Bilateral Posterior Cricoarytenoid Myoneurectomy for Abductor Spasmodic Dysphonia.

OBJECTIVE: To discuss the utility and outcomes of bilateral myoneurectomy for treatment of abductor spasmodic dysphonia. METHODS: Bilateral myoneurectomy is a known treatment option for patients with adductor spasmodic dysphonia. Its use for treatment of abductor spasmodic dysphonia, however, has not been documented previously. In this case report, treatment and long-term outcomes of abductor spasmodic dysphonia with bilateral myoneurectomy are discussed. RESULTS: A 50-year-old male presented with abductor spasmodic dysphonia. His initial Voice Handicap Index-10 (VHI-10) score was 29, and he had breathy breaks during 60 series. He had no improvement in vocal quality after 6 botulinum toxin injections over 21 months. He underwent staged bilateral posterior cricoarytenoid partial myoneurectomy, with the left posterior cricoarytenoid myoneurectomy performed 33 months after presentation and right posterior cricoarytenoid myectomy 11 months later. Eight years postoperatively, his VHI-10 score was 12. During postoperative 60 series, the patient demonstrated few breathy breaks. Overall, the patient reports improved quality of life and satisfaction with his voice. CONCLUSION: This is the first report of a long-term follow-up data for bilateral, endoscopic, partial posterior cricoarytenoid muscle myoneurectomy to treat refractory abductor spasmodic dysphonia. Long-term VHI-10 results suggest improvement of symptoms, despite mild difficulty with 60 series. While botulinum toxin therapy is the mainstay of management for abductor spasmodic dysphonia, surgical treatment is a potential alternative at least for refractory cases.

Identifying eustachian tube dysfunction prior to hyperbaric oxygen therapy: Who is at risk for intolerance?

PURPOSE: Determine whether specific risk factors, symptoms and clinical examination findings are associated with hyperbaric oxygen therapy (HBOT) intolerance and subsequent tympanotomy tube placement. MATERIALS AND METHODS: A retrospective case series with chart review was conducted from 2007 to 2016 of patients undergoing HBOT clearance at a tertiary care university hospital in an urban city. Eighty-one (n=81) patient charts were reviewed for risk factors, symptoms and clinical examination findings related to HBOT eustachian tube dysfunction and middle ear barotrauma. Relative risk was calculated for each variable to determine risk for HBOT intolerance and need for tympanotomy tube placement. Risk factor, symptom, physical examination and HBOT complication-susceptibility scores were calculated for each patient. RESULTS: Mean risk factor, clinical and HBOT complication-susceptibility scores were significantly higher in patients who did not tolerate HBOT compared to patients who tolerated HBOT. Patients reporting a history of otitis media, tinnitus, and prior ear surgery were at a higher risk for HBOT intolerance. Patients reporting a history of pressure intolerance and prior ear surgery were more likely to undergo tympanotomy tube placement. Patients noted to have otologic findings prior to HBOT were at a higher risk for both HBOT intolerance and tympanotomy tube placement. CONCLUSIONS: A thorough otolaryngological evaluation can potentially predict and identify patients at risk for HBOT intolerance and tympanotomy tube placement.

Laryngotracheal mucormycosis: Report of a case.

Airway mucormycosis is a deadly opportunistic infection that affects immunocompromised persons, particularly diabetics and those undergoing chemotherapy. Although it is typically a pulmonary or sinonasal infection, mucormycosis can affect the larynx and trachea, with devastating results. We report the case of a 46-year-old man with human immunodeficiency virus infection, hepatitis C infection, neurosyphilis, and recently diagnosed Burkitt lymphoma who presented with dysphonia and stridor after receiving one dose of intrathecal chemotherapy. Flexible laryngoscopy detected the presence of fibrinous material that was obstructing nearly the entire glottis. Surgical debridement revealed a firm mucosal attachment; there was little bleeding when it was removed. After debridement, the patient's dyspnea improved only to recur 2 days later. After an awake tracheotomy, laryngoscopy and bronchoscopy identified necrosis extending from the supraglottic area to the carina tracheae. Biopsies demonstrated hyphal architecture consistent with mucormycosis. Despite continued debridements, the fibrinous material reaccumulated. The patient was placed in hospice care; his airway remained patent, but he died from other causes several weeks after presentation. The management of airway mucormycosis is challenging and complex. Fungal airway infections should be considered in the differential diagnosis of an immunosuppressed patient who presents with dyspnea, dysphonia, and vocal fold immobility. Timely diagnosis and management are critical for a successful outcome, although the prognosis is poor if the infection is widespread, even with the best of efforts.

Vocal fold paresis and paralysis.

Diagnosis and treatment of the immobile or hypomobile vocal fold are challenging for the otolaryngologist. True paralysis and paresis result from vocal fold denervation secondary to injury to the laryngeal or vagus nerve. Vocal fold paresis or paralysis may be unilateral or bilateral, central or peripheral, and it may involve the recurrent laryngeal nerve, superior laryngeal nerve, or both. The physician's first responsibility in any case of vocal fold paresis or paralysis is to confirm the diagnosis and be certain that the laryngeal motion impairment is not caused by arytenoid cartilage dislocation or subluxation, cricoarytenoid arthritis or ankylosis, neoplasm, or other mechanical causes. Strobovideolaryngoscopy, endoscopy, radiologic and laboratory studies, and electromyography are all useful diagnostic tools.