Airway Anomalies

a, b
April M. Landry, MD *, Michael J. Rutter, MD

KEYWORDS
 Airway anomalies  Laryngeal cleft  Complete tracheal rings
 Congenital subglottic stenosis  Laryngeal atresia  Glottic web

KEY POINTS
 Airway anomalies are potential life-threatening and life-altering abnormalities that require
a high degree of suspicion in diagnosis.
 Anomalies of the airway are frequently found in association with other system abnormal-
ities, as well as several common syndromes.
 There is a wide range of management and surgical options based on the severity and type
of airway abnormality.
 Close communication of postoperative care and potential complications are required
following surgical treatment of these diseases.

INTRODUCTION

Congenital airway anomalies are rare but potentially life-threatening conditions. The
focus of this article is on anomalies of the larynx, subglottis, and trachea. These anom-
alies often present with noisy breathing, cyanosis, apneas, retractions, feeding diffi-
culties, and recurrent aspiration. Failure to recognize and diagnose the cause of the
symptoms could lead to failure to thrive, recurrent or persistent respiratory distress,
chronic aspiration with resultant lung damage, and possible death.
Embryology
A review of the embryology of the aerodigestive tract helps us to understand the for-
mation of these abnormalities. The respiratory diverticulum develops from the primi-
tive foregut. The tracheoesophageal folds invaginate to form the tracheoesophageal
septum. This septum divides the foregut from the respiratory diverticulum and fusion
occurs in the caudal to cranial direction.1 Incomplete formation of the tracheoesopha-
geal septum leads to laryngotracheal clefts.2 When the embryo is in development, an
epithelial structure called the epithelial lamina obliterates the lumen of the primitive lar-
ynx. The laryngeal lumen begins recanalization after obliteration from caudal to cranial

Disclosure Statement: A.M. Landry: No disclosures. M. Rutter: Consultant and patent holder
Aeris Balloon Dilator, Bryan Medical Rutter Suprastomal Stent, Boston Medical Products.
a
Department of Otolaryngology Head and Neck Surgery, Emory University, 1600 Tullie Road
NE, Atlanta, GA 30329, USA; b Department of Otolaryngology Head and Neck Surgery, Uni-
versity of Cincinnati, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
* Corresponding author. 590 Lakeshore Drive Northeast, Atlanta, GA 30307.
E-mail address: april.marie.landry@emory.edu

Clin Perinatol - (2018) -–-

https://doi.org/10.1016/j.clp.2018.07.002 perinatology.theclinics.com
0095-5108/18/ª 2018 Elsevier Inc. All rights reserved.
2 Landry & Rutter

during the eighth week of gestation.3 Failure of the larynx to undergo recanalization
results in a spectrum of glottic web and laryngeal atresia.

Congenital Subglottic Stenosis

Subglottic stenosis (SGS) is a narrowing of the region extending from the infraglottic
cavity to the inferior margin of the cricoid without history of intubation. Stenosis of
the subglottis is defined as a diameter of 4 mm or less in full-term infants (normal diam-
eter 4.5–5.5 mm) and 3 mm or less in premature infants (normal diameter is 3.5 mm).4
SGS is separated into congenital or acquired in nature.
Congenital SGS is diagnosed when the stenosis is noted without a history of endotra-
cheal intubation. If the infant has been intubated, one cannot determine if the manipula-
tion of the airway has caused or contributed to the stenosis and it is then determined to
be acquired. The true incidence of congenital stenosis is difficult to determine because
many of these infants are intubated at birth. The suspected incidence of congenital SGS
is 5% of all cases of SGS.4,5 Patients with congenital SGS are at risk of developing an
acquired stenosis, even when an age-appropriate endotracheal tube is used.
Congenital SGS can be due to abnormal cartilage shape or membranous thick-
ening. The cricoid cartilage is nearly equal in diameter in the anterior-posterior and
transverse dimensions. An elliptical cricoid in which the anterior-posterior diameter
is greater than the transverse diameter may be found in congenital SGS. The stenosis
can also be membranous where there is a circumferential, soft narrowing arising from
thickening of the submucosa due to a fibrous tissue and mucous gland hyperplasia.6,7

Anterior Glottic Webs and Laryngeal Atresia

Anterior glottic webs and laryngeal atresia are a result of failure of the laryngeal lumen
to recannulate after epithelial obliteration. These abnormities are a spectrum of dis-
ease determined by the amount of recanalization that occurred before the embryo-
logic process was interrupted. The spectrum of anterior webs range from thin webs
with little glottic involvement (Fig. 1) to thick webs with near complete glottic fusion
and subglottic extension (Fig. 2).8 If the recanalization process is interrupted early in

Fig. 1. Thin anterior glottic web.

 Airway Anomalies 3

Fig. 2. Thick glottic web with subglottic extension.

its course, laryngeal atresia may occur in which there is complete obliteration of the
lumen and the glottis is a fused, firm membrane and is often associated with a distal
tracheoesophageal fistula. Webs are partial laryngeal atresia.
Laryngeal atresia is 1 cause of congenital high airway obstruction syndrome
(CHAOS), in which lung fluid is unable to be eliminated owing to complete obstruction
of the upper airway. The tracheobronchial tree and lungs fill with lung fluid and these
structures subsequently dilate. CHAOS due to laryngeal atresia can be recognized
prenatally owing to advances in antenatal imaging, including fetal MRI.9 If recognized
prenatally, the infant may be delivered via a planned ex utero intrapartum treatment
procedure in which a tracheostomy is placed while the infant receives oxygenation
via the placental circulation. If not recognized prenatally, complete laryngeal atresia
will present at birth with aphonia, cyanosis, and death if a tracheostomy is not per-
formed emergently.10
An association between anterior glottic webs and chromosome 22q11.2 deletion
syndrome has been described by several groups.11–14 As many as 65% of patients
with anterior glottic webs have an associated 22q11.2 deletion syndrome.11 It is rec-
ommended that all patients with anterior glottic webs should be tested by fluorescent
in situ hybridization analysis, especially those with cardiac abnormalities.

Laryngeal Cleft
Laryngeal clefts are thought to be a result of the failure of the midline formation of tra-
cheoesophageal septum. The septum forms in a caudal to cranial direction, thus the
depth of the cleft is determined by the timing of the interruption in the formation of the
septum. The Benjamin and Inglis system is the most commonly used classification
system of laryngeal clefts.15 The type I cleft extends to the level of the vocal cords.
Type II clefts extend past the vocal cords and into the posterior cricoid cartilage
(Fig. 3). Type III and IV clefts extend through the posterior cricoid cartilage, with the
former extending into the cervical trachea and the latter into the thoracic trachea
(Fig. 4). Management depends on the severity of the cleft. Type I clefts may be able
to be managed medically with feeding therapy and thickening of feeds. Type II, III,
and IV clefts typically require surgical treatment.
4 Landry & Rutter

Fig. 3. Type 2 laryngeal cleft with extension into but not through the cricoid cartilage.

Laryngeal clefts are associated with other congenital abnormities in 58% to 68% of
cases.16,17 Most commonly, these anomalies occur in the digestive tract and include
esophageal atresia with tracheoesophageal fistula or tracheoesophageal fistula alone.
Cardiac, urogenital, and craniofacial anomalies are also commonly found in associa-
tion with laryngeal clefts.18 Laryngeal cleft have also been associated with other
syndromes (Table 1).1,18

Congenital Tracheal Stenosis

Congenital tracheal stenosis is most commonly a result of complete tracheal rings
in which a complete ring of tracheal cartilage forms instead of a C-shaped

Fig. 4. Type III laryngeal cleft with extension through the cricoid and into cervical trachea.
 Airway Anomalies 5

Table 1
Syndrome associated with laryngeal clefts

CHARGE Coloboma, heart disease, choanal atresia, growth and mental retardation,
genital anomalies, ear anomalies
VACTERL or Vertebral anomalies, anal atresia, cardiac defects, tracheoesophageal fistula
VATER and/or esophageal atresia, renal or radial anomalies, and limb defects
Pallister Hall Hypothalamic hamartoblastoma, hypopituitarism, polydactyly and
syndactyly, cardiac, renal, and pulmonary abnormities
Opitz-Frias or Hypertelorism, hypospadias, cleft lip and palate, and other midline
G syndrome malformations

cartilage with a posterior membranous trachea (Fig. 5). The cause of this abnor-
mality is not known but may be due to an unequal or abnormal partitioning of the
foregut. Complete tracheal rings may form at any point along the tracheobronchial
tree in short or long segments. Long-segment disease is typically considered to
be greater than 50% of the trachea.19,20 Narrowed segments can be as small
as 1 mm and involve the length of the trachea, whereas other patients may
have a short segment of mild narrowing. This is a rare disease that is estimated
to affect 1 in 64,500 live births.21 Approximately two-thirds those with complete
tracheal rings will have an associated cardiac abnormality.19,21 Pulmonary artery
slings or an aberrant left pulmonary artery are the most common cardiac anomaly
noted in 50% of patients with complete rings.22 Complete rings are associated
with bronchial branching abnormities, including an anomalous right upper lobe
(bronchus suis), bronchial trifurcation, or a single lung.23 If complete tracheal rings
are suspected or found, echocardiograph should be performed due to the high
possibility of cardiac abnormalities. Computed tomography with angiogram of
the chest and reconstructions are useful to assess vascular anatomy and surgical
planning. Conservative management is appropriate for patients with short-
segment stenosis and the most stenotic segment is not less than 60% of normal
tracheal diameter.24

Fig. 5. Complete tracheal rings.

6 Landry & Rutter

EVALUATION FOR SURGICAL REPAIR, INDICATIONS, AND CONTRAINDICATIONS

An evaluation of the airway is indicated in an infant with noisy breathing. Stertor is a

snoring type of noise from obstruction of the nasopharynx and oropharynx. Stridor
is a high-pitched noise made from the larynx or trachea. Stridor can be inspiratory,
expiration, or biphasic. The phase of stridor helps determine if the concerning area
is supraglottic (inspiratory), glottic or subglottic (biphasic), or tracheal (expiratory).
Other concerning symptoms include retractions, cyanosis, acute life-threatening
events, coughing and choking with feedings, and recurrent pneumonias.
Physical examination should include an awake flexible laryngoscopy. The physician
should pass the scope into bilateral nasal cavities to ensure there are no lesions of the
nasal cavities or nasopharynx. The scope is passed into the oropharynx where the
base of tongue and pharyngeal walls are examined for masses or cysts. The supra-
glottis and glottis are then examined. An awake examination allows for visualization
of vocal cord movement.
Infants who are in respiratory distress or critically ill can potentially decompensate
during an awake flexible examination. In these patients, the flexible examination
should be done in a controlled setting with pulse oximetry, oxygen, and instrumenta-
tion for possible intubation and resuscitation. Instrumentation of the airway with a rigid
scope should be deferred in the setting of an active or recent respiratory infection if at
all possible (Table 2).

SURGICAL TECHNIQUE OR PROCEDURE

To fully evaluate the larynx and trachea, a direct laryngoscopy and bronchoscopy is
required. If a subglottic or tracheal anomaly is suspected, this operative procedure
is indicated. Direct laryngoscopy and bronchoscopy is also used to confirm abnormal-
ities noted on a flexible examination, such as a glottic web. The following is a descrip-
tion of direct laryngoscopy and bronchoscopy, followed in turn by specific surgical
procedures based on diagnosis.

PROCEDURE: DIRECT LARYNGOSCOPY AND BRONCHOSCOPY

Preoperative planning
 Communicate suspicions of airway abnormality with anesthesiology, nursing
team, and surgical technician

Table 2
Signs or symptoms of airway anomalies

Congenital SGS Stridor, airway distress, unable to accommodate appropriately sized

endotracheal tube
Recurrent croup-like symptoms may be seen in older infants
Anterior glottic Small webs: high-pitched cry or harsh voice with or without airway
web compromise; possibly no symptoms
Thick webs associated with SGS: abnormal cry, airway distress, stridor
Laryngeal atresia Aphonia, cyanosis and death if endotracheal tube not placed at birth
Laryngeal cleft Shorter clefts: likely to present later with chronic aspiration
Longer clefts: florid aspiration, stridor, cyanosis, respiratory distress,
gastric distension with positive pressure
Tracheal stenosis Depending on severity of stenosis, may present with only stridor, or with
near-death episodes or inability to ventilate, requiring extracorporeal
membrane oxygenation
 Airway Anomalies 7

 Review steps of the procedure with the anesthesia staff to aid in sharing of the
airway
 Ensure the appropriately sized rigid ventilating bronchoscope, Hopkins rod, and
light sources are available
Prep and patient positioning
 Equipment and all staff should be ready on induction of the patient if the patient
cannot be mask ventilated
 Spontaneous breathing is preferred
 Turn the table 90 with the anesthesia team on the left side and surgical techni-
cian on the right side
Surgical procedure
 A preferred laryngoscope blade is placed on the right side of the oral cavity and
the tongue is swept to the left
 Topical lidocaine is applied to the vocal cords
 A rigid 0 Hopkins rod is brought into the field and used to examine the supraglot-
tis and glottis, then passed into the subglottis and trachea to the right and left
mainstem bronchi
 As the scope is withdrawn, the posterior tracheal wall should be evaluated for
normal trachealis musculature
 The posterior larynx is evaluated for a cleft by distracting the interarytenoid area
with a microlaryngeal instrument
 Stenosis is graded by passing an endotracheal tube of known size through the
narrowest point and evaluating for a leak at a pressure less than 20 cm of water.
Comparison is then made with the expected normal size for age. The Myer-
Cotton grade system is accepted is the most common means of determining
the degree of stenosis (Box 1).25
After direct laryngoscopy and bronchoscopy has resulted in a definitive diagnosis,
further management and surgical treatment varies widely depending on diagnosis and
severity of disease.

LARYNGOTRACHEAL RECONSTRUCTION WITH CARTILAGE GRAFTING

High-grade congenital SGS may require a laryngotracheal reconstruction (LTR). A wide

variety of cartilage grafts have been described, including costal, thyroid, auricular, hyoid,
and hyoid. In infants, the upper portion of the thyroid cartilage (ala) is most commonly
used. The cricoid and upper tracheal rings are divided in the midline to open the airway.
The posterior cricoid may also be divided to increase the diameter. The thyroid alar graft is
then placed between the anterior cricoid rings to distract and enlarge the subglottic
airway. However, the workhorse is the costal cartilage graft LTR, whether anterior, pos-
terior, or anterior and posterior grafts. Posterior cartilage grafts may also be used to
manage posterior glottic stenosis and vocal cord mobility problems.

Box 1
Myer-Cotton grading system

Grade 1: less than 50% obstruction

Grade II: 51%–70% obstruction
Grade III: 71%–99% obstruction
Grade IV: total obstruction
8 Landry & Rutter

ANTERIOR GLOTTIC WEBS

A wide variety of endoscopic and external treatments have been proposed. The goal
of surgery is to relieve airway obstruction and preserve voice quality for the future. The
difficulty in treating anterior webs is that dividing the web leads to raw edges that will
readhere to each other.
Endoscopic procedures can include excision of the web in a single or staged pro-
cedure. A folded piece of silastic material may be placed into the anterior commissure
to prevent reformation of the web. Other surgeons may leave the patient intubated to
allow for remucosalization of the edges.
In thicker webs with subglottic extension, a tracheostomy may be performed to
allow for laryngeal growth before definitive management with reconstruction via
an open approach. A laryngofissure (midline division of the thyroid cartilage) is
performed and the web is divided. The web edges are then sutured laterally to
eliminate the raw edges. The subglottic component of the disease can be
addressed with cartilage grafts as needed. A keel or stent may again be used
to aid in prevention of restenosis at the anterior commissure.3,10,26,27

LARYNGEAL CLEFT REPAIR

Type I and II clefts are managed endoscopically in most cases. The patient is
placed in suspension laryngoscopy and the cleft edges are demucosalized by a
cold or laser technique. Sutures are placed for a single or 2-layer closure.
Type III and IV clefts are mostly commonly managed via an open approach. Both
anterior and lateral approaches to the cervical or thoracic trachea and esophagus are
used. To fully visualize the repair site, some surgical teams will perform the surgery
with extracorporeal membrane oxygenation or cardiopulmonary bypass. The surgery
aims to recreate separate tracheal and esophageal lumens. Two suture lines are
required, thus there is a greater chance of anastomotic leak. Various interposition grafts
are used, including periosteal and muscle flaps, to reinforce the suture lines.1,17,28–30

SLIDE TRACHEOPLASTY

A slide tracheoplasty has become a preferred method of treating long-segment

tracheal stenosis. In this procedure, the trachea is transected at the midpoint of the
stenosis. The upper and lower segments are incised longitudinally (1 segment is
incised anteriorly and 1 is incised posteriorly). The segments are then slid together
and sutured. This results in an oblique suture line and quadrupling of the cross-
sectional area of the trachea.19–21,31

COMPLICATIONS AND MANAGEMENT

A plan should be determined on sign-out between the surgical and medical teams in
the case of accidental extubation or decannulation. Accidental extubation or decan-
nulation in these patients may be especially life-threatening in the setting of a compro-
mised upper airway.
In the case of tracheostomy decannulation, the most direct way of reestablishing an
airway in these patients is replacement of the tracheostomy tube. If this is unsuccessful,
teams should be aware of the ability to orally reintubate or mask ventilate the patient.
The mucociliary clearance of the airway is disrupted with surgery; humidification is key
in preventing crusting and mucous plugging, which can lead to respiratory compromise.
Granulation tissue and restenosis are common concerns in airway surgery. Patients
will likely require repeat visits to the operating room for direct laryngoscopy and
 Airway Anomalies 9

bronchoscopy with endoscopic interventions for removal of granulation tissue and/or

dilation of stenotic segments.
Anastomotic leaks and wound dehiscence can occur that may first present with
crepitus and infection of the neck. Further wound breakdown can result in pneumo-
thorax or pneumomediastinum and eventual loss of the airway.

POSTOPERATIVE CARE

Timing of intubation and extubation following airway surgery is variable and based on
patient factors, airway abnormalities, type of surgery, surgeon preference, and site
experience. The surgeon determines the size and position of the endotracheal tube
or tracheostomy based on the patient’s specific anomaly.
Patients may require intubation for several days to stabilize the reconstruction site
and/or wait for edema to subside. In other airway surgeries, prolonged intubation may
compromise the site of healing, so immediate or next-day extubation is preferred.
Systemic antibiotics and reflux medications are commonly given perioperatively. Mul-
tiple adjuvant therapies, such as helium, racemic epinephrine, topical medications, and
positive pressure ventilation, may be required. Positive pressure ventilation should be dis-
cussed before being started because it may be contraindicated in some airway surgeries.
Feeding difficulties are frequently encountered these patients. They frequently
require feeding via a direct gastric route. Oral stimulation and feeding therapies should
be initiated early in the process to avoid oral aversion.

SUMMARY

Congenital airway anomalies should be suspected in the setting of noisy breathing,

cyanosis, apneas, retractions, feeding difficulties, recurrent aspiration, and inability
to place the appropriate size endotracheal tube on intubation. The embryologic
processes that are interrupted during development can be used to understand
these anomalies and their wide range of severities. Airway abnormalities are
commonly associated with anomalies of other systems, including but not limited
to the digestive and cardiac symptoms. Anterior webs and laryngeal clefts have
strong associations with several syndromes. Because respiratory compromise
and an abnormal airway diagnosis may occur shortly after birth, airway anomalies
may be the first sign of an underlying syndrome. Awake flexible laryngoscopy and
direct laryngoscopy or bronchoscopy are the mainstays of diagnosing airway
anomalies. Management options and surgical treatment are varied depending on
the patient and disease severity. Airway surgery requires precise communication
between surgical, anesthetic, and medical teams both preoperatively and postop-
eratively. Multidisciplinary teams are commonly needed to best serve these com-
plex patients.

Best practices

 Infants with stridor, abnormal cry, feeding difficulties, and signs of airway obstruction should
be evaluated with an awake flexible laryngoscopy and, if necessary, a direct laryngoscopy or
bronchoscopy.
 The diagnosis of congenital airway anomalies requires a high degree of suspicion.
 Treatment often involves a multidisciplinary team approach given the rate of associated
abnormalities and complexity of disease.
10 Landry & Rutter

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