Laryngomalacia

Allison M. Dobbie,

MD*,

David R. White,

MD

KEYWORDS
 Stridor  Laryngomalacia  Upper airway obstruction  Supraglottoplasty
 Aryepiglottoplasty
KEY POINTS
 Laryngomalacia is the most common congenital laryngeal anomaly, accounting for up to
70% of patients who present with stridor. Most cases are mild and self-resolve, but severe
symptoms require investigation and treatment.
 Laryngomalacia presents as a spectrum of disease, from mild intermittent stridor to
life-threatening airway compromise.
 There is a strong association of laryngomalacia with gastroesophageal reflux disease
(GERD), which warrants medical treatment of GERD in many cases.
 In children with severe laryngomalacia, supraglottoplasty is the preferred surgical option,
which can achieve improvement in both airway and feeding symptoms.
 Laryngomalacia can play a role in sleep-disordered breathing and obstructive sleep
apnea.

Videos of flexible fiberoptic laryngoscopy and supraglottoplasty accompany

this article at http://www.pediatric.theclinics.com/

INTRODUCTION: NATURE OF THE PROBLEM

Laryngomalacia is the most common congenital laryngeal anomaly and accounts for
60% to 70% of cases of stridor in neonates and infants.1 The physical finding of stridor
is a manifestation of upper airway obstruction caused by collapse of the supraglottic
tissue because of excess mucosa, and abnormal and/or reduced laryngeal tone.
Symptoms generally become apparent after the first 2 weeks of life, and, in most
cases, resolve between 12 and 18 months of age. Most cases resolve with minimal
or no treatment; approximately 10% of cases require surgical intervention.
The term laryngomalacia, or soft larynx in Latin, replaced the more antiquated
term congenital laryngeal stridor, which had previously been used to describe the

Division of Pediatric Otolaryngology, Department of Otolaryngology-Head and Neck Surgery,

Medical University of South Carolina, 135 Rutledge Avenue, MSC 550, Charleston, SC 29425, USA
* Corresponding author.
E-mail address: allison.dobbie@gmail.com
Pediatr Clin N Am 60 (2013) 893902
http://dx.doi.org/10.1016/j.pcl.2013.04.013
pediatric.theclinics.com
0031-3955/13/$ see front matter 2013 Elsevier Inc. All rights reserved.

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condition. First coined by Jackson and Jackson2 in 1942, the term differentiated the
condition from other causes of stridor and more clearly depicted the flaccidity of
the larynx.3
THE INFANT LARYNX: ANATOMIC CONSIDERATIONS

A review of laryngeal anatomy aids in the understanding of pathophysiology in laryngomalacia. The structure of the larynx is divided into 3 areas: the supraglottis, glottis,
and subglottis. Laryngomalacia affects the supraglottic structures, which include
the portions of the larynx above the level of the vocal cords. Important supraglottic
structures that can be involved in laryngomalacia include the epiglottis, arytenoid cartilages, and aryepiglottic folds (which connect the epiglottis to the arytenoids).
Neonatal and infantile larynges have several important differences from those of
older children and adults. At birth, the position of the larynx is higher than in older children and adults.4 The growth of the larynx is accelerated during the first 3 years of
postnatal life and gradually achieves its final shape. Postnatal descent of the hyoid
and larynx is unique to humans. The high position of the larynx at the time of birth
facilitates transition to spontaneous breathing and prevention of aspiration, and this
also accounts for obligate nasal breathing in neonates. The descent of the larynx is
crucial for appropriate development of speech. Major postnatal changes to the larynx
occur in the first year of life.
The infantile epiglottis is longer than the laryngeal length in older children, which
may predispose it to posterior displacement. The cartilage of the infantile larynx is
also more pliable than that of the larynx later in life, a property that has been proposed
to play a role in the collapsibility of the laryngeal airway.
CLINICAL PRESENTATION

Inspiratory stridor is the primary feature of laryngomalacia. Characterized by a harsh,

high-pitched sound, stridor as it presents in laryngomalacia often worsens while the
infant is supine, feeding, or crying. Feeding difficulties also often accompany the presence of stridor in patients with laryngomalacia, because the delicate balance between
the suck-swallow sequence and respiration is often disrupted.5 Coughing, choking,
regurgitation with feedings, and slow oral intake are all common symptoms. There
is thought to be a close relationship between laryngomalacia and gastroesophageal/laryngopharyngeal reflux, although the exact mechanism has yet to be fully
elucidated.
Other causes of stridor must also be considered when evaluating a patient with
these symptoms (Table 1). One of the most useful ways to differentiate between
causes of noisy breathing is to identify in which phase of the respiratory cycle the
sound is heard. Different causes of airway obstruction can lead to stridor during
different phases of respiration: inspiration, expiration, or both (biphasic).
Stridor present during inspiration is usually caused by partial obstruction at the level
of the supraglottic tissues. Variable extrathoracic obstruction results in primarily inspiratory stridor. During inspiration, atmospheric pressure is greater than extrathoracic
intraluminal airway pressure, leading to collapse of supraglottic structures. During
the expiratory phase, the exhalatory breath increases extrathoracic airway pressure
such that it overcomes the collapse. Stridor primarily present during expiration is usually caused by obstruction in the lower tracheal airway. Negative intrathoracic pressure during inspiration allows air movement into the lungs, but the increase in
intrathoracic pressure during expiration causes affected portions of the tracheal
airway to collapse, leading to expiratory stridor.

Laryngomalacia

Table 1
Causes of infantile stridor
Inspiratory Phase

Expiratory Phase

Biphasic

Laryngomalacia

Tracheomalacia

Subglottic stenosis

Vallecular cyst

Complete tracheal rings

Subglottic cyst

Epiglottitis

Vascular anomalies
 Pulmonary artery sling
 Double aortic arch
 Aberrant innominate artery

Subglottic hemangioma

Vocal cord paralysis

Laryngeal web

Respiratory papillomatosis

WORK-UP: PATIENT HISTORY

A complete patient history should be obtained when evaluating a patient with stridor.
History should include a focus on antenatal and perinatal events, as well as current
symptoms (Table 2).
WORK-UP: PHYSICAL EXAMINATION

A complete physical examination should be performed, taking special note of the

following:






Vital signs
Weight
General appearance
Presence of upper airway sounds and their timing within the respiratory cycle
Work of breathing, such as the presence of suprasternal retractions or abdominal
muscle usage
 Auscultation of lung fields
 Chest wall structural abnormalities (eg, pectus excavatum)
WORK-UP: DIAGNOSTIC TESTING

When laryngomalacia is suspected, diagnosis is confirmed with flexible fiberoptic

laryngoscopy (Video 1). Flexible laryngoscopy can, in most cases, be performed easily
Table 2
Key components in patient history
Antenatal/Perinatal Events

Respiratory Symptoms

Other Symptoms

Prenatal complications

Stridor

Weight gain

Gestational age and

weight at birth

Ameliorating or aggravating
factors (positioning, sleep,
crying)

Feeding problems (coughing,

choking, gagging)

History of endotracheal
intubation

Cyanosis

Prolonged feeding time

Other congenital
anomalies

Apneas

Reflux

History of pneumonias
(suspected aspiration)

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in the otolaryngologists office or at the bedside without sedation. A small, flexible

fiberoptic endoscope is passed from the childs nostril through the nasal cavity and
is positioned just above the larynx, allowing observation of the dynamic states of
the larynx. Topical anesthetic such as lidocaine has been shown to exaggerate laryngomalacia6 and should not be used during flexible laryngoscopy in patients suspected
to have the disease. Flexible fiberoptic laryngoscopy has been found to have good
reliability (88%) for diagnosis of laryngomalacia, regardless of physician experience.7
The key findings on flexible laryngoscopy, which may be present in any combination, are:





A tightly curled, omega-shaped epiglottis

Retroflexion (posterior displacement) of epiglottis
Short aryepiglottic folds
Redundant, prolapsing arytenoid mucosa and cartilage

Formal direct laryngoscopy and bronchoscopy under general anesthesia is not

necessary in every patient with findings of laryngomalacia on flexible endoscopy.
Most patients only require confirmation of diagnosis by flexible endoscopy alone.
Rigid direct laryngoscopy should be performed in the following situations:
 Absence of any abnormality in a patient with clinical stridor
 When the symptom severity does not correlate with laryngoscopic examination,
raising suspicion for another cause or secondary lesion
 Clinical signs and symptoms of severe disease, in patients for whom surgical
intervention is considered
 Significant aspiration symptoms that cause concern for a posterior laryngeal cleft
or tracheoesophageal fistula
Other diagnostic tests may be considered, including modified barium swallow or
functional endoscopic evaluation of swallowing, particularly if concern for aspiration
exists. In addition, esophageal pH probe studies should be considered if moderate
to severe laryngomalacia symptoms persist despite antireflux treatment. Some investigators propose formal pH studies on all patients with laryngomalacia.8
CLASSIFICATION

Many classification schemes have been proposed for laryngomalacia, but no single
system has been universally adopted. All schemes center on defining the site at which
the supraglottic collapse is present.913 There are 4 main categories:
 Posterior collapse: primarily caused by redundant arytenoid mucosa and/or
excess cuneiform cartilage that prolapses into the airway
 Lateral collapse: from foreshortened aryepiglottic folds
 Anterior collapse: obstruction from retroflexed epiglottis
 Combined: 2 or more of the patterns coexistent
If surgical intervention becomes necessary, classification of anatomic site of
collapse can help direct surgical approach.12
ETIOLOGIC THEORIES

The exact pathophysiology of laryngomalacia has yet to be fully elucidated and is the
subject of much ongoing research. Since the original description of this disease process, several theories have been proposed to explain its pathogenesis, which include
anatomic, cartilaginous, and neurologic theories. The anatomic theory purports that

Laryngomalacia

the cause of laryngomalacia is abnormal shape and structure of the larynx. In a prospective study by Manning and colleagues,14 laryngeal dimensions were compared
between patients with laryngomalacia and controls. The mean ratio of aryepiglottic
fold/glottic length of patients with severe laryngomalacia was significantly lower
than that of controls without laryngomalacia. Within the group of patients with severe
laryngomalacia, the ratio for those without associated neurologic conditions did not
differ from that of the other patients.
The cartilaginous theory attributes the cause to an intrinsic structural difference in
the laryngeal cartilages of infants with laryngomalacia, but this has been refuted by
recent studies that showed histologically normal fibroelastic arytenoid cartilage from
patients with laryngomalacia.15
At present, the neurologic theory has the most support in recent studies. The neurologic theory proposes that neurosensory dysfunction leads to lack of neuromuscular
coordination of the supraglottic airway. Increased laryngopharyngeal sensory thresholds were observed in patients with laryngomalacia,16 indicating that peripheral
afferent function of laryngeal sensation is altered. This is a plausible clinical explanation for the weak laryngeal tone seen in infants with laryngomalacia, because studies
have shown that alteration of laryngeal afferents is associated with changes in laryngeal motor function.
A recent histopathologic study lends support to this theory. Munson and colleagues17 showed that nerve perimeter and surface area of the superior laryngeal
nerve branches of the vagal nerve within supra-arytenoid tissue obtained from
patients with severe laryngomalacia are significantly greater compared with agematched autopsy tissue, thereby providing histologic confirmation of altered vagal
nerve function in this patient population.
Gastroesophageal reflux disease (GERD) has also been implicated as a causative
factor because of the high prevalence of reflux seen in patients with laryngomalacia.18,19 GERD is observed in about 70% of patients with laryngomalacia.20 Despite
this strong association, systematic review of the literature has not found support for
a direct causal relationship.21 Nevertheless, laryngomalacia and extraesophageal
reflux disease seem to have a propagating relationship. First, the negative intrathoracic pressure generated by breathing against an airway obstruction likely encourages contents of the stomach to be drawn into the esophagus, larynx, and
pharynx. This mechanism has been proved in an animal model.22 Second, supporters
of the neuromuscular theory of laryngomalacia16 point out that the same efferent
vagal signals responsible for laryngeal muscular tone, which are thought to be underdeveloped in patients with laryngomalacia, control the tone of the lower esophageal
sphincter.23
There is some evidence to support that the presence of extraesophageal reflux may
in turn worsen symptoms of laryngomalacia by causing edema and inflammation of
laryngeal tissues. In a study of specimens taken from patients with laryngomalacia
of tissue excised during supraglottoplasty, histologic analysis revealed marked submucosal edema and dilated lymphatic channels.15 In addition, laryngopharyngeal
reflux may lead to impaired laryngopharyngeal sensation with resultant swallowing
dysfunction and microaspiration in children.24
NONPHARMACOLOGIC TREATMENT

In patients in whom disease presentation is mild, with only intermittent stridor and
absence of feeding difficulty, no intervention other than periodic monitoring is warranted (Fig. 1). Even mild cases can be treated with alterations in feeding techniques.

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Fig. 1. Algorithm for management of laryngomalacia.

Feeding modifications include pacing, texture change by thickening the formula, and
upright positioning during feeding.
PHARMACOLOGIC TREATMENT

The association between laryngomalacia and GERD is well established; however, the
role of antireflux medications remains controversial.25 There is a paucity of good
evidence evaluating efficacy of antireflux medical treatment, because nearly all of
the studies are limited by patient selection bias as well as the lack of randomization
and control groups.8,20
However, acid suppression therapy should be implemented in patients with laryngomalacia who have a confirmed diagnosis of GERD. In patients with laryngomalacia
with feeding difficulties and GERD-related symptoms, infants with laryngomalacia
have improved feeding symptoms with high-dose H2-blocker therapy (ranitidine
3 mg/kg, 3 times a day).16 Proton pump inhibitors (PPI) should be considered for
refractory or breakthrough symptoms. They should also be implemented in patients
who undergo surgical therapy, in the immediate perioperative and postoperative
period until complete healing has occurred. Those with refractory symptoms may
benefit from combined daytime PPI therapy and nighttime H2-blocker therapy.
SURGICAL MANAGEMENT

The decision to proceed with surgical management of laryngomalacia is determined

by the severity of the patients symptoms rather than by the severity of the endoscopic
appearance of the airway (Table 3). Before the development of supraglottoplasty, tracheostomy was the standard treatment of severe laryngomalacia. Although tracheostomy is effective in bypassing the laryngeal obstruction, there are numerous risks,
complications, and challenges associated with pediatric tracheostomy.

Laryngomalacia

Table 3
Indications for surgical intervention
Absolute Indications

Relative Indications

Cor pulmonale and/or pulmonary

hypertension

Weight loss with feeding difficulty

Pectus excavatum

Aspiration

Hypoxia/hypercapnea

Obstructive sleep apnea/sleep-disordered breathing

Respiratory compromise

Failure to thrive

Supraglottoplasty, also termed aryepiglottoplasty, is an endoscopic procedure

designed to modify the anatomy of the supraglottic larynx to reduce collapse and
prolapse into the airway. It has become the preferred primary surgical intervention
for laryngomalacia. Supraglottoplasty typically involves division of the aryepiglottic
folds and excision of arytenoid mucosa and/or cartilage (Video 2). A wide variety of
techniques have been used. The first reported procedure of this type was in 1984
by Lane and colleagues26 using cold steel instruments, followed by Seid and colleagues27 using carbon dioxide laser.
Subjective improvement of stridor is seen in almost all patients after supraglottoplasty. Success rates of the procedure are around 90%. Polysomnography has
recently been used as an objective test to evaluate success of the procedure, with
postsurgical improvement in most measures.28
Supraglottoplasty has also been shown to reduce gastroesophageal reflux. In one
study, all patients with laryngomalacia and coexistent GERD had significant reduction
in reflux indices (defined as the percentage of time the pH is below 4 during pH probe
study; P 5 .02).23 Growth curves after supraglottoplasty have been studied as well. A
study by Meier and colleagues29 noted that within 3 months after surgery, significant
improvement on the growth curve was seen in patients treated with supraglottoplasty
(P 5 .009) compared with those either observed or treated with acid suppression therapy. After 12 months, all 3 groups approached the mean on the growth curve.
Risk factors for supraglottoplasty failures have been studied. Most often, lower success rates are seen in patients with other medical comorbidities.30,31 In one recent
study,32 prematurity was an independent risk factor for a poor outcome after supraglottoplasty, even after correction for age and weight.
Complications of supraglottoplasty are rare, but include laryngeal edema, granuloma formation, and supraglottic stenosis.30 Aspiration after supraglottoplasty has
also been studied as a potential complication of the procedure.33,34 However, postsupraglottoplasty aspiration recently has been found to be a continuation of aspiration
that was present preoperatively rather than as a consequence of the operation.5
Contraindications for supraglottoplasty are few, but include presence of multilevel
airway obstruction and severe neurodevelopmental comorbidities. Moreover, supraglottoplasty should be postponed if possible when upper or lower respiratory tract
infections are present.
STATE-DEPENDENT AND LATE-ONSET LARYNGOMALACIA

Laryngomalacia has also been reported in children presenting with sleep-induced stridor, upper airway obstruction, and apnea.35,36 In these patients, diagnosis is often
much later, because in many cases there are no symptoms of laryngomalacia while

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the patient is awake. Many undergo adenotonsillectomy on diagnosis with obstructive

sleep apnea as the standard first-line surgical treatment. On failure of improvement
after adenotonsillectomy, sedated flexible bronchoscopy or sleep endoscopy can
reveal the presence of laryngomalacia. Supraglottoplasty can be implemented to treat
obstructive sleep apnea in patients with laryngomalacia observed during sleep
endoscopy.
Another subtype of laryngomalacia is the exercise-induced variant.37,38 This has
been observed most often in older children and teenagers. Endoscopic findings in
older children with laryngomalacia usually show collapse of supra-arytenoid tissue
with normal-appearing epiglottis and aryepiglottic folds, in contrast with what is often
observed in congenital laryngomalacia.39
SUMMARY

Laryngomalacia is a common disease of infancy and childhood and is certain to be

encountered by the pediatrician. Most patients have a benign disease course; however, some present with more severe symptoms and develop life-threatening airway
obstruction and failure to thrive. Proper identification of those patients who require
medical and surgical intervention is key to treatment proceeding in timely fashion
with successful outcomes. Additional consideration of the role of laryngomalacia in
feeding disorders and sleep-disordered breathing aids in comprehensive care of patients with this disease.
SUPPLEMENTARY DATA

Supplementary data related to this article can be found online at http://dx.doi.org/10.

1016/j.pcl.2013.04.013
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