Bilateral tapia syndrome after maxillomandibular advancement surgery

Lesions of the hypoglossal and laryngeal nerve, recurrent in its unilateral or bilateral extracranial pathways, cause a motor deficit in the tongue with transient, partial or total loss of speech, which may be associated with mild or severe dysphagia, characterizing Tapia syndrome. This unusual condition is usually related to airway manipulation during anesthetic-surgical surgery, and few cases in the literature are correlated with maxillofacial surgeries, which partly explains the ignorance of this complication by a significant number of professionals. We describe a case report of bilateral Tapia syndrome established after a procedure for maxillomandibular advancement. This is a 55-year-old male patient diagnosed with retrognatism and retromaxillism. The patient underwent a maxillomandibular advancement with nasotracheal intubation. He evolved with bilateral Tapia syndrome, recovering from the signs and symptoms of this complication, being reoperated to correct aesthetic results obtained in the first intervention that was below acceptable, not evolving after this second surgery with the syndrome. We conclude that preventive measures should be taken, such as avoiding sudden movements in the head region and prolonged hyperextension of the neck during surgery, minimizing the trauma of the tracheal cannula on the tissues covering the hypoglossal and recurrent laryngeal nerves.

A preoperative predictive study of advantages of airway changes after maxillomandibular advancement surgery using computational fluid dynamics analysis

The purpose of this study was to develop a simulation approach for predicting maxillomandibular advancement-induced airway changes using computational fluid dynamics. Eight patients with jaw deformities who underwent maxillomandibular advancement and genioglossus advancement surgery were included in this study. Computed tomography scans and rhinomanometric readings were performed both preoperatively and postoperatively. Computational fluid dynamics models were created, and airflow simulations were performed using computational fluid dynamics software; the preferable number of computational mesh points was at least 10 million cells. The results for the right and left nares, including simulation and postoperative measurements, were qualitatively consistent, and surgery reduced airflow pressure loss. Geometry prediction simulation results were qualitatively consistent with the postoperative stereolithography data and postoperative simulation results. Simulations were performed with either the right or left naris blocked, and the predicted values were similar to those found clinically. In addition, geometry prediction simulation results were qualitatively consistent with the postoperative stereolithography data and postoperative simulation results. These findings suggest that geometry prediction simulation facilitates the preoperative prediction of the postoperative structural outcome.

Effects of maxillomandibular advancement surgery on a skeletal Class III patient with obstructive sleep apnea: A case report

This case report describes the successful surgical treatment of a patient diagnosed with obstructive sleep apnea (OSA). A 55-year-old Caucasian male patient with a body mass index (BMI) of 25.6 kg/m2 sought treatment with a chief concern of excessive daytime sleepiness and fatigue. An initial polysomnography report showed moderate OSA with an apnea-hypopnea index (AHI) of 21.2 events/h, and Epworth Sleepiness Score (ESS) of 12/24. The patient was initially prescribed with CPAP treatment but was unable to tolerate treatment after a few months. Clinical and radiographic examination revealed a concave facial profile with maxillary retrognathism. Intraoral examination revealed generalized gingival recession, missing upper lateral incisors and lower first premolars, anterior crossbite, and maxillary transverse deficiency with bilateral posterior crossbite. The lateral cephalogram showed a narrow posterior airway space at the level of the base of the tongue. The patient was treated with maxillomandibular advancement (MMA) surgery to improve airway obstruction. Results showed balanced facial esthetic and stable occlusion with a complete resolution of the patient’s OSA and a post-operative improvement of AHI from 21.2 to 0.7 events/h and ESS from 12/24 to 3/24. The lowest oxyhemoglobin saturation during sleep was improved to 97%, and the BMI decreased from 25.6 to 25.2 kg/m2. These results suggest that MMA surgical procedure can be used as a definitive treatment for patients with maxillomandibular deficiency and OSA.

822 Apnea every 5 minutes

Introduction Vagal Nerve Stimulators (VNS) are used in refractory epilepsy and depression. VNS are known to decrease airflow, oxygen saturation, and respiratory amplitude during sleep. We present a case of VNS induced OSA that was overlooked for 6 years. Report of case(s) A 63-year-old Caucasian female with refractory depression, hypothyroidism, and obesity presented with snoring and excessive daytime sleepiness (EDS). She had VNS implanted in a research trial for depression. She was on bupropion, duloxetine, lithium carbonate, lamotrigine, olanzapine, and levothyroxine. Polysomnography (PSG) showed moderate OSA with apnea-hypopnea index (AHI) of 25.8 and SpO2 nadir of 83%, and was titrated to bi-level positive airway pressure (PAP). She tried different masks and pressures but her leak and PAP intolerance persisted. There was no improvement in her EDS, and Armodafinil was prescribed for wake promotion. She struggled with bi-level PAP therapy for five years before being considered for hypoglossal nerve stimulator. But was turned down because of VNS presence. She was then recommended maxillomandibular advancement (MMA) but decided against it. She continued PAP therapy until a repeat PSG revealed mild to moderate OSA (AHI 10.9, RDI 17.8, and SpO2 nadir 79%), and it was noted that most of her respiratory events appeared in a regular fashion at 300-second intervals corresponding with the firing of VNS. PSG performed with VNS turned off showed no OSA (AHI 0.8 and SpO2 nadir 85%). PAP therapy was discontinued and subsequent nocturnal pulse oximetry showed normal oxygenation (ODI 15, RDI 17.8, SpO2 <88% for only 1.7 minutes). Her EDS resolved and VNS was eventually removed as per patient’s preference. She was started on a new medical therapy for depression. She continues to be asymptomatic. Conclusion Ascertainment bias led to delay in recognition of the cause of OSA as focus was on treatment only. Lowering the VNS frequency, increasing cycle time, turning it off during sleep or removal can improve respiratory events. The decision to do so depends on perceived benefit and harm of continuing VNS therapy. This case highlights the importance of re-evaluation of causes and treatment strategies when the standard of care is ineffective. Support (if any):