In an infant a circumferential oedema of 1mm reduces the cross sectional area in an
infant subglottis by 60%.
7. In an infant the larynx is placed at a higher level i.e. the superior border of infantile
larynx is located at the level of first cervical vertebrae and the cricoid at the level of 4th
cervical vertebra.
8. Infantile larynx is more pliable than adult larynx, more elastic making it more
susceptible to narrowing due to mucosal oedema.
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Embryology of laryngotracheal system:

Embryologically speaking the respiratory system should be considered as an outgrowth of

primitive pharynx. The development of lower respiratory system begins at 26 days after
conception as the laryngotracheal groove at the ventral aspect of foregut. This groove deepens
to form the laryngotracheal diverticulum and is separated from the oesophagus by tracheo
oesophageal folds which fuse to form the tracheo oesophageal septum. This septum divides the
foregut into a ventral laryngotracheal tube and a dorsal oesophagus. Failure of fusion of
tracheo oesophageal folds will lead to tracheo oesophageal fistula.

Larynx develops from the 4th & 5th branchial arches. The laryngotracheal opening lies
between these arches. This opening becomes T shaped due to growth of hypobranchial
eminence and arytenoids. These masses progressively grow between the 5th & 7th weeks
obliterating the laryngeal lumen. Recanalization of laryngeal introitus occurs during the 10th
week. Failure of the process of recanalization causes atresia / stenosis / web formation in the
larynx.
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The arytenoid masses are separated by interarytenoid notch which later gets obliterated.
Failure of this obliteration will cause posterior laryngeal cleft resulting in aspiration in new born
infants.

Congenital subglottic stenosis: is defined as a subglottic diameter of 4mm or less in a full term
neonate and less than 3.5 mm in a preterm neonate. Though rare congenital subglottic
stenosis accounts for 5% of all cases of subglottic stenosis. This is the third most common
congenital airway problem next only to tracheomalacia and vocal cord palsy. Subglottic
stenosis is considered congenital when there is no history of endotracheal intubation or other
forms of laryngeal trauma. It is often associated with other congenital malformations.

Causes of congenital subglottic stenosis:

Membranous stenosis: Could be caused due to

1. increased fibrous connective tissue

2. Hyperplastic submucosal glands

3. Granulation tissue

Cartilaginous stenosis: could be caused due to

1. Cricooid cartilage deformity which includes small cricoid, elliptical cricoid, Large anterior
lamina, large posterior lamina, generalized thickening involving the cricoid, and submucosal
cleft.

2. Trapped first trachea ring: The first tracheal ring in this condition gets trapped within the
cricoid cartilage leading on to subglottic narrowing of the airway.
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Acquired subglottic stenosis: 95% of all subglottic stenosis belong to the acquired variety. Most
common cause for acquired stenosis is endotracheal intubation.

Causes of acquired subglottic stenosis:

1. Intubation: Factors like period of intubation, size of the tube, vibrations caused by ventilator,
and infections during intubation are important

2. Laryngeal trauma due to surgery to airway like high tracheostomy, cricothyroidotomy, airway
surgery for laryngeal papillomatosis, and prior surgery for subglottic stenosis

3. Accidental: Could be inhalational (thermal/caustic)

Trauma: Blunt or penetrating

4. Autoimmune

5. Infection

6. GERD: Is known to cause exacerbation of laryngo tracheal stenosis, restenosis after repair, or
may be the sole cause of subglottic / tracheal stenosis in patients with no h/o intubation /
tracheal injury.

Postma's criteria for diagnosing GERD:

a. a decrease in the pH level to less than 4

b. a decrease in the pharyngeal pH level immediately following distal esophageal acid exposure

c. no decrease in the pH level during eating or swallowing

d. a rapid and sharp decrease in the proximal sensor pH level rather than a gradual one
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Laryngopharynx is more susceptible to inflammatory effects of acid / pepsin because the lining
mucosa lacks the protective mechanisms possessed by stomach and lower end of esophagus

7. Inflammatory diseases: sarcoidosis, SLE

8. Neoplasms

Idiopathic subglottic stenosis

Pathogenesis of subglottic stenosis: Is not clearly understood. The most commonly accepted
theory proposes that it results from wound healing in the areas of the airway that have
undergone compression by the endotracheal tube or by its cuff resulting in necrosis of mucosa
and underlying cartilage. Necrosis is caused by ischemia resulting from the pressure exerted by
the cuff cutting off the blood supply to the underlying mucosa. This causes a disruption to the
normal mucociliary clearance of secretions causing perichondritis of the underlying cartilage.
The underlying cartilage may weaken, undergo necrosis causing tracheomalacia. Healing of this
area can occur only by second intention.

Healing classically passes through three stages:

1. Inflammatory stage

2. Proliferative stage

3. Stage of contraction & remodelling

These stages may overlap.

Stage of inflammation: This stage is characterized by blood vessel contraction followed by

vasodilatation. These effects are mediated by prostaglandins. Platelets could be seen adhered
to exposed collagen. Platelets release proteolytic enzymes that activate the complement
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system. This activated complement system destroys the bacteria and facilitates wound
debridement. Polymorphs enter this area at the 6th hour phagocytizes the bacteria and wound
debris. They also release proteases that lyses devitalized tissue. The concentration of
polymorphs reaches the maximum within 48 hours and disappears within 72 hours. T cells and
B cells enter the area after polymorphs. T cells secrete regulatory lymphokines.

Helper T cells are necessary for wound healing while suppressor T cells down regulate wound
healing.

Macrophages enter the wound 3-4 days after injury. They can be present in the area for weeks
together. These are the only cells capable of functioning under low oxygen tension present in
these areas. Macrophages direct the proliferative and synthetic activity in the wound. This is
due to the secretion of interleukin 1 and tumor necrosis factor alpha both being secreted by
macrophages. Interleukin 1 directly stimulates fibroblastic activity and collagen synthesis.

Proliferative phase: Lasts for about 10 - 14 days. It starts with re-epithelization. This process of
resurfacing of the defect begins about 12 hours after injury. The epithelial cells around the
edges of the wound start to proliferate. The replication rate of these cells increases by 17 fold.
This stage is also associated with neovascularization. During neovascularization there is
migration of endothelial cells. This endothelial cell migration is stimulated by the release of
angiogenic factors from macrophages. Macrophages release angiogenic factors in response to
hypoxia and high levels of lactate in the wound area. Endothelial cell migration results in
capillary bud formation. Conditions like diabetes mellitus and irradiation can affect
neovascularization. Collagen deposition begins with migration of fibroblasts to the area of
injury. The migration of fibroblasts begins after 48-76 hours after injury. The collection of
fibroblasts, inflammatory cells and capillary buds is known as the granulation tissue.

Stage of contraction and remodelling: This is the final phase of wound healing. It begins
roughly after 1 week of injury. Wound contraction reduces the size of the wound by 50 - 60%.
Wound contraction is made possible by the presence of modified fibroblasts known as
myofibroblasts. These myofibroblasts provide the contractile force required for wound
contraction. These myofibroblasts histologically resemble smooth muscle cells and are present
throughout the wound. Collagen levels present in the wound reaches the maximum level by
the 3rd week of injury, but its strength is just about 5% of the unwounded area. This is known
as the neomatrix of the wound. This neomatrix is replaced by stronger interwoven type I
collagen during the first year of healing process. A fully remodelled scar tissue has about 80%
of normal tissue strength.
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Clinical features:

If tracheal stenosis is congenital it will present as acute respiratory distress in the new born
child.

Acquired tracheal stenosis in an infant is commonly seen when the new born has been
intubated for respiratory distress and the process of extubation has failed.

Infants with mild tracheal / subglottic stenosis may present with croup like symptoms with
history of poor feeding.

When tracheal / subglottis stenosis is suspected in an infant or child then history must be
sought for:

1. Prematurity

2. Intubation - extubation records - size of the endotracheal tube, duration of intubation,

number of intubations and trauma during intubation

3. Noisy breathing

4. Poor feeding

5. Growth chart should be reviewed for evidence of failure to thrive

Adults usually present with history of:

1. Shortness of breath

2. Stridor

3. History of intubation
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Classically stridor in a patient with subglottic / tracheal stenosis is biphasic. The patient should
be examined for respiratory distress, irritability, tachypnoea and cyanosis. Direct laryngoscopy
should be performed to look out for vocal cord anomalies, supraglottic and subglottic
anomalies. Flexible nasopharyngoscope examination would clinch the diagnosis in most
patients.

If stenosis involves supraglottic voice is muffled, severe inspiratory stridor, severe feeding
problems. There is no cough.

If stenosis involves glottis the voice becomes hoarse, sometimes the patient may become
aphonic. These patients have biphasic stridor. There are feeding abnormalities. Cough is
usually absent.

If stenosis involves subglottis patients may have normal voice, sometimes hoarseness may be
present. Stridor is usually biphasic. There is no feeding abnormality. Barking cough is
commonly present.

Direct laryngoscopy under general anesthesia should be performed in all these patients. Things
to document during this procedure include:

1. Size of the largest scope that can be passed through the stenotic segment

2. Location and length of the stenotic segment

3. Any other airway abnormalities like webs, clefts, mass lesions etc.

4. Fixation of cricoarytenoid joints

5. Changes due to reflux

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After the procedure oedema of the stenotic segment of the airway should be anticipated and
managed by steroid injections or tracheostomy.

Differential diagnosis: Can be grouped under four heads:

1. Congenital - Tracheomalacia, laryngomalacia, vocal cord palsy, laryngeal clefts, congenital

cysts, external compression of the airway due to mass lesion or vascular anomalies.

2. Infections / inflammation - Croup, Retropharyngeal abscess, GERD, tracheitis

3. Neoplasms- Subglottic hemangioma and recurrent respiratory papillomatosis

4. Traumatic - External compression, foreign body

Staging subglottic / tracheal stenosis: Two staging systems are in use. They are Myer - Cotton
staging system and McCaffrey system.

Myer-Cotton staging system: This system is useful to stage mature, firm, circumferential
stenosis confined to subglottis. It classifies stenosis based on the relative reduction of the cross
sectional subglottic area. This area can easily be determined by differing sized endotracheal
tubes that could be used for intubating these patients. This system uses 4 grades to classify
subglottic stenosis.

Grade I: Lesions causing less than 50% obstruction to the subglottic airway.

Grade II: Lesions causing subglottic obstruction between 51 - 70%

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Grade III: Lesions causing 71 - 99% obstruction

Grade IV: Complete stenosis

McCaffrey system: This system classifies laryngotracheal stenosis based on the subsites
involved and the length of the stenotic segment. This is also a 4 stage classification.

Stage I: Lesions are confined to the subglottis / trachea and are less than 1cm long

Stage II: Lesions belonging to this stage are isolated to subglottis and are greater than 1cm long

Stage III: Are subglottic / tracheal lesions without involvement of glottis

Stage IV: Stenosis with involvement of glottis

Lano's classification to predict patient prognosis: Lano et.al. In 1998 proposed this
classification. This classification is useful to predict prognosis in adult patients with air way
stenosis. This system of classification is based on the number of subsites involved in the
stenotic segment including glottis, subglottis and trachea.

Stage I: Lesions involving one subsite are classified under this group

Stage II: Lesions involving two subsites

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Stage III: Involves all three subsites (glottis, subglottis and trachea)

Radiological evaluation:

Imaging plays a vital role in identification and measurement of the stenosed segment.

Plain x-ray chest:

Plain chest radiographs are very useful in pediatric age group of patients. It helps to rule out
foreign bodies, narrowing of subglottis / trachea due to croup, subglottic cysts & hemangioma.
Both inspiratory and expiratory views should be taken. Main advantage of plain x-ray chest is
that it is cheap and freely available and the patient need not be sedated to perform it.

Barium swallow: Should always be performed to rule out tracheo oesophageal fistula. It helps
to identify congenital anomalies causing compression to oesophagus and tracheal like vascular
rings, oesophageal masses, and reflux oesophagitis.

Airway fluoroscopy: Is indicated when inspiratory and expiratory chest x-rays cannot be
performed. This is a dynamic imaging modality and is helpful in ruling out tracheomalacia.

CT scan: Helps in identifying the site and extent of stenotic segment in adults. It is of very
limited use in an infant. In infants it can only be used as an adjunct to bronchoscopy. Thin cuts
1.5mm should be performed for precise location of the stenotic segment and for assessing its
length.
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MRI scan: Is useful in identifying soft tissue masses. It is difficult to perform MRI in an infant /
child. Children need to be sedated before performing CT / MRI scans.

MRI Neck lateral view showing subglottic stenosis

MRI Neck AP view showing stenotic segment

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Management: Depends on the severity of stenosis. Patient's with Cotton's grade I and II
stenosis can be managed empirically by keeping them under close observation for evidence of
airway compromise. Periodical bronchoscopy should be performed to look for progressive
airway narrowing.

1. Securing the airway: This is of prime importance. Tracheostomy should be performed in all
patients with air way compromised due to subglottic / tracheal stenosis.

2. Gastro oesophageal reflux should be ruled out in all these patients prior to tracheal
reconstruction. This can be done by performing a 24 hours pH probe. Even if pH probe does
not demonstrate reflux it is always better to treat these patients for GERDS empirically.

3. In pediatric age group it is advisable to wait till the child is at least 10 kg weight before
proceeding to perform tracheal reconstruction.

Factors responsible for laryngotracheal stenosis:

1. Prolonged intubation
2. High tracheotomies
3. Excessive cartilage removal during tracheostomy
4. Infection following tracheostomy
5. Use of improper sized ET/tracheostomy tubes for air way maintenance
6. Laryngotracheal trauma
7. GERD
8. Wegner's granulomatosis

a. Endoscopic dilatation
b. Endoscopic scar removal
c. These two provide temporary relief.
d. Open surgical techniques:
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Anterior cricoid split

Laryngotracheal expansion surgery

Anterior laryngofissure with anterior lumen augmentation

Laryngofissure with division of posterior cricoid lamina

Laryngofissure with division of posterior cricoid lamina with anterior and posterior
grafts

Resection with anastomosis

Laryngotracheal reconstruction with stenting

Choice of procedure depends on:

1. Age of the patient

2. Site of stenosis

3. Nature of stenosis

4. Cause of stenosis

5. General condition of the pt

Incidence of laryngotracheal stenosis is maximal in the age group between 20-40yrs

Endoscopic dilatation: Mild stenosis Cotton's Grade I and II can be treated with endoscopic
dilatation / laser resection of the scar tissue. Endoscopic repair may fail in patients with:

1. Circumferential stenosis

2. Exposure and damage to cartilage tissue.

3. Scarring of posterior inlet of larynx

4. Arytenoid fixation

5. Vertical scar length of more than 1 cm

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Endoscopic dilatation is contraindicated in patients with Grade III and Grade IV stenosis

Anterior cricoid split: This procedure was originally used in an infant who had failed multiple
extubations. This procedure was performed in lieu of tracheostomy. Later on this procedure
was used to treat patients with congenital subglottic stenosis. Lesions responsive to this
procedure are mild subglottic narrowing with extensive fibrosis and a normal cricoid, subglottic
cysts.

Cotton's criteria for performing anterior cricoid split:

1. Extubation failure on two occasions

2. Patient should not be in assisted ventilation for 10 days prior to the procedure

3. No acute respiratory tract infection

4. No other airway pathology should be present other than subglottic stenosis

Procedure:

This procedure is performed via a midline neck incision. The cricoid cartilage and the first two
tracheal rings are incised anteriorly. The cartilages are laid open facilitating drainage of
odematous mucosa. The cricoid and the first two tracheal rings are laid open by prolene stay
sutures anchored to the soft tissues of the neck. The skin wound is closed after placing a drain.
The child is left intubated at least for a week following the procedure.

Laryngotracheal expansion surgery: This procedure involves division of scar tissue with
separation of the edges by interposition of graft material. This widens the airway and keeps it
patent. The scar tissue should not be completely stripped off, as it would cause a large surface
area of denuded mucosa leading on to restenosis. Silastic sheet rolls, laryngeal stents,
Montgomery T tubes, endotracheal tubes can be used to augment the airway. Use of
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autologous costal cartilage is ideal to provide structural support as this tissue does not undergo
complete resorption.

Anterior laryngofissure with anterior lumen augmentation: This procedure is very useful in
managing patients with anterior subglottic stenosis / anterior tracheal wall collapse. This
procedure should not be performed in patients in whom the glottis is involved, or when the
cricoid cartilage is deformed / weak. During this procedure the larynx and the first two rings of
trachea are opened up via an anterior incision. Care should be taken while incising the anterior
wall of cricoid cartilage not to injure the posterior wall of cricoid. The perichondrium should be
carefully elevated and should be oriented to the luminal side in order to allow epithelialization.
The perichondrium also serves as a barrier against infection. Grafts can be used to hold the
perichondrium in place and also to keep the incised walls apart. The graft material used for
anterior grafting should be thicker and larger with a flange to prevent it from prolapsing into
the airway.

Laryngofissure with division of posterior cricoid lamina:

Indications for this procedure include:

1. Posterior subglottic stenosis

2. Posterior glottic stenosis

3. Complete / circumferential stenosis

4. Significant damage to cricoid cartilage

In this procedure both anterior and posterior cricoid walls should be divided. Care must be
taken not to damage anterior commissure. The incision should extend superiorly to includes
inter arytenoid area and inferiorly it should include about 5 - 10mm in to the membranous
trachea. Grafting of posterior cricoid lamina should be done with great care as improper
grafting can lead to aspiration. The graft should be elliptical in shape and must not be too thick.
The width of the graft needed should be calculated according to the desired distraction of the
cut edges of the incised posterior cricoid cartilage. The graft should be anchored using
appropriately placed sutures extraluminally. If knot is present intraluminally, it could lead to
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granulation formation and restenosis may develop at a later date. These patients should be put
on long term stenting.

Laryngofissure with division of posterior cricoid lamina and interposition of anterior and
posterior grafts:

This procedure is ideal for patients with significant degree of posterior stenosis. Grafting is
absolutely necessary to maintain adequate degree of separation of airway walls. This
procedure can also be performed in two stages i.e. anterior and posterior stages. It is better to
perform the anterior stage to begin with and the posterior stage can be deferred for a period of
8 weeks.

Shiann Yann Lee's technique:

This method of laryngotracheal reconstruction involves creation of a tracheal trough by splitting

the anterior wall of trachea, lateralization of tracheal wall, followed by insertion of T tube in the
tracheal trough. This is covered by skin anteriorly.

Advantages:

More conservative

Higher success rate

Selection criteria:

1. Pts with subglottic / tracheal benign stenosis

2. Pts with good laryngeal function / normal vocal cord mobility

3. Good pulmonary reserve

4. Fit to undergo the procedure under general anesthesia

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Procedure:

General anesthesia is administered via tracheostomy tube.

A midline vertical incision is given extending between the superior border of stoma to the
cricoid cartilage. If subglottic stenosis is present the cricoid is divided. The stenotic segment is
exposed. Accurate measurement of stenotic area was taken. Fibrous tissue in the tracheal
lumen was released and lateralized with 3-0 vicryl by suturing it to the lateral soft tissues of the
neck. This is known as open lateropexy. Mitomycin C solution is prepared by diluting 2mg in
1ml of normal saline. Cotton patties soaked in this solution are applied to the stenotic segment
for 5 minutes. The T tube is cut to appropriate size; the sharp edges are rounded by filing them.
Tracheostomy tube is removed and the stent is introduced through the stenotic segment. The
upper portion of the tube should lie below the level of vocal cords while the lower portion of
the vertical limb should lie at least 1cm above the level of carina. If it comes into contact with
carina it would cause irritation and coughing. The horizontal tube is brought out through the
tracheostome. A 14 gauge Foley’s catheter can be negotiated through the proximal end of the
T tube and its balloon is inflated causing an air tight obstruction at the upper end so that
anesthesia can be maintained through the horizontal limb of the tube by connecting it to the
Boyles apparatus.

Skin is separated from the subcutaneous tissue and sutured over the T tube with 4-0 Ethilon.
Horizontal portion of the T tube is plugged after extubation to enable the patient to breathe
through the nose. Pt also regains the ability to speak on the table. The T tube stent can be
removed after 9 months.

Resection & anastomosis:

This method was popularized by Montgomery. He said that a tracheal gap of up to 3cms can be
closed primarily without resorting to any release technique in a majority of patients. The crucial
factor is that anastomosis should be performed without tension. Even if there is minimal
tension, it can cause restenosis. Tension of anatomotic site can be avoided by performing
tracheal release procedures.
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Figure showing skin flap being elevated in the neck

Image showing isthmus being sectioned

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Image showing stenosed segment of trachea being excised

Image showing dense fibrosis in the subglottic area

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Image showing body of hyoid being sectioned to lengthen the trachea (Laryngeal drop)
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Image showing tracheal anastomosis being performed

Image showing Montgomery T tube inserted to stent the anastomosed area

Image showing Montgomery T tube

Release procedures:

1. Release of distal trachea from the thorax (6 cms mobilization is possible)

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2. Annular ligament release

3. Suprahyoid release technique of Montgomery

4. Infrahyoid release technique of Dido

5. Intralaryngeal release technique

Release of thoracic trachea

This involves mediastinal dissection and is performed with the assistance of cardiothoracic
surgeon. It has all the inherent risks of mediastinal dissection. This procedure causes about 6
cms lengthening of trachea.

One more cm can be added by keeping the neck of the patient flexed for a period of 2 weeks.

Annular ligament release: This technique can increase the length of the trachea by 1.5 cms.

Annular ligaments should not be sectioned completely as it could disrupt the blood supply to
the tracheal rings from both superior and inferior thyroid arteries. Sectioning of annular
ligament should be performed in a staggered manner sectioning the ligament on either side of
the anastomosis.
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Figure showing staggered (Castellated) incision of trachea

Suprahyoid release technique of Montgomery: This method involves release of larynx /Hyoid
bone from its superior attachments. This can be easily be performed and well tolerated by the
patient. This release method will increase the length of trachea by 4 cms.

Infrahyoid release technique of Dedo: This procedure involves separation of thyroid cartilage
from that of hyoid bone. This method produces a similar increase in the length of larynx as that
of Suprahyoid release.

Intralaryngeal release technique:

The unique advantage of this technique is that it doesn’t in any way interfere with any of the
other laryngeal release techniques. In this procedure the larynx and trachea is skeletonized
through neck incision. Thyroid cartilage is exposed and is held between retractors. The
stenosed segment of the trachea is excised. Sternohyoid and thryohyoid muscles are elevated
with the perichondrium of the thyroid cartilage until the posterior margin of the ala of thyroid
cartilage is reached. A transverse cut over the perichondrium of the thyroid cartilage is
outlined above the level of vocal cords. A Stryker saw is used to cut the ala of thyroid cartilage.
The inner perichondrium is excised exposing the thick inner thyroid membrane. This
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membrane is a confluence of inner laryngeal mucosa and the inferior extent of thyroepiglottic
ligament. This highly elastic thyroid membrane stretches and drops the larynx. The interior of
larynx is undisturbed and the nerve supply of larynx is left intact. Post op neck flexion for a
period of 10 days would be of further help. This technique is not preferred in children because
of the danger to the laterally placed thyroid cartilage growth centre.

Figure showing larynx and trachea being skeletonized

Figure showing ala of thyroid cartilage being cut

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Prevention of subglottic / tracheal stenosis:

Prevention is always better than cure. Since prolonged intubation is the commonest acquired
cause of airway stenosis it is better to take the following precautions:

1. While intubating a patient appropriate size endotracheal tube should be chosen

2. High volume low pressure cuffed tube should be chosen

3. Multiple traumatic intubations should be avoided

4. GRDS in intubated patients should be treated aggressively

5. The duration of intubation should be monitored and tracheostomy should be resorted to in

patients with more than 2 weeks of intubation

6. Care must be taken to prevent laryngo tracheal infections

7. Blind intubations should be avoided at all costs.

8. After intubation proper care should be taken to secure the tube as movements of the tube
may traumatize the delicate airway. The ventilator used should have minimal vibrations as this
could easily be transmitted via the ET tube to the delicate mucosa of the airway

9. Care should be taken to avoid accidental extubation

10. All intubated patients with ryles tube should be treated for reflux prophylactically

11. Head end of intubated patients should always be kept elevated as this could minimize the
risk of reflux
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