Microdebrider Assisted Lingual Tonsillectomy

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.

Endoscopic Excision of Concha Bullosa

Contributors: Gresham Richter

Here we present endoscopic excision of a concha bullosa (a pneumatized middle turbinate) that was causing obstruction in the left nasal cavity.  This particular patient failed medical management of his chronic sinusitis including antibiotic and steroid therapy. The concha bullosa was causing obstruction of the maxillary sinus ostium and deviation of the nasal septum. Resection of the concha bullosa was necessary in order to complete a functional endoscopic sinus surgery afterward and septoplasty (not shown).

DOI # 10.17797/pyzfxehca8

Author Recruited by: Gresham Ritcher

Congenital Nasal Pyriform Aperture Stenosis (CNPAS): Sublabial Approach to Surgical Correction

Congenital nasal pyriform aperture stenosis (CNPAS) is defined as inadequate formation of the pyriform apertures forming the bony nasal openings resulting in respiratory distress and cyanosis soon after birth. Some clues such as worsening distress during feeding and improvement during crying may indicate a nasal cause of respiratory distress rather than distal airway etiology. Inability or difficulty passing a small tube through the nasal cavities may suggest CNPAS. The presenting clinical features of CNPAS can be  similar to other obstructive nasal airway anomalies such as choanal atresia. Diagnosis is confirmed via CT scan with a total nasal aperture less than 11mm.

CNPAS may occur in isolation or it may be a sign of other developmental abnormalities such as holoprosencephaly, anterior pituitary abnormalities, or encephalocele. Some physical features of holoprosencephaly include closely spaced eyes, facial clefts, a single maxillary mega incisor, microcephaly, nasal malformations, and brain abnormalities (i.e. incomplete separation of the cerebral hemispheres, absent corpus callosum, and pituitary hormone deficiencies). It is important to rule out other associated abnormalities to ensure optimal treatment and intervention.

Conservative treatment of CNPAS includes humidification, nasal steroids, nasal decongestants and reflux control. Failure of conservative treatment defined by respiratory or feeding difficulty necessitates more aggressive intervention. The most definitive treatment for CNPAS is surgical intervention to enlarge the pyriform apertures.

Contributors:

Adam Johnson MD, PhD
Abby Nolder MD

Mandibular Distraction for Micrognathia in a Neonate

Introduction

Patients with Pierre-Robin Sequence (PRS) suffer from micrognathia, glossoptosis, and upper airway obstruction, which is sometimes associated with cleft palate and feeding issues.  To overcome these symptoms in our full-term male neonate patient with PRS, mandibular distraction osteogenesis was performed.

Methods

The patient was intubated after airway endoscopy.  A submandibular incision was carried down to the mandible. A distractor was modified to fit the osteotomy site that we marked, and its pin was pulled through an infrauricular incision.   Screws secured the plates and the osteotomy was performed.  The mandible was distracted 1.8 mm daily for twelve days.

Results

During distraction, the patient worked with speech therapy.  Eventually, he adequately fed orally.  He showed no further glossoptosis or obstruction after distraction was completed.

Conclusion

In our experience, mandibular distraction is a successful way to avoid a surgical airway and promote oral feeding in children with PRS and obstructive symptoms.

By: Ravi W Sun, BE

Surgeons:

Megan M Gaffey, MD

Adam B Johnson, MD, PhD

Larry D Hartzell, MD

Department of Otolaryngology – Head and Neck Surgery, University of Arkansas for Medical Sciences, Little Rock, AR, USA
Arkansas Children’s Hospital, Little Rock, AR, USA

Recruited by: Gresham T Richter, MD

Superiorly Based Pharyngeal Flap for Velopharyngeal Dysfunction

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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