European Annals of Otorhinolaryngology, Head and Neck diseases (2012) 129, 257—263

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Pathophysiology and diagnostic approach tolaryngomalacia in infants

S. Ayari a, G. Aubertinb, H. Girschigc, T. Van Den Abbeeled, M. Mondaine,∗

a Service ORL pédiatrique, hôpital femme-mère-enfant, 59, boulevard Pinel, 69500 Bron, Franceb Service de pneumo-pédiatrie, hôpital Armand-Trousseau, 26, rue du Docteur-Arnold-Netter, 75012 Paris, Francec 173, Route de Desvres, 62280 Saint-Martin-Boulogne, Franced Service ORL, hôpital Robert-Debré, 48, boulevard Sérurier, 75935 Paris, Francee Service ORL, CHU de Montpellier, 37, avenue du Doyen Gaston-Giraud, 34295 Montpellier cedex 5, France

KEYWORDSLaryngomalacia;Stridor;Fibroscopy;Infant

Summary Laryngomalacia is defined as collapse of supraglottic structures during inspiration.It is the most common laryngeal disease of infancy. Laryngomalacia presents in the form ofstridor, a high-pitched, musical, vibrating, multiphase inspiratory noise appearing within thefirst 10 days of life. Signs of severity are present in 10% of cases: poor weight gain (probably themost contributive element), dyspnoea with permanent and severe intercostal or xyphoid retrac-tion, episodes of respiratory distress, obstructive sleep apnoea, and/or episodes of suffocationwhile feeding or feeding difficulties. The diagnosis is based on systematic office flexible laryn-goscopy to confirm laryngomalacia and exclude other causes of supraglottic obstruction. Rigidendoscopy under general anaesthesia is only performed in the following cases: absence of laryn-gomalacia on flexible laryngoscopy, presence of laryngomalacia with signs of severity, search

for any associated lesions prior to surgery, discrepancy between the severity of symptoms andthe appearance on flexible laryngoscopy, and/or atypical symptoms (mostly aspirations). Thework-up must be adapted to each child; however, guidelines recommend objective respiratoryinvestigations in infants presenting signs of severity.© 2012 Elsevier Masson SAS. All rights reserved.

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Laryngomalacia is defined as collapse of supraglottic struc-tures during inspiration. Clinical practice guidelines forcongenital laryngomalacia were published by the SFORL in2011. This article describes the diagnostic approach to con-genital laryngomalacia.

∗ Corresponding author.E-mail address: m-mondain@chu-montpellier.fr (M. Mondain).

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1879-7296/$ – see front matter © 2012 Elsevier Masson SAS. All rights redoi:10.1016/j.anorl.2012.03.005

athophysiological mechanisms ofaryngomalacia in infants

ot all neonates have the same laryngeal anatomy, butll neonates potentially present supraglottic structureshat can invaginate during inspiration. The developmentf symptoms results from variable combinations of thenfant’s specific laryngeal anatomy, poor control of the tone

f supraglottic structures (either pathological neurologi-al mechanisms or simple physiological variations relatedo changes in tone during sleep), mucosal oedema, andncreased airflow (Fig. 1).

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258 S. Ayari et al.

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Figure 2 Course of the length of the supraglottis duringgrowth. Post-mortem anatomical study of four larynges [2] —t

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igure 1 Pathophysiology of laryngomalacia. Larynx aGERD) + Airflow = Symptoms.

The anatomy of the neonatal larynx presents a number ofpecificities, as the epiglottis is relatively longer (comparedo the length of the larynx) than in older children and cane tubular, or even omega-shaped. The infant’s epiglottisan therefore prolapse posteriorly and participate in col-apse of the supraglottis. Aryepiglottic folds are long, withelatively large, flaccid mucosa. These folds may be shortn the anteroposterior plan, drawing the epiglottis posteri-rly. Aryepiglottic folds can prolapse medially and inferiorlynto the supraglottis, narrowing its lumen. They can alsoibrate. Manning et al. showed that the aryepiglottic foldsre significantly shorter in infants with severe laryngoma-acia than in infants with no signs of severe laryngomalacia1]. The corniculate cartilages and the superior part of therytenoid cartilages are clearly visible in the posterior partf the supraglottis, giving the impression of a deep supra-lottic interarytenoid groove. These cartilages can prolapsenteriorly and inferiorly into the airway and can also vibrate.uring the first 18 months of life, the supraglottis lengthens

ess rapidly than the rest of the larynx (while the growthf the supraglottic and subglottic airways is identical) [2]:he anatomical structure predisposing to laryngomalaciaherefore disappears around the age of 18 to 24 monthsFig. 2).

Mucosal oedema has been demonstrated histologically3] and participates in narrowing of the airway. Thisedema is related either to pharyngolaryngeal refluxPLR) or mucosal trauma during inspiration. Severe laryn-omalacia induces intercostal retraction with increasedntrathoracic depression, which, in turn, predisposeso gastro-oesophageal reflux disease (GERD), increasing

he mucosa oedema, creating a self-perpetuating pro-ess.

The clinical features can be influenced by disorders ofeuromuscular tone. Some forms of laryngomalacia are

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he supraglottis grows less rapidly than the larynx as a whole.

ore severely (or exclusively) symptomatic during sleep.he concept of laryngeal immaturity is contested, as laryn-omalacia is not more frequent in preterm infants [4] [5].ocumented neuromuscular disease (congenital or acquiredith hypotonia and/or psychomotor retardation) can beresent with a prevalence varying according to the seriesetween 8 and 50% [6]. The prevalence of neuromuscu-ar disease is higher in the case of severe laryngomalaciand influences the results of surgery [7]. In this setting,aryngomalacia may not be isolated, but part of a broaderyndrome of pharyngolaryngomalacia. Moreover, acquiredaryngomalacia due to an acquired neurological abnormal-

ty (stroke, degenerative disease, tumour) is well known8].

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Pathophysiology and diagnostic approach to laryngomalacia

What is known about the epidemiology oflaryngomalacia in infants and associatedlesions?

The real incidence of laryngomalacia is unknown, althoughit is the most common cause of stridor in infants. The inci-dence has been estimated in cohorts of infants with stridorreferred for specialist consultation: these studies did notinclude infants with mild permanent or intermittent stridor.For example, Zoumalan et al. [9] published a series of 202infants under the age of 12 months examined for stridor in aspecialized unit: stridor was present at birth in 157 infantsand 94% of them had laryngomalacia.

The prevalence of associated airway lesions has beenmore clearly documented: such lesions are present in 18.9%of cases according to Mancuso et al. [10]. Associatedlaryngotracheal lesions (laryngeal dyskinesia, vocal cordparalysis, subglottic stenosis, tracheomalacia) are morefrequent in infants with severe laryngomalacia: Dicksonet al. [11] reported associated lesions in 79% of cases ofsevere laryngomalacia (including 73.3% of subglottic steno-sis and 55.3% of tracheomalacia) and in 28.8% of cases oflaryngomalacia with few signs of severity. Schoeder et al.reported similar figures [5]. Other airway lesions may alsobe observed: pharyngeal obstruction (including microretrog-nathism, glossoptosis, vallecular cyst, palatal anomaly) ornasal obstruction (choanal atresia) [6]. These anomalies canbe part of a syndrome (Down syndrome, CHARGE). For exam-ple, laryngomalacia is observed in 50% of trisomic infants[12].

Cardiac anomalies may also be observed in 31% of cases,according to some authors [13], in line with the 51% ofcardiac anomalies reported in patients with congenitallaryngeal diseases (ASD, VSD, patent ductus arteriosus, PHT)by Sakakura et al. [14].

Clinical presentation of laryngomalacia

Although variants of laryngomalacia have been described inolder children and adolescents [6], laryngomalacia usuallypresents rapidly, during the first 10 days of life. It is charac-terized by stridor which is a high-pitched, musical, vibrating,multiphase inspiratory noise. A hoarser tone or later onsetof stridor should raise the suspicion of another aetiology.The stridor of laryngomalacia is often worsened by agita-tion, crying, feeding, and flexion of the cervical spine, andis often improved by extension of the cervical spine, theprone position and quiet breathing. The intensity of stridoris variable during sleep, increasing or decreasing accordingto the infant. Stridor usually deteriorates during the firstmonths of life, followed by slow improvement after the ageof one year, but stridor can sometimes persist for severalyears [15].

Laryngomalacia with no signs of severity

Most forms of laryngomalacia are minor (70—90%) caus-ing isolated and intermittent stridor, with no changes ofcrying or coughing, no dyspnoea, and no swallowing disor-ders [16]. These minor forms have no consequences on the

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fants 259

nfant’s growth. The loudness of stridor does not appear toe proportional to the severity of laryngomalacia and somenfants can have very severe laryngomalacia with no realtridor. Moreover, parents must be warned that stridor usu-lly becomes louder between the ages of 0 and 4 months.racheal tug is frequent, but is not a sign of severity. Thislinical presentation is not pathognomonic of laryngoma-acia. Other diseases requiring specific management mayresent with the same clinical features: only systematicffice flexible endoscopy performed in visit can confirm theiagnosis of laryngomalacia.

igns of severity of laryngomalacia

igns of severity are:

poor weight gain (probably the most contributive ele-ment);dyspnoea with permanent and severe intercostal orxyphoid retraction;episodes of respiratory distress;obstructive sleep apnoea;episodes of suffocation while feeding or feeding difficul-ties.

Ten to 20% of cases present signs of upper airway obstruc-ion due to the supraglottic obstacle: episodes of cyanosisarticularly while feeding, dyspnoea with intercostal retrac-ion, progressive chest deformity (pectus excavatum) [17].part from signs of GERD (regurgitation, vomiting, malaises,tc.), feeding disorders can also comprise micro-aspirationsnd slow feeding. When feeding disorders are predominant,n associated disease must be excluded. Chronic airwaybstruction induces an increase in the infant’s energy expen-iture, which, combined with feeding disorders, results inoor weight gain or even muscle atrophy. The most severeorms present features of chronic respiratory failure, some-imes responsible for pulmonary artery hypertension andeart failure [18].

linical and complementary work-up strategy

he work-up has a triple objective:

to confirm the diagnosis of laryngomalacia by systematicflexible laryngoscopy whenever laryngomalacia is sus-pected;

to identify associated lesions by clinical examination; to determine the severity of laryngomalacia and its reper-

cussions by complementary examinations, in the presenceof clinical signs of severity.

o confirm the diagnosis of laryngomalacia

espite the specific features of the stridor usually associatedith laryngomalacia, clinical diagnosis based on listening to

he infant’s breathing is not absolutely reliable [19] and muste confirmed by direct visualization of the larynx.

260

Figure 3 Examples of endoscopic findings in laryngomala-cia. A. Supraglottic stenosis with tubular epiglottis and shortaryepiglottic folds. B. Anterior laryngomalacia with completecollapse of the marginal zone of the epilarynx totally maskingthe glottis. C. Posterior laryngomalacia with anterior prolapseof the corniculate cartilages (right photograph).

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alva sign of severity (expert opinion). Standard radiographyis no longer indicated since the availability of fiberoptic

Flexible laryngoscopy must be performed systematically:he positive diagnosis of laryngomalacia requires dynamicxamination of the larynx in a conscious infant.

In the great majority of cases, this examination is per-ormed in the office via the nose with or without localnaesthesia (5% lidocaine is not approved for children underhe age of 6 years — do not exceed one puff per 10 kg ofody weight), or via the mouth, without entering the glot-is. The presence of stridor during laryngoscopy is necessaryo confirm the diagnosis.

In an infant with a risk of cardiorespiratory malaise, flex-ble laryngoscopy must be performed in an environmentquipped with resuscitation equipment.

The usual endoscopic findings are (Fig. 3):

visualization of more or less complete collapse of thesupraglottis concomitant with stridor, during inspiration,which can obstruct visualization of the glottis with shortaryepiglottic folds;

anterior prolapse of the arytenoid cartilages and possiblythe corniculate cartilages (accessory or sesamoid carti-lages);

posterior prolapse of the epiglottis which can be curled up

to form a tubular structure. An omega-shaped epiglottisis not necessarily pathological [20].

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S. Ayari et al.

Classifications of the various types of laryngomalaciaave been proposed. Holinger’s classification is indicatedelow [20]:

Type 1: anterior prolapse of the arytenoid and corniculatecartilages;

Type 2: tubular epiglottis which curls on itself, often asso-ciated with type 1;

Type 3: anteromedial collapse of the arytenoids; Type 4: posterior prolapse of the epiglottis; Type 5: short aryepiglottic folds.

Flexible laryngoscopy must exclude associated glottic orupraglottic obstruction. Visualization of the glottis, partic-larly the essential evaluation of mobility of the glottis, canometimes be difficult. Video recording allowing review ofhe examination provides a major contribution.

Rigid endoscopy under general anaesthesia must not beerformed systematically, but is necessary to investigate theubglottis and the entire airways in the following situations:

absence of laryngomalacia during fiberoptic laryngoscopy;presence of laryngomalacia with signs of severity: investi-gation of any associated lesions is part of the anatomicalwork-up prior to surgery;

discrepancy between the severity of the symptoms andthe appearance on fiberoptic laryngoscopy;

atypical symptoms suggestive of laryngeal diastema(predominant aspirations) or oesophagotracheal fistula(aspirations, abdominal bloating, associated pneumonia,etc.).

Subglottic and tracheal examination is usually performednder general anaesthesia with spontaneous breathing,enerally using a rigid laryngoscope or possibly a rigid bron-hoscope. Some teams perform fiberoptic laryngotrachealndoscopy under local anaesthesia in a specialized environ-ent.Examination under general anaesthesia does not allow

precise diagnosis of laryngomalacia and may miss associ-ted laryngeal palsy. When fiberoptic laryngoscopy in theonscious infant does not reveal any obvious laryngomala-ia, the presence of sleep-induced laryngomalacia may bebserved during the general anaesthetic induction phase.

One study reported a false-negative rate of about 8%or fiberoptic laryngoscopy performed without anaesthesia21] (based on double-blind reading of 140 silent videosf laryngoscopy performed either in a conscious infant ornder general anaesthesia; control videos of infants witho laryngeal lesion were also analysed). The double-blindethodology of this study is attractive, but the absence

f audio information associated with the videos may havencreased the false-negative rate.

No strict correlation has been established between particular of type laryngomalacia and the severity ofaryngomalacia. However, complete laryngeal collapse pre-enting visualization of the glottis can be considered to be

aryngoscopy. A bayonet appearance of the trachea is notathological.

Pathophysiology and diagnostic approach to laryngomalacia in infants 261

Confirmation of th e diagnosis

No signs of severi ty Signs of s everi ty

Rigid endos copy

- Confi rmation of th e diagnos is- Sea rch f or oth er l esions

Management

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Office flexible laryngoscopy

Susp icion of laryngoma lacia

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To identify associated lesions by clinicalexamination

Clinical interview must detect the presence of symptoms ofGERD. Flexible laryngoscopy provides arguments in favourof pharyngolaryngeal reflux (PLR): oedema or erythema ofthe posterior wall of the larynx. The association betweenlaryngomalacia and PLR has been largely demonstrated andis sufficiently significant not to require systematic investi-gations [22]. However, persistence of indirect endoscopicsigns of PLR or clinical symptoms of GERD despite medicaltreatment may be an indication for oesophageal pHmetry.

A complete paediatric clinical examination is essentialto detect associated comorbidities: retardation, multiplemalformation syndrome (CHARGE, Pierre Robin sequence,Down syndrome, 22q11 deletion). The incidence of associ-ated malformations is 8 to 50% [5,11,23].

To determine the severity of laryngomalacia andits repercussions by complementary examinations,in the presence of clinical signs of severity

No data are available concerning the indications forpolysomnography in laryngomalacia.

The task force proposed polysomnography to guide ther-apeutic management in infants with cardiac or neurologicalor complex multiple malformation syndrome, as this exam-ination can distinguish between the repercussions relatedto airway obstruction and those related to the associatedcomorbidity. It should also be performed in the case of fail-ure of surgical management of laryngomalacia.

Measurement of PO2 and PCO2 evaluates the conse-

quences on gas exchange in severe forms of laryngomalacia.Echocardiography is performed in infants with associatedcardiac malformations or hypoxia (PHT). The other comple-mentary investigations are discussed case by case (Fig. 4).

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— Decision flow-chart.

typical laryngomalacia: clinical features andrinciples of treatment

ate onset laryngomalacia

cquired laryngomalacia has been occasionally describedn the literature and can occur in both older children anddults. It has usually been described in the context of neu-ological events or coma and can be reversible in someases, reinforcing the neuromuscular hypothesis of congen-tal laryngomalacia, although these acquired cases usuallyxclusively concern the epiglottis that becomes flaccid andble to invaginate between the vocal cords [24]. Some formsf laryngomalacia are induced by effort.

haryngolaryngomalacia (PLM)

linical featuresn addition to the signs usually described in laryngomalacia,hildren with PLM also experience sleep-disordered breath-ng, usually associated with feeding difficulties related towallowing disorders with aspirations and/or disorders ofoordination of the suckling-swallowing reflex. GERD isrequently present, ideally demonstrated by dual-channelHmetry. In the literature, few authors have specifically dis-inguished these cases of PLM, which are generally includedn the group of laryngomalacia. When PLM is identified, its rarely isolated and is usually part of a known or unknownongenital syndrome: neonatal brainstem dysfunction [25].n the series reported by Froehlich et al. [26], 27 out of2 infants presented PLM: three infants present an isolatedorm, 15 infants presented an identified syndrome (CHARGE,own syndrome, neonatal anoxia, Ondine’s curse) and nine

nfants presented a combination of anomalies not corre-ponding to a known syndrome. Furthermore, 18 infants67%) presented neurological anomalies. The most commoneurological anomaly was axial hypotonia, observed in 12

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ut of 18 cases. Radiological abnormalities (brain CT or MRI)ere detected in eight cases of this series, consisting of cor-

ical atrophy or microcephaly. PLM is frequently observed inHARGE syndrome. In the review by Roger et al. [27], basedn 45 infants with CHARGE syndrome, PLM was present in1.4% of cases.

ndoscopic featuresuring rigid endoscopy under general anaesthesia, flexi-le fiberoptic laryngoscopy performed at the beginning ofhe procedure during induction of anaesthesia is essen-ial to allow dynamic analysis of the larynx that mayometimes reveal abnormalities not identified during nasalberoptic laryngoscopy in the conscious patient. In PLM,

nspiratory collapse of the lateral walls of the pharynxs observed in the absence of any tonsillar hypertrophy,nd may be associated with glossoptosis. In the larynx,aryngomalacia with collapse of the supraglottic larynx dueo anteroposterior flattening of the larynx with prolapsef the arytenoids anteriorly and the epiglottis posteriorlys associated with PLM. Direct laryngoscopy of cases ofLM does not reveal short aryepiglottic folds or redundantupraarytenoid mucosa, thereby allowing the distinctionith ‘‘peripheral’’ forms of laryngomalacia with an anatom-

cal substratum.

anagement general work-up looking for associated abnormalities muste performed in all cases of PLM. Brain MRI and pHme-ry must be performed. Depending on the clinical findings,his work-up may be completed by cardiological, ophthalmo-ogical, genetic assessment, etc. Polysomnography must beerformed to assess the severity of PLM and especially theegree of obstructive syndrome, in order to guide treatmentn a context of noninvasive ventilation.

PLM has a variable course. Some forms, particularlysolated forms, can improve with time. Deterioration ofreathing and/or feeding and/or neurological disorders havelso been observed with no correlation between the coursef these three spheres [26].

onclusion

aryngomalacia is the most common laryngeal disease innfants, although its epidemiology has been poorly defined.he diagnosis is essentially based on office flexible laryn-oscopy, which confirms laryngomalacia and excludes otherauses of supraglottic obstruction. Laryngomalacia is usu-lly well tolerated and has a favourable course in mostases. In 10% of cases, it is poorly tolerated with theresence of signs of severity: an assessment is thenerformed to guide treatment, which is usually surgi-al.

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