Residency · Residency · Otolaryngology

Pediatric Airway: Stridor and Laryngomalacia

Overview

Stridor in the infant is one of the most common referrals to the pediatric otolaryngologist. Laryngomalacia is the most frequent cause of neonatal stridor, accounting for 60-70% of cases. Understanding the differential diagnosis, evaluation framework, and indications for surgical intervention (supraglottoplasty) is essential for the ENT resident.

Stridor: General Concepts

Definition and Classification

Stridor: audible, turbulent airflow through a narrowed segment of the airway.

Inspiratory stridor: supraglottic or glottic obstruction (flaccid supraglottic tissue collapses on inspiration). Expiratory stridor/wheeze: intrathoracic tracheal or bronchial obstruction. Biphasic stridor: fixed subglottic or upper tracheal obstruction (not affected by respiratory phase).

Differential Diagnosis by Level

Supraglottic

Laryngomalacia (most common overall), Vallecular cyst, epiglottic cyst, Lingual thyroid, Epiglottitis (rare in post-Hib vaccine era).

Glottic

Vocal fold paralysis (second most common cause of neonatal stridor). Congenital glottic web, Posterior glottic stenosis, Laryngeal papillomatosis (usually presents later).

Subglottic

Subglottic stenosis (congenital or acquired; third most common). Subglottic hemangioma, Croup (viral laryngotracheobronchitis), Complete tracheal rings.

Tracheal

Tracheomalacia. Vascular ring/sling (innominate artery compression, double aortic arch, pulmonary artery sling). Tracheal stenosis (complete rings), Extrinsic compression (mediastinal mass).

Evaluation of the Stridulous Infant

History

Age of onset (birth vs. weeks-months of age). Positional changes: worse supine (laryngomalacia), worse prone (tracheomalacia). Feeding difficulties, failure to thrive, Cyanotic episodes, apnea, History of intubation (acquired stenosis), Associated anomalies (cardiac, neurologic), Progression vs. stable vs. improving.

Physical Examination

Observation: respiratory rate, retractions (suprasternal, subcostal, intercostal), nasal flaring. Quality and phase of stridor. Cry quality: weak cry suggests vocal fold paralysis; normal cry with stridor suggests laryngomalacia. Growth parameters: failure to thrive suggests significant airway or feeding compromise. Cutaneous hemangiomas: >50% of infants with subglottic hemangioma have cutaneous hemangiomas (especially in a "beard" distribution).

Flexible Nasopharyngolaryngoscopy

First-line diagnostic tool; performed awake in the office. Assesses dynamic airway: supraglottic collapse (laryngomalacia), vocal fold mobility, subglottic narrowing. Can identify most supraglottic and glottic pathology.

Airway Fluoroscopy

Lateral and AP views during respiration, Dynamic assessment of tracheomalacia, Can identify vascular compression.

Direct Laryngoscopy and Bronchoscopy (DLB)

Gold standard for complete airway assessment. Performed under general anesthesia with spontaneous ventilation. Systematic evaluation: nasopharynx, supraglottis, glottis, subglottis, trachea, mainstem bronchi. Sizing the airway with endotracheal tubes (subglottic stenosis grading). Indicated when: Diagnosis is uncertain after office evaluation. Multiple levels of obstruction suspected. Preoperative planning for surgical intervention. Worsening symptoms despite observation.

Additional Imaging

CT/MRI with angiography: vascular anomalies, extrinsic compression. Chest X-ray: evaluate lungs, mediastinum. Echocardiogram: if vascular ring suspected or cardiac anomaly.

Laryngomalacia

Pathophysiology

Collapse of supraglottic structures during inspiration. Traditionally attributed to "floppy" tissue from cartilage immaturity. Current understanding: neuromuscular dysfunction (altered laryngeal sensorimotor function, laryngopharyngeal reflux). Associated with GERD in 65-100% of cases.

Types of Supraglottic Collapse

Type 1: prolapse of mucosa overlying the arytenoid cartilages (redundant arytenoid mucosa). Type 2: short aryepiglottic folds pulling the epiglottis posteriorly (omega-shaped or tubular epiglottis). Type 3: posterior displacement of the epiglottis against the posterior pharyngeal wall (rare). Often a combination of types.

Clinical Features

Inspiratory stridor beginning in the first 2 weeks of life, Worsens with feeding, crying, supine position, agitation, Peaks in severity at 6-8 months, Self-resolves in most cases by 12-24 months, Normal cry and voice. Feeding difficulties: reflux, choking, prolonged feeding, failure to thrive.

Severity Classification

Mild: inspiratory stridor without feeding difficulty or growth problems; no oxygen desaturations. Moderate: feeding difficulty, occasional desaturations, mild retractions, slow weight gain. Severe: failure to thrive, significant desaturations/apnea, cyanotic episodes, cor pulmonale, severe dysphagia.

Management

Conservative (Mild-Moderate)

Observation and parental reassurance: 90% of cases resolve spontaneously. Anti-reflux therapy: PPI or H2 blocker (controversy regarding efficacy). Upright positioning during and after feeds, Thickened feeds if reflux-related feeding difficulty, Close follow-up with growth monitoring.

Surgical: Supraglottoplasty

Indications: Failure to thrive. Significant oxygen desaturations or apneic episodes. Cor pulmonale. Severe feeding difficulty despite medical management. Approximately 10-20% of patients require surgery.

Technique: Suspension microlaryngoscopy. Cold steel or CO2 laser. Type-specific intervention: Type 1: trimming redundant arytenoid mucosa. Type 2: division of short aryepiglottic folds. Type 3: epiglottopexy (suture epiglottis to tongue base; rarely needed). Avoid bilateral aggressive arytenoid mucosal excision (risk of supraglottic stenosis). Avoid damage to the interarytenoid area.

Outcomes: Success rate: 85-95% improvement in stridor and feeding. Revision supraglottoplasty needed in 10-15%. Lower success rate in patients with neurologic comorbidities, Down syndrome, cardiac disease.

Other Important Pediatric Airway Conditions

Subglottic Hemangioma

Infantile hemangioma of the subglottic airway. Presents at 2-6 months with biphasic stridor (proliferative phase). 50% have associated cutaneous hemangiomas (beard distribution). Treatment: oral propranolol (first-line; 2-3 mg/kg/day for 6-12 months); CO2 laser, systemic steroids, open excision for refractory cases.

Vocal Fold Paralysis

Second most common congenital laryngeal anomaly. Unilateral: often idiopathic or birth-related (cardiac surgery, Arnold-Chiari malformation). Bilateral: more concerning; may require tracheotomy; evaluate for central neurologic pathology (MRI brain). Spontaneous recovery possible (up to 60% for unilateral by 12 months).

Congenital Subglottic Stenosis

Third most common congenital laryngeal anomaly. Elliptical cricoid cartilage or thickened subglottic soft tissue. Mild cases outgrow (cricoid growth); severe cases require LTR or CTR.

<image>Flexible laryngoscopic views of laryngomalacia types. Panel A: Type 1 with redundant arytenoid mucosa prolapsing over the arytenoids during inspiration, partially obscuring the glottis. Panel B: Type 2 with short aryepiglottic folds and an omega-shaped epiglottis curling posteriorly and inferiorly toward the glottis during inspiration. Panel C: Type 3 with the epiglottis prolapsing posteriorly against the posterior pharyngeal wall. Panel D: Normal infant larynx for comparison during quiet inspiration, with clearly visible vocal folds, arytenoids, and epiglottis in neutral position. Each panel labels the arytenoids, epiglottis, aryepiglottic folds, and direction of tissue collapse.</image>

<image>Supraglottoplasty surgical technique. Panel A: Suspension laryngoscopy view showing redundant arytenoid mucosa and short aryepiglottic folds causing airway obstruction. Panel B: Division of the left aryepiglottic fold with CO2 laser or cold scissors to release the epiglottis. Panel C: Excision of redundant arytenoid mucosa on one side using cup forceps, preserving the interarytenoid mucosa. Panel D: Post-procedure view showing a widely patent supraglottic airway with visible vocal folds, released aryepiglottic fold, and trimmed arytenoid tissue. Dotted lines indicate tissue to be excised; labels identify structures at risk (interarytenoid area, arytenoid cartilage).</image>

<image>Differential diagnosis of neonatal stridor organized by anatomic level. Sagittal cross-section of the infant upper airway from nasopharynx to trachea with pathology illustrated at each level. Supraglottic: laryngomalacia (collapsed arytenoids), vallecular cyst. Glottic: vocal fold paralysis (medialized cord), glottic web. Subglottic: subglottic stenosis (narrowed cricoid), subglottic hemangioma (asymmetric soft tissue mass). Tracheal: tracheomalacia (collapsed posterior wall), vascular ring (extrinsic compression from double aortic arch). Each condition is labeled with typical stridor phase (inspiratory, biphasic, or expiratory) and age of presentation.</image>

Clinical Pearls

Laryngomalacia accounts for 60-70% of neonatal stridor; 90% of cases resolve spontaneously by 12-24 months; only 10-20% require supraglottoplasty. A normal cry in the presence of stridor strongly suggests laryngomalacia; a weak or absent cry should raise concern for vocal fold paralysis. Cutaneous hemangiomas in a "beard" distribution (chin, lower lip, anterior neck) should prompt evaluation for subglottic hemangioma even before respiratory symptoms develop. Oral propranolol has replaced surgery as the first-line treatment for subglottic hemangioma; treatment duration is typically 6-12 months through the proliferative phase. Bilateral vocal fold paralysis in a neonate requires MRI of the brain to evaluate for Arnold-Chiari malformation or other central pathology. During supraglottoplasty, avoid bilateral aggressive excision of arytenoid mucosa and preserve the interarytenoid area to prevent supraglottic stenosis -- a challenging complication to manage.

References

• Thompson DM. "Abnormal sensorimotor integrative function of the larynx in congenital laryngomalacia: a new theory of etiology." Laryngoscope. 2007;117(S114):1-33.
• Richter GT, Thompson DM. "The surgical management of laryngomalacia." Otolaryngol Clin North Am. 2008;41(5):837-864.
• Rahbar R, Nicollas R, Roger G, et al. "The biology and management of subglottic hemangioma: past, present, future." Laryngoscope. 2004;114(11):1880-1891.
• Leung AKC, Cho H. "Diagnosis of stridor in children." Am Fam Physician. 1999;60(8):2289-2296.

Read this lecture as Markdown