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Microdebrider Assisted Lingual Tonsillectomy Adrian Williamson, Michael Kubala MD, Adam Johnson MD PhD, Megan Gaffey MD, and Gresham Richter MD The lingual tonsils are a collection of lymphoid tissue found on the base of the tongue. The lingual tonsils along with the adenoid, tubal tonsils, palatine tonsils make up Waldeyer’s tonsillar ring. Hypertrophy of the lingual tonsils contributes to obstructive sleep apnea and lingual tonsillectomy can alleviate this intermittent airway obstruction.1,2 Lingual tonsil hypertrophy can manifest more rarely with chronic infection or dysphagia. A lingual tonsil grading system has been purposed by Friedman et al 2015, which rates lingual tonsils between grade 0 and grade 4. Friedman et al define grade 0 as absent lingual tonsils and grade 4 lingual tonsils as lymphoid tissue covering the entire base of tongue and rising above the tip of the epiglottis in thickness.3 Lingual tonsillectomy has been approached by a variety of different surgical techniques including electrocautery, CO2 laser, cold ablation (coblation) and microdebridement.4-9 Transoral robotic surgery (TORS) has also been used to improve exposure of the tongue base to perform lingual tonsillectomy.10-13 At this time, there is not enough evidence to support that one of these techniques is superior. Here, we describe the microdebrider assisted lingual tonsillectomy in an 8 year-old female with Down Syndrome. This patient was following in Arkansas Children's Sleep Disorders Center and found to have persistent moderate obstructive sleep apnea despite previous adenoidectomy and palatine tonsillectomy. Unfortunately, she did not tolerate her continuous positive airway pressure (CPAP) device. The patient underwent polysomnography 2 months preoperatively which revealed an oxygen saturation nadir of 90%, an apnea-hypopnea index of 7.7, and an arousal index of 16.9. There was no evidence of central sleep apnea. The patient was referred to otolaryngology to evaluate for possible surgical management. Given the severity of the patient’s symptoms and clinical appearance, a drug induced sleep state endoscopy with possible surgical intervention was planned. The drug induced sleep state endoscopy revealed grade IV lingual tonsil hypertrophy causing obstruction of the airway with collapse of the epiglottis to the posterior pharyngeal wall. A jaw thrust was found to relieve this displacement and airway obstruction. The turbinates and pharyngeal tonsils were not causing significant obstruction of the airway. At this time the decision was made to proceed with microdebrider assisted lingual tonsillectomy. First, microlaryngoscopy and bronchoscopy were performed followed by orotracheal intubation using a Phillips 1 blade and a 0 degree Hopkins rod. Surgical exposure was achieved using suspension laryngoscopy with the Lindholm laryngoscope and the 0 degree Hopkins rod. 1% lidocaine with epinephrine is injected into the base of tongue for hemostatic control using a laryngeal needle under the guidance of the 0 degree Hopkins rod. 1. The 4 mm Tricut Sinus Microdebrider blade was set to 5000 RPM and inserted between the laryngoscope and the lips to resect the lingual tonsils. Oxymetazoline-soaked pledgets were used periodically during resection to maintain hemostasis and proper visualization. A subtotal lingual tonsillectomy was completed with preservation of the fascia overlying the musculature at the base of tongue. She was extubated following surgery and there were no postoperative complications. Four months after postoperatively the patient followed up at Arkansas Children's Sleep Disorders Center and was found to have notable clinical improvement especially with her daytime symptoms. A postoperative polysomnography was not performed given the patient’s clinical improvement.
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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