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CME · 0.5 cr Craniofacial and Pediatric Plastic Surgery

Superiorly Based Pharyngeal Flap for Velopharyngeal Dysfunction

Dr. Adrian Williamson, Dr. Adam Johnson, Dr. Larry Hartzell ·December 30, 2021 ·1,033 views f 𝕏 in

Velopharyngeal dysfunction (VPD) refers to the improper control of airflow through the nasopharynx. The term VPD denotes the clinical finding of incomplete velopharyngeal closure. Other terms used to describe VPD include velopharyngeal insufficiency, inadequacy and incompetence. However, the use of VPD has gained popularity over these terms as they may be used to infer a specific etiology of impaired velopharyngeal closure.1

Control of airflow through the nasopharynx is dependent on the simultaneous elevation of the soft palate and constriction of the lateral and posterior pharyngeal walls. Disruptions of this mechanism caused by structural, muscular or neurologic pathology of the palate or pharyngeal walls can result in VPD. VPD can result in a hypernasal voice with compensatory misarticulations, nasal emissions and aberrant facial movements during speech.2

The assessment of velopharyngeal function is best preformed by a multispecialty team evaluation including speech-language pathologists, prosthodontists, otolaryngologists and plastic surgeons. The initial diagnosis of VPD is typically made with voice and resonance evaluation conducted by a speech-language pathologist. To better characterize the patient’s VPD, video nasopharyngeal endoscopy or speech videofluoroscopy can be used to visualize the velopharyngeal mechanism during speech.

VPD may first be managed with speech-language therapy and removable prostheses. For those who are good surgical candidates and do not fully respond to speech-language therapy, surgical intervention may be pursued.

Surgical management of VPD is most commonly accomplished by pharyngeal flap procedures or sphincter pharyngoplasty. In this video, a superiorly based pharyngeal flap with a uvular mucosal lining flap was preformed for VPD in a five-year-old patient with 22q11 Deletion Syndrome and aberrantly medial internal carotid arteries.

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