Paediatric Laryngeal Pathology

66 Paediatric Laryngeal Pathology


66.1 Laryngomalacia


66.1.1 Incidence and Aetiology


• Most common cause of stridor in newborn


• May be autosomal dominant


• 68% have other respiratory disorders (as seen on flexible bronchoscopy)


66.1.2 Clinical Features


• 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%)


66.1.3 Investigations


• Direct laryngobronchoscopy if failure to thrive


66.1.4 Treatment


• Observation sufficient in most cases


• 10 to 15% (failure to thrive/>1 lesion) may need intervention


• Supraglottoplasty and anterior epiglottoplexy


66.2 Absent/Rudimentary Epiglottis


• Rare bifid epiglottis can be associated with stridor and aspiration


• Multiple congenital anomalies common


• Direct laryngoscopy ± tracheostomy


66.3 Laryngeal Atresia


• 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


66.3.1 Laryngeal Webs


• 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


66.4 Saccular Cysts


• 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)


66.5 Laryngoceles


• See Chapter 56: Benign Neck Disease


66.6 Laryngeal Clefts


• Characterized by a deficiency in separation between oesophagus and larynx/trachea


• Posterior glottic (laryngeal/tracheal) wall


• Associated with high mortality


• Autosomal dominant inheritance


66.6.1 Embryology


• 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


66.6.2 Types


• I: interarytenoid


• II: into cricoid


• III: through posterior cricoid


• IV: membranous trachea


66.6.3 Clinical Features


• Aspiration and cyanosis—53%


• Postpartum asphyxia—33%


• Increased mucus production—23%


• Recurrent pneumonia—16%


• Voiceless crying—16%


• Stridor—10%


• Impaired swallowing—5%


66.6.4 Investigations


• Contrast swallow


• MRI


• Laryngoscopy


66.6.5 Treatment


• Poor prognosis—due to other congenital anomalies


• 50% need a tracheostomy


• Surgical repair options include anterior laryngofissure (with rib graft)


66.7 Vocal Fold Paralysis


• Congenital (10% of all congenital) or acquired


• Bilateral more frequent


• Common association with:


figure Hydrocephalus


figure Meningomyelocoele


figure Arnold–Chiari malformation


figure Other CNS lesions


66.7.1 Incidence and Aetiology


• 1.5 to 23% = frequency


• Congenital lesions more common


Acquired Causes

• Traumatic


figure Vaginal delivery


figure Surgery for congenital malformation, e.g., TOF


• Infectious


figure Whooping cough


figure Encephalitis


figure Poliomyelitis


figure Syphilis


• Neoplastic—tumours of brain and spinal column


Congenital Causes

• 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


66.7.2 Treatment


• 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


66.8 Subglottic Stenosis


66.8.1 Incidence and Aetiology


Figs. 66.1 and 66.2


• Congenital—cricoid cartilage deformity


• Acquired:


figure External injury (including trachy too high)


figure 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.


Stay updated, free articles. Join our Telegram channel

Jul 4, 2016 | Posted by in OTOLARYNGOLOGY | Comments Off on Paediatric Laryngeal Pathology

Full access? Get Clinical Tree

Get Clinical Tree app for offline access