– CAMILO REYES GELVES, MD
Obstructive sleep apnea (OSA) is a state-dependent sleep disorder that involves complete interruption or significant decrease in airflow in the presence of a breathing effort caused by repetitive upper airway collapse which results in oxygen desaturation and arousals. Consequences of untreated OSA include adverse cardiovascular and metabolic outcomes, decline in quality of life, and neurocognitive impairment. Moderate-to severe OSA, defined as an apnea–hypopnea index (AHI) score of 15 or more events per hour, is an independent risk factor for insulin resistance, dyslipidemia, vascular disease, and death1. Patients usually have nocturnal (snoring, apneas, choking sensation, arousal and awakening) and daytime symptoms (morning headaches, nonrestorative sleep, fatigue, cognitive deficits, mood changes, decreased libido and hypertension among others). In our practice, we use the Epworth sleepiness scale and the STOP BANG questionnaire to screen our patients. Patients undergo a comprehensive Otolaryngologic evaluation, medical history and physical examination. As
OSA is a state-dependent disease, at AUMC Otolaryngology, our patients also undergo a Drug Induced Sleep Endoscopy (DISE) which is the closest resemblance to Non-REM sleep2. We asses airway collapse while under simulated sleep at the palate, tongue and epiglottis3. After our evaluation, we assess patients for a hypoglossal nerve stimulator.
Indications for a hypoglossal nerve stimulator are as follow: Age > 22 y/o, Body Mass Index < 35, Diagnosed OSA with AHI 15-65, Positive Airway Pressure (PAP) failure or inability to tolerate PA. PAP failure is defined as an inability to eliminate OSA (AHI of greater than 15 despite PAP usage), and PAP intolerance is defined as: Inability to use PAP (greater than 5 nights per week of usage; usage defined as greater than 4 hours of use per night), or unwillingness to use PAP (for example, a patient returns the PAP system after attempting to use it). Finally, appropriate airway anatomy based on DISE findings4.
The system is placed under the skin of the neck and chest through 3 small incisions; a neck incision, an upper chest incision for the implant and a lower chest incision for the sense lead. The hypoglossal nerve is identified. Using a nerve stimulator, the “functional breakpoint” is identified (transition from exclusion to inclusion branches). The cuff is placed to stimulate branches to the genioglossus (oblique and horizontal), geniohyoid and transverse muscle fibers. The stimulation lead is then tunneled and sutured to the digastric muscle. After this, the implant pocket is created superficial to the pectoralis fascia. A tunnel and a pocket is created between the internal and external intercostal muscles for the sense lead which should be facing the pleura. Tunnels are created for the sense and stimulator leads towards the implant for connection. The device is placed in the pocket and sutured into the pectoralis major fascia. The chest sensor and tongue movement is then verified using telemetry. If there is no adequate response, the leads must be repositioned.
Wounds are closed in usual fashion and pressure dressing is applied. Patients must avoid any strenuous activities and avoid shoulder abduction for more than 90 degrees for one month. Four to 6 weeks postop, the implant is activated and its settings are customized during an overnight sleep study.
We present the case of a 65 y/o female with OSA apnea-hypopnea index (AHI) of 34 diagnosed in 2007 who was on CPAP therapy with a pressure between 4-18 cm H2O with a nasal mask from which she achieved improvement of her symptoms. However, she complained of nasal congestion, choking sensation, aerophagia and difficulty tolerating the mask. She underwent an uvulopalatopharyngoplasty, septoplasty and inferior turbinate reduction. Postoperative sleep study failed to show improvement on her AHI and she had significant problems using the device throughout the night with multiple awakenings. She was evaluated and stated that she would like to be “completely off the machine”. A DISE was performed and showed 1) Velopharynx – complete lateral collapse, 2) Oropharynx – complete lateral collapse, 3) Tongue base – partial A/P collapse, 4) Epiglottis – no collapse, 5) O2 nadir of 90% while on nasal cannula. She underwent a hypoglossal nerve stimulator device implant. Careful selection of extrusion branches was selected and NIM monitoring confirmed proper stimulation of extrusion branches (Figure 1). Extrusion of the tongue was seen immediately intraoperative. She was admitted overnight for observation and discharged the next day without complications. Chest X-ray was ordered to rule out pneumothorax and assess proper implant location (Figure 2). Incisions healed well and her device was activated 6 weeks postoperatively. As of now, she is sleeping 8-9 hours a night compared to less than 3 hours straight before the implant. She is not snoring and feels increased daytime level of energy.
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Stimulation for Obstructive Sleep Apnea: The STAR Trial. Otolaryngol–Head Neck Surg Off J Am Acad Otolaryngol-Head
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