Laryngomalacia is the most common cause of stridor in infants, causing a variable degree of airway obstruction.  Supraglottoplasty as a treatment for severe laryngomalacia has become more widely implemented in the last two decades. Traditional indications for supraglottoplasty are applied during infancy and include severe dyspnea, hypoxia or cyanotic episodes, and failure to thrive.  These indications permit surgery on only the most severely affected infants.  Within the last several years, supraglottoplasty has been shown to be very effective for the treatment of laryngomalacia causing obstructive sleep apnea, exercise-induced stridor, and aspiration in older children.  Substantial improvement in OAHI is seen in infants undergoing supraglottoplasty for severe laryngomalacia. 

Subjective improvement of stridor and work of breathing are seen in nearly all neurologically normal patients who undergo supraglottoplasty.  Reliable improvements are noted in objective measurements such as weight gain/growth and apnea/hypopnea index, and swallowing mechanics.  Failure rates of 8-16% are reported, with most reported failures associated with underlying neurodevelopmental delay, syndromes, or prematurity.  The most common reported complications of supraglottoplasty include rare cases of supraglottic stenosis and more common cases of aspiration.  Most cases of supraglottic stenosis are responsive to revision surgery requiring no further treatment. Post-supraglottoplasty aspiration more recently has been demonstrated to be a continuation of aspiration that was present preoperatively, rather than a consequence of the operation itself.  When present, postoperative aspiration is managed conservatively (i.e. thickening of oral liquid intake) and is generally transient (resolving in nearly 100% of cases within a few months). Postoperative recovery is rapid but requires a brief overnight observation period.  Overall, the success rates and morbidities of supraglottoplasty compare favorably to those of more common airway procedures such as adenotonsillectomy even though the typical patient with severe laryngomalacia is failing to thrive and in some degree of chronic respiratory distress.

Laryngomalacia encountered during sleep endoscopy in a child with obstructive sleep apnea (OSA).  (A) During exhalation, short aryepiglottic folds are noted in an otherwise normal-appearing larynx. (B) During inhalation, prolapse of supra-arytenoid tissue is noted.  Supraglottoplasty corrected the OSA in this patient.

Laryngomalacia has been associated with obstructive sleep apnea in infants, but sleep-disordered breathing is more commonly associated with the diagnosis of adenotonsillar hypertrophy in children.  Sleep disordered breathing (SDB) in infants is associated with sudden infant death syndrome (SIDS) and is possibly related to decreased intelligence.  In children, SDB is associated with decreased intelligence, memory performance, attention, and school performance as well as increased systemic inflammatory response.  It also causes increased neuronal loss in the developing brain and results in decreased spatial task learning and retention in rodent models.  Given the developing state of the infant brain, one could argue that our criteria for the treatment of SDB in infants with laryngomalacia should more closely represent our criteria for SDB in children with adenotonsillar hypertrophy.