Hypoglossal Stimulation Device

Anatomy and Physiology

During respiration, negative inspiratory airway pressure (P_ins) exerts a pulling force on the soft tissues of the airway, moving them inward. If the P_ins is lower than the critical closing pressure (P_crit), the airway will collapse, and obstruction will occur.[15] Activation of upper airway musculature decreases P_crit and counteracts airway collapse.

However, upper airway musculature activation decreases during normal sleep, the airway narrows, and the P_crit increases.[3] Additionally, factors that contribute to airway narrowing, such as obesity and anatomical variations, can further elevate the P_crit. The P_crit will vary among populations during sleep. The P_crit can be as low as -25 cm H₂O in non-snorers, while it may be nearer to -10 cm H₂O in snorers. The P_crit is typically >0 cm H₂O in apneic patients.[15]

Among the upper airway muscles responsible for maintaining airway patency, the most crucial is the genioglossus muscle.[13] The large genioglossus muscle comprises a substantial portion of the tongue and is innervated by the hypoglossal nerve. Stimulation of the hypoglossal nerve and the subsequent contraction of the genioglossus muscle moves the tongue anteriorly, helping to maintain airway patency.[16] However, during sleep, reduced activation of the genioglossus results in the tongue falling backward into the airway, increasing the risk of airway obstruction. The risk of airway obstruction is further heightened when combined with other factors that lead to airway collapse, such as obesity.[7]

A hypoglossal nerve stimulator senses inspiratory effort via a pressure lead placed between the intercostal muscles. Changes in P_ins trigger stimulation of the hypoglossal nerve resulting in contraction of the genioglossus muscle, anterior movement of the tongue, widening of the airway, a reduction in the P_crit, and prevention of airway collapse.[9][17]

Indications

Candidates for HGNS must be 18 years or older, have moderate or severe OSA by AHI standards, have failed or cannot tolerate CPAP therapy, and have no complete concentric collapse (CCC) of the soft palate.

Contraindications

The HGNS procedure is contraindicated for patients with a BMI ≥32, specific anatomic abnormalities, severe obstructive or restrictive lung disease, neurologic conditions that limit upper airway control, or have >25% central or mixed apnea on the AHI. Additionally, patients with an inability to operate the HGNS system, who are pregnant, or who plan to become pregnant are not candidates for the HGNS procedure.

Equipment

Standard equipment for the HGNS procedure includes the following:

• Head and neck surgical set
• Microdissectors
• Nerve stimulator
• Bipolar stimulation electrodes
• MDT tunneler
• MDT catheter passer
• Operating microscope
• Surgical loupes

Personnel

Personnel typically include the following:

• Surgeon
• Surgical first assistant
• Anesthetist
• Circulator or operating room nurse
• Surgical technologist or operating room nurse

Preparation

A preoperative evaluation by a sleep medicine provider or an otolaryngologist (ENT) is required for all patients considering HGNS. If all inclusion criteria are met and no contraindications are found, a drug-induced sleep endoscopy (DISE) is performed to determine if complete concentric collapse (CCC) of the soft palate is present.[13] The DISE is an essential step in the preoperative evaluation; the presence of CCC results in poor outcomes compared to patients without CCC.[18] If CCC is absent, the HGNS procedure may proceed.

Informed consent should be obtained and documented. In addition to discussing the risks, benefits, and alternatives to the HGNS procedure, patients must consent to a specific follow-up appointment schedule. Typically patients are seen 1 week after the procedure by the otolaryngologist and 4 weeks after the procedure by the sleep medicine clinician. Activation of the stimulator is generally performed at this sleep medicine appointment. Additionally, titration polysomnography is performed 12 to 16 weeks after the HGNS procedure. Finally, patients will need to engage in long-term follow-up; attending 1 or 2 sleep medicine appointments per year is typical.

Technique or Treatment

The placement of a hypoglossal nerve stimulator is typically performed in the outpatient surgical setting, takes 2 to 3 hours to complete, and the stimulator is traditionally placed on the right side of the patient. The procedure comprises three distinct sections corresponding to the three incisions made.[19]

The first surgical incision is for the stimulator lead and is made approximately 2 cm below the mandibular border and anterior to the submandibular gland. After locating and dissecting the hypoglossal nerve, a bipolar stimulator is used to identify the distal branches of the hypoglossal nerve innervating the muscles of tongue protrusion, particularly the genioglossus muscle. The stimulation cuff must be implanted in the correct branches of the hypoglossal nerve, or the procedure will be unsuccessful. If the cuff incorrectly stimulates the styloglossus or hyoglossus muscles responsible for tongue retraction, the procedure will fail to maintain airway patency. Once the correct distal branches of the hypoglossal nerve are identified via stimulation or electromyography, the stimulation cuff is attached, and an anchoring suture is placed.[19][20]

The second surgical incision allows for the placement of the neuro-stimulation generator and is made approximately 3 cm below the clavicle. A pocket is created to house the neurostimulation generator, which is subsequently sutured to the pectoralis fascia.[19]

The third surgical incision is made on the inferolateral chest wall to accommodate the pressure sensor lead. The internal intercostal muscle is identified via tissue dissection, the internal and external intercostal muscles are separated, and the pressure sensor is placed between them. A tunneling catheter is used to connect the stimulator lead and the sensor lead to the neuro-stimulation generator. The device is tested to ensure adequate tongue protrusion and accurate sensing of respirations. All incisions are closed and dressed in the standard fashion. Typically, patients will be discharged home the same day.[19]

While studies have evaluated implanting the device and pressure sensor through a single shared incision, the standard approach using three incisions remains the most widely used technique.[21]

Complications

In the Stimulation Therapy for Apnea Reduction (STAR) multicenter prospective trial, 2% of patients had a severe adverse event following device placement that resulted in the need for repositioning or fixations of the stimulator.[14] Other major surgical complications, such as hematoma formation and pneumothorax, have occurred but are rare.[19]

The STAR trial also reported several nonserious adverse events related to the device or the placement procedure.

Procedure-related events included incisional postoperative discomfort in 26% of patients and nonincisional postoperative discomfort in 25%. Other reported events included temporary tongue weakness (18%), intubation effects (12%), headache (6%), other symptoms (11%), and mild infection (1%).[14] These complications were demonstrated to be transient in the five-year follow-up study. This follow-up study reported that only 1 or 2 incisional discomfort events occurred per year after the first year, while only 1 nonincisional discomfort event was reported in the third year. None of the other postoperative complications were noted after the first year.[22]

Device-related complications reported in the STAR trial included discomfort from electrical stimulation (40%), tongue abrasion (21%), dry mouth (10%), mechanical pain due to device presence (6%), temporary internal device functionality issues (10%), temporary external device use or function issues (6%), other symptoms (15%), and mild or moderate infection (1%).[14] These complications also became less common after the first year, particularly when looking at the most common complication, namely discomfort from electrical stimulation. In the fifth year following device placement, only 5 events of discomfort due to electrical stimulation were reported, compared to 81 in the first 12 months.[22] 

The prospective Adherence and Outcome of Upper Airway Stimulation for OSA International Registry (ADHERE Registry) indicates that the most common complication associated with HGNS was discomfort due to stimulation, which decreased from 12% at 6 months to 8% at 12 months.[23] The reduced incidence of discomfort due to stimulation during later postoperative visits is likely attributable to adjustments in the level of stimulation provided.[22]

Clinical Significance

The STAR trial was a prospective, multicenter, single-group trial that examined 126 patients with OSA who had a mean baseline AHI of 32 events per hour, ODI of 28.9 events per hour, Epworth Sleepiness Scale (ESS) score of 11.6, and a Functional Outcomes of Sleep Questionnaire score (FOSQ) of 14.3.[14] Following device placement, 98% of patients completed a 12-month follow-up, which found an improvement in mean AHI to 15.3 events per hour (median, 29.3-9), ODI to 13.9 events per hour (median, 25.4-7.4), ESS score of 7 (median, 11-6), and a FOSQ of 18.2 (median, 14.6-18.2).

Additionally, 46 STAR trial participants who had a response to treatment took part in a therapy withdrawal study. Patients were randomized to continue or discontinue treatment for 7 days after the 12-month follow-up. In patients who discontinued therapy, the AHI increased from a mean of 7.6 events per hour to 25.8 events per hour, and the ODI increased from 6 events per hour to 23 events per hour. In comparison, no notable change was seen in the patients who continued therapy.[14]

A five-year follow-up to the STAR trial evaluated 97 participants, of which 71 chose to undergo voluntary in-lab polysomnography. In these 71 patients, the mean AHI was 12.4 events per hour and ODI 9.9 events per hour, demonstrating maintenance of initial improvements seen at the 12-month follow-up in the STAR trial.[22] Ninety-two patients completed the evaluation of patient subjective measures, with a mean ESS score of 6.9 and a FOSQ of 18. These results demonstrate the maintenance of improvements seen in the initial trial. This five-year evaluation did find a higher rate of serious adverse events, with 6% of the initial 126 participants requiring repositioning or replacement of the neurostimulator.[22]

The prospective observational ADHERE registry evaluated 1017 patients, of which 640 completed a 6-month posttitration follow-up and 382 completed a 12-month follow-up.[23] This study found significant improvements in AHI and ESS scores, with baseline AHI falling from 32 events per hour at baseline to 6.3 and 9.5 events per hour at 6 and 12 months, respectively. At the same time, the ESS score improved from a baseline score of 11 to 7 at the 6-month evaluation and 6 at the 12-month evaluation. In addition, 93% of participants reported being satisfied with the treatment, 95% preferred it over CPAP, 94% would choose HGNS again, and median device use was 5.7 hours per night.[23]

These extensive trials demonstrate significant improvements in objective and subjective measures evaluating the severity of OSA, a low rate of significant adverse events, and that HGNS is well tolerated by patients in whom CPAP was ineffective or intolerable.

Enhancing Healthcare Team Outcomes

The primary management of OSA has traditionally been CPAP. Unfortunately, many patients do not tolerate CPAP and often go untreated. In these patients, HGNS represents a safe and viable alternative.[23] (level III).

However, the stimulator placement involves a surgical procedure, multiple follow-up visits, and titration polysomnography. Therefore, the decision to utilize HGNS as a treatment for OSA should be based on robust discussion between the patient and an interdisciplinary healthcare team of primary care, sleep medicine, and otolaryngology providers.