I am currently searching the literature on the impact of adenoid hypertrophy on pediatric dysphagia. I welcome, and appreciate any recent contributions to the field, ideally with objective findings from VFSS. Thank you in advance.
Our ENTs tell me that they commonly see nasal congestion, mouth breathing and LPR (laryngopharyngeal reflux) in those infants/children who present with adenoid hypertrophy, and it often presents as tonsillaradenoid hypertrophy. It becomes most worrisome to them when it provokes OSA and/or chronic cough and there is associated clinical presentation of dysphagia. To their knowledge and mine, no one has published about this diagnosis related to objective data from VFSS but my impressions in radiology include nasopharyngeal narrowing, swallow-breathe incoordination leading to retrograde flow into the nasopharynx, which appeared due to the adverse effect of the obstructed nasal airflow on breathing, and, for 2 of them, incidental findings of LPR were witnessed during the VFSS. Post adenoidectomy follow-up VFSS results with infants who had isolated adenoid hypertrophy (without other co-morbidities) noted greater improvement in the integrity of swallowing physiology post-op than those with other associated co-morbidities (craniofacial anomalies, Down Syndrome, hypotonia).
I suspect the setting or “bigger picture” when there is tonsillaradenoid hypertrophy (or adenoid hypertrophy) is likely to be a critical factor for our index of suspicion, and for the nature of our radiological data. I also suspect that if the adenoid hypertrophy provoked significant mouth breathing, that could readily alter the anterior seal on the bolus, and there might also be a pathway for laryngeal airway invasion due the need for urgent breaths during dynamic swallowing. The co-occurring LPR might also lead to diminished laryngeal sensation which has been shown to be a risk factor for airway invasion as well. Partnership with ENT is so valuable at all ages for our pediatric patients, for optimal outcomes.