Laryngomalacia

the most common congenital cause of upper airway obstruction.

supraglottic structures collapse into the airway during the inspiratory phase of respiration which produces inspiratory stridor

The presentation is usually within 2 weeks of birth with inspiratory stridor which is made worse by feeding (a/w GORD) and lying supine.

The condition is caused by collapse of the supralaryngeal structures during inspiration.
Characterised by:

Short aryepiglottic folds,
redundant arytenoid tissue,
- prolapsing into airway during inspiration
a long curled epiglottis

Infants with laryngomalacia may have a difficult time coordinating the suck swallow breath sequence needed for feeding as a result of their airway obstruction

Many children require no treatment with the condition worsening for ==6–9 months ==and then abating. Most resolve by 12-24 mo.

Those with severe progressive or atypical symptoms should be formally assessed by rigid bronchoscopy under general anaesthesia. This also allows examination for a second lesion which occurs in 20–30% of cases.

5-10% require treatment

Aetiology

Theories of etiology include the anatomic, cartilaginous, and neurologic theories

Anatomical

The anatomic theory proposes that there is an abnormal placement of flaccid tissue resulting in stridor. The challenge with the anatomic theory is there are infants who have the typical anatomic laryngeal findings of laryngomalacia who do not have symptoms of airway obstruction

Cartilaginous

The cartilaginous theory proposes that the cartilages of the larynx are immature and abnormally pliable. This theory has been refuted by the finding of histologically normal cartilage in infants with symptomatic laryngomalacia

Neurological

The neurologic theory recognizes that laryngomalacia may be a consequence of an underdeveloped or abnormally integrated CNS system, particularly the peripheral nerves and brainstem nuclei responsible for breathing and airway patency.

As the infant matures laryngomalacia likely resolves secondary to the maturation of the CNS system

The laryngeal adductor reflex is a vagal nerve reflex responsible for laryngeal function and tone. The afferent activation of the reflex is mediated by the superior laryngeal nerve which is located in the aryepiglottic fold

Sensory information from this nerve is then transmitted to the brainstem nuclei that regulate respiration and swallowing.

A motor response to sensory stimulation is mediated by the vagus nerve resulting in glottic closure, inhibition of respiration, and swallow. An alteration in this pathway has a role in the etiology of laryngomalacia and the associated feeding symptoms

Comorbidities

GORD

The airway obstruction of laryngomalacia generates negative intrathoracic pressure which promotes gastric acid reflux onto the laryngopharyngeal tissues leading to laryngopharyngeal reflux

The laryngeal tissues are sensitive to the acid exposure and become edematous as a response. Increased supraglottic edema results in further collapsing of these tissues into the airway and further obstructive symptoms

CHD

Congenital heart disease is reported in 10% of infants with laryngomalacia

References

Anaesthesia for complex airway surgery in children | BJA Education | Oxford Academic

Laryngomalacia: Disease Presentation, Spectrum, and Management - PMC