Authors: Freitas S et al.
Cureus, June 17, 2026.
Summary
This case report describes how drug-induced sleep endoscopy changed the treatment plan for a 10-year-old girl with severe obstructive sleep apnea, obesity, and neurocognitive impairment.
The patient had habitual snoring, witnessed apneas, excessive daytime sleepiness, an obstructive apnea-hypopnea index of 15 events per hour, and an oxygen saturation nadir of 85%. Awake examination suggested inferior turbinate hypertrophy, grade II adenotonsillar hypertrophy, and a Mallampati class III airway.
Based on the awake examination, adenotonsillectomy with inferior turbinate reduction was initially planned. However, because obesity and developmental impairment increase the risk of persistent obstructive sleep apnea after adenotonsillectomy, the team performed drug-induced sleep endoscopy before proceeding.
Sedation was designed to reproduce sleep-like airway conditions while preserving spontaneous ventilation. The patient received oral midazolam, brief sevoflurane only to obtain intravenous access, and then a propofol target-controlled infusion. Bispectral index monitoring and cerebral oximetry were used as adjuncts. Topical anesthetics, nasal decongestants, and airway maneuvers were avoided so that the airway findings would not be artificially altered.
At a bispectral index value of 67, the patient had reproducible snoring with preserved spontaneous ventilation. A brief oxygen desaturation to 74% occurred but resolved without airway intervention.
Drug-induced sleep endoscopy showed:
• No collapse at the velum
• No collapse of the oropharyngeal lateral walls
• An enlarged but non-obstructing tongue base
• Marked isolated posterior trapdoor collapse of the epiglottis
Mandibular advancement did not improve the obstruction, but lateral head rotation completely relieved the epiglottic collapse. This indicated that the obstruction was primarily positional and supraglottic rather than adenotonsillar.
Because adenotonsillar tissue was not causing meaningful dynamic obstruction, adenotonsillectomy was avoided. The patient underwent only bilateral inferior turbinate reduction during the same anesthetic.
The epiglottic collapse was managed conservatively with positional therapy, weight-management referral, nasal irrigation, sleep-hygiene measures, and nutritional counseling. At one year, the patient had partial improvement in snoring and daytime somnolence, although repeat polysomnography was not available.
What You Should Know
Awake airway examination may not accurately identify the true site of obstruction in pediatric obstructive sleep apnea.
Drug-induced sleep endoscopy allows dynamic assessment of the airway under sleep-like conditions and may be especially useful in children with obesity, craniofacial abnormalities, neuromuscular disease, or neurodevelopmental impairment.
In this patient, awake examination suggested adenotonsillar obstruction, but drug-induced sleep endoscopy demonstrated isolated positional epiglottic collapse.
The findings prevented an adenotonsillectomy that was unlikely to treat the actual cause of obstruction.
Carefully titrated anesthesia is essential because excessive sedation or inappropriate drug selection may alter airway behavior and produce misleading findings.
Spontaneous ventilation should be maintained during the examination whenever possible.
Drug-induced sleep endoscopy is not a perfect substitute for natural sleep. Differences in sedative agents, sedation depth, scoring systems, and clinician interpretation can affect the findings.
This was a single case, and the patient did not undergo repeat polysomnography, so the long-term physiologic benefit of the revised treatment plan remains uncertain.
The report supports a more individualized, anatomy-based approach to pediatric obstructive sleep apnea rather than relying solely on awake examination or assuming that adenotonsillectomy is always the correct first operation.
Thank you to Cureus for allowing us to summarize this article.