Alternative interventions for obstructive sleep apnea

September 3, 2019|Cleveland Clinic Journal of Medicine
Tina Waters, MD
Author and Disclosure Information

Tina Waters, MD
Sleep Disorders Center, Neurological Institute, Cleveland Clinic

Correspondence: Tina Waters, MD, Medical Principal, Cigna; tina.waters@cigna.com

Dr. Waters reported no financial interests or relationships that pose a potential conflict of interest with this article.

This article is based on Dr. Waters’ “Alternative Interventions for Obstructive Sleep Apnea” webcast released May 23, 2019, part of the “Obstructive Sleep Apnea: A Cleveland Clinic State-of-the-Art Review” online series (available at www.clevelandclinicmeded.com/online/sleep-apnea). The article was drafted by Cleveland Clinic Journal of Medicine staff and was then reviewed, revised, and approved by Dr. Waters.

Release date: September 1, 2019
Expiration date: August 31, 2022
Estimated time of completion: 0.75 hour

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ABSTRACT

Positive airway pressure (PAP) therapy is the gold standard treatment for patients with obstructive sleep apnea (OSA) and has been shown to positively impact quality of life and cardiovascular outcomes. However, not all patients with OSA can use or tolerate PAP therapy. Alternative interventions to PAP include lifestyle measures, surgical interventions, hypoglossal nerve stimulation, oral appliance therapy, and expiratory PAP devices for OSA. While these alternative interventions may benefit patients and have demonstrated improvements in OSA and quality-of-life measures, the cardiovascular impact of these interventions is uncertain as data are limited.

KEY POINTS

  • Alternative interventions for OSA are available for patients who cannot use PAP therapy.
  • Lifestyle interventions that may benefit patients with OSA are weight loss, exercise, change in sleep position, alcohol avoidance, and a review of concomitant medications.
  • Surgical interventions for OSA target the airway obstruction and include uvulopalatopharyngoplasty, maxillomandibular advancement, and bariatric surgery. Drug-induced sleep endoscopy is increasingly used to locate airway obstruction in patients with OSA.
  • Alternative device therapies for OSA are the implanted hypoglossal nerve stimulation system, oral appliances, and nasal expiratory PAP therapy valves.

HYPOGLOSSAL NERVE STIMULATION

Figure 1. Hypoglossal nerve stimulation consists of an implanted pulse generator, sensing lead, and stimulation lead.
Used with permission from Inspire Medical Systems, Inc.
Figure 1. Hypoglossal nerve stimulation consists of an implanted pulse generator, sensing lead, and stimulation lead.
HNS, or upper airway stimulation, is a new, fully implantable treatment for patients with OSA. The system consists of an implanted pulse generator (IPG), sensing lead, and stimulation lead.17 The device is implanted unilaterally via incisions under the clavicle for the IPG, on the chest for the sensing lead, and on the neck for the stimulation lead (Figure 1).

The IPG contains a battery, computer, and lead connector block. It receives information from the sensing lead, operates timing and output algorithms, conveys energy to the stimulation lead, and also serves as a return electrode for advanced stimulation configurations. The sensing lead monitors breathing during sleep and detects pressure changes in the respiratory cycle and conveys this information to the IPG. The stimulation lead encircles the medial branch of the hypoglossal nerve (cranial nerve XII) with an electrode cuff. Stimulation as generated from the IPG is delivered to key airway muscles, which are controlled by the hypoglossal nerve, primarily the genioglossus muscle responsible for tongue protrusion. The device can be turned on and off with a handheld sleep remote.

Indications and contraindications

The indications and contraindications for HNS are shown in Table 2.

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Efficacy and outcomes

Stimulation of the hypoglossal nerve results in a multilevel mechanism of action: activation and protrusion of the tongue opens the oropharyngeal airway directly but also affects the retropalatal airway by a palatoglossal coupling action.19 Sleep lab testing with polysomnography is used to titrate the voltage of HNS to achieve an open airway that resolves apneic events and normalizes airflow, breathing patterns, and oxygen saturation levels.

Approval of HNS for OSA by the US Food and Drug Administration was based on findings in the Stimulation Therapy for Apnea Reduction (STAR) trial,17 a prospective trial of 126 patients at 22 centers in the United States and Europe with the primary outcomes of AHI and oxygen desaturation index. Secondary outcomes included quality of life as measured by the Functional Outcomes of Sleep Questionnaire and Epworth Sleepiness Scale (ESS). Patient demographics included mean age 54.5, 83% men, mean BMI of 28 kg/m2, and mean baseline AHI of 34 (ie, severe OSA).

Data at 5 years for 97 of the 126 patients on HNS in the STAR trial is available.20 The AHI was reduced an average of 70% to levels in the mild OSA range.20,21 Overall, 85% of the patients had improved quality-of-life measures after HNS implantation, with increased Functional Outcomes of Sleep Questionnaire scores and ESS scores in the normal range over time. Consistent HNS therapy demonstrated sustained benefits at 5 years. The AHI improved by 50% or to less than 20 in 75% of patients, with 44% having resolved OSA and 78% improved to mild OSA (AHI < 15). Device-related adverse events occurred in 6% (9 of 126) of patients requiring replacement or repositioning of the stimulator or leads.20

Moderate to severe snoring was prevalent at baseline in the STAR trial, but over the course of 5 years, 85% of bed partners of patients on HNS reported no or soft snoring.17,21 Nightly use averaged 80% over 60 months based on patient reporting, with 87% reporting use at least 5 nights per week at 36 weeks.20

In terms of predictors of response to HNS therapy, the oxygen desaturation index is the only characteristic that reached a level of statistical significance; patients with higher levels of oxygen desaturation tended to improve and tolerate therapy better long-term.20 A randomized controlled trial of withdrawal of HNS therapy demonstrated increased AHI and oxygen desaturation index when therapy was withdrawn, followed by improvement when therapy resumed.22

A clinical trial of 20 patients implanted with HNS after its approval in 2014 reported that the mean AHI decreased from 33 before implant to 5.1 after implant.23 The ESS also improved from 10.3 before implant to 6 after implant. Mean adherence to device use was 7 (± 2) hours per night. The average stimulation amplitude was 1.89 (± 0.5) volts after the titration sleep study was completed. Similar reductions in AHI were reported by Huntley et al24 for patients receiving HNS implant at 2 academic centers, with no differences between the 2 cohorts in postoperative AHI.

Adverse events

The adverse events reported with HNS are related to the implant procedure or the device.21 Procedure-related adverse events are incision discomfort, temporary tongue weakness, headache, and mild infection of incisions. The most common device-related adverse event is discomfort from the electrical stimulation. Tongue abrasion can also occur if the tongue protrudes and rubs against a sharp tooth. Dry mouth is also commonly reported.

HNS compared with UPPP

Outcomes in patients with moderate to severe OSA matched for BMI, demographics, and preoperative AHI were evaluated comparing patients undergoing HNS (n = 20) with patients receiving UPPP (n = 20).25 The AHI decreased 29% postoperatively in patients with UPPP compared with 88% in patients with HNS, 65% of which had normalization of their AHI. Surgical success was achieved in 40% of patients in the UPPP group compared with 100% in the HNS group. Greater improvement in daytime sleepiness was noted in patients in the HNS group compared with the UPPP group.