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Table 11.1 Comparison of severity classication, symptoms, and treatment options in pediatric
and adult obstructive sleep apnea (OSA)
Pediatric OSA
Severity
classication
Symptoms • Snoring • Snoring
Sleep study
ndings
First-line
treatment
Mild: AHI 1 to <5 Mild: AHI 5 to <15
Moderate: AHI: 5 to <10 Moderate: AHI 15 to <30
Severe: AHI 10 or greater Severe: AHI 30 or greater
• Discrete apneas less common • Apnea more commons
• Daytime sleepiness less
common
• Hyperactivity • Headache
• Aggressive behavior
• Subcortical arousals • Arousals
Tonsillectomy and adenoidectomy CPAP, weight loss
Adult OSA
• Daytime sleepiness very
common
A. L. Soaper et al.
have persistent OSA after adenotonsillectomy. Children with other comorbidities
such as Down syndrome, obesity, craniofacial anomalies or neuromuscular disorders have even higher rates of residual OSA [3–5]. Both congenital and sleepdependent laryngomalacia have been implicated as causes of OSA in infants and in
children before and after adenotonsillectomy. In a retrospective study by Verkest
etal. of 42 infants, 77% of patients with laryngomalacia who underwent PSG had
OSA [6]. While it is likely that this number is overestimated due to the retrospective
nature of the study and selection bias, this study suggests that the incidence of OSA
is signicant in these infants.
Congenital laryngomalacia is the most common cause of stridor in neonates and
affects males more than females [7]. It is classically dened as a condition of
dynamic collapse of the supraglottic airway based on movement of the arytenoid
and epiglottic tissues. This causes symptoms including inspiratory stridor, which is
typically worse with feeding and agitation, feeding intolerance, coughing, choking,
and regurgitation. Stridor is present at birth in up to 75% of neonates with laryngomalacia and is explained by the Bernoulli effect, in which negative pressure from
upper airway obstruction contributes to dynamic collapse of the larynx [7]. In severe
cases, which account for 5–10% of all cases, upper airway obstruction can cause
failure to thrive, cor pulmonale, pectus excavatum, and even death [8]. Typical
endoscopic ndings noted in congenital laryngomalacia include redundant or prolapsed arytenoid tissue, shortened aryepiglottic folds, and an omega-shaped, infantile epiglottis (Fig.11.1).
Most cases present in the rst few weeks of life and are self-limited, with symptoms typically resolving by 12–24 months of age (Table11.2). There is a close
association between laryngomalacia and gastroesophageal reux disease (GERD),
with GERD reported in 64% of patients with laryngomalacia [9]. Moreover, several
studies have found that infants with laryngomalacia and concomitant GERD have
more severe symptoms than those infants with laryngomalacia alone [8, 9].
Sleep-dependent laryngomalacia, also known by multiple monikers including
late-onset laryngomalacia, sleep exclusive laryngomalacia, state-dependent
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163
a
b
c
Fig. 11.1 (a, b) Congenital laryngomalacia on direct laryngoscopy, characterized with shorted
aryepiglottic folds and redundant arytenoid tissue, completely obstructing the view of the true
vocal folds (c) immediately after supraglottoplasty with division of the aryepiglottic folds and
removal of redundant arytenoid tissue (► https://doi.org/10.1007/000-bfa)
laryngomalacia, occult laryngomalacia, and sleep-dependent laryngomalacia, was
rst described by Amin etal. in 1997 [10]. It is characterized by stridor and upper
airway obstruction during sleep, without daytime stridor and normal anatomic ndings while awake [7]. However, most children determined to have sleep-dependent
laryngomalacia present primarily with snoring as reports of stridor during sleep are
uncommon. In contrast to congenital laryngomalacia, sleep-dependent laryngomalacia occurs in the absence of the anatomic features seen in children with congenital
disease, such as a retroexed and omega-shaped epiglottis (Fig. 11.2). Sleepdependent laryngomalacia is also commonly diagnosed in children (2–18years) and
is noted in 3.9% of children who present with sleep-disordered breathing [11]
(Table11.2). Boudewyns etal. noted a 5.4% prevalence of sleep-state laryngomalacia in a group of 37 children who underwent drug-induced sleep endoscopy
(DISE) [12].
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Table 11.2 Comparison of clinical presentation, diagnosis, and treatment for congenital versus
sleep-state laryngomalacia
Congenital laryngomalacia
Age at
presentation
Clinical
symptoms
Diagnosis Flexible laryngoscopy Drug-induced sleep
Exam ndings • Supraglottic collapse • Supraglottic collapse
Nonsurgical
management
Surgical
management
Several weeks after birth > 2years old
While asleep and awake: Only while asleep:
• Mild symptoms • Snoring
– Stridor exacerbated by agitation,
supine position, feeding
– Difculty feeding • Apneic episodes
• Severe symptoms
– Failure to thrive
– Apnea
– Cyanosis
– Apparent life-threatening event
– Cor pulmonale
– Pectus excavatum
• Shortened aryepiglottic folds • Redundant arytenoid
• Redundant arytenoid mucosa
• Prone positioning • Supplemental oxygen
• Supplemental oxygen • Positive pressure
• Positive pressure
• Antireux medications
• Supraglottoplasty • Supraglottoplasty
• Epiglottopexy • Epiglottopexy
• Tracheostomy • Tracheostomy
Sleep-state laryngomalacia
• Stridor (less
commonly)
endoscopy
mucosa
A. L. Soaper et al.
There have been several theories proposed to explain the etiology of laryngomalacia. These include the anatomic or cartilage theory, which suggested that malpositioned or lax laryngeal cartilage was the cause of airway obstruction. In contrast, the
neurologic theory of laryngomalacia suggests that reduced tone is the reason for
airway collapse and this theory is supported by observations in adults with central
nervous system injury who develop laryngomalacia postinjury [10]. More recently,
this condition has been hypothesized to be caused by abnormal sensorimotor function which leads to decreased tone, impaired neuromuscular coordination, and accidity of the larynx. Based on these last two theories, improvement in congenital
laryngomalacia is presumed to occur as the laryngeal reexes mature [8]. Regardless
of mechanism, children with laryngomalacia develop symptoms due to oppiness
of the cartilage/soft tissue of the supraglottic larynx with prolapsing of the epiglottis
and or the aryepiglottic folds into the airway during inhalation which leads to the
symptoms detailed below.
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Fig. 11.2 Sleep-state laryngomalacia during a drug-induced sleep endoscopy with demonstration
of redundant arytenoid mucosa collapsing into the airway (► https://doi.org/10.1007/000-bf9)
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11.2 Evaluation andDiagnosis
Congenital laryngomalacia is a clinical diagnosis often managed with observation
by the primary care physician. For children with signicant daytime and/or nighttime symptoms who may benet from further evaluation or management, referral to
an otolaryngologist is typically recommended. In the otolaryngology clinic, the
diagnosis of congenital laryngomalacia can be conrmed with a exible beroptic
laryngoscopy examination. During this assessment, specic attention is placed on
the identication of dynamic collapse of the supraglottic structures including ndings such as shortened aryepiglottic folds, omega-shaped epiglottis, and prolapse of
arytenoid tissue. These ndings may be conrmed during laryngoscopy in the operating room when surgical therapy is considered (Fig.11.1). Congenital laryngomalacia is a major risk factor for OSA in children under one-year of age [13].
Considering this, oximetry and PSG are often used in the workup for those children
with laryngomalacia and signicant daytime or nighttime signs or symptoms.
Sleep-dependent laryngomalacia is not observed during awake evaluation and
typically can only be conrmed during sedated evaluations like DISE.Typical ndings on DISE would include redundant arytenoid mucosa with dynamic supraglottic
prolapse which obstructs the airway. Experts who created the 2021 expert consensus statement from the American Academy of Otolaryngology—Head and Neck
Surgery noted that DISE is useful for assessment of children with OSA after adenotonsillectomy and should be performed prior to additional surgery. Cine magnetic
resonance imaging (MRI) may also be a helpful adjunct for diagnosis of patients
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with this condition. DISE and cine MRI are frequently used to assess patients with
persistent OSA.In addition to its use for children with persistent OSA, these assessments are also indicated to evaluate children with small tonsils, those with suspected multilevel airway obstruction, and those unable to tolerate PSG (e.g.,
developmental delay) [14]. The challenge of these modalities is obtaining the proper
level of anesthesia to mimic sleep so that the dynamic movement of the airway can
be assessed. While propofol is commonly used to assess adults with OSA, there is
currently no consensus regarding the ideal pediatric anesthetic protocol for DISE or
cine MRI.We prefer a combination of dexmedetomidine and ketamine. Typically,
inhalational agents are used to place an intravenous catheter. They are discontinued
once the patient is asleep and a loading dose of dexmedetomidine (2μg/kg) is given
over 10min, followed by an infusion of 2μg/kg/h. Once the loading dose of dexmedetomidine is started, ketamine 1 mg/kg is administered. If the patient is inadequately sedated, a second bolus of ketamine 1mg/kg is administered at the end of
the 10-min bolus and the dexmedetomidine is increased to 3μg/kg/h. If the patient
is still moving (e.g., not yet in Ramsay 5 level of sedation) [15], a propofol infusion
(50μg/kg/min) can be started [16]. This must be titrated carefully in order to avoid
respiratory depression which may exaggerate airway collapse [14]. During the
DISE, the neck should be in a neutral position (without pillows or extension/exion). We do not typically examine the airway in alternate positions as our sleep lab
does not report on positional data. The upper airway should be examined with and
without a jaw thrust (at the choana/velum and at base of tongue to assess retroglossal airway), and an oral airway and supplemental oxygen should be removed prior
to the evaluation. While children with positional OSA are more likely to demonstrate obstruction at the tongue base or velum, we do not routinely perform DISEs.
A. L. Soaper et al.
11.3 Management ofLaryngomalacia
Because most children with congenital laryngomalacia have mild symptoms, they
can often be managed conservatively (e.g., with observation) with symptom resolution by 12–24months of age. Repositioning into a prone position or extending the
child’s neck during sleep may be used during this period, although caution should
be given about prone sleep positioning for infants. In addition, children with signs
and symptoms of GERD are treated with either a type 2 histamine antagonist or
proton pump inhibitor. It is thought that reux causes irritation and edema in the
airway, worsening the airway obstruction. Treatment of reux has been associated
with improved symptoms and shortened disease course of congenital laryngomalacia [6]. However, evidence supporting causality between GERD and laryngomalacia or benet from antireux therapy in patients without GERD symptoms is
limited [17].
Nonsurgical treatment for OSA due to congenital or sleep-dependent laryngomalacia can be considered if OSA is mild, if symptoms are mild, or if the patient is not
a surgical candidate. For children with congenital laryngomalacia, supplemental
oxygen is considered the primary nonsurgical treatment for infants with OSA and
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has been shown to lower AHI without signicant hypoventilation or hypercapnia
[18]. Alternatively, for children with sleep-dependent laryngomalacia, continuous
positive airway pressure (CPAP) may be considered. Unfortunately, CPAP compliance is low in children (less than 50%) and is not frequently used for children
younger than 1year of age [19]. Common side effects of CPAP include dry mouth,
frequent awakening, and poor mask tting. Mask tting can be an especially big
problem as many masks are too large for young children. Additionally, there is concern that long-term mask use may result in midface attening in the developing
child. For children with mild sleep-dependent laryngomalacia, pharmacologic
agents like intranasal steroids and oral montelukast have shown some short-term
benet in children with mild and moderate OSA though evidence is limited.
While most children with congenital laryngomalacia do not require surgical
intervention, 5–10% will have severe symptoms (e.g., failure to thrive, feeding difculties) (Table11.2) and may benet from operative intervention [20]. The surgery
is typically performed within 1–2weeks, however occasionally symptoms may be
so severe (severe OSA, recurrent acute life-threatening events (ALTEs), inability to
coordinate feeding and breathing) that it may be performed urgently [7]. The most
common surgery performed to treat laryngomalacia is supraglottoplasty.
Epiglottopexy may also be considered for children with independent epiglottic collapse that is severe. Though tracheostomy is rarely performed, it is an option for
children with severe disease and comorbid conditions, making resolution of their
symptoms unlikely. This may be the case for children with craniofacial abnormalities and those with neurological impairment [7].
Supraglottoplasty involves trimming tight aryepiglottic folds to release the epiglottis and reduce the lateral aryepiglottic fold collapse. It may also include the
removal or reduction of redundant arytenoid mucosa. This procedure can be safely
performed with the child spontaneously breathing or while intubated. The senior
author typically performs this intubated after the administration of an intraoperative
dose of intravenous steroid. Intubation puts the aryepiglottic folds on tension, allowing for easier access to trim these tissues. The patient is then placed into suspension
with a laryngoscope. This can be performed with several different laryngoscopes
(including a Lindholm); however, the senior author prefers a Parsons side-slot
laryngoscope and suspension. Using a rigid endoscope, the arytenoid mucosa is
grasped, and the tight aryepiglottic folds are trimmed. This can be done with microscissors, although the senior author prefers sharp sinus true cuts [21]. It is important
to keep the cut closely associated to the epiglottis. Other techniques include the use
of a microscope and alternative methods of tissue removal including the carbon
dioxide laser and microdebrider [20]. The redundant arytenoid and aryepiglottic
fold mucosa are then trimmed on the lateral side of the arytenoids/folds (using a
microdebrider or scissor). Care must be taken to leave a rim of intact mucosa
between the aryepiglottic fold cuts and any cut on the arytenoid mucosa to prevent
supraglottic scarring. Similarly, it is critical to avoid denuding the interarytenoid
mucosa to avoid supraglottic stenosis.
Supraglottoplasty results in improvement in the AHI for children with congenital
and sleep-dependent laryngomalacia. A 2016 meta-analysis by Camacho etal. of
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A. L. Soaper et al.
138 children with OSA who underwent supraglottoplasty reported that for children
with sleep-dependent laryngomalacia, the mean AHI decreased from 14 to
3.3events/hour and the lowest oxygen saturation increased from 85 to 88%. For
those children with congenital laryngomalacia, the mean AHI decreased from 20 to
4.0events/hour and the lowest oxygen saturation increased from 74 to 88% [22]. A
second meta-analysis from 2016 by Lee etal. examined pooled data of 121 patients
who underwent a supraglottoplasty, regardless of the type of laryngomalacia, and
found a mean decrease in AHI of 8.9 [23].
Epiglottopexy can be considered when addressing OSA-independent epiglottis
collapse (epiglottic retroexion); this is more commonly considered for children
with sleep-dependent laryngomalacia [24] (Fig.11.3). It is performed under general
anesthesia with nasotracheal or endotracheal intubation. The lingual surface of the
epiglottis, vallecula, and base of tongue are all typically denuded, with either a
radiofrequency ablation, electrocautery, or laser, taking care to leave a rim of
mucosa along the lateral edges and tip of the lingual epiglottis to prevent swallow
dysfunction as recommended by Oomen etal. [25]. The epiglottis may be left to
scar to the base of tongue or may be secured to the base of tongue with absorbable
interrupted sutures to promote scarring of the epiglottis to the tongue base. The
suturing to the tongue base can be technically challenging and it is unclear if outcomes are better than doing it without the suture, so our preference is not to suture.
If lingual tonsil hypertrophy is also present, a lingual tonsillectomy can be performed together with the epiglottopexy [25], which we believe can help facilitate
scar band formation between the epiglottis and tongue base. Though there are few
studies on the effects of epiglottopexy alone on the airway, Zalzal et al. demonstrated a decrease in mean AHI from 5.1 to 1.5in a cohort of ten patients [24]. The
same study also showed similar outcomes in 18 patients who received an epiglottopexy and division of aryepiglottic folds, with an improvement in mean AHI from
5.7 to 3.1. In another series of 19 patients, Baljosevic et al. demonstrated
Fig. 11.3 Epiglottic
retroexion on druginduced sleep endoscopy
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improvements in oxygen desaturations and weight gain after both epiglottic suture
placement and laser epiglottopexy [26]. The preoperative oxygen desaturation index
(ODI) was a mean of 5.8, which improved to 1.2 postoperatively. Preoperative mean
oxygen saturation was 89.4 ± 4.3% which improved postoperatively to
96.7±1.1% [26].
Another option for treatment is the epiglottic suture, described in a case series of
eight children to specically address the omega shape of the epiglottis [27]. Under
general endotracheal anesthesia, a small strip of mucosa is excised from the lingual
surface of the epiglottis and a resorbable suture is placed transversely, bringing
together the lateral edges of the cut mucosa, unfurling the epiglottis in the process.
Seven of the eight patients demonstrated improved breathing and feeding after the
procedure, with one requiring a revision surgery.
Tracheostomy is considered denitive treatment for OSA and laryngomalacia
and was previously a mainstay of treatment. Its use has since decreased to avoid the
morbidity and mortality associated with tracheostomy. It is most utilized for select
patients who have severe laryngomalacia and OSA with signicant comorbidities
(such as genetic abnormalities, craniofacial syndromes, or neuromuscular disease)
[8]. Pediatric tracheostomy is performed in an intubated patient and may be carried
out before or after microlaryngoscopy and bronchoscopy. An incision is made either
vertically or with a horizontal incision one nger breadth inferior to the cricoid
cartilage. The strap muscles are divided in the midline and the thyroid gland is
either retracted or divided at the midline. Once the trachea is identied, two stay
sutures (we prefer a 4–0 prolene) are placed on either side of midline and spanning
1–2 tracheal rings (often rings 2–3). A midline, vertical incision is made in the trachea spanning two tracheal rings, typically involving tracheal rings 2, 3, or 4.
Inferior and superior maturation sutures (we prefer a 4–0 chromic) may be placed
in a half horizontal mattress fashion, making a bite into the skin, around a tracheal
ring, and back through the skin to mature the skin to the tracheal cartilage. Some
providers choose not to use maturation sutures, but they make it easier to replace a
tracheostomy tube if it is displaced prior to maturation of the stoma. The endotracheal tube is then pulled back, the tracheostomy tube is placed into the tracheotomy
incision with an obturator in place, and tracheostomy ties are placed.
In cases where there is both adenotonsillar hypertrophy and mild laryngomalacia, resolution of the laryngomalacia may occur following adenotonsillectomy
alone. In these instances, laryngomalacia is thought to be due to negative inspiratory
pressure needed to overcome the upstream obstruction, as explained by the Bernoulli
effect [6].
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11.4 Postoperative Management
Following supraglottoplasty or epiglottopexy, we recommend overnight admission
with continuous pulse oximetry monitoring, which can occur on a hospital oor,
stepdown unit, or high-dependency unit (HDU). Once they emerge from anesthesia,
the children can resume their normal home diet. An antireux medication, like a
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proton pump inhibitor or type 2-histamine blocker, is often given in the postoperative period. No antibiotic therapy is typically given, but a second dose of steroid is
frequently given 8 h after surgery. If there are persistent feeding difculties, a
speech language pathology consult may also be requested. For children with OSA,
a PSG is recommended at least 1month after supraglottoplasty or epiglottopexy.
Because children at this age typically do not snore, it is important to get objective
data to conrm resolution of moderate to severe OSA.In cases of congenital laryngomalacia, a repeat sleep study can be performed as soon as 2–3weeks after surgery
to determine if oxygen or other therapies are needed in these newborns and infants.
Children who undergo tracheostomy are commonly monitored in an intensive
care unit (ICU). In our institution, children are in the ICU for at least 5days while
the tracheostomy stoma matures. We also perform the rst tracheostomy tie change
on postoperative day 3 to minimize skin breakdown and the rst tracheostomy tube
change on postoperative day 5. The stay sutures are also removed on day 5. If the
stoma is healing well and the tracheostomy change is uncomplicated, care of the
tracheostomy tube, tracheostomy tube changes, and family education are turned
over to the nursing teams.
A. L. Soaper et al.
11.5 Complications
The risk of complications following supraglottoplasty is low, and includes aspiration, supraglottic stenosis, cartilage damage, granuloma formation, and need for
revision surgery. Temporary aspiration or dysphagia can occur in 14–25% of
patients [6]. A review by Denoyelle etal. (2003) quotes an overall complication rate
of 7.4% and major complication rate of 3.7%. Minor complications included granuloma formation, edema, and a posterior brous web. Major complications included
supraglottic stenosis and need for revision surgery [20]. Another study by Reddy
et al. found a 4% rate of supraglottic stenosis following supraglottoplasty [28].
Following supraglottoplasty, children with comorbidities, especially neurologic
conditions, tend to have worse feeding and persistent upper airway obstruction than
children without comorbidities [8]. For children with multiple comorbidities, one
review found that these children had a signicantly smaller improvement in their
AHI than children without multiple comorbidities [11].
Complications after epiglottopexy are also rare, but because it is less commonly
performed, outcomes data are limited. These complications are like those listed above
for supraglottoplasty and include aspiration, dysphagia, cartilage damage, granuloma
formation, and need for revision surgery. Given the role of the epiglottis in airway
protection and swallowing, there is a concern for postoperative dysphagia or aspiration. In a series of ve patients, Kanotra etal. studied the swallowing function following an epiglottopexy and found that it did not severely impact swallowing [29]. In a
study by Baljosevic etal., 89% of children had preoperative dysphagia and symptoms
of GERD (n= 17), and postoperatively following epiglottopexy, the dysphagia had
resolved in all children and two children had continued GERD symptoms [26].
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11.6 Current Gaps inKnowledge
There is much yet to be understood in regard to the impact of laryngomalacia or
independent epiglottic collapse on pediatric OSA. Predictors of sleep-dependent
laryngomalacia are not yet known. Further investigation is needed into risk factors
for sleep-dependent laryngomalacia and whether congenital laryngomalacia carries
an increased risk of developing sleep-dependent laryngomalacia in the future.
Moreover, little is also known about the efcacy and long-term outcomes of supraglottoplasty or epiglottopexy for the treatment of pediatric sleep apnea and laryngomalacia. Many of the studies evaluating laryngomalacia and OSA are small, single
center studies and there is a need for large, multicenter studies to further understand
these diagnoses.
11.7 Summary
Overall, congenital laryngomalacia is a common cause of stridor in the neonate and
typically presents with stridor with feeding and agitation. This is related to short
aryepiglottic folds and an infantile, omega-shaped epiglottis. Sleep-state laryngomalacia is more commonly seen in older children and requires DISE for diagnoses.
Both can be important contributors to pediatric OSA and children with persistent
OSA following tonsillectomy and adenoidectomy should be evaluated for sleepdependent laryngomalacia. Most patients with congenital laryngomalacia will
improve with conservative measures over time. For those children with sleepdependent laryngomalacia and children with severe congenital laryngomalacia, surgical management is indicated which can include supraglottoplasty, epiglottopexy,
and rarely, tracheostomy.
References
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