Laryngomalacia

Airway collapse under anesthesia - Loss of upper airway tone at induction turns intermittent supraglottic collapse into real obstruction. These patients often need increased PEEP with mask ventilation or through a supraglottic airway to stent the airway open.

Severity assessment - Flexible fiberoptic laryngoscopy in the awake infant is the gold standard and shows which structures are collapsing; pair it with the weight-gain curve for failure to thrive and, in older children with suspected sleep-exclusive disease, the polysomnogram AHI. Severe symptoms go to the OR for direct laryngoscopy and bronchoscopy.

Preop airway exam - Confirm choanal patency and look for cleft lip or palate, glossoptosis, micrognathia, or Pierre Robin sequence. Those findings, more than the laryngomalacia itself, are what make the intubation hard.

Silent aspiration - Aspiration in these infants is often silent and missed clinically, so a modified barium swallow is what detects it. Suspect it when feeding difficulty or a swallowing deficit is part of the picture.

Reflux - Nearly 60% have concomitant acid reflux and many are on a proton pump inhibitor. Plan for a full stomach and for the extra supraglottic edema reflux brings.

Laryngospasm risk - Laryngomalacia sits on the list of airway anomalies that raise laryngospasm risk. Keep the plane deep through instrumentation and have succinylcholine and atropine drawn.

Shared airway for supraglottoplasty - 10% to 20% of these infants have severe symptoms and need surgery, done through direct laryngoscopy with laser, cold steel, microdebrider, or coblator. Steroids during and after the case are the usual adjunct to limit airway edema, and these patients are observed in hospital afterward.

Synchronous airway lesions - Look for the second lesion: subglottic stenosis, tracheomalacia or bronchomalacia, vocal fold paralysis, laryngeal papillomatosis, or subglottic hemangioma (suspect it with a beard-distribution cutaneous hemangioma). Bronchoscopy to the mainstem bronchi is what finds them.

Comorbidities that predict trouble - Neurologic comorbidity (hypotonia, seizures, cerebral palsy) carries the highest revision rate after supraglottoplasty at nearly 70%, with 60% needing tracheostomy for persistent obstruction. Cardiac comorbidity means septal defects, aortic or pulmonary stenosis, or pulmonary hypertension — get the echo report before you induce.

Postoperative aspiration - Aspiration after supraglottoplasty is uncommon but clusters in infants under 18 months, revision cases, and those with neurologic comorbidity.

Laryngomalacia is the most common cause of stridor in an infant — dynamic inspiratory collapse of the supraglottic airway from shortened aryepiglottic folds that tether the epiglottis posteriorly, an omega-shaped epiglottis, and redundant arytenoid tissue that prolapses over the glottis. The leading causal theory is neurologic: altered laryngeal tone from abnormal integration of the laryngeal nerves, supported by increased supraglottic nerve diameter in severe disease. Estimated incidence is 1 in 2,000 to 3,000. Nearly 60% of these infants also carry acid reflux, which irritates and edematizes the upper airway and worsens the obstruction. Stridor is worse supine and with feeding. It matters to us because anesthesia strips away the pharyngeal and laryngeal tone that was already marginal, so collapse that is intermittent awake becomes obstruction once the child is asleep.