66 Paediatric Laryngeal Pathology • Most common cause of stridor in newborn • May be autosomal dominant • 68% have other respiratory disorders (as seen on flexible bronchoscopy) • Inspiratory stridor • Feeding problems • Gastric reflux (80%), regurgitation (40%) • Worsens with increased respiratory effort • Begins shortly after birth getting worse until 6 to 8 months • Plateau at 9 months and steadily improve after • Flaccid epiglottis with short and redundant aryepiglottic folds • OSA (23%), CSA (10%) • Aspiration pneumonitis in 7% • May be concurrent laryngeal congenital lesions (18–60%) • Direct laryngobronchoscopy if failure to thrive • Observation sufficient in most cases • 10 to 15% (failure to thrive/>1 lesion) may need intervention • Supraglottoplasty and anterior epiglottoplexy • Rare bifid epiglottis can be associated with stridor and aspiration • Multiple congenital anomalies common • Direct laryngoscopy ± tracheostomy • Rarest laryngeal lesion • Child makes strong respiratory efforts at birth but no air movement, cry, or stridor • Marked cyanosis when cord clamped • Most die without emergency tracheostomy • If large TOF present they may survive • Mostly occur in glottis • Most located anteriorly and extend towards arytenoids • Vary in thickness • 5% of all congenital laryngeal lesions • Acquired lesions more common • Symptoms present at birth in 75% and all at 1 year • Many asymptomatic until stressed, have an infection, or are intubated • Vocal dysfunction and airway obstruction (inspiratory stridor) • Needs direct laryngoscopy • 60% require surgical intervention • 30 to 40% require tracheostomy • 4 types of lesions • Most arise in infancy • Stridor in 90%—inspiratory (occ. biphasic) • Respiratory difficulty in 55% • Failure to thrive due to feeding difficulties • Direct laryngoscopy required • May require emergency tracheostomy • Definitive treatment is endoscopic I&D (laryngofissure if required) • See Chapter 56: Benign Neck Disease • Characterized by a deficiency in separation between oesophagus and larynx/trachea • Posterior glottic (laryngeal/tracheal) wall • Associated with high mortality • Autosomal dominant inheritance • 4/52 gestation primordium of respiratory system appears as outgrowth from the foregut • The outgrowth expands in a caudal direction and becomes separated from the foregut by the development of 2 longitudinal ridges (oesophagotracheal ridges), which fuse to form the septum • Failure of fusion results in a cleft • I: interarytenoid • II: into cricoid • III: through posterior cricoid • IV: membranous trachea • Aspiration and cyanosis—53% • Postpartum asphyxia—33% • Increased mucus production—23% • Recurrent pneumonia—16% • Voiceless crying—16% • Stridor—10% • Impaired swallowing—5% • Contrast swallow • MRI • Laryngoscopy • Poor prognosis—due to other congenital anomalies • 50% need a tracheostomy • Surgical repair options include anterior laryngofissure (with rib graft) • Congenital (10% of all congenital) or acquired • Bilateral more frequent • Common association with: Hydrocephalus Meningomyelocoele Arnold–Chiari malformation Other CNS lesions • 1.5 to 23% = frequency • Congenital lesions more common • Traumatic Vaginal delivery Surgery for congenital malformation, e.g., TOF • Infectious Whooping cough Encephalitis Poliomyelitis Syphilis • Neoplastic—tumours of brain and spinal column • Probably due to compression of vagus through foramen magnum—improves when hydrocephalus of Arnold–Chiari malformation decompressed • Brainstem dysgenesis and traction of vagal nerve roots are other theories • Secure airway (ETT/tracheostomy) if bilateral • Relieve compression—if within 24 h—nerve will regain function in 2 weeks; otherwise may take 1.5 years • Periodic examinations to assess VF function • Figs. 66.1 and 66.2 • Congenital—cricoid cartilage deformity • Acquired: External injury (including trachy too high) Internal injury, e.g., prolonged intubation (90%) – ETT that allows a leak at pressure <20 cm H2O should be chosen to avoid problem – Predisposing factors include repeat intubation, local/systemic infection, GORD, other systemic factors such as anaemia, dehydration, etc.
66.1 Laryngomalacia
66.1.1 Incidence and Aetiology
66.1.2 Clinical Features
66.1.3 Investigations
66.1.4 Treatment
66.2 Absent/Rudimentary Epiglottis
66.3 Laryngeal Atresia
66.3.1 Laryngeal Webs
66.4 Saccular Cysts
66.5 Laryngoceles
66.6 Laryngeal Clefts
66.6.1 Embryology
66.6.2 Types
66.6.3 Clinical Features
66.6.4 Investigations
66.6.5 Treatment
66.7 Vocal Fold Paralysis
66.7.1 Incidence and Aetiology
Acquired Causes
Congenital Causes
66.7.2 Treatment
66.8 Subglottic Stenosis
66.8.1 Incidence and Aetiology
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Paediatric Laryngeal Pathology
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