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:
[email protected] Pediatr Clin N Am 60 (2013) 893–902
http://dx.doi.org/10.1016/j.pcl.2013.04.013 pediatric.theclinics.com
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894 Dobbie & White
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 laryng-
omalacia. 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 car-
tilages, 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 chil-
dren 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 pres-
ence 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 gastroesopha-
geal/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 inspi-
ratory 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 usu-
ally caused by obstruction in the lower tracheal airway. Negative intrathoracic pres-
sure 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.
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Laryngomalacia 895
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 Subglottic hemangioma
Pulmonary artery sling
Double aortic arch
Aberrant innominate artery
— — 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 Ameliorating or aggravating Feeding problems (coughing,
weight at birth factors (positioning, sleep, choking, gagging)
crying)
History of endotracheal Cyanosis Prolonged feeding time
intubation
Other congenital Apneas Reflux
anomalies
— — History of pneumonias
(suspected aspiration)
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896 Dobbie & White
in the otolaryngologist’s office or at the bedside without sedation. A small, flexible
fiberoptic endoscope is passed from the child’s 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 laryng-
omalacia6 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 combina-
tion, 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 inves-
tigators 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.9–13 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 pro-
cess, several theories have been proposed to explain its pathogenesis, which include
anatomic, cartilaginous, and neurologic theories. The anatomic theory purports that
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Laryngomalacia 897
the cause of laryngomalacia is abnormal shape and structure of the larynx. In a pro-
spective 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 neuro-
logic theory proposes that neurosensory dysfunction leads to lack of neuromuscular
coordination of the supraglottic airway. Increased laryngopharyngeal sensory thresh-
olds were observed in patients with laryngomalacia,16 indicating that peripheral
afferent function of laryngeal sensation is altered. This is a plausible clinical explana-
tion for the weak laryngeal tone seen in infants with laryngomalacia, because studies
have shown that alteration of laryngeal afferents is associated with changes in laryn-
geal motor function.
A recent histopathologic study lends support to this theory. Munson and col-
leagues17 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 age-
matched 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 laryngomala-
cia.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 intratho-
racic pressure generated by breathing against an airway obstruction likely encour-
ages 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 under-
developed 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 sub-
mucosal 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 war-
ranted (Fig. 1). Even mild cases can be treated with alterations in feeding techniques.
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898 Dobbie & White
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 laryng-
omalacia 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 patient’s symptoms rather than by the severity of the endoscopic
appearance of the airway (Table 3). Before the development of supraglottoplasty, tra-
cheostomy was the standard treatment of severe laryngomalacia. Although tracheos-
tomy is effective in bypassing the laryngeal obstruction, there are numerous risks,
complications, and challenges associated with pediatric tracheostomy.
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Laryngomalacia 899
Table 3
Indications for surgical intervention
Absolute Indications Relative Indications
Cor pulmonale and/or pulmonary Weight loss with feeding difficulty
hypertension
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 col-
leagues27 using carbon dioxide laser.
Subjective improvement of stridor is seen in almost all patients after supraglotto-
plasty. 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 ther-
apy. After 12 months, all 3 groups approached the mean on the growth curve.
Risk factors for supraglottoplasty failures have been studied. Most often, lower suc-
cess 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 supra-
glottoplasty, even after correction for age and weight.
Complications of supraglottoplasty are rare, but include laryngeal edema, granu-
loma formation, and supraglottic stenosis.30 Aspiration after supraglottoplasty has
also been studied as a potential complication of the procedure.33,34 However, postsu-
praglottoplasty 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, supra-
glottoplasty 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 stri-
dor, 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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900 Dobbie & White
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; how-
ever, 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 pa-
tients 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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