Laryngomalacia

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1. Overview

Laryngomalacia (from Greek: larynx + malakia meaning "softness") is the most common cause of stridor in newborns and infants, accounting for 60-75% of all cases of congenital stridor¹².

It involves the dynamic collapse of immature supraglottic structures (arytenoid cartilages and epiglottis) into the airway during inspiration, creating characteristic inspiratory stridor.

The hallmark laryngoscopic finding is the omega-shaped (Ω) epiglottis, which represents inward curling of the lateral epiglottic margins³.

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2. Visual Summary Panel

Image Integration Plan

[!NOTE] Image Generation Status: Diagrams illustrating the Bernoulli effect on the floppy epiglottis are queued.

Clinical Severity Grading

Based on validated scoring systems⁴:

• Mild (Grade I): Auditory stridor only. No recession. Normal feeding and growth.
• Moderate (Grade II): Stridor + Retractions (subcostal/sternal) + Feeding difficulties. Some growth faltering.
• Severe (Grade III): ALTE (Apparent Life Threatening Event), Cyanosis, Failure to Thrive, Cor Pulmonale. Requires surgical intervention.

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3. Epidemiology

Incidence and Prevalence

Laryngomalacia is the most common congenital laryngeal anomaly, representing:

• 60-75% of all congenital laryngeal lesions¹²
• 45-75% of all cases of infant stridor⁵
• Incidence: Estimated 1 in 2,500-3,000 live births⁶
• True prevalence likely higher due to mild cases that resolve without medical attention⁷

Demographics

Age Distribution:

• Onset: Typically within first 2 weeks of life (median onset 7-10 days)⁸
• Peak severity: 4-8 months of age (median 6 months)¹⁹
• Resolution: 12-24 months in most cases (80% by 18 months)¹⁰
• Late-onset laryngomalacia (> 6 months) described in ~5% of cases¹¹

Sex Distribution:

• Male predominance: Male:Female ratio = 1.5-2.0:1²¹²
• Rationale for male predominance unclear; possibly related to narrower infant airways in males

Associated Conditions

Laryngomalacia has significant associations with¹³¹⁴:

Neurological (20-30%):

• Hypotonia/neuromuscular disorders (15-20%)
• Down syndrome (trisomy 21) - up to 10-fold increased risk
• Cerebral palsy
• Arnold-Chiari malformation

Gastrointestinal (60-80%):

• Gastro-oesophageal reflux disease (GORD) - present in 60-100% of severe cases¹⁵
• Bidirectional relationship: GORD worsens laryngomalacia; increased work of breathing worsens GORD

Cardiac (5-10%):

• Congenital heart disease
• Pulmonary hypertension in severe cases

Genetic Syndromes:

• 22q11.2 deletion syndrome (DiGeorge/velocardiofacial)
• CHARGE syndrome
• Pierre Robin sequence

Synchronous Airway Lesions (10-30%):

• Second airway pathology present in 10-30% of cases requiring endoscopy¹⁶
• Most common: subglottic stenosis, tracheomalacia, vocal cord paralysis
• Higher prevalence in severe laryngomalacia requiring surgery (up to 40%)¹⁷

Risk Factors

• Prematurity (increased incidence and severity)¹⁸
• Low birth weight (less than 2500g)
• Family history of laryngomalacia or other airway anomalies
• Maternal GORD during pregnancy
• Genetic syndromes (particularly those affecting connective tissue)

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4. Pathophysiology

Anatomical Defects

Laryngomalacia results from immaturity and structural abnormalities of the laryngeal cartilaginous framework and supraglottic tissues¹⁹²⁰. Three primary anatomical findings:

1. Omega-Shaped Epiglottis (Ω-Epiglottis):

• Inward curling of lateral epiglottic margins
• Tubular/cylindrical rather than flat configuration
• Short, tight epiglottis that folds on itself
• Most common anatomical variant (60-80% of cases)³²¹
• Epiglottis may be long and posteriorly positioned

2. Redundant Arytenoid Mucosa:

• Excessive, prolapsing arytenoid tissue (particularly cuneiform cartilages)
• Redundant aryepiglottic folds
• Present in 40-60% of cases²²
• Arytenoid tissues collapse anteriorly into the laryngeal inlet during inspiration

3. Shortened Aryepiglottic Folds:

• Foreshortened aryepiglottic folds tether the epiglottis posteriorly
• Creates increased tension on epiglottis during inspiration
• Prevents normal epiglottic elevation
• Present in 20-40% of cases²³

Many patients exhibit combination patterns involving 2 or all 3 anatomical variants²⁴.

Biomechanical Mechanisms

Dynamic Airway Collapse:

The pathophysiology involves dynamic supraglottic collapse during inspiration through the Bernoulli principle²⁵:

1. Inspiration initiates: Diaphragm contracts, intrathoracic pressure decreases
2. Negative pressure generation: Sub-atmospheric pressure develops in trachea and larynx
3. Bernoulli effect: High-velocity airflow through narrowed laryngeal inlet creates lateral suction forces
4. Supraglottic collapse: Floppy supraglottic structures drawn into airway lumen
5. Airflow turbulence: Vibration of prolapsed tissues generates stridor
6. Cycle repeats: With each inspiration, particularly vigorous breaths

Cartilage Immaturity:

The fundamental defect is immature laryngeal cartilage²⁶²⁷:

• Decreased cartilage rigidity and structural integrity
• Histology shows immature chondrocytes with altered matrix composition
• Reduced neural control and coordination of laryngeal muscles
• Proprioceptive dysfunction of laryngeal mechanoreceptors
• Delayed neuromuscular maturation of the supraglottic larynx

Neuromuscular Factors:

Emerging evidence suggests central neurological dysregulation²⁸:

• Impaired laryngeal sensory feedback mechanisms
• Abnormal central integration of airway protective reflexes
• Higher association with neurological conditions supports central component
• May explain association with hypotonia and neuromuscular disorders

Gastro-Oesophageal Reflux Interaction

Bidirectional vicious cycle¹⁵²⁹:

GORD worsens laryngomalacia:

• Acid/pepsin exposure causes laryngeal inflammation and oedema
• Oedematous tissues increase supraglottic mass → more collapse
• Airway hyperreactivity and increased laryngospasm
• Tissue friability and increased mucus production

Laryngomalacia worsens GORD:

• Increased work of breathing generates greater negative intrathoracic pressure
• Negative pressure enhances gastric-to-oesophageal reflux
• Frequent crying and agitation increase intra-abdominal pressure
• Feeding difficulties lead to smaller, more frequent feeds → more reflux episodes

Age-Related Natural History

Why symptoms improve with age:

• Progressive cartilage maturation and stiffening (12-24 months)³⁰
• Growth of laryngeal framework enlarges airway diameter
• Improved neuromuscular control and coordination
• Reduction in relative tongue size (tongue smaller relative to oropharynx)
• Maturation of central respiratory control mechanisms
• Resolution of associated GORD in many cases

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5. Clinical Presentation

Cardinal Symptom: Inspiratory Stridor

Characteristics of the Noise:

• High-pitched inspiratory stridor - classic presentation in 95-100%³¹
• Sound described as "squeaky," "crowing," or "harsh"
• Monophasic inspiratory (vs biphasic in subglottic stenosis, expiratory in tracheomalacia)
• Intensity varies from barely audible to very loud
• May have fluttering quality due to tissue vibration

Positional Variation (Highly Characteristic):

• Worse supine (lying on back) - gravity causes posterior displacement of tongue and supraglottic tissues³²
• Better prone (tummy time) - gravity pulls tissues anteriorly, opening airway
• Improved when held upright or with neck extension
• Symptoms often disappear completely in prone position (diagnostic clue)

Situational Triggers:

• Worse during:
  • Feeding/sucking (increased respiratory effort)
  • Crying or agitation (increased inspiratory flow)
  • Upper respiratory tract infections (mucosal oedema)
  • Active/excited states (increased ventilatory demand)
• Better during:
  • Deep/quiet sleep (reduced inspiratory effort)
  • Calm, relaxed states
  • Prone positioning

Feeding Difficulties

Present in 40-70% of cases; hallmark of moderate-to-severe disease³³:

Mechanisms:

• Difficulty coordinating sucking-swallowing-breathing triad
• Increased work of breathing during feeds (inspiratory effort against obstruction)
• Fatigue during feeds → incomplete feeds → inadequate caloric intake
• Aspiration risk due to laryngeal dysfunction

Clinical manifestations:

• Prolonged feeding times (> 30-40 minutes per feed)
• Frequent pauses/breaks during feeds
• Sweating, tachypnoea, increased work of breathing during feeds
• Choking, coughing, or gagging episodes
• Preference for small, frequent feeds rather than large volume
• Maternal report of "noisy eating" or "gulping"

Failure to Thrive (FTT):

• Present in 10-20% of laryngomalacia cases³⁴
• Occurs due to:
  • Inadequate caloric intake (feeding difficulties)
  • Excessive caloric expenditure (increased work of breathing)
  • Energy balance becomes negative
• Defined as weight less than 3rd centile or crossing 2 major centile lines downward
• Major indication for surgical intervention

Respiratory Symptoms

Work of Breathing Signs:

• Suprasternal retractions (tracheal tug)
• Subcostal and intercostal retractions
• Sternal retractions
• Tracheal tug
• Nasal flaring

Chronic Complications:

• Pectus excavatum (sunken chest) - develops in severe chronic cases from persistent negative intrathoracic pressure³⁵
• Barrel chest deformity
• Paradoxical breathing pattern

Obstructive Sleep Apnoea (OSA):

• Present in 10-45% of cases³⁶
• Obstructive events during sleep (central apnoea less common)
• Desaturations, particularly in supine position
• Sleep fragmentation, restless sleep
• Polysomnography may show obstructive apnoea-hypopnoea index (OAHI) > 5

Acute Life-Threatening Events

ALTE/BRUE (Apparent Life-Threatening Event/Brief Resolved Unexplained Event):

• Occurs in 5-10% of laryngomalacia cases³⁷
• Episodes of:
  • Cyanosis or pallor
  • Apnoea (cessation of breathing)
  • Marked change in muscle tone (limpness)
  • Choking or gagging
• Typically associated with feeding or sleep position
• Often precipitated by URI or increased reflux
• Absolute indication for urgent ENT assessment

Associated Symptoms from GORD

Present in majority of moderate-severe cases¹⁵:

• Frequent regurgitation or vomiting
• Irritability, especially post-feeding
• Back-arching during or after feeds (Sandifer syndrome)
• Chronic cough or choking
• Failure to thrive

Natural History Timeline

Typical progression¹¹⁰:

• 0-2 weeks: Onset of symptoms (may be present from birth)
• 2-8 weeks: Increasing stridor intensity
• 4-8 months: Peak severity (maximum stridor)
• 8-12 months: Gradual improvement begins
• 12-24 months: Resolution in 80% of cases
• Persistent beyond 24 months: Consider other diagnoses or severe laryngomalacia

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6. Differential Diagnosis

Stridor in infancy has numerous causes. Key differential diagnoses include³⁸³⁹:

Vocal Cord Paralysis

Second most common cause of congenital stridor (15-20%):

Bilateral Vocal Cord Paralysis:

• Inspiratory stridor (similar to laryngomalacia)
• Weak cry or aphonia (voice absent)
• Severe respiratory distress, often requiring tracheostomy
• Caused by: birth trauma, Arnold-Chiari malformation, CNS lesions
• Does NOT improve with positioning (key difference)

Unilateral Vocal Cord Paralysis:

• Breathy, weak cry
• Aspiration (liquid more than solids)
• Mild inspiratory stridor
• Left-sided more common (longer recurrent laryngeal nerve course)
• Causes: iatrogenic (post-cardiac surgery), birth trauma, idiopathic

Distinguishing features:

• Abnormal cry quality (vs normal cry in laryngomalacia)
• No positional variation
• Laryngoscopy: immobile vocal cord(s) vs dynamic supraglottic collapse

Subglottic Stenosis

Third most common cause of congenital stridor:

Presentation:

• Biphasic stridor (both inspiratory and expiratory) - key feature
• Stridor less positional than laryngomalacia
• Recurrent/persistent croup
• Respiratory distress with URTIs
• Barking cough

Types:

• Congenital: cartilaginous narrowing, complete tracheal rings
• Acquired: post-intubation (most common), trauma, inflammatory

Distinguishing features:

• Biphasic stridor (vs purely inspiratory)
• History of prolonged intubation in acquired cases
• Fixed obstruction (not positional)
• Laryngoscopy: narrowing at level of cricoid cartilage

Vascular Ring/Sling

Anomalous vascular structures compressing trachea/oesophagus:

Types:

• Double aortic arch (most common complete ring)
• Right aortic arch with aberrant left subclavian
• Pulmonary artery sling
• Innominate artery compression

Presentation:

• Biphasic or expiratory stridor
• Dysphagia (difficulty swallowing) - key associated feature
• Symptoms worsen with feeding (oesophageal compression)
• Recurrent respiratory infections
• Chronic cough

Distinguishing features:

• Dysphagia prominent (rare in laryngomalacia)
• Expiratory component to stridor
• Diagnosis: CT angiography, bronchoscopy shows pulsatile external compression

Tracheomalacia

Weakness of tracheal cartilage causing tracheal collapse:

Presentation:

• Expiratory stridor or wheeze (key feature)
• Barking/brassy cough ("TOT cough")
• Expiratory prolongation
• Recurrent respiratory infections
• Symptoms worse with crying, agitation

Types:

• Primary: intrinsic cartilage weakness
• Secondary: external compression (e.g., vascular ring, mediastinal mass)

Distinguishing features:

• Expiratory stridor (vs inspiratory in laryngomalacia)
• Can coexist with laryngomalacia (synchronous lesion in 10-15%)
• Bronchoscopy: > 50% collapse of tracheal lumen during expiration

Laryngeal Web/Atresia

Congenital membrane across larynx:

Presentation:

• Immediate respiratory distress at birth (complete atresia)
• Weak, abnormal cry
• Biphasic stridor
• Severity depends on degree of obstruction

Distinguishing features:

• Symptoms from birth (vs onset at 2 weeks)
• Severe respiratory distress requiring immediate intervention
• Laryngoscopy: membrane across glottis

Subglottic Haemangioma

Benign vascular tumor in subglottis:

Presentation:

• Onset typically 1-3 months (vs 0-2 weeks in laryngomalacia)
• Biphasic stridor, progressive
• May have cutaneous haemangiomas (50% of cases) - "beard distribution"
• Barking cough
• Symptoms progressively worsen (vs improvement after peak in laryngomalacia)

Distinguishing features:

• Progressive worsening without plateau
• Cutaneous haemangiomas (when present)
• Laryngoscopy: subglottic compressible mass
• Peak age 3-6 months (proliferative phase of haemangioma)

Laryngeal Papillomatosis

Recurrent respiratory papillomatosis (HPV 6/11):

Presentation:

• Progressive hoarseness (most common symptom)
• Stridor (late finding)
• Recurrent/persistent cough
• Onset typically > 1 year (rare in neonates)

Distinguishing features:

• Progressive voice changes predominate
• Maternal history of genital warts
• Laryngoscopy: exophytic papillomatous lesions on vocal cords

Foreign Body Aspiration

Acute airway obstruction from inhaled object:

Presentation:

• Sudden onset stridor/respiratory distress (key history)
• Witnessed/suspected choking episode
• Unilateral wheeze (if lodged in bronchus)
• Age typically > 6 months (when infant developing pincer grasp)

Distinguishing features:

• Acute onset (vs gradual in laryngomalacia)
• History of choking event
• Chest X-ray may show radiopaque foreign body or air trapping

Laryngeal Cleft

Posterior laryngeal defect allowing communication with oesophagus:

Presentation:

• Aspiration with feeds (hallmark) - coughing, choking, cyanosis
• Recurrent pneumonias
• Stridor (variable)
• Failure to thrive

Grading:

• Type 1: above vocal cords (most common, 75%)
• Type 2: extends to cricoid
• Type 3: into cervical trachea
• Type 4: into thoracic trachea

Distinguishing features:

• Aspiration predominates over stridor
• Recurrent pneumonias
• Diagnosis challenging; requires high index of suspicion on laryngoscopy

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7. Investigations

Flexible Nasendoscopy (Awake Laryngoscopy)

Gold standard diagnostic test⁴⁰⁴¹:

Procedure:

• Performed in outpatient clinic by ENT specialist
• Infant awake, usually held by parent or nurse
• Flexible fibreoptic scope passed through nostril
• Topical anaesthetic (lidocaine) and decongestant may be used
• Visualisation of larynx during spontaneous breathing

Key Findings:

1. Omega-Shaped Epiglottis (60-80%):

• Inward curling of lateral epiglottic margins
• Tubular/"omega" (Ω) configuration
• May be elongated and retroflexed posteriorly

2. Prolapsing Arytenoid Mucosa (40-60%):

• Redundant arytenoid tissue (cuneiform and corniculate cartilages)
• Prolapse anteriorly into glottic inlet during inspiration
• May completely obscure glottis during peak inspiration

3. Shortened Aryepiglottic Folds (20-40%):

• Foreshortened, tight aryepiglottic folds
• Draw epiglottis posteriorly
• Prevent normal epiglottic elevation

Dynamic Assessment:

• Critical: Observation during spontaneous breathing
• Supraglottic structures collapse inward during inspiration
• Degree of collapse correlates with severity
• Visualisation of vocal cords moving normally (excludes vocal cord paralysis)

Advantages:

• Awake examination allows assessment of dynamic airway
• Office-based, no anaesthesia required
• Direct visualisation of pathology
• Can assess laryngeal sensation and reflexes

Limitations:

• Cannot assess subglottis or trachea adequately
• May not identify synchronous lesions
• Infant cooperation variable

Microlaryngoscopy and Bronchoscopy (MLB)

Indications⁴²:

• Diagnosis uncertain after flexible laryngoscopy
• Atypical presentation
• Severe disease requiring surgical intervention
• Suspected synchronous airway lesion
• Failed conservative management

Procedure:

• Performed under general anaesthesia in operating theatre
• Rigid laryngoscope and bronchoscope
• Systematic examination: nasopharynx → larynx → trachea → bronchi
• Allows palpation of laryngeal structures

Findings:

• Confirms laryngomalacia anatomy (omega epiglottis, redundant arytenoids)
• Identifies synchronous lesions (10-30% of cases)¹⁶:
  • Subglottic stenosis (most common)
  • Tracheomalacia
  • Complete tracheal rings
  • Vocal cord paralysis
• Excludes other pathology
• Allows assessment of entire airway

Limitation:

• General anaesthesia eliminates spontaneous breathing dynamics
• Positive pressure ventilation can mask dynamic collapse
• Some advocate for spontaneous ventilation MLB to better assess dynamics⁴³

Polysomnography (Sleep Study)

Indications³⁶:

• Suspected obstructive sleep apnoea (OSA)
• Desaturation episodes
• Apnoeas witnessed by parents
• Assessment of severity prior to surgery
• Post-operative assessment of resolution

Findings in Laryngomalacia:

• Obstructive apnoeas/hypopnoeas
• Oxygen desaturations (particularly supine)
• Increased arousal index (sleep fragmentation)
• Paradoxical breathing patterns
• OAHI (Obstructive Apnoea-Hypopnoea Index) often > 5 events/hour in severe cases

Clinical utility:

• Quantifies severity of obstruction
• Documents hypoxemia
• Provides objective measure for surgical decision-making
• Useful for pre/post-operative comparison

pH-Metry/Impedance Study

Indications⁴⁴:

• Suspected GORD contributing to symptoms
• Failed medical management of presumed GORD
• Pre-operative assessment

Findings:

• Acid reflux episodes
• Proximal extent of reflux (pharyngeal reflux)
• Correlation of symptoms with reflux episodes
• Weakly acidic/non-acid reflux (impedance)

Clinical utility:

• Confirms GORD diagnosis (present in 60-100% severe laryngomalacia)
• Guides anti-reflux therapy
• May influence surgical decision (concurrent fundoplication consideration)

Barium Swallow/Upper GI Series

Indications:

• Suspected vascular ring (causes extrinsic oesophageal compression)
• Aspiration concerns
• Dysphagia prominent

Findings:

• Extrinsic oesophageal compression (vascular ring)
• Posterior indentation (vascular ring)
• Aspiration events
• GORD (less sensitive than pH-metry)

CT/MRI Angiography

Indications:

• Suspected vascular anomaly (vascular ring/sling)
• Atypical stridor pattern
• Dysphagia with feeding difficulties
• Pulsatile external compression seen on bronchoscopy

Findings:

• Vascular anatomy (double aortic arch, aberrant vessels)
• Relationship of vessels to airway
• Surgical planning for vascular ring division

Echocardiography

Indications:

• Suspected cardiac disease
• Severe laryngomalacia with chronic hypoxia
• Assessment for pulmonary hypertension/cor pulmonale
• Syndrome workup (CHARGE, 22q11.2 deletion)

Findings:

• Congenital heart disease (present in 5-10%)
• Pulmonary hypertension (severe cases)
• Right ventricular dysfunction (cor pulmonale)

Genetic Testing

Indications:

• Dysmorphic features
• Syndromic presentation
• Developmental delay/hypotonia
• Multiple congenital anomalies

Tests:

• Chromosomal microarray
• 22q11.2 deletion testing (DiGeorge/velocardiofacial syndrome)
• Targeted gene panels (if specific syndrome suspected)

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8. Management

Management is stratified by severity. 80% of cases are mild and managed conservatively; 20% require intervention¹⁴⁵.

A. Conservative Management (80% of Cases)

Indications:

• Mild-to-moderate stridor
• Normal weight gain/growth
• No feeding difficulties
• No apnoea or cyanotic episodes
• No significant work of breathing at rest

Components:

1. Parental Reassurance and Education:

• Explanation of self-limiting nature (resolves 12-24 months)
• "It will sound worse before it gets better"

• peak at 6 months

• Natural history: improvement expected after peak
• Safety netting advice (red flags to return)

2. Positioning Advice:

• Prone positioning during supervised awake periods ("tummy time")
• Elevate head of bed 30-45° for sleep (reduces reflux and improves stridor)
• Avoid supine flat positioning when possible
• Upright positioning during and after feeds

3. Anti-Reflux Measures:

Aggressive treatment of GORD critical (present in 60-100% of moderate-severe cases)¹⁵⁴⁶:

Lifestyle/Feeding Modifications:

• Smaller, more frequent feeds
• Thickened feeds (add rice cereal or commercial thickener)
• Upright positioning during feeds and 30 minutes post-feed
• Avoid overfeeding
• Consider trial of hypoallergenic formula (cow's milk protein allergy association)

Pharmacological:

• Alginates (Gaviscon Infant):

  • First-line in UK
  • Forms protective barrier on gastric contents
  • Dose: Half to one sachet mixed with feeds

• H2-Receptor Antagonists (Ranitidine - withdrawn in many countries; Famotidine):

  • Alternative first-line or second-line
  • Famotidine 0.5-1 mg/kg/day divided BID

• Proton Pump Inhibitors (Omeprazole, Lansoprazole):

  • Second-line or severe GORD
  • Omeprazole 0.7-1.4 mg/kg/day (max 20mg) once daily
  • Lansoprazole 0.7-3 mg/kg/day once daily
  • More effective acid suppression than H2-antagonists
  • Studies show improvement in stridor severity with PPI therapy⁴⁷

4. Monitoring:

• Regular weight checks (every 2-4 weeks initially)
• Plot on growth charts (must maintain centile)
• Monitor for development of feeding difficulties
• Assess work of breathing, retractions
• Parental diary of symptoms helpful

5. Infection Prevention:

• Avoid exposure to respiratory infections when possible
• Early treatment of URTIs (can precipitate acute deterioration)
• Consider palivizumab (RSV prophylaxis) in high-risk infants

6. Follow-Up Schedule:

• Initial: 4-6 weeks post-diagnosis
• Subsequently: every 2-3 months until resolution
• Discharge: when stridor resolved and growth normal

Outcomes with Conservative Management:

• 80-90% spontaneous resolution by 18-24 months¹⁰
• Vast majority require no intervention
• Close monitoring essential to identify the 10-20% requiring surgery

B. Surgical Management: Supraglottoplasty

Indications (Severe Disease - 10-20%)⁴⁸⁴⁹:

Absolute Indications:

1. Failure to Thrive - weight less than 3rd centile or crossing 2 major centile lines
2. Severe obstructive sleep apnoea - OAHI > 10, severe desaturations
3. Cor pulmonale - right heart failure from chronic hypoxia
4. Recurrent ALTE/BRUE - cyanotic episodes

Relative Indications:

1. Severe feeding difficulties despite anti-reflux therapy
2. Moderate-severe pectus excavatum deformity
3. Significant chest wall retractions at rest
4. Persistent hypoxia (oxygen saturations less than 90%)
5. Failed conservative management > 12 months

Pre-Operative Assessment:

• Microlaryngoscopy and bronchoscopy (if not already performed)
• Assessment for synchronous lesions
• Polysomnography (document severity)
• GORD assessment/treatment optimisation
• Echocardiography if cor pulmonale suspected
• Informed consent (including risks)

Surgical Technique:

Procedure: Endoscopic Supraglottoplasty⁵⁰⁵¹

Approach:

• General anaesthesia with spontaneous ventilation (preferred) or jet ventilation
• Suspension laryngoscopy
• Microlaryngeal instruments and/or laser (CO2 laser, KTP laser, cold steel)

Specific Procedures Based on Anatomy:

1. Division of Short Aryepiglottic Folds:

• Most common procedure (performed in ~80% of cases)
• Bilateral division/excision of aryepiglottic folds
• Releases posterior tethering of epiglottis
• Allows epiglottis to elevate and spring open
• Division extends from arytenoids to lateral epiglottic margin

2. Excision of Redundant Arytenoid Tissue:

• Arytenoidectomy (partial)
• Removal of redundant cuneiform cartilages
• Excision of prolapsing arytenoid mucosa
• Reduces bulk of tissue prolapsing into airway
• Care to preserve underlying arytenoid cartilage and vocal cord function

3. Epiglottopexy:

• Less commonly required
• Fixation of omega-shaped epiglottis in anterior position
• Partial epiglottectomy (removal of redundant epiglottis)
• Reserved for severe omega epiglottis contributing significantly

Goal: Enlarge supraglottic inlet by removing/releasing obstructing tissues

Post-Operative Care:

Immediate (First 24-48 Hours):

• Observation in high-dependency or ICU setting
• Continuous pulse oximetry
• Humidified oxygen
• Head elevation 30-45°
• NPO (nil by mouth) for 4-6 hours, then gradual feeding advancement
• Steroids (dexamethasone 0.15 mg/kg) to reduce oedema
• Analgesia (paracetamol, ibuprofen)

Subsequent Days:

• Monitor for airway oedema (peaks 24-48 hours)
• Advance feeds as tolerated
• Continue PPI/anti-reflux therapy
• Discharge typically 24-72 hours post-op (if uncomplicated)

Follow-Up:

• Review 2 weeks post-op (assess healing, symptoms)
• Repeat polysomnography at 6-8 weeks (if pre-op study abnormal)
• Flexible laryngoscopy at 6-8 weeks (assess healing, residual pathology)
• Long-term follow-up to ensure resolution

Success Rates:

• Overall success: 85-95% in appropriately selected patients⁴⁸⁵²
• Resolution of stridor: 85-95%
• Improvement in feeding/weight gain: 80-90%
• Resolution of OSA: 75-85%
• Improvement in oxygen saturations: > 90%

Revision Surgery:

• Required in 5-15% of cases⁵³
• Indications: incomplete initial procedure, re-scarring, residual pathology
• Success rates for revision similar to primary surgery

C. Tracheostomy

Indications (Very Rare):

• Failed supraglottoplasty (persistent severe symptoms after revision)
• Severe synchronous airway lesions (e.g., complete tracheal rings)
• Profound neurological impairment preventing airway protection
• Concurrent complex cardiac disease preventing supraglottoplasty
• Multi-level airway obstruction not amenable to supraglottoplasty

Incidence: less than 1% of laryngomalacia cases require tracheostomy⁵⁴

Considerations:

• Major morbidity (mortality 1-5%, morbidity 40-50%)
• Negative impact on speech/language development
• Requires extensive family training and support
• Home nursing care requirements
• Generally avoided if possible; supraglottoplasty preferred

D. Adjunctive Therapies

Fundoplication:

• Anti-reflux surgery (Nissen fundoplication)
• Considered if severe refractory GORD despite maximal medical therapy
• May be performed concurrently with supraglottoplasty in select cases
• Studies show benefit in neurologically impaired children⁵⁵
• Controversial in isolated laryngomalacia; medical GORD management preferred

Non-Invasive Ventilation (NIV):

• CPAP (Continuous Positive Airway Pressure)
• Bridge to surgery or temporising measure
• Provides pneumatic splinting of airway
• Compliance challenges in infants
• Limited role; surgical intervention preferred for definitive management

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9. Complications

Untreated/Severe Laryngomalacia

Nutritional/Growth:

• Failure to Thrive (10-20% of cases)
• Malnutrition
• Developmental delay secondary to malnutrition

Respiratory:

• Cor Pulmonale (right heart failure from chronic hypoxia)⁵⁶
  • Pulmonary hypertension
  • Right ventricular hypertrophy and failure
  • Hepatomegaly, peripheral oedema
  • Rare but serious complication
• Pectus Excavatum (sunken chest deformity)³⁵
  • Develops from chronic negative intrathoracic pressure
  • May require surgical correction if severe
• Chronic Hypoxia:
  • Desaturations during sleep/feeds
  • Neurodevelopmental impact

Aspiration:

• Aspiration pneumonia (5-10% of cases)⁵⁷
• Recurrent pneumonias
• Chronic lung disease
• Associated with GORD and feeding incoordination

Acute Events:

• ALTE/BRUE (Apparent Life-Threatening Events)
• Cyanotic spells
• Apnoea episodes
• Sudden Infant Death Syndrome (SIDS) - theoretical risk, extremely rare

Psychosocial:

• Parental anxiety and stress
• Sleep deprivation (frequent feeds, monitoring)
• Impact on family quality of life

Surgical Complications (Supraglottoplasty)

Intra-Operative (Rare):

• Bleeding (usually minor)
• Airway fire (with laser)
• Dental/lip trauma
• Anaesthetic complications

Early Post-Operative:

• Airway oedema (most common, 5-10%)⁵⁸
  • Managed with steroids, observation
  • May require re-intubation (1-2%)
• Aspiration (transient, 5-8%)
  • Due to supraglottic oedema/altered anatomy
  • Usually resolves within weeks
• Supraglottic stenosis (less than 2%)
  • Scarring with airway narrowing
  • May require revision surgery

Late Post-Operative:

• Persistent stridor (5-15%)⁵³
  • Incomplete initial procedure
  • Residual redundant tissue
  • Synchronous lesion
  • Requires revision supraglottoplasty
• Granulation tissue (3-5%)
  • At excision sites
  • May require endoscopic removal
• Supraglottic stenosis (rare, less than 2%)
• Voice changes (transient, usually resolves)

Overall Complication Rate: 10-15% (mostly minor)⁵²

---

10. Prognosis & Outcomes

Natural History

Spontaneous Resolution:

• 80-90% of cases resolve spontaneously without surgery¹¹⁰
• Median age of resolution: 12-18 months
• By 24 months: > 95% have resolved or significantly improved
• Persistent symptoms beyond 24 months warrant re-evaluation (may be misdiagnosis)

Timeline:

• Onset: 0-2 weeks
• Peak: 4-8 months (median 6 months)
• Improvement: 8-12 months
• Resolution: 12-24 months (80%)

Factors Affecting Resolution:

• Severity (mild cases resolve earlier)
• Presence of neurological comorbidity (delayed resolution)
• Effective GORD management (earlier resolution)
• Anatomical subtype (omega epiglottis alone resolves better than multi-component)

Surgical Outcomes

Success Rates:

• Symptom resolution: 85-95%⁴⁸⁵²
• Improvement in stridor: 90-95%
• Resolution of FTT: 80-90% (catch-up growth)
• Resolution of OSA: 75-85%
• Quality of life improvement: > 90%

Revision Surgery:

• Required in 5-15% of cases
• Success rate of revision similar to primary surgery (80-90%)
• Reasons: incomplete initial procedure, re-scarring, synchronous lesion

Time to Improvement:

• Immediate improvement in most (within days)
• Maximal benefit by 6-8 weeks (after oedema resolves)
• Some patients have gradual improvement over 3-6 months

Long-Term Outcomes

Voice and Speech:

• Normal voice development in vast majority (> 95%)⁵⁹
• Transient dysphonia post-supraglottoplasty (resolves in weeks)
• Long-term voice quality normal
• Speech and language development appropriate for age

Respiratory:

• Normal respiratory function long-term
• Exercise tolerance normal
• No increased risk of asthma (beyond population baseline)
• Pectus deformity may persist if severe (can require surgical correction)

Growth and Development:

• Catch-up growth occurs after supraglottoplasty in FTT patients⁶⁰
• Normal neurodevelopment in isolated laryngomalacia
• Developmental delays more related to comorbidities (neurological) than laryngomalacia itself

Recurrence:

• Recurrence after resolution extremely rare
• Symptoms of upper airway obstruction with URTIs not uncommon (similar to normal children)

Prognostic Factors

Good Prognosis (Spontaneous Resolution Likely):

• Isolated laryngomalacia (no comorbidities)
• Mild symptoms
• Normal weight gain
• Single anatomical finding (omega epiglottis alone)
• No neurological impairment

Poor Prognosis (Surgery Likely Required):

• Severe symptoms from onset
• Neurological comorbidity (hypotonia, CP, Down syndrome)⁶¹
• Multiple anatomical findings
• Synchronous airway lesions
• Severe GORD refractory to medical management
• FTT at presentation

Mortality:

• Extremely rare in isolated laryngomalacia (less than 0.1%)
• Deaths typically associated with severe comorbidities or misdiagnosis
• ALTE/BRUE episodes concerning but usually not fatal if recognised

---

11. Exam Pearls & High-Yield Points

OSCE/Clinical Exam Scenarios

History-Taking Station:

Key Questions to Ask:

• Onset: "When did the noisy breathing start?" (typically 0-2 weeks)
• Character: "Does it happen breathing in or out?" (inspiratory = laryngomalacia)
• Positional: "Is it better on the tummy or back?" (better prone = laryngomalacia)
• Feeding: "How long do feeds take? Any difficulty?" (prolonged feeds/FTT = severe)
• Sleep: "Any pauses in breathing? Blue spells?" (apnoea/cyanosis = severe)
• Growth: "Is weight gain normal?" (FTT = surgical indication)
• Triggers: "Worse with crying or when upset?" (yes = laryngomalacia)
• PMH: Neurological problems? Premature birth? Cardiac issues?

Red Flags to Identify:

• Failure to thrive (weight loss or faltering growth)
• Cyanotic episodes/ALTE
• Severe feeding difficulties
• Cor pulmonale features (hepatomegaly, oedema)

Physical Examination Station:

Structured Approach:

1. General Inspection:

   • Alert vs lethargic
   • Dysmorphic features (syndromic association?)
   • Cyanosis (peripheral vs central)
   • Nutritional status (thin, wasted?)

2. Respiratory Examination:

   • Listen for stridor (inspiratory, high-pitched)
   • Count respiratory rate
   • Work of breathing signs:
     • Suprasternal retractions (tracheal tug)
     • Subcostal/intercostal retractions
     • Nasal flaring
   • Chest deformity: Pectus excavatum (sunken sternum)
   • Auscultation: transmitted upper airway sounds, chest usually clear

3. Positional Testing (KEY):

   • "Let me position the baby prone" → stridor improves/disappears
   • "Now supine" → stridor worsens
   • Document positional variation (diagnostic)

4. Growth Assessment:

   • Plot weight on growth chart (must maintain centile)
   • Assess for failure to thrive

5. Cardiovascular:

   • Signs of cor pulmonale (rare):
     • Hepatomegaly
     • Peripheral oedema
     • Loud P2 (pulmonary hypertension)

Viva/Oral Exam Scenarios:

Classic Viva Questions:

Q: "What is the most common cause of stridor in an infant?"

• A: Laryngomalacia (60-75% of congenital stridor)¹

Q: "Describe the classical laryngoscopy findings in laryngomalacia."

• A: Three main findings:
  1. Omega-shaped epiglottis (Ω) - inward curling of lateral epiglottic margins
  2. Prolapsing arytenoid mucosa - redundant arytenoid tissue collapsing anteriorly
  3. Shortened aryepiglottic folds - tethering epiglottis posteriorly
• Dynamic collapse of supraglottic structures during inspiration³⁴⁰

Q: "What are the indications for supraglottoplasty?"

• A: Absolute indications:
  1. Failure to thrive
  2. Severe obstructive sleep apnoea
  3. Cor pulmonale
  4. Recurrent ALTE/BRUE (cyanotic episodes)
• Relative indications: Severe feeding difficulties, pectus excavatum, failed conservative management > 12 months⁴⁸⁴⁹

Q: "Describe the surgical technique of supraglottoplasty."

• A: Endoscopic procedure under general anaesthesia:
  • Division of aryepiglottic folds (bilateral) - releases posterior epiglottic tethering
  • Excision of redundant arytenoid mucosa - removes prolapsing tissue
  • Epiglottopexy (if needed) - for severe omega epiglottis
• Goal: enlarge supraglottic inlet by removing obstructing tissues
• Success rate: 85-95%⁵⁰⁵¹

Q: "A 3-month-old with laryngomalacia is failing to gain weight. What is your management?"

• A: Failure to thrive is an absolute indication for surgery
  • Optimise anti-reflux therapy first (aggressive GORD management)
  • Refer to ENT urgently
  • Perform microlaryngoscopy and bronchoscopy (assess for synchronous lesions)
  • Supraglottoplasty indicated
  • Nutritional support (high-calorie feeds, possible NG feeds pre-operatively)

Q: "What is the differential diagnosis of inspiratory stridor in an infant?"

• A:
  • Laryngomalacia (most common, 60-75%)
  • Vocal cord paralysis (bilateral)
  • Subglottic stenosis (usually biphasic)
  • Laryngeal web
  • Subglottic haemangioma (progressive, age 1-3 months onset)
  • Vascular ring (usually biphasic + dysphagia)
  • Foreign body (sudden onset, witnessed event)

Q: "What is the relationship between GORD and laryngomalacia?"

• A: Bidirectional vicious cycle:
  • GORD → laryngeal inflammation/oedema → worsens laryngomalacia
  • Laryngomalacia → increased work of breathing → greater negative intrathoracic pressure → worsens GORD
  • Present in 60-100% of severe cases
  • Aggressive GORD treatment improves laryngomalacia symptoms
  • PPI therapy (omeprazole) first-line pharmacological management¹⁵⁴⁶

Q: "When does laryngomalacia typically resolve?"

• A:
  • Self-limiting condition
  • Peak symptoms: 4-8 months (median 6 months)
  • Resolution: 12-24 months in 80-90% of cases
  • Mechanism: laryngeal cartilage maturation and stiffening, airway growth¹¹⁰

ExamDetail Pearls:

Laryngoscopy Findings - High-Yield Details:

1. Omega-Shaped Epiglottis:

   • Greek letter Ω configuration
   • Lateral epiglottic margins curl inward creating tubular shape
   • Epiglottis may be elongated and retroflexed
   • Most common finding (60-80%)
   • Best visualised on direct/suspended laryngoscopy

2. Dynamic Collapse:

   • Critical finding: collapse occurs during inspiration (dynamic)
   • Supraglottic structures drawn into laryngeal inlet
   • Degree of collapse correlates with symptom severity
   • Must observe during spontaneous breathing (why awake flexible laryngoscopy preferred)

3. Arytenoid Prolapse:

   • Cuneiform and corniculate cartilages prolapse anteriorly
   • May completely obscure glottic view during peak inspiration
   • "Ball-valve" effect

4. Exclusions to Make:

   • Vocal cords mobile bilaterally (excludes vocal cord paralysis)
   • No subglottic narrowing (excludes subglottic stenosis)
   • No masses (excludes haemangioma, papilloma)
   • No laryngeal cleft (posterior commissure intact)

Surgical Technique - Examinable Details:

Supraglottoplasty Steps:

1. Positioning:

   • General anaesthesia (spontaneous ventilation preferred vs jet ventilation)
   • Suspension laryngoscopy (anterior commissure laryngoscope)

2. Division of Aryepiglottic Folds:

   • Bilateral incisions along aryepiglottic folds
   • From arytenoid cartilage to lateral epiglottic margin
   • Instrument: cold steel microlaryngeal scissors or CO2/KTP laser
   • Releases posterior tethering of epiglottis
   • Allows epiglottis to "spring open"

3. Excision of Redundant Arytenoid Mucosa:

   • Removal of redundant cuneiform cartilages (partial arytenoidectomy)
   • Excise prolapsing mucosa
   • Preserve underlying arytenoid cartilage (maintains vocal cord function)
   • Reduces bulk of tissue obstructing airway

4. Epiglottopexy (If Needed):

   • For severe omega epiglottis
   • Partial resection of redundant epiglottis
   • Or fixation of epiglottis to base of tongue
   • Less commonly performed (only if significant contribution)

5. Haemostasis:

   • Ensure meticulous haemostasis (prevent postoperative bleeding)
   • Laser cautery or epinephrine-soaked pledgets

Post-Op Immediate Care:

• HDU/PICU observation (airway oedema risk)
• Dexamethasone 0.15 mg/kg (reduce oedema)
• Humidified oxygen
• Pulse oximetry monitoring
• NPO 4-6 hours, then gradual feeds

Success Rate: 85-95% (key number to remember)

Mnemonics

**"OMEGA"

• Key Features of Laryngomalacia:**

• Omega-shaped epiglottis
• Male predominance (2:1)
• Expiratory stridor absent (inspiratory only)
• GORD association (60-100%)
• Ages 12-24 months for resolution

**"STRIDOR"

• Differential Diagnosis:**

• Subglottic stenosis (biphasic)
• Tracheomalacia (expiratory)
• Ring (vascular) - dysphagia
• Infection (croup, epiglottitis - acute)
• Down syndrome association
• Omega epiglottis = laryngomalacia
• Recurrent nerve palsy (vocal cord paralysis)

**"FLOPPY"

• Indications for Surgery:**

• Failure to thrive
• Life-threatening events (ALTE)
• Obstructive sleep apnoea (severe)
• Pectus excavatum (severe)
• Pulmonale (cor)
• Years of conservative management failed (> 12 months)

---

12. Patient & Layperson Explanation

What is Laryngomalacia? It means "Soft Voice Box". The cartilage in your baby's larynx (voice box) is floppy and immature. Think of it like soft, bendy straws instead of rigid ones.

Why is my baby noisy? When your baby breathes in, the floppy tissue gets sucked into the airway, vibrating and making a squeaking noise (called "stridor"). It sounds scary, but the airway doesn't block completely - your baby is still getting enough air.

Is it dangerous? In 9 out of 10 babies, it is harmless. It sounds worse when they are excited, crying, or feeding. As long as your baby is growing well and gaining weight, they are getting enough air and oxygen.

Will it go away? Yes, it always goes away. It usually gets louder until about 6 months old, then slowly disappears by age 1 to 2 as the voice box becomes firmer and bigger.

What can I do to help?

• Tummy time (when awake and supervised) - lying on stomach helps open the airway
• Keep baby upright during and after feeds
• Smaller, more frequent feeds if they struggle with large feeds
• Give medicines if prescribed (usually for acid reflux, which makes it worse)

What should I watch for and when should I worry? Call your doctor urgently if you notice:

• Blue spells - lips or skin turning blue
• Weight loss - if baby is too tired to finish feeds and stops gaining weight
• Pauses in breathing - stopping breathing for 10+ seconds
• Severe difficulty breathing - chest sucking in with each breath

If these happen, your baby may need a small operation to trim the floppy tissue. This is very successful and helps immediately.

The operation (if needed):

• Called "supraglottoplasty"

• trimming the floppy tissue in the voice box

• Done through the mouth (no cuts on the skin)
• Takes about 30-60 minutes
• Success rate over 90% - most babies go home in 1-3 days
• Baby's breathing improves immediately
• Normal voice development - won't affect speech

What about feeding?

• Feeding can be tiring for babies with laryngomalacia
• Offer frequent small feeds rather than large feeds
• Keep baby upright during feeding
• Burp frequently
• If baby is struggling and losing weight, tell your doctor immediately

Bottom Line: Laryngomalacia sounds scary but is almost always harmless. Your baby will outgrow it. As long as they are growing well, just monitor closely and use positioning to help. If growth falters or breathing becomes severely difficult, excellent surgical treatment is available.

---

13. References

Footnotes

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8. Landry AM, Thompson DM. Laryngomalacia: disease presentation, spectrum, and management. Int J Pediatr. 2012;2012:753526. PMID: 22611412 ↩

9. Zafereo M, Taylor RJ, Pereira KD. Supraglottoplasty for laryngomalacia with obstructive sleep apnea. Laryngoscope. 2008;118(10):1873-1877. PMID: 18622316 ↩

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12. Senders CW, Navarrete EG. Laser supraglottoplasty for laryngomalacia: are specific anatomical defects more influential than associated anomalies on outcome? Int J Pediatr Otorhinolaryngol. 2001;57(3):235-244. PMID: 11223455 ↩

13. Giannoni C, Sulek M, Friedman EM, Duncan NO 3rd. Gastroesophageal reflux association with laryngomalacia: a prospective study. Int J Pediatr Otorhinolaryngol. 1998;43(1):11-20. PMID: 9597460 ↩

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51. Zalzal GH, Anon JB, Cotton RT. Epiglottoplasty for the treatment of laryngomalacia. Ann Otol Rhinol Laryngol. 1987;96(1 Pt 1):72-76. PMID: 3813389 ↩ ↩²

52. Preciado D, Zalzal G. A systematic review of supraglottoplasty outcomes. Arch Otolaryngol Head Neck Surg. 2012;138(8):718-721. PMID: 22801886 ↩ ↩² ↩³

53. Denoyelle F, Mondain M, Gresillon N, Roger G, Chaudre F, Garabedian EN. Failures and complications of supraglottoplasty in children. Arch Otolaryngol Head Neck Surg. 2003;129(10):1077-1080. PMID: 14568791 ↩ ↩²

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56. Avelino MA, Maunsell R, Valera FC, Neto JF, Schweiger C, Miura CS, Magna LA. Predicting supraglottoplasty outcomes using pulmonary artery pressure in patients with laryngomalacia and obstructive sleep apnea. Int J Pediatr Otorhinolaryngol. 2012;76(12):1781-1785. PMID: 22981295 ↩

57. Giannoni C, Sulek M, Friedman EM, Duncan NO 3rd. Gastroesophageal reflux association with laryngomalacia: a prospective study. Int J Pediatr Otorhinolaryngol. 1998;43(1):11-20. PMID: 9597460 ↩

58. Zalzal GH, Collins WO. Microdebrider-assisted supraglottoplasty. Int J Pediatr Otorhinolaryngol. 2005;69(3):305-309. PMID: 15733587 ↩

59. Zafereo M, Taylor R, Pereira KD. Supraglottoplasty for laryngomalacia with obstructive sleep apnea. Laryngoscope. 2008;118(10):1873-1877. PMID: 18622316 ↩

60. Roger G, Denoyelle F, Triglia JM, Garabedian EN. Severe laryngomalacia: surgical indications and results in 115 patients. Laryngoscope. 1995;105(10):1111-1117. PMID: 7564846 ↩

61. Senders CW, Navarrete EG. Laser supraglottoplasty for laryngomalacia: are specific anatomical defects more influential than associated anomalies on outcome? Int J Pediatr Otorhinolaryngol. 2001;57(3):235-244. PMID: 11223455 ↩