Dental Clinical Policy Bulletins (2024)

Number: 018
(Updated)

Subject: Obstructive Sleep Apnea

Reviewed: December 4, 2012

Important Note

This Clinical Policy Bulletin expresses our determination of whether certain services or supplies are medically necessary. We have reached these conclusions based on a review of currently available clinical information including:

Clinical outcome studies in peer-reviewed published medical and dental literature
Regulatory status of the technology
Evidence-based guidelines of public health and health research agencies
Evidence-based guidelines and positions of leading national health professional organizations
Views of physicians and dentists practicing in relevant clinical areas
Other relevant factors

We expressly reserve the right to revise these conclusions as clinical information changes, and welcome further relevant information.

Each benefits plan defines which services are covered, which are excluded and which are subject to dollar caps or other limits. Members and their dentists will need to consult the member's benefits plan to determine if any exclusions or other benefits limitations apply to this service or supply. The conclusion that a particular service or supply is medically necessary does not guarantee that this service or supply is covered (that is, will be paid for by Aetna) for a particular member. The member's benefits plan determines coverage. Some plans exclude coverage for services or supplies that we consider medically necessary. If there is a discrepancy between this policy and a member's plan of benefits, the benefits plan will govern. In addition, coverage may be mandated by applicable legal requirements of a state, the federal government or CMS for Medicare and Medicaid members.

Policy:

Aetna considers the diagnosis and treatment of obstructive sleep apnea (OSA)in adults aged 18 and oldermedically necessary according to the criteria outlined below.

1. Diagnosis

Aetna considers attended full-channel nocturnal polysomnography (NPSG) (Type I device) performed in a healthcare facilitymedically necessary for diagnosis in members with symptoms suggestive of obstructive sleep apnea, when attended NPSG isused as part of a comprehensive sleep evaluation, and member hasone or more ofthe following indications for attended NPSG:

1. Member has at least one of the following comorbid medical conditions that degrade the accuracy of portable monitoring:

moderate to severe pulmonary disease (with pO2 lessthan 60 or pCO2 greater than 45),
neuromuscular disease (e.g., Parkinson'sdisease, spina bifida, myotonic dystrophy, amyotrophic lateralsclerosis),
stroke,
epilepsy,
congestive heart failure (NYHA class III or IV or LVEFless than 45%),
super obesity (BMI greater than 45); or

2. Member hasone or moreof the following comorbid sleep disorders:

periodic limb movement disorder,
parasomnias,
narcolepsy,
central sleep apnea or complex sleep apnea; or

Member is less than 18 years of age; or
Member has negative or technically inadequate portable monitoring results; or
Member has low pretest probability of obstructive sleep apnea (normal BMI (less than 30), normal airway (Mallampati score1 or 2), no snoring, and normal neck circumference (less than 17 inches in men, and less than 16 inches in women)); or
Member lacks the mobility or dexterity to useportable monitoring equipment safely at home.Note: Where attended NPSG is indicated, a split-night study NPSG is considered medically necessary,in which the final portion of the NPSG is used to titrate continuous positive airway pressure (CPAP), where if Apnea Hypopnea Index (AHI) is greater than15 in first 2 hours of a diagnostic sleep study; an additional full-night CPAP titration NPSG may be necessary if the AHI is less than or equal to 15 during the first 2 hours, orif the split-night study did not allow for the abolishment of the vast majority of obstructive respiratory events (see section III below).

2. Aetna considers unattended (home) sleep studies using any of the following diagnostic techniques medically necessary formembers with symptoms suggestive of OSA (see Appendix B for definition of device types), when the home sleep studyis used as part of a comprehensive sleep evaluation:

Sleep monitoring using aType II device; or
Sleep monitoring using a Type III device, or
Sleep monitoring using a Type IV(A) device, measuring airflow and at least2 other channels and providing measurement of apnea-hypopnea index (AHI); or
Sleep monitoring using a device that measures 3 or more channels that include pulse oximetry, actigraphy, and peripheral arterial tone (e.g., Watch-PAT device).Note: Sleep studies using devices that do not provide a measurement of apnea-hypopnea index (AHI) and oxygen saturation are considered not medically necessary because they do not provide sufficient information to prescribe treatment. Examples include the BiancamedSleepMinder, SNAP testing with fewer than three channels,and the SleepImage Sleep Quality Screener.Note that the ApneaLinkdoes not meetcriteria as acovered type IV device because it does not measure airflow;however, the ApneaLink Plus records 5 channels, including airflow, and meets criteria for a covered sleep study device.

3. Attended full-channel nocturnal polysomnography (NPSG) (Type I device) performed in a healthcare facility is considered medically necessaryfor persons diagnosed with obstructive sleep apneawho haveany ofthe following indications for attended NPSG:

To titrate CPAP in persons diagnosed with clinically significant OSAfor whom in-laboratory NPSG was medically necessary, but whowere unable to undergo a split-night study because they had an insufficientAHI (less than 15) during the first two hours ofan attended NPSG; or
To titrate CPAP in persons with clinically significant OSA for whom in-laboratoryNPSG was medically necessary,andwho underwent a split-night study that did notabolish the vast majority of obstructive respiratory events; or
To monitor results from CPAP in persons with OSA who havepersistent significant symptoms (disturbed sleep with significant arousals) despite documented AHI less than 5 on CPAP and documented compliance with CPAP (CPAP used for 70 percent of nights for four or more hours per night, for two or more months); or
To confirm diagnosis of obstructive sleep apnea prior to surgical modifications of the upper airway.

4. It may be necessary to perform repeat sleep studies up to twice a year for any of the following indications (Note: where repeat testing is indicated, attended full-channel nocturnal polysomnography (NPSG) (Type I device) performed in a healthcare facility is considered medically necessary for persons who meet criteria for attended NPSGin section I above; in all other cases,unattended (home) sleep studies are considered medically necessary):

To determine whether positive airway pressure treatment (i.e., CPAP, bilevel positive airway pressure (BiPAP), demand positive airway pressure (DPAP), variable positive airway pressure (VPAP), or auto-titrating positive airway pressure (AutoPAP)) continues to be effective; or
To determine whether positive airway pressure treatment settings need to be changed; or
To determine whether continued treatment with positive airway pressure treatment is necessary; or
To assess treatment response after upper airway surgical procedures and after initial treatment with oral appliances.

5. Video-EEG-NPSG (NPSG with video monitoring of body positions and extended EEG channels) is considered medically necessary to assist with the diagnosis of paroxysmal arousals or other sleep disruptions that are thought to be seizure related when the initial clinical evaluation and results of a standard EEG are inconclusive.

6. Aetna considers any of the following diagnostic techniques experimental and investigational in members with symptoms suggestive of OSA because their effectiveness for this indication has not been established:

Acoustic pharyngometry. SeeCPB 0336 - Acoustic Pharyngometers and SNAP Testing System; or
Actigraphy testing when used alone. Actigraphy, which consists of a small portable device that senses physical motion and stores the resulting information, has been used in research studies for the evaluation of rest-activity cycles. This technique, when used alone (single channel study), has not been validated as a method of diagnosing OSA. SeeCPB 0710 - Actigraphy and Accelerometry; or
Cephalographic X-rays for diagnosis of OSA. Lateral cephalographic X-rays andorthopantograms may be medically necessary for evaluating persons for oral appliances; lateral cephalographic X-rays may also be necessary to evaluate persons for OSA surgery; or
Laryngeal function studies; or
Sonography; or
The static charge sensitive bed; or
Tomographic X-ray; or
X-rays of the temporomandibular joint or sella turcica.

Note: SNAP testing using 3 or more channels is considered a medically necessary method of home sleep testing; SNAP testing using less than 3 channels is considered experimental and investigational. See CPB 0336 Acoustic Pharyngometers and SNAP Testing System.

7. Treatment

Treatment of snoring alone, without significant OSA, is not considered medically necessary.

1. Continuous Positive Airway Pressure (CPAP)

It is expected that members receive lifestyle advicewhere applicable (i.e., helping people to lose weight, stop smoking and/or decrease alcohol consumption).

Aetna considersCPAPor autoPAP medically necessary DMEfor members with a positive facility-based NPSG*, orwith a positive home sleep test* includingType II, III, IV(A) or Watch-PAT devices, as definedby either of the following criteria:

Member's AHI is greater than or equal to 15 events/hour with a minimum of 30 events; or

2. AHI greater than 5 and less than15 events/hour with a minimum of 10 events and at least one of the following is met:

Documented history of stroke; or
Documented hypertension (systolic blood pressure greater than 140 mm Hg and/or diastolic blood pressure greater than 90 mm Hg); or
Documented ischemic heart disease; or
Documented symptoms of impaired cognition, mood disorders, or insomnia; or
Excessive daytime sleepiness (documented by either Epworth greater than 10 or Multiple Sleep Latency Test (MSLT) less than 6); or
Greater than 20 episodes of oxygen desaturation (i.e., oxygen saturation of less than 85 %) during a full night sleep study, or any one episode of oxygen desaturation (i.e., oxygen saturation of less than 70 %).

*The sleep study is based on a minimum of 2 hours of continuous recorded sleep or shorter periods of continuous recorded sleep if the total number of recorded events during that shorter period is at least the number of events that would have been required in a 2-hour period.

Notes: The AHI is equal to the average number of episodes of apnea and hypopnea per hour of sleep. The respiratory disturbance index (RDI) is equal to the episodes of apnea and hypopnea per hour of measurement. Forpurposes of this policy, apnea is defined as a cessation of airflow for at least 10 seconds. Hypopnea is defined as an abnormal respiratory event lasting at least 10 seconds with at least a 30% reduction in thoraco-abdominal movement or airflow as compared to baseline, and with at least a 4% oxygen desaturation. Leg movement, snoring, respiratory event related arousals (RERAs), and other sleep disturbances that may be included by some polysomnographic facilities are not considered to meet theAHI and/or RDI definition in this policy. Although AHI and RDI have been used interchangeably, some facilities use the term RDI to describe a calculation that includes these other sleep disturbances. Requests for CPAP will be considered not medically necessary if based upon an index that does not score apneas and hypopneas separately from other sleep disturbance events. Only persons with an AHI and/or RDI, as defined in this policy that meets medical necessity criteria may qualify for a CPAP device.

Aetna considers CPAP experimental and investigational for the treatment ofpersons with upper airway resistance syndrome (UARS) or for the improvement of seizure control in persons with epilepsy.

BiPAP without a backup rate feature, DPAP, and VPAP are considered medically necessary DME for members who are intolerant to CPAP or AutoPAP. These alternatives to CPAP may also be considered medically necessary for OSA members with concomitant breathing disorders, which include restrictive thoracic disorders, COPD, and nocturnal hypoventilation. An oral pressure appliance (OPAP) is considered medically necessary DME only on an exception basis for members who are unable to tolerate a standard nasal/face mask due to facial discomfort, sinus pain, or claustrophobia from masks. A BiPAP device with a backup rate feature (e.g., adaptive servoventilation, VPAP Adapt SV) is considered experimental and investigational for obstructive sleep apnea (seeCPB 0452 - Noninvasive Positive Pressure Ventilation).

The following accessories and supplies are considered medically necessary for members who meet criteria for positive airway pressure devices:

Chinstrap
Disposable or non-disposable filters
Full face mask with positive airway pressure device*
Headgear
Heated or non-heated humidifier
Nasal interface (mask or cannula type) for positive airway pressure device
Oral interface for positive airway pressure device
Replacement cushions and pillows for nasal application device
Replacement interface for full face mask
Tubing for heated or non-heated humidifier.

* Nasal interface (mask or cannula type) may be used with positive airway pressure device, with or without head strap is an alternative to full face mask. However, upgraded face maskis considered medically necessary only if there is documentation that the member needs a different mask because he/she can not maintain CPAP pressures or that in order to get the pressure the mask needs to be so tight as to generate pressure sores.

Note: Aetna follows Medicare DME MACrules with respect to the usual medically necessary quantity of supplies for positive airway pressure devices.

Upon individual review, positive airway pressure devices are considered a medically necessary form of non-invasive ventilation for members with lung disease without OSA. Requests for these devices for non-invasive ventilation of members with lung disease are subject to medical review.

2. Oral Appliances

Custom-fitted and prefabricated oral appliances to reduce upper airway collapsibility are considered medically necessary for members with OSA who meet the medical necessity criteria for CPAP or AutoPAP. Oral appliances to reduce upper airway collapsibility are considered experimental and investigational for indications other than OSA. The diagnosis must be made by the patient's physician and/or qualified alternate medical professional (sleep specialist) and not by the patient's dentist.

Oral appliances for OSA that are available over-the-counter without a prescription are not considered medically necessary because they have not been shown to be as effective as prefabricated or custom-fitted oral appliances in the treatment of OSA.

Note

: Dental rehabilitation services (dentures, bridgework, etc.) as treatment for OSA, even if medically necessary, are not available benefits under standard Aetna health insurance plans. Members should review their dental benefits plan, if any.

Uvulopalatopharyngoplasty (UPPP)

Uvulopalatopharyngoplasty is used to treat OSA by enlarging the oropharynx; it is considered medically necessary for OSA members who meet the criteria for CPAP orAutoPAP(see above), but who are intolerant to CPAP or AutoPAP. The medical records must document that the member has attempted CPAP or AutoPAPbefore considering surgery.

Uvulopalatopharyngoplasty has been found to be most reliably effective in OSA members who have adequately responded to a trial of CPAP or AutoPAP. If CPAP or AutoPAPis unsuccessful in relieving a member's symptoms, this indicates that apnea is not due to obstruction. Aetna considers this procedure experimental and investigational for persons who do not respond to CPAP or AutoPAPbecause this surgical approach has not been shown to be effective in non-obstructive apnea.

4. Uvulectomy and Laser Assisted Uvuloplasty (LAUP)

Cold knife uvulectomy and laser assisted uvuloplasty (LAUP, laser uvulectomy) are considered experimental and investigational for OSA because they have not been shown to be as effective as UPPP for this indication. However, Aetna may consider these procedures medically necessary, upon individual case review, for members with severe OSA who have other medical conditions that make them unable to undergo UPPP and have failed a trial of CPAP or AutoPAPor the use of an oral appliance or device. Note: Uvulectomy is considered medically necessary as an emergent treatment for acute edema of the uvula causing acute respiratory distress. Uvulectomy is considered experimental and investigational as a treatment for recurrent throat infections and for all other indications.

According to guidelines from the American Academy of Sleep Medicine (Chesson et al, 1997), polysomnography with video recording and additional EEG channels in an extended bilateral montage may be indicated to assist with the diagnosis of paroxysmal arousals or other sleep disruptions that are thought to be seizure related when the initial clinical evaluation and results of a standard EEG are inconclusive.

Accepted guidelines indicate that nocturnal pulse oximetry alone is not appropriately used as a case finding or screening method to rule out OSA. Pulse oximetry, when used alone, has not been shown to have an adequate negative predictive value to rule out OSA (i.e., all patients with symptoms suggestive of OSA would require polysomnography regardless of whether the pulse oximetry was positive or negative).

The MESAM and the static charge sensitive bed have not been proven to be valid devices for screening or diagnosing OSA. Actigraphy has not been validated as a method of screening or diagnosing OSA although it may be a useful adjunct to other procedures in the evaluation of sleep disorders.

Although the cephalometric x-ray is not necessary for the diagnosis of OSA, it is necessary for certain non-surgical and surgical treatments. A lateral cephalometric x-ray is very helpful if an anterior mandibular osteotomy is being performed for genioglossus advancement, or if maxillomandibular surgery is being planned for surgical correction of OSA. It is also helpful in analyzing hyoid position, posterior airway space, and other cephalometric parameters used in the treatment of OSA. For sleep apnea appliances for OSA, a pre-treatment lateral cephalometric x-ray and a second cephalometric X-ray with the bite registration or appliance in place may be necessary to visualize the mandibular repositioning and the changes in the airway space.

Uvulopalatopharyngoplasty, jaw realignment surgery, positive airway pressure devices (e.g., CPAP, BiPAP, etc.), tracheostomy, tonsillectomy and adenoidectomy, and orthodontic devices such as the tongue retaining device, may be effective treatments for properly selected patients with OSA.

Several small scale studies have examined adult tonsillectomy as treatment for tonsil hypertrophy. Martinho et al (2006) evaluated seven moderately obese obstructive sleep apnea-hypopnea syndrome (OSAHS) with obstructive palatine tonsil hypertrophy patients who were treated with tonsillectomy. The authors reported that tonsillectomy resulted in a significant reduction in AHI post-operatively and concluded that tonsillectomy could be considered an option for obese OSAHS patients with significant tonsil hypertrophy when CPAP is not possible as the first choice of treatment.

Verse et al (2000) evaluated11 patients with substantial tonsilar hypertrophy who had undergone tonsillectomy as single-treatment. The patient population included 5 patients with severe OSA, 4 with mild OSA, and 2 patients who were simple snorers with an AHI below 10. The results of 3 to 6 months of follow-up showed surgical response rates were 80 % in severe apneics and 100 % in mild apneics. However, Verse et al also noted that substantial tonsilar hypertrophy can rarely cause OSA in adults and that their patient population was carefully selected to determine if tonsillectomy was an effective and safe surgical option in treating this disorder.

With respect to simple tonsillectomy as a treatment for adult OSA, updates to the American Academy of Sleep Medicine practice parameters for the treatment of OSA state that classic upper airway surgical techniques such as nasal-septal reconstruction, cauterization, and tonsillectomy frequently fail to correct OSA (Aurora et al, 2010).

The Food and Drug Administration (FDA) has cleared numerous types of CPAP devices under the 510(k) process. These include but are not limited to many devices that allow a patient to wear a device that collects airflow and other patient measurements into a device that records data, while treating OSA with that device. The patient then takes the device to the physician and the physician downloads information that determines whether the patient has apnea sleep-related breathing disorder including OSA or needs further sleep studies or assessment. There are currently many sleep assessment devices on the market cleared by the FDA through the 510(k) process for use in the home. Patients may have a 3-month trial period of CPAP to assess appropriate therapeutic use and response. Reports obtained via a compliance monitor may be included when making this determination.

A variety of oral appliances and prostheses, including tongue retainers and mandibular advancing devices, have been used to treat patients with OSA. These devices modify the airway by changing the posture of the mandible and tongue. A task force of the Standards of Practice Committee of the ASDA concluded that, despite the considerable variation in the design of these devices, their clinical effects in improving OSA have been consistent (Kushida et al, 2006). These devices have been shown to be effective in alleviating OSA, and present a useful alternative to CPAP or surgery (Ferguson et al, 2006; Gotsopoulos et al, 2002). Oral appliances, however, have been shown to be less reliable and effective than CPAP, and therefore the literature suggests that their use should generally be reserved for patients who are intolerant of CPAP. Oral appliances can be pre-fabricated or custom-fabricated. There is evidence of the efficacy of both pre-fabricated and custom-fabricated appliances for OSA (Vanderveken et al, 2008; Henke et al, 2000).

Patients with OSA suffer from numerous apneic events while sleeping, due to collapse of the upper airway during inspiration. Continuous positive airway pressure, and more recently, BiPAP, DPAP, VPAP, and AutoPAP, have been used in the treatment of OSA as a means of serving as a "pneumatic splint" in order to prop open the airways during inspiration.

Bilevel positive airway pressure, DPAP, and VPAP have been shown to be effective alternatives to CPAP, but are indicated only as second line measures for patients who are intolerant to CPAP. These alternatives to CPAP may also be indicated for OSA patients with concomitant breathing disorders to include restrictive thoracic disorders, COPD, and nocturnal hypoventilation. Long-term adherence to CPAP therapy was initially reported to range from 65 to 80 % (Nino-Murcia et al, 1989; Waldhorn et al, 1990; Rolfe et al, 1991; Hoffstein et al, 1992) with 8 to 15 % of patients refusing to accept treatment (Waldhorn, 1990; Krieger, 1992) after a single night's use. Other studies have evaluated compliance as regular CPAP use. More recent studies have shown up to 80 % of patients falling into the category of regular users (Pepin et al, 1999).

OPAP(Oral Pressure Appliance) is a custom fabricated intra-oral device that is used with a positive airway pressure device (e.g., CPAP, BiPAP, etc.) in place of a standard nasal mask. The oral pressure appliance positions the lower jaw forward to maximize the forward movement of the tongue and soft tissues of the back of the throat. In addition, the device has a chamber that, according to the manufacturer, allows air flow and pressure to be delivered into the back of the throat and thereby "splint" the soft tissues of the upper airway and prevent their collapse during sleep. The oral pressure appliance is custom fitted by a dentist specializing in dental appliances for sleep disorders. The OPAP method of treatment is similar to nasal mask delivery of air pressure with CPAP or BiPAP. The oral pressure appliance is connected to the end of the hose coming from the CPAP or BiPAP, and the pressure is adjusted in the same way as through the nose. OPAP differs from nasal masks in that it does not require head gear to hold it in place. It is inserted into the mouth and held in place by the upper and lower teeth. At present, no studies of OPAP have been published in peer-reviewed medical journals. Therefore, one is unable to draw any conclusions about the effectiveness of OPAP compared to a standard nasal mask in treatment of patients with obstructive sleep apnea.

In contrast to fixed CPAP, flexible positive airway pressure (C-Flex, Respironics, Murraysville, PA) (also known as pressure-relief CPAP) is characterized by a pressure reduction at the beginning of expiration. Flexible positive airway pressure is intended to improve patient satisfaction and compliance over standard CPAP. To compare adherence and clinical outcomes between flexible positive airway pressure CPAP, Aloia et al (2005) conducted a nonrandomized, open-label controlled trial of CPAP therapy versus therapy using the C-Flex device in persons with moderate-to-severe OSA. Study participants received either therapy with CPAP (n = 41) or with the C-Flex device (n = 48), depending on the available treatment at the time of recruitment, with those recruited earlier receiving CPAP therapy and those recruited later receiving therapy with the C-Flex device. The mean (+/- SD) treatment adherence over the 3-month follow-up period was higher in the C-Flex group compared to the CPAP group (weeks 2 to 4, 4.2 +/- 2.4 versus 3.5 +/- 2.8, respectively; weeks 9 to 12, 4.8 +/- 2.4 versus 3.1 +/- 2.8, respectively). The investigators reported that change in subjective sleepiness and functional outcomes associated with sleep did not improve more in one group over the other. Self-efficacy showed a trend toward being higher at the follow-up in those patients who had been treated with the C-Flex device compared to CPAP treatment. The investigators concluded that therapy with the C-Flex device may improve overall adherence over 3 months compared to standard therapy with CPAP. The investigators stated that clinical outcomes do not improve consistently, but C-Flex users may be more confident about their ability to adhere to treatment. The investigators concluded that randomized clinical trials are needed to replicate these findings.

A study by Nilius et al (2006) found no significant differences between C-Flex and CPAP in effectiveness and compliance. During the first night of treatment, patients receiving C-Flex had less dryness of the mouth, but this difference disappeared over a period of 7 weeks. The investigators conducted a study to compare polysomnographic data and compliance in sleep apnea patients receiving continuous positive airway pressure (CPAP) and C-Flex. A total of 52 persons newly diagnosed withOSA underwent conventional CPAP titration. Thereafter, polysomnography was performed at the titrated pressure using both the fixed CPAP pressure mode and the C-Flex mode in a randomized crossover approach. The patients were then discharged home for 7 weeks of treatment with the last-applied treatment mode, and compliance data were established at the end of that time. The average AHI was 5.8/hour with CPAP, and 7.0/hour with C-Flex. The investigators reported that compliance after 7 weeks was, on average, 9.4 mins longer with C-Flex than with CPAP, a difference that was not statistically significant. Evaluation of a 13-item questionnaire (the fewer the complaints, the lower the score) showed no significant difference between scores for C-Flex (16.4) and CPAP (18.1). With regard to oral dryness, the score with C-Flex (1.4) was significantly lower than with CPAP (1.9) (p < 0.05). The investigators reported that this difference in oral dryness score was no longer detectable after 7 weeks. The investigators concluded that further studies are needed.

According to the Standard of Practice Committee of the American Academy of Sleep Medicine (Littner et al, 2002), central apnea may occur in some OSA patients with congestive heart failure (CHF) during CPAP titration after the airway obstruction of OSA is treated. Other patients with OSA may have central apneas after arousals as they fall back to sleep or which are the result of excessive CPAP pressure. Attempts to identify central apnea by detecting cardiac oscillations in the airflow tracing during polysomnography are not reliable because the airway can close during central apnea and the oscillations may not appear.

Adaptive servo-ventilation (ASV), a novel method of ventilatory support, is considered a bilevel positive airway pressure with a backup rate feature, and uses an automatic, minute ventilation-targeted device (VPAP Adapt, ResMed, Poway, CA) that performs breath to breath analysis and adjusts its settings accordingly. Depending on breathing effort, the device will automatically adjust the amount of airflow it delivers in order to maintain a steady minute ventilation. Most studies on the use of ASV have investigated its use for heart failure patients with central apnea or Cheyne-Stokes respiration (Teschler et al, 2001; Pepperell et al, 2003; Töpfer et al, 2004; Pepin et al, 2006; Kasai et al, 2006; Zhang et al, 2006;Banno et al, 2006; Morrell et al, 2007; Morgenthaler et al, 2007; Hastings et al, 2010). Consistent withDurable Medical Equipment Medicare Administrative Carrier (DME MAC)policy, bilevel positive airway pressure with a backup rate feature is considered experimental and investigational for OSA (NHIC, 2008).

While virtually all studies report that surgical treatment of OSA improves snoring and daytime sleepiness, improvements in objective outcomes have been inconsistent with successful results of UPPP ranging from 50 % to 75 %. Fujitais credited with developing the UPPP as a method of enlarging the oropharynx (Fujita et al, 1985). He based the UPPP on his observation that patients with OSA, without other obvious sites of obstruction, often have a large edematous uvula, wide posterior tonsillar pillar mucosa and redundant mucosal folds in the lateral posterior pharyngeal walls extending from the nasopharynx to the hypopharynx. The surgery attempts to remove the redundant tissue but preserve the underlying muscular layer. In brief, the mucosae and submucosae of the soft palate, tonsillar fossa and the lateral aspect of the uvula are resected. The posterior pillar may be resected if contributing to the narrowing. In essence the amount of tissue removed is individualized for each patient, determined by the potential space and the width of the tonsillar pillar mucosa between the2 palatal arches (Fujita et al, 1985). For a detailed discussion of the UPPP technique and its variants see the review by Koopmannand Moran (1990).

The UPPP enlarges the oropharynx but cannot correct obstructions in the hypopharynx. Early on it was recognized that UPPP failed in about 50 % of unselected patients with OSA. Riley et al(1990) and Crumley et al(1987) proposed that these failures may have been caused by an obstruction at the base of the tongue. The surgical approach to this problem has been to either modify the tongue itself or reposition the tongue by repositioning the mandible and/or maxilla.

Riley and Guilleminault and colleagues at the Sleep Disorders Center at Stanford University (Palo Alto CA) have been the primary early advocates of maxillofacial surgery for those patients who fail other treatment approaches. A stepwise protocol has been described (Riley et al, 1986; Riley et al, 1989; Riley et al, 1990). For example a hyoid resuspension can be done at the time of a UPPP. In this procedure the hyoid is resuspended anteriorally and superiorally from the mandible with strips of fascia lata harvested from the thigh. In this way the tongue is moved anteriorally.If the patient fails this treatment, he/she then becomes eligible for the maxillary and mandibular osteotomy (MMO). While the purpose of this procedure is to enlarge the hypopharynx by advancing the mandible, the maxilla is also advanced to permit greater advancement of the mandible and to provide optimal esthetics. The maxilla is advanced by a Le Fort I osteotomy with rigid fixation and the mandible by a bilateral sagittal ramus split. The fixation must be maintained for one to three weeks. If a dental malocclusion is created by this surgery, the MMO must be preceeded by a total mandibular subapical osteotomy with retropostioning of the dentition and bilateral repositioning of the inferior alveolar nerve. All3 of the above procedures are frequently preformed in conjunction with removal of fatty tissue of the neck.

Jaw realignment is an aggressive, multi-step procedure requiring a3- to6-month interval between each step. According to the medical literature, jaw realignment surgery is generally reserved for those patients who fail other treatment approaches for OSA. An NIH Statement (1995) and American Sleep Disorders Association Guidelines (1996) state that jaw realignment surgery is a promising treatment for OSA. A systematic review of the evidence prepared for the American Sleep Disorders Association by Scher et al (1996), concluded that inferior sagittal mandibular osteotomy and genioglossal advancement with or without hyoid myotomy and suspension appears to be the most promising of procedures directed at enlarging the retrolingual region. The ASDA assessment stated that most of the experience with genioglossal advancement with or without hyoid suspension has been in conjunction with or following UPPP. Jaw fixation is necessary for2 to3 weeks following surgery, and a soft diet is necessary for a total of6 weeks. Patients undergoing jaw realignment surgery must usually also undergo orthodontic therapy to correct changes in occlusion associated with the surgery. Jaw realignment surgery is generally reserved for those patients who fail other treatment approaches for OSA. According to the medical literature, patients undergoing jaw realignment surgery must usually also undergo orthodontic therapy to correct changes in occlusion associated with the surgery.

Tracheostomy, which simply bypasses the obstructing lesion of the upper airways, has been shown to be the most effective and predictable surgical approach to OSA. However, the social and medical morbidities of a permanent tracheostomy and the advent of surgical alternatives have made tracheostomy an unpopular solution to OSA, reserved for those patients with the most severe sleep apnea not manageable by other interventions.

Laser-assisted uvulopalatoplasty (LAUP) is an outpatient surgical procedure, which has been used as a treatment for snoring. LAUP has also been used as a treatment for sleep-related breathing disorders, including obstructive sleep apnea. The American Academy of Sleep Medicine Standards of Practice Committee reviewed the evidence supporting the use of LAUP in obstructive sleep apnea, and found that adequate controlled studies on the LAUP procedure for sleep-related breathing disorders were not found in the peer-reviewed literature (Littner et al, 2001). The AASM concluded that "LAUP is not recommended for treatment of sleep-related breathing disorders."

There is some evidence for the use of uvulectomy or uvuloplasty as a treatment for snoring, but Aetna does not consider treatment of snoring medically necessary because snoring, in itself, is not associated with functional limitations. Most of the published literature on uvulectomy have to do with ritual removal of the uvula at birth in Africa, a practice that is associated with significant complications. Uvulectomy is also performed, again primarily in Africa, as a treatment for recurrent throat infections. However, there is no reliable evidence to support this practice. Acute edema of the uvula causing respiratory distress is an accepted indication for uvulectomy. Hawke and Kwok (1987) reported on uvulectomy in treating a patient with acute inflammatory edema of the uvula (uvulitis) associated with asphyxiation. Waeckerle et al (1976) reported on uvulectomy for hereditary angioneurotic edema. There is no evidence to support the use of uvulectomy as a treatment for gagging. Dawodu (2007) reported that gagging may occur as a complication of uvulectomy.

Radiofrequency ablation may be used to reduce and tighten excess tissues of the soft palate, uvula and tongue base (Somnoplasty) or nasal passages and soft palate (Coblation or Coblation channeling). These procedures are performed in an outpatient setting under local anesthesia. Current literature does not support their efficacy and applicability for OSA. Most published studies have been nonrandomized and have enrolled highly selected patients. These studies also fail to report long-term outcomes or recurrence rates. Woodson et al (2003) reported on the results of radiofrequency ablation of the turbinates and soft palate in patients with mild to moderate obstructive sleep apnea (AHI of 10 to 30 on screening sleep study).A total of 90subjects were randomly assigned to radiofrequency ablation, CPAP, or sham-placebo. Subjects assigned to radiofrequency ablation had a moderate decrease in AHI that did not reach statistical significance. The AHI of subjects assigned to radiofrequency ablation decreased by an average of 4.5 events/hour, whereas the AHI of subjects assigned to sham-placebo decreased by an average of 1.8 events/hour, a difference that did not achieve statistical significance. However, compared with sham-placebo, subjects assigned to radiofrequency ablation reported statistically significant improvements in quality of life, airway volume, apnea index and respiratory arousal index. In addition to the modest impact of radiofrequency ablation on AHI, this study has a number of other important limitations. First, it is a relatively small study, and improvements were not consistently seen among each of the measured parameters. Second, a significant number of subjects were lost to follow-up, and data were incomplete on 25 % of study subjects. Third, the study does not report on long-term clinical outcomes or recurrence rates. Fourth, although this study did not involve a direct comparison with UPPP, which is the current surgical standard treatment for OSA, studies of UPPP have reported much more substantial improvements in AHI, AI and other relevant parameters. Finally, this study involved a single investigator group and is the only published randomized clinical study of radiofrequency ablation for OSA; this study needs to be replicated by other investigators and in larger numbers of subjects.

A recent study (Garrigue et al, 2002) reported on the results of an uncontrolled case series examining the impact of atrial overdrive pacing in 15 patients with central orOSA syndrome who had received permanent atrial-synchronous ventricular pacemakers for symptomatic sinus bradycardia. With atrial overdrive pacing, achieved by increasing the atrial base rate, patients had a significantly reduced the number of episodes of central or OSA (from an average AHI of 28 with spontaneous rhythm to an average AHI of 11 with atrial overdrive pacing) without a significant reduction in total sleep time. The authors, however, concluded that further studies are needed to elucidate the mechanisms involved in achieving these reductions and to assess the precise role of cardiac pacing in preventing symptoms, disability, and death in patients with sleep apnea syndrome. In a randomized controlled trial, Luthje et al (2005) aimed to reproduce the finding of a recent study that atrial overdrive pacing markedly improved SDB. These investigators found that neither the primary endpoint AHI, nor the apnea index, oxygen desaturation, ventilation, biomarkers were affected by the nocturnal atrial overdrive pacing. They concluded that the lack of effect on the AHI means that atrial overdrive pacing is inappropriate for treating SDB. This is in agreement with the findings of a randomized controlled study by Pepin et al (2005) who reported that atrial overdrive pacing has no significant effect on OSA.

In a randomized controlled study, Simantirakis et al (2005) reported that atrial over-drive pacing had no significant effect in treating OSA-hypopnea syndrome. In another randomized controlled study, Krahn et al (2006) evaluated the impact of prevention of bradycardia with physiologic pacing on the severity of OSA. The authors concluded that temporary atrial pacing does not appear to improve respiratory manifestations of OSA, and that permanent atrial pacing in this patient population does not appear to be justified.

Upper airway resistance syndrome (UARS) is characterized by a normal AHI, but with sleep fragmentation related to subtle airway resistance. Guilleminault and colleagues (1993) considered UARS clinically significant if it entails greater than 10 episodes of EEG arousals/hour of sleep in patients with a documented history of excessive daytime sleepiness. They described UARS as multiple sleep fragmentations resulting from very short alpha EEG arousals, which in turn are related to an increase in resistance to airflow. According to Guilleminault et al (1993), the resistance to airflow is subtle enough that it is not detected by routine sleep analysis, but can be detected with esophageal pressure tracings. In addition, UARS may not be associated with snoring, the classic symptom of OSA. However, there is no consensus on the criteria for diagnosis or indications for treatment of UARS. Neither the American Sleep Disorders Association nor any other professional medical organization has issued guidelines for the diagnosis and treatment of UARS.

Cautery-assisted palatal stiffening operation (CAPSO) is an office-based procedure performed with local anesthesia for the treatment of palatal snoring. A midline strip of soft palate mucosa is removed, and the wound is allowed to heal by secondary intention. The flaccid palate is stiffened, and palatal snoring ceases. Wassmuth et al (2000) evaluated the ability of CAPSO to treat OSA syndrome (OSAS). A total of 25 consecutive patients with OSAS underwent CAPSO. Responders were defined as patients who had a reduction in AHI of 50 % or more and an AHI of 10 or less after surgery. By these strict criteria, 40 % of patients were considered to have responded to CAPSO. Mean AHI improved significantly from 25.1 +/- 12.9 to 16.6 +/- 15.0. The Epworth Sleepiness Scale improved significantly from 12.7 +/- 5.6 to 8.8 +/- 4.6. Mair and Day (2000) analyzed data on CAPSO with regard to extent of surgery, need for repetition of procedure, results, complications, predictors of success. A totalof 206 consecutive patients underwent CAPSO over an 18-month period, followed by office examination and telephone evaluation. The success rate was initially 92 % and dipped to 77 % after 1 year. CAPSO eliminates excessive snoring caused by palatal flutter and has success rates that were comparable with those of traditional palatal surgery. The authors stated that CAPSO is a simple and safe office procedure that avoids the need for multiple-stage operations and does not rely on expensive laser systems or radiofrequency generators and hand pieces. The results of these studies appear to be promising; however their findings need to be verified by randomized controlled studies.

In a prospective, non-randomized study, Pang and Terris (2007) evaluated the effectiveness of CAPSO in treating snoring and mild OSA. A total of 13 patients with simple snoring and mild OSA underwent the modified CAPSO under local anesthesia. Patients had pre-operative polysomnography and at 3 months post-operatively; they were Friedman stage II and III, with tonsil size 0, 1, or 2. All patients had improvement in their snoring; 84 % had improvement in the Epworth Sleepiness Scale, from 12.2 to 8.9. Objective success on the polysomnogram was noted in 75 % of patients (6/8) with mild OSA. The AHI improved from 12.3 % to 5.2 % (p < 0.05), and the lowest oxygen saturation improved from 88.3 % to 92.5 % (p < 0.05). The authors concluded that the modified CAPSO is a simple, low-cost, and effective office-based method to treat snoring and mild OSA. The findings of this small study are promising. Randomized controlled trials with larger sample size and longer follow-up are needed to ascertain the clinical value of CAPSO.

The PillarPalatal Implant System (Restore Medical, Inc.) is intended as a treatment option for snoring and OSA. The System consists of an implant and a delivery tool. The implants are designed to stiffen the tissue of the soft palate reducing the dynamic flutter which causes snoring. According to the manufacturer, the implants reduce the incidence of airway obstruction caused by the soft palate. The implant is a cylindrical shaped segment of braided polyester filaments. The delivery tool is comprised of a handle and needle assembly that allows for positioning and placement of the implant submucosally in the soft palate. The implant is designed to be permanent while the delivery tool is disposable.

Clinical information on Restore's website reported that with the Pillar Procedure, AHI was reduced in 13 of 16 patients (81.3 %) with a 53.4 % mean decrease for those 13 patients. Six of the 13 patients (46.2 %) experienced an AHI decrease of greater than 50 % along with a 90-day AHI of less than 10. Ten of the 13 patients (76.9 %) decreased to an AHI less than 10. While these data appeared promising, larger prospective clinical studies with longer follow-up are needed in the peer-reviewed published literature to validate the effectiveness of this procedure for OSA.

In a retrospective review of 125 patients who underwent the Pillar implant for snoring and obstructive sleep apnea/hypopnea syndrome (OSAHS), Friedman and colleagues (2006) found that the Pillar implant is an effective treatment for snoring and OSAHS in selected patients and can be combined with adjunctive procedures to treat OSAHS. The major drawback of this study was that it was a short-term study. Well-designed studies with long-term follow-up are needed to determine the real value of this technique.

A structured assessment of the evidence for the Pillar procedure by Adelaide Health Technology Assessment for the Australian Department of Health and Ageing (Mundy et al, 2006) concluded: "Further investigation is required to establish which patients (mild or moderate obstructive sleep apnoea) would benefit the most from this procedure, and whether greater success would be achieved in conjunction with more invasive surgical procedures. In addition, long-term follow-up of obstructive sleep apnoea patients may indicate whether or not the observed reductions in AHI delivered a clinical benefit to these patients".

This is in agreement with the conclusions of an assessment by the Canadian Agency for Drugs and Technologies in Health (CADTH, 2007), which stated that there is currently insufficient published evidence to ascertain if palatal implants (e.g., the Pillar System) are an effective treatment option for patients with mild to moderate OSA due to palatal obstruction. The CADTH report further stated that larger, randomized controlled studies are needed to determine the long-term safety and effectiveness of the implants in a more diverse patient population, including those who are obese or those with co-morbid medical conditions. Comparisons with existing treatments for OSA are also needed.

An assessment by the National Institute for Health and Clinical Excellence (NICE, 2007) reached similar conclusions about the lack of reliable evidence of the effectiveness of palatal implants as a treatment for obstructive sleep apnea. The assessment concluded: "Current evidence on soft-palate implants for obstructive sleep apnoea (OSA) raises no major safety concerns, but there is inadequate evidence that the procedure is efficacious in the treatment of this potentially serious condition for which other treatments exist. Therefore, soft-palate implants should not be used in the treatment of this condition".

In a prospective study, Nordgard et al (2007) assessed the long-term effectiveness of palatal implants for treatment of mild-to-moderate OSA. A total of 26 referred patients with a pre-treatment AHI of 10 to 30 and a BMI of less than or equal to 30, representing an extended follow-up of a subset of 41 patients enrolled in previous short-term trials were included. Twenty-one of 26 patients (80.8 %) experienced a decrease in AHI. Fifteen of 26 patients (57.7 %) had a follow-up AHI less than 10 at 1 year, whereas 13 patients (50 %) had a 50 % or greater reduction to an AHI less than 10 at 1 year. Mean AHI was reduced from 16.5 +/- 4.5 at baseline to 12.5 +/- 10.5 at 3 months (p < 0.014) and to 12.3 +/- 12.7 at 1 year (p < 0.019). The authors concluded that patients initially responding to palatal implants with improved AHI maintained improvement through long-term follow-up at 1 year. The main drawback of this study was its small sample size. The authors noted that additional studies with longer follow-up would be appropriate.

In a continuation of a prospective case series, Walker et al (2007) assessed the long-term safety and outcomes of palatal implants for patients with mild-to-moderate OSA. Polysomnography, daytime sleepiness, and snoring intensity were measured at baseline, 90 days, and extended follow-up. A total of 22 (42 %) patients from the previous study were followed for a median of 435.5 days. Thirteen were classified as responders, based on their 90-day evaluation; 76.9 % of initial responders maintained improvements in AHI, daytime sleepiness, and snoring at extended follow-up. Nine patients were initial non-responders for AHI and daytime sleepiness and remained unchanged at extended follow-up. However, snoring for these 9 patients initially improved, and the improvement continued through extended follow-up. The authors concluded that initial response or non-response to palatal implants remains stable over an extended period. However, they noted that the generalizability of these results is unknown because of significant loss to follow-up (31 of 53 or 58 %). Other drawbacks of this study were small sample size, lack of randomization, as well as selection bias that can occur among patients who chose to participate in a follow-up study.

In a multi-institution, randomized, placebo-controlled study, Steward and colleagues (2008) examined the effectiveness of Pillar palate implants for OSA. A total of 100 patients with mild-to-moderate OSA and suspected retropalatal obstruction were randomly assigned treatment with three palatal implants or sham placebo. Final AHI increased for both groups at 3 months, correlating with increased percentage of supine sleep but was less in the implant group (p = 0.05). A clinically meaningful reduction in AHI (greater than or equal to 50 % reduction to less than 20) was more common in the implant group (26 % versus 10 %, p = 0.05). Significant differences were noted for changes in lowest oxyhemoglobin saturation (p = 0.007) and Functional Outcomes of Sleep Questionnaire (p = 0.05). Improvement in Epworth Sleepiness Score did not differ from that of sham (p = 0.62). Partial implant extrusion occurred in 2 patients (4 %). The authors concluded that palate implants for mild-to-moderate OSA showed effectiveness over placebo for several important outcomes measures with minimal morbidity, but overall effectiveness remains limited. They stated that further study is needed.

In a randomized, double-blind, placebo-controlled study, Gillespie et al (2011) examined if the Pillar palatal implant system reduces CPAP pressure and improves patient compliance with CPAP therapy. Subjects with mild-to-moderate sleep apnea dissatisfied with CPAP because of pressure-related complaints were randomized to receive Pillar implants or a sham procedure performed in double-blind fashion. Active and sham groups were compared for changes in therapeutic CPAP pressures (primary outcome) with a 90-day follow-up sleep study and CPAP compliance (secondary outcome) with a 90-day smart card report. A total of 26 subjects were randomized to Pillar implants and 25 to a sham implant procedure. There were no differences between groups with regard to demographics and baseline parameters. Both sham and active groups had reduced mean CPAP pressure (-1.1 versus -0.5 cm H(2)O) with no difference between groups (p = 0.32) at 90-day follow-up. In addition, there was no difference in average daily CPAP use between groups (p = 0.80). Both groups experienced improvements in Epworth sleepiness scores and Functional Outcome of Sleep Questionnaire scores at 90 days with no differences between groups. The active group reported significantly higher CPAP satisfaction scores than the sham group (p = 0.04). The authors concluded that Pillar implants do not significantly reduce CPAP pressure or increase CPAP compliance compared to sham controls but marginally improve subjective CPAP satisfaction (but the reason for this is unclear). These findings do not presently support the use of Pillar implants as an adjunctive treatment to improve CPAP compliance.

In a Cochrane review, Smith et al (2006) ascertained the effectiveness of drug therapies in the treatment of OSA. The authors concluded that there is insufficient evidence to recommend the use of drug therapy in the treatment of OSA. They noted that small studies have reported positive effects of certain agents on short-term outcome. Certain agents have been shown to reduce the AHI in largely unselected populations with OSA by between 24 and 45 %. For fluticasone, mirtazipine, physostigmine and nasal lubricant, studies of longer duration are needed to establish if this has an impact on daytime symptoms. Individual patients had more complete responses to particular drugs. It is likely that better matching of drugs to patients according to the dominant mechanism of their OSA will lead to better results and this also requires more investigation.

Transpalatal advancement pharyngoplasty (TAP) changes the retro-palatal airway by advancing the palate forward without excising the soft palate. The TAP procedure has been employed alone or in combination with other soft tissue surgeries for patients with narrowing in the retro-palatal airway, in particular, narrowing proximal to the point of palatal excision using traditional UPPP techniques. A transpalatal approach and advancement has also been advocated for individuals with obstructions in the nasopharynx that can not be accessed through traditional techniques. However, to date, there is very little published outcomes data for patients with OSA. Woodson (2005) described the findings of 30 subjects who underwent TAP; 20 of them also had various tongue-base procedures performed at the same time as TAP. Only 10 had TAP alone. Post-operative AHI in these 30 patients was better than a comparable group of 44 patients undergoing UPPP, 26 of whom had UPPP as the sole procedure. In addition, for the patients in each group who did not have additional tongue base surgery, the AHI improved significantly more in the TAP-treated subjects (n = 10) than the UPPP-treated subjects (n = 26). Larger studies are needed to establish the safety and effectiveness of the TAP procedure, together with prospective comparisons with established palate-based surgical techniques.

It has been suggested that nasal surgery may improve subjective daytime complaints in patients with OSA. However, published reports have not demonstrated that reducing nasal obstruction and resistance from various causes and using various methods, (e.g., polypectomy, septoplasty, turbinectomy, and radiofrequency ablation of inferior nasal turbinates) correlates with a significant reduction in objective OSA indicators (e.g., AHI or nocturnal oxygen desaturation). In this regard, Kohler and colleagues (2007) stated that the impact of treating nasal obstruction in patients with snoring and OSA on long-term outcome remains to be defined through randomized controlled studies of medical as well as surgical treatments.

Koutsourelakis et al (2008) stated that although nasal surgery has limited effectiveness in OSA treatment, some patients experience improvement. These researchers tested the hypothesis that post-surgery improvement is associated with increased nasal breathing epochs. A total of 49 OSA patients (mean AHI 30.1 +/- 16.3 events x h(-1)) with symptomatic fixed nasal obstruction due to deviated septum were randomly assigned to either septoplasty (surgery group; n = 27) or sham surgery (placebo group; n = 22). The breathing route was examined during over-night polysomnography. All patients in the placebo group were non-responders, whereas in the surgery group 4 (14.8 %) patients were responders and exhibited considerable increase in nasal breathing epochs (epochs containing more than 3 consecutive phasic nasal signals), and 23 patients were non-responders, presenting a modest increase in nasal breathing epochs. The change in AHI was inversely related to the change in nasal breathing epochs, with responders exhibiting among the greatest increases in nasal breathing epochs. Baseline nasal breathing epochs were positively related to percent change in AHI. Responders had among the lowest baseline nasal breathing epochs; a cut-off value of 62.4 % of total sleep epochs best separated (100 % sensitivity, 82.6 % specificity) responders/non-responders. The authors concluded that nasal surgery rarely treats OSA effectively; but baseline nasal breathing epochs can predict the surgery outcome.

Lin and associates (2008) provided an overview of the literature on multi-level surgery for patients with OSA/hypopnea syndrome (OSAHS) patients. Articles were included only if the surgical intervention involved at least two of the frequently involved anatomical sites: nose, oropharynx, and hypopharynx. After applying specific inclusion criteria, 49 multi-level surgery articles (58 groups) were identified. There were 1,978 patients included in the study. The mean minimal follow-up time was 7.3 months (range of 1 to 100 months). A meta-analysis was performed to re-define the success rate to be consistent with the commonly agreed upon criteria, namely "a reduction in the AHI of 50 % or more and an AHI of less than 20". "Success" implies an improved condition and is not meant to imply cure. The re-calculated success rate was 66.4 %. The overall complication rate was 14.6 %. The evidence-base medicine (EBM) level of these 49 studies revealed that only 1 study was EBM level 1, 2 papers were EBM level 3, and the other 46 papers were ranked as level 4 evidence. The authors concluded that multi-level surgery for OSAHS is associated with improved outcomes, although this benefit is supported largely by level 4 evidence. They stated that future research should focus on prospective and controlled studies. This is in agreement with the observation of Randerath et al (2007) who noted that combined surgeries in the sense of multi-level surgery concepts are of increasing interest in the secondary treatment of OSA following failure of nasal ventilation therapy although more evidence from prospective controlled trials are needed.

In a prospective, randomized cross-over study, Thomas et al (2003) compared the effectiveness of 2 tongue-base surgical procedures in the treatment of patients with moderate-to-severe sleep-disordered breathing. A total of 17 patients with moderate-to-severe sleep-disordered breathing and Fujita type II upper airway collapse for whom conservative treatment failed were enrolled in this study. They were randomly assigned to undergo palatopharyngoplasty combined with either tongue advancement (mandibular osteotomy) or tongue suspension. Parameters assessed included severity of sleep-disordered breathing (polysomnography), sleepiness (Epworth Sleepiness Scale [ESS]), and anatomic changes (upper airway endoscopy), as well as demographic factors. Patients not achieving satisfactory improvement in their condition were offered non-surgical management or additional surgical treatment that varied based on the post-operative assessment but included crossing-over to the other tongue surgical procedure. Nine of the 17 patients were randomized to the tongue suspension group, and 8 to the tongue advancement group. In the 9 tongue suspension patients, ESSscores fell from 12.1 to 4.1 (p = 0.007). Airway collapse for all 9 patients measured on Müller maneuver improved, by a mean of 64 % (p = 0.0006) at the palate and 83 % (p = 0.0003) at the base of the tongue. In the 8 tongue advancement patients, ESS scores fell from a mean of 13.3 to 5.4 (p = 0.004). Airway collapse for 5 of 8 patients measured on Müller maneuver improved by a mean of 31 % (p = 0.1) at the palate and 75 % (p = 0.03) at the base of the tongue. The authors concluded that prospective, randomized trials of tongue-base surgery for sleep-disordered breathing are possible. Preliminary findings from the current protocol reveal a slight advantage of tongue suspension over tongue advancement.

In a Cochrane review on surgery for OSA that included tongue advancement and tongue suspension, Sundaram et al (2005) concluded that the review do not provide evidence to support the use of surgery in sleep apnea/hypopnea syndrome, as overall significant benefit has not been demonstrated. Subjects recruited to the studies had mixed levels of AHI, but tended to suffer from moderate daytime sleepiness where this was measured. Short-term outcomes are unlikely to consistently identify suitable candidates for surgery. Long-term follow-up ofindividuals who undergo surgical correction of upper airway obstruction is needed. This would help to determine whether surgery is a curative intervention, or whether there is a tendency for the signs and symptoms of sleep apnea to re-assert themselves, prompting patients to seek further treatment for sleep apnea.

In a pilot study, Hamans etal (2008) examined the effectiveness of adjustable tongue advancement for the treatment of OSA.A total of 10patients (mean age of 44 years) with moderate-to-severe OSA, i.e., an AHI between 15 and 50, with CPAP intolerance were included inthis prospective, non-randomized, multi-center study to evaluate the feasibility, safety, andeffectiveness ofthis novel procedure, whichconsists of the implantation of a tissue anchor in the tongue base and an adjustment spool at the mandible. Titration of this tissue anchor results in advancement of the tongue and a patent upper airway. The mean AHI decreased from 22.8 at baseline to 11.8 at the 6-month follow-up (p = 0.007). The ESS score decreased from 11.4 at baseline to 7.7 at the 6-month follow-up (p = 0.094), and the snoring score decreased from 7.5 at baseline to 3.9 at the 6-month follow-up (p = 0.005). Four technical adverse events were noted, and 1 clinical adverse event occurred. The authors concluded that adjustable tongue advancement is a feasible and relatively safe way to reduce the AHI and snoring in selected patients with moderate-to-severe OSA and CPAP intolerance. Technical improvements and refinements to the procedure are ongoing.

In a phase II, prospective,multi-center, case series study, Woodson and colleagues (2010) examined the safety and effectiveness of a new surgical device for tongue suspension for OSA -- the Advance System (an adjustable tongue-advancement device). Surgically naive patients with moderate-to-severe OSA and tongue base obstruction (BMI less than32, AHI 15 to 60) underwent surgical insertion of a mid-line tissue anchor into the posterior tongue and connected to an adjustable mandibular bone anchor with a flexible tether. Outcomes included changes in AHI, sleepiness (Epworth Sleepiness Scale), sleep-related quality-of-life (Functional Outcomes of Sleep Questionnaire), snoring, swallowing, speech, and pain (0 to 10 visual analog scale [VAS]). Followingimplantation of the device, 42 patients (mean age of 50 years, BMI 28) noted improvement at6 months for AHI (mean [SD]: 35.5 [20.4] to 27.3 [18.8]), Epworth Sleepiness Scale (11.5 [3.9] to 7.8 [4.7]), and Functional Outcomes of Sleep Questionnaire (15.5 [2.6] to 17.5 [2.6], allp < 0.01). Snoring VAS scores improved (7.3 [2.1] to 4.7 [2.9],p < 0.01). Post-implantation pain scores were mild-to-moderate (4.4) at day1 and resolved by day 5. Post-titration pain scores were mild (less than2). Device-related adverse events included wound infection (7 %) and edema or seroma (5 %), which resolved. However, in 31% of patients, asymptomatic tissue anchor barb fractures were observed radiographically. The authors concluded that the tissue anchor failure rate of the tested device precludes its clinical use; however, the study results support that a titratable, tongue-suspension device with low direct surgical morbidity in patients with moderate-to-severe OSA significantly improves multiple measures of sleep apnea. They stated that further investigation is warranted.

Obstructive sleep apnea has been reported to be common in medically refractory epileptic patients. Chihorek and colleagues (2007) examined if OSA is associated with seizure exacerbation in older adults with epilepsy. Polysomnography was performed in older adult patients with late-onset or worsening seizures (group 1, n = 11) and those who were seizure-free or who had improvement of seizures (group 2, n = 10). Patients in group 1 had a significantly higher AHI than patients in group 2 (p = 0.002). Group 1 patients also had higher Epworth Sleepiness Scale scores (p = 0.009) and higher scores on the Sleep Apnea Scale of the Sleep Disorders Questionnaire (p = 0.04). The two groups were similar in age, BMI, neck circumference, number of anti-epileptic drugs currently used, and frequency of nocturnal seizures. The authors concluded that OSA is associated with seizure exacerbation in older adults with epilepsy, and its treatment may represent an important avenue for improving seizure control in this population. Moreover, they noted that large, prospective, placebo-controlled studies are needed to ascertain if treatment of OSA (e.g., CPAP) improves seizures control in patients with epilepsy.

Malow and colleagues (2008) stated that small, uncontrolled case series suggested that treatment of OSA in patients with epilepsy may improve seizure control. These researchersaddressed critical design issues in a pilot study before conducting a definitive, randomized, controlled trial.They identified a cohort of adult patients with medically refractory epilepsy and co-existing OSA, documented by PSG. After an 8-week baseline period, subjects with OSA were randomized to therapeutic or sham CPAP for 10 weeks. Subjects maintained seizure calendars and anti-epileptic drug dosages were held constant. A total of 68 subjects with suspected OSA were enrolled and 35 subjects randomized to therapeutic CPAP (n = 22) or sham CPAP (n = 13). Male gender and an elevated sleep apnea questionnaire score were predictive of OSA on PSG. Nineteen subjects in the therapeutic group and all 13 subjects in the sham group completed the trial. Baseline AHI and CPAP adherence were comparable between groups. A significant reduction in AHI was observed in the therapeutic CPAP group as compared to the sham group. Subjects, study co-ordinators, and principal investigators were unable to predict treatment allocation. The authors concluded that the findings of this pilot study provided critical information related to study design and feasibility for planning a comprehensive trial to test the hypothesis that treatingOSA in patients with epilepsy improves seizure control. They stated that randomized, large-scale, multi-center clinical trials are needed to confirm these results.

The Provent sleep apnea therapy is a non-invasive treatment for OSA. The Provent nasal device uses a novel MicroValve design that attaches over the nostrils and is secured in place with hypo-allergenic adhesive. The MicroValve opens and closes, redirecting air through small holes to create resistance upon breathing out.

In a pilot study, Colrain and associates (2008) tested the hypothesis that the application of expiratory resistance via a nasal valve device would improve breathing during sleep in subjects with OSA and in primary snorers.A total of 30men and women were recruited from the community and from the Stanford University Sleep Disorders Clinic; 24 had at least mild OSA (AHI greater than 5), and 6 were primary snorers. Subjects underwent 2 nights of polysomnographic evaluation, one with and one without a new nasal resistance device with the order of nights counter-balanced across participants. The device consisted of a small valve inserted into each nostril calibrated to provide negligible inspiratory resistance, but increased expiratory resistance with a back pressure between 60 and 90 cm H2O*sec/Liter (at 100 ml/sec flow). StandardPSG was conducted to compare participants' sleep both with and without the device, with the scoring conducted blind to treatment condition. The AHI (p < 0.001) and oxygen desaturation (O2DI) (p < 0.01) indices both significantly decreased, and the percentage of the night spent above 90 % saturation (p < 0.05) significantly increased with device use. The observed amount of snoring (p < 0.001) was significantly decreased with device use, and there were no significant changes in measures of sleep architecture. The authors concluded that these findings were suggestive of a therapeutic effect of expiratory nasal resistance for some OSA patients and indicated that this technique is worthy of further clinical study. This trial examined the effect of the device over1 day, and thusdid not provide any information on the durability of the effect of the device in OSA.

In a multi-center study, Rosenthal et al (2009) evaluated the effectiveness of a novel device placed in the nares that imposes an expiratory resistance for the treatment of OSA and assessed adherence to the device over a 30-day in-home trial period. One diagnostic and 3 treatment polysomnograms were administered in a Latin-square design to identify the optimal expiratory resistance to be used during the 30-day in-home trial. Subjects had repeatPSG with the prescribed device at the end of the 30-day trial. Subjects (n = 34; aged 27 to 67 years) with a baseline AHIgreater than or equal to5 were included in this study. The AHI was reduced from 24.5 +/- 23.6 (mean +/- SD) to an average of 13.5 +/- 18.7 (p < 0.001) across initial treatment nights. The AHI was 15.5 +/- 18.9 (p = 0.001) for the prescribed device at the end of the 30-day trial. Of 24 subjects with an AHIgreater than10 at baseline, 13 achieved an AHI less than 10 on the initial treatment nights; 10 had a similar response on the final treatment night. Percent of the night snoring decreased from 27.5 +/- 23.2 to 11.6 +/- 13.7 (p < 0.001) on initial treatment nights and 14.6 +/- 20.6 (p = 0.013) at the end of the trial; Epworth Sleepiness scores decreased from 8.7 +/- 4.0 at baseline to 6.9 +/- 4.4 (p < 0.001) at the end of the trial; the Pittsburgh Sleep Quality Index improved from 7.4 +/- 3.3 to 6.5 +/- 3.6 (p = 0.042). Mean oxygen saturation increased from 94.8 +/- 2.0 to 95.2 +/- 1.9 (p = 0.023) on initial treatment nights and 95.3 +/- 1.9 (p = 0.003) at the end of the trial. Sleep architecture was not affected. Participants reported using the device all night long for 94 % of nights during the in-home trial. The authors concluded that treatment with this novel device was well-tolerated and accepted by the participants. An overall reduction in AHI was documented; however, therapeutic response was variable among the participants. They stated that further research isneeded to identify the ideal candidates for this new therapeutic option in the management of OSA. This small, uncontrolled trial, which showed a statistically significant impact on one of the primary endpoints, AHI, but a non-significant result for another endpoint, oxygen desaturation index. In addition, Provent has not been either compared to CPAP, or evaluated in persons who have failed CPAP. Although reduction in AHI with Provent was significant, patients on average still had clinically significant OSA (AHIgreater than5); by contrast, studies of CPAP have shown success in getting AHI below 5.

Walsh et al (2011) evaluated the short-term efficacy of and adherence with a convenient expiratory positive airway pressure (EPAP) nasal device was evaluated in OSA patients non-adherent with CPAP. Participants were OSA patients who refused CPAP or used CPAP less than 3 hrs/night. After demonstrating tolerability to the EPAP device during approximately 1 week of home use, patients underwent a screening/baseline polysomnogram (PSG1) and a treatment PSG (PSG2). Patients meeting pre-specified efficacy criteria underwent PSG3 after about 5 weeks of EPAP treatment. Forty-seven of 59 eligible patients (80 %) tolerated the device and underwent PSG1. Forty-three patients (27 males, 16 females; 53.7 ± 10.9 years) met apnea-hypopnea index (AHI) entry criteria and underwent PSG2. Mean AHI decreased from 43.3 ± 29.0 at baseline to 27.0 ± 26.7 (p < 0.001) at PSG2. Twenty-four patients (56 %) met efficacy criteria; their mean AHI was 31.9 ± 19.8, 11.0 ± 7.9, 16.4 ± 12.2 at PSG1, PSG2, and PSG3, respectively (p < 0.001, PSG1 versus both PSG2 and PSG3). Mean Epworth Sleepiness Scale (ESS) scores were 12.3 ± 4.8 at baseline, 11.1 ± 5.1 at PSG1, and 8.7 ± 4.4 at PSG3 (p = 0.001 compared to baseline). Device use was reported an average of 92 % of all sleep hours. The authors concluded that the improvements in AHI and ESS, combined with the high degree of treatment adherence observed, suggested that the convenient EPAP device tested may become a useful therapeutic option for OSA. Limitations of this study included lack of a sham or other comparative treatment, lack of objective method for measuring adherence data, small sample size and short duration of study, as well as frequent interaction by study staff.

Berry et al (2011) examined the efficacy of a novel nasal expiratory positive airway pressure (EPAP) device as a treatment for OSA. Patients were treated with a nasal EPAP device (n = 127) or similar appearing sham device (n = 123) for 3 months. Polysomnography (PSG) was performed on 2 non-consecutive nights (random order: device-on, device-off) at week 1 and after 3 months of treatment. Analysis of an intention- to-treat group (ITT) (patients completing week 1 PSGs) (EPAP n = 119, sham n = 110) was performed. At week 1, the median AHI value (device-on versus device-off) was significantly lower with EPAP (5.0 versus 13.8 events/hr, p < 0.0001) but not sham (11.6 versus 11.1 events/h, p = NS); the decrease in the AHI (median) was greater (-52.7 % versus -7.3 %, p < 0.0001) for the ITT group. At month 3, the percentage decrease in the AHI was 42.7 % (EPAP) and 10.1 % (sham), p < 0.0001. Over 3 months of EPAP treatment the Epworth Sleepiness Scale decreased (9.9 ± 4.7 to 7.2 ± 4.2, p < 0.0001), and the median percentage of reported nights used (entire night) was 88.2 %. The authors concluded that nasal EPAP device significantly reduced the AHI and improved subjective daytime sleepiness compared to the sham treatment in patients with mild to severe OSA with excellent adherence. The results of this study suggested that nasal EPAP is an effective treatment alternative for a substantial percentage of OSA patients. Limitations of this study included large number of exclusion criteria, and lack of objective method for measuring adherence data. Also, no baseline predictors of treatment success were identified by post hoc analysis.

Patel et al (2011) examine characteristics predictive of therapeutic response to the device and provided pilot data as to its potential mechanisms of action. A total of 20 subjects (15 males, 5 females, aged 54 ± 12 years, BMI 33.5 ± 5.6 kg/m²) with OSAHS underwent 3 nocturnal polysomnograms (NPSG) including diagnostic, therapeutic (with a Provent® nasal valve device), and CPAP. Additional measurements included intra-nasal pressures and PCO, closing pressures (Pcrit), and awake lung volumes in different body positions. In 19/20 patients who slept with the device, RDI was significantly reduced with the nasal valve device compared to the diagnostic NPSG (27 ± 29/hr versus 49 ± 28/hr), with 50 % of patients having an acceptable therapeutic response. Among demographic, lung volume, or diagnostic NPSG measures or markers of collapsibility, no significant predictors of therapeutic response were found. There was a suggestion that patients with position-dependent SDB (supine RDI greater than lateral RDI) were more likely to have an acceptable therapeutic response to the device. Successful elimination of SDB was associated with generation and maintenance of an elevated end expiratory pressure. No single definitive mechanism of action was elucidated. The authors concluded that the present study shows that the nasal valve device can alter SDB across the full spectrum of SDB severity. There was a suggestion that subjects with positional or milder SDB in the lateral position were those most likely to respond (but this observation needs to be confirmed in a larger study). An important limitation of this study was that these researchers did not directly assess lung volume during sleep. The authors noted that this pilot study was not able to establish predictors of success or a single definitive mechanism of action; but does help define a restricted list of candidates for further investigation.

Kryger et al (2011) evaluated the long-term durability of treatment response and safety of a nasal EPAP device used to treat OSA. Patients in the EPAP arm of the EPAP versus sham randomized study who used the EPAP device ≥ 4 hrs/night, ≥ 5 nights/week on average during months 1 and 2 of the 3-month trial and had ≥ 50 % reduction in AHI or AHI reduction to < 10 documented by polysomnography, comparing the 3-month device-on PSG to the week-one device-off PSG. Treatment with a nasal EPAP device (n = 41) for 12 months. Polysomnography (PSG) on the patients wearing the device was performed after 12 months of treatment. The month 12 device-on PSG data from the analyzable subject cohort (n = 34) was compared to the week 1 device-off PSG from the EPAP versus sham trial. Of the 51 patients eligible, 34 were still using the EPAP device at the end of 12 months. Median AHI was reduced from 15.7 to 4.7 events/hr (week 1 device-off versus month 12 device-on). The decrease in the AHI (median) was 71.3 % (p < 0.001). The median proportion of sleep time with snoring was reduced by 74.4 % (p < 0.001). Over 12 months of EPAP treatment, the Epworth Sleepiness Scale decreased (11.1 ± 4.2 to 6.0 ± 3.2, p < 0.001), and the median percentage of reported nights used (entire night) was 89.3 %. The authors concluded that nasal EPAP significantly reduced the AHI, improved subjective daytime sleepiness and reduced snoring after 12 months of treatment. Long-term adherence to EPAP was excellent in those who had a positive clinical response at month 3 of the EPAP versus sham study. (This appeared to be the same study as reported by Berry et al, 2011 and exhibitedsimilar limitations as that study).

The Zzoma positional device is a cervical pillow designed to prevent positional sleep apnea patients from rolling onto their backs. The device was cleared by the FDA based upon a 510(k) premarket notificationdue toits substantial equivalence to another positional device, a Sona pillow, which is one of several cervical pillows that have been cleared for treatment of mild obstructive sleep apnea and snoring.

A number of studies have examined various positioning devices for treatment of positional obstructive sleep apnea. Skinner et al (2008) studied a thoracic anti-supine band (TASB), which mimics the 'tennis-ball technique' in a randomized cross-over trial of 20 adults with mild to moderate positional obstructive sleep apnea. Portable sleep studies measuring AHI were performed at start of treatment and at 1-month follow-up. Mean AHI (+/- SD) was 12.0 +/- 14.5/H for TASB and 4.9 +/- 3.9/H for nasal CPAP (nCPAP). No significant difference was founding sleep efficiency or subjective responses. The investigators concluded that "control of body position during sleep using an anti-supine device mimicking the so-called 'tennis ball technique' provides benefit in the management of position-dependent [obstructive sleep apnea hypopnea syndrome] in subjects who meet strict inclusion criteria. The overall improvement is, however, less than for nCPAP.

Lee et al (2009) evaluated optimal sleep positions in 16 patients, including lateral position, cervical vertebral support with head tilting (CVS-HT), scapula support (SS), and LP, through use of polysomnography for2 successive nights. Lateral position was found to have the most dominant effect (p = 0.0319) and SS (p = 0.0265) for AHI. The study did not, however, specify any particular positional device for cervical support.

The Zzoma positional device has been examined in a clinical trial. Permut et al (2010) randomly assigned 38 patients to either the Zzoma positional device (PD) OR CPAP. They found no significant different between PD and CPAP in their ability to normalize their AHI (p = 0.16). However, the mean SaO2 during the night was unchanged compared with baseline with the use of PD but was increased with CPAP therapy from 95 % to 96 % (p < 0.001). The lowest SaO2 increased during the night for both PD and CPAP groups. The investigators concluded that positional therapy is equivalent to CPAP at normalizing the AHI in patients with positional OSA, with similar effects on sleep quality and nocturnal oxygenation.They noted that positional therapy is effective at maintaining sleep in the non-supine position during the night and is similar to CPAP therapy in its effects on sleep quality and nocturnal oxygenation. Whether more prolonged use will maintain these effects and how positional therapy compares with CPAP in regard to cognitive function, compliance, and quality of life awaits further study. Drawbacks of this study included (i) it only studied the acute 1-night effects of the PD, as compared with CPAP. Assessment of effectiveness would require the use of other outcome measures, such as daytime sleepiness, cognitive function, and quality of life, all of which would have to be evaluated in a randomized trial after more prolonged use and would be influenced by compliance, and (ii) this study did not include patients with severe OSA.

No studies were found in the peer-reviewed literature comparing the Zzoma device to other positional devices. The Clinical Guideline for the Evaluation, Management and Long-term Care of Obstructive Sleep apnea in Adults released by the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine (Epstein et al, 2009) state that "positional therapy, consisting of a method that keeps the patient in a non-supine position, is an effective secondary therapy or can be a supplement to primary therapies for OSA in patients who have a low AHI in the non-supine versus that in the supine position". The guideline does not, however, specify a particular positional device. The guidelines state "[a] positioning device (e.g., alarm, pillow, back pack, tennis ball) should be used when initiating positional therapy".

Valbuza et al (2010) stated that treatment of OSA using methods for increasing upper airway muscle tone has been controversial and poorly reported. These investigators reviewed the evidence to evaluate the effectiveness of these methods. Data sources are from the Cochrane Library, Medline, Embase and Scielo, registries of ongoing trials, theses indexed at Biblioteca Regional de Medicina/Pan-American Health Organization of the World Health Organization and the reference lists of all the trials retrieved. This was a review of randomized or quasi-randomized double-blind trials on OSA. Two reviewers independently applied eligibility criteria. One reviewer assessed study quality and extracted data, and these processes were checked by a second reviewer. The primary outcome was a decrease in the AHI of below 5 episodes per hour. Other outcomes were subjective sleep quality, sleep quality measured by NPSG, quality of life measured subjectively and adverse events associated with the treatments. Three eligible trials were included -- 2 showed improvements through the objective and subjective analyses, and 1 showed improvement of snoring, but not of AHI while the subjective analyses showed no improvement. The adverse events were reported and they were not significant. The authors concluded that there is no accepted scientific evidence that methods aiming to increase muscle tone of the stomatognathic system are effective in reducing AHI to below 5 events per hour. They stated that well-designed randomized controlled trials are needed to assess the effectiveness of such methods.

The European Respiratory Society's task force on non-CPAP therapies in sleep apneas (Randerath et al, 2011) summarized the effectiveness of alternative treatment options in OSAS. The task force evaluated the scientific literature according to the standards of evidence-based medicine. Evidence supports the use of mandibular advancement devices in mild-to-moderate OSAS. Maxillo-mandibular osteotomy seems to be as efficient as CPAP in patients who refuse conservative treatment. Distraction osteogenesis is usefully applied in congenital micrognathia or mid-face hypoplasia. There is a trend towards improvement after weight reduction. Positional therapy is clearly inferior to CPAP and long-term compliance is poor. Drugs, nasal dilators and apnea triggered muscle stimulation can not be recommended as effective treatments of OSAS at the moment. Although tongue muscle training improves snoring, it is not efficacious in the treatment of sleep apnoea in general. Nasal surgery, radiofrequency tonsil reduction, tongue base surgery, uvulo-palatal flap, laser mid-line glossectomy, tongue suspension and genioglossus advancement can not be recommended as single interventions. Uvulopalatopharyngoplasty, pillar implants and hyoid suspension should only be considered in selected patients and potential benefits should be weighed against the risk of long-term side-effects. Multi-level surgery is only a salvage procedure for OSA patients.

Percutaneous submental electrical stimulation during sleep has been suggested as a method for treating patients with OSA. Electrical stimulation to the submental region during OSA is reported to break the apnea without arousal and to diminish apneic index, time spent in apnea, and oxygen desaturation. The mode of breaking the apnea by electrical stimulation has not yet been shown. Moreover, genioglossus is supposed to be the muscle responsible for breaking the apnea by forward movement of the tongue. However, the therapeutic value of transcutaneous electrical stimulation of the genioglossus muscle in patients with OSA to reduce sleep-disordered breathing is stillunclear. The European Respiratory Society's task force on non-CPAP therapies in sleep apneas (Randerath et al, 2011) noted that "[t]here are conflicting results on the clinical efficacy of apnoea triggered neurostimulation. Intraneural stimulation of the hypoglossus nerve and transcutaneous electrical stimulation of the genioglossus muscle showed significant improvements of respiratory disturbances and sleep parameters without adverse effects. In contrast, other groups failed to find an enlargement of the upper airways by transcutaneous or intramuscular stimulation during wakefulness or sleep. However, undesirable contractions of the platysma or tongue were observed and arousals were induced".

Appendix A

Epworth Sleepiness Scale

Indicate the likelihood of falling asleep in the following commonly encountered situations. Assign the following scores to the patient's responses:

Likelihood of dozing	Score
None	0
Low Chance	1
Moderate Chance	2
High Chance	3

Sitting and reading
Watching TV
Sitting, inactive, in a public place, i.e., theater
As a passenger in a car for an hour without a break
Lying down to rest in the afternoon when circ*mstances permit
Sitting and talking to someone
In a car, while stopped for a few minutes in traffic.

Sum the scores. A total greater than 10 is considered abnormal.

Multiple Sleep Latency Test (MSLT)

The MSLT, most commonly used in the evaluation of narcolepsy, is also used to document daytime sleepiness in OSA. The MSLT evaluates the rapidity with which a patient falls asleep during daytime nap opportunities at 2-hour intervals throughout the day. The test is typically administered after an overnight polysomnogram. Similar to the polysomnogram, the EEG, EOG and EMG are routinely recorded. A sleep latency of less than 6 mins is considered clinically significant. Although the polysomnogram is always part of the work-up of OAS, the MSLT is considered expensive and time consuming and is infrequently performed. However, with the recent emphasis on excessive daytime sleepiness as an initial symptom of an obstructive sleep disorder, evaluating a patient's daytime sleepiness becomes more important, in order to distinguish true excessive daytime sleepiness from the occasional sleepiness that almost every one experiences.

According to the Standards of Practice Committee of the American Academy of Sleep Medicine (Littner et al, 2005), the MSLT is indicated as part of the evaluation of patients with suspected narcolepsy and may be useful in the evaluation of patients with suspected idiopathic hypersomnia. The MSLT is not routinely indicated in the initial evaluation and diagnosis of OSAS, or in assessment of change following treatment with nasal CPAP. The MSLT is not routinely indicated for evaluation of sleepiness in medical and neurological disorders (other than narcolepsy), insomnia, or circadian rhythm disorders.

Assessment of Adequacy of Response to CPAP

In an article on the use of oral appliance therapy for OSA, Ferguson (2001) used a conservative definition of treatment success. A complete response is defined as a reduction in AHI to less than 5/hour. A partial response was defined as an improvement in symptoms combined with a greater than or equal to 50 % reduction in AHI but the AHI remained greater than 5/hour. Treatment failures were defined as having ongoing symptoms and/or a less than 50 % reduction in AHI. By this definition, a reduction of 55 events/hour of sleep to 33 events/hour of sleep (40 % reduction in AHI) would not be considered as a good response to CPAP.

Wassmuth et al (2000) evaluated the ability of cautery-assisted palatal stiffening operation (CAPSO) to treat OSA syndrome. Twenty-five consecutive patients with OSA syndrome underwent CAPSO. Responders were defined as patients who had a reduction in AHI of 50 % or more and an AHI of 10 or less after surgery.

Furthermore, Heinzer et al (2001) noted that a good response to CPAP treatment is defined as an AHI of less than 10 events/hour.

Javaheri (2000) concluded that an AHI of 4 +/- 3 per hour signifies complete elimination of disordered breathing. The author prospectively studied 29 men with heart failure whose initial polysomnograms showed 15 or more episodes of apnea and hypopnea per hour (AHI). Twenty-one patients had predominately central and 8 patients OSA. All were treated with CPAP during the subsequent night. In 16 patients, CPAP resulted in virtual elimination of disordered breathing. In these patients, the mean AHI (36 +/- 12 [SD] versus 4 +/- 3 per hour, p = 0.0001), arousal index due to disordered breathing (16 +/- 9 versus 2 +/- 2 per hour, p = 0.0001), and percent of total sleep time below saturation of 90 % (20 +/- 23 % to 0.3 +/- 0.7 %, p = 0.0001) decreased, and lowest saturation (76 +/- 8 % versus 90 +/- 3 %, p = 0.0001) increased with CPAP. In 13 patients who did not respond to CPAP, these values did not change significantly. In patients whose sleep apnea responded to CPAP, the number of hourly episodes of nocturnal premature ventricular contractions (66 +/- 117 versus 18 +/- 20, p = 0.055) and couplets (3.2 +/- 6 versus 0.2 +/- 0.21, p = 0.031) decreased. In contrast, in patients whose sleep apnea did not respond to CPAP, ventricular arrhythmias did not change significantly. The author concluded that in 55 % of patients with heart failure and sleep apnea, first-night nasal CPAP eliminates disordered breathing and reduces ventricular irritability. Based on this study, an AHI of 4 +/- 3 per hour signifies complete elimination of disordered breathing.

Appendix B

Monitoring Devices
Type I:	Comprehensive standard overnight polysomnography in a sleep center or laboratory with a sleep technician in constant attendance	Minimum of 7 parameters including EEG, EOG, chin EMG, ECG or heart rate, airflow, respiratory effort, oxygen saturation
Type II:	Comprehensive, portable sleep study	Minimum of 7 parameters including EEG, EOG, chin EMG, ECG or heart rate, airflow, respiratory effort, oxygen saturation
Type III:	Modified portable sleep apnea testing	Minimum of 4 parameters, including ventilation (at least 2 channels of respiratory movement, or respiratory movement and airflow), heart rate or ECG, oxygen saturation
Type IV(A):	Three or more bioparameters	Airflow and at least 2 other parameters (for example, EOG, peripheral arterial tonometry (PAT), snoring, actigraphy, pulse oximetry)
Type IV(B):	Continuous single- or dual-bioparameter recording	Minimum of 1 parameter (for example, overnight oximetry) and does not meet criteria for Types I to III or Type IV(A) device.


CPT Codes / HCPCS Codes / ICD-9 Codes
Diagnosis:
CPT codes covered if selection criteria are met:
70350	Cephalogram, orthodontic
70355	Orthopantogram(eg, panoramic X-Ray)
95800	Sleep study, unattended, simultaneous recording; heart rate, oxygen saturation, respiratory analysis (eg, by airflow or peripheral arterial tone) and sleep time
95801	minimum of heart rate, oxygen saturation, and respiratory analysis (eg, by airflow or peripheral arterial tone)
95806	Sleep study, simultaneous recording of ventilation, respiratory effort, ECG or heart rate, and oxygen saturation, unattended by a technologist
95807	Sleep study, simultaneous recording of ventilation, respiratory effort, ECG or heart rate, and oxygen saturation, attended by a technologist
95808	Polysomnography; sleep staging with 1-3 additional parameters of sleep, attended by a technologist
95810	sleep staging with 4 or more additional parameters of sleep, attended by a technologist
95811	sleep staging with 4 or more additional parameters of sleep, with initiation of continuous positive airway pressure therapy or bilevel ventilation, attended by a technologist
95951	Monitoring for localization of cerebral seizure focus by cable or radio, 16 or more channel telemetry, combined EEG and video recording and interpretation (e.g., for presurgical localization), each 24 hours [to assist with the diagnosis of paroxysmal arousals or other sleep disruptions thought to be seizure related when EEG is inconclusive]
CPT codes not covered for indications listed in the CPB:
70100	Radiologic examination, mandible; partial, less than 4 views
70110	complete, minimum of 4 views
70240	Radiologic examination, sella turcica
70332	Temporomandibular joint arthrography, radiological supervision and interpretation
76101	Radiologic examination, complex motion (i.e., hypercycloidal) body section (e.g., mastoid polytomography), other than urography; unilateral
76102	bilateral
76536	Ultrasound, soft tissues of head and neck (e.g., thyroid, parathyroid, parotid), real time with image documentation
78300	Bone and/or joint imaging; limited area
92520	Laryngeal function studies (i.e., aerodynamic testing and acoustic testing)
94760 - 94762	Noninvasive ear or pulse oximetry for oxygen saturation; single determination; multiple determinations (e.g., during exercise); or by continuous overnight monitoring (separate procedure) [as a screening method to rule out OSA]
95803	Actigraphy testing, recording, analysis, interpretation, and report (minimum of 72 hours to 14 consecutive days of recording)
Other CPT codes related to the CPB:
95805	Multiple sleep latency or maintenance of wakefulness testing, recording, analysis and interpretation of physiological measurements of sleep during multiple trials to assess sleepiness
HCPCS codes covered if selection criteria are met:
G0398	Home sleep study test (HST) with type II portable monitor, unattended; minimum of 7 channels: EEG, EOG, EMG, ECG/heart rate, airflow, respiratory effort and oxygen saturation
G0399	Home sleep test (HST) with type III portable monitor, unattended; minimum of 4 channels: 2 respiratory movement/airflow, 1 ECG/heart rate and 1 oxygen saturation
G0400	Home sleep test (HST) with type IV portable monitor, unattended; minimum of 3 channels
HCPCS codes not covered for indications listed in the CPB:
D0320	Temporomandibular joint arthrogram, including injection
D0321	Other temporomandibular joint films, by report
D0322	Tomographic survey
D0330	Panoramic film
D0340	Cephalometric film
E0445	Oximeter device for measuring blood oxygen levels non-invasively [as a screening method to rule out OSA]
ICD-9 codes covered if selection criteria are met:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances
786.03	Apnea
786.09	Other dyspnea and respiratory abnormality
Other ICD-9 codes related to the CPB:
278.00 - 278.01	Overweight and obesity
291.82	Alcohol induced sleep disorders (parasomnia)
292.85	Drug induced sleep disorders (parasomnia)
307.47	Other dysfunctions of sleep stages or arousal from sleep [parasomnias]
332.0	Paralysis agitans (Parkinson's disease)
335.20	Amyotrophic lateral sclerosis
345.00 - 345.91	Epilepsy and recurrent seizures
347.00 - 347.11	Narcolepsy
359.21	Myotonic dystrophy
428.0	Congestive heart failure
433.00 - 434.91, 436	Stroke
741.00 - 741.93	Spina Bifida
780.39	Other convulsions
780.79	Other malaise and fatigue
V85.42 - V85.45	BMI greater than 45
Treatment:
Oral Appliances:
HCPCS codes covered if selection criteria are met:
E0485	Oral device/appliance used to reduce upper airway collapsibility, adjustable or non-adjustable, prefabricated, includes fitting and adjustment [covered only for obstructive sleep apnea in persons that meet criteria for CPAP but who are intolerant to positive airway pressure devices]
E0486	Oral device/appliance used to reduce upper airway collapsibility, adjustable or non-adjustable, custom fabricated, includes fitting and adjustment
ICD-9 codes covered if selection criteria are met:
327.23	Obstructive sleep apnea (adult) (pediatric)
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.09	Organic disorders of initiating and maintaining sleep (organic Insomnia)
327.20	Organic sleep apnea, unspecified
327.21	Primary central sleep apnea
327.22	High altitude periodic breathing
327.24	Idiopathic sleep related nonobstructive alveolar hypoventilation
327.25	Congenital central alveolar hypoventilation syndrome
327.26	Sleep related hypoventilation/hypoxemia in conditions classified elsewhere
327.27	Central sleep apnea in conditions classified elsewhere
327.29	Other organic sleep apnea
327.30 - 327.39	Circadian rhythm sleep disorder
780.50 - 780.59	Sleep disturbances [unspecified sleep disorders that remain a general symptom without a specifically identified sleep disorder diagnosis]
786.03	Apnea
Continuous Positive Airway Pressure (CPAP):
CPT codes covered if selection criteria are met:
94660	Continuous positive airway pressure ventilation (CPAP), initiation and management
HCPCS codes covered if selection criteria are met:
A7027	Combination oral/nasal mask, used with continuous positive airway pressure device, each
A7028	Oral cushion for combination oral/nasal mask, replacement only, each
A7029	Nasal pillows for combination oral/nasal mask, replacement only, pair
A7030	Full face mask used with positive airway pressure device, each
A7031	Face mask interface, replacement for full face mask, each
A7032	Cushion for use on nasal mask interface, replacement only, each
A7033	Pillow for use on nasal cannula type interface, replacement only, pair
A7034	Nasal interface (mask or cannula type) used with positive airway pressure device, with or without head strap
A7035	Headgear used with positive airway pressure device
A7036	Chinstrap used with positive airway pressure device
A7037	Tubing used with positive airway pressure device
A7038	Filter, disposable, used with positive airway pressure device
A7039	Filter, non-disposable, used with positive airway pressure device
A7044	Oral interface used with positive airway pressure device, each
A7045	Exhalation port with or without swivel used with accessories for positive airway devices, replacement only
A7046	Water chamber for humidifier, used with positive airway pressure device, replacement, each
E0470	Respiratory assist device, bi-level pressure capability, without back-up rate feature, used with noninvasive interface, e.g., nasal or facial mask (intermittent assist device with continuous positive airway pressure device) [for OSA members intolerant of CPAP]
E0472	Respiratory assist device, bi-level pressure capability, with back-up rate feature, used with invasive interface, e.g., tracheostomy tube (intermittent assist device with continuous positive airway pressure device) [for OSA members intolerant of CPAP]
E0561	Humidifier, non-heated, used with positive airway pressure device
E0562	Humidifier, heated, used with positive airway pressure device
E0601	Continuous airway pressure (CPAP) device [for OSA with AHI 15 or > = to 15 events per hour with minimum of 30 or AHI > 5 and < 15 events per hour with minimum of 10 + one related diagnosis] [not covered for C-Flex]
HCPCS codes not covered for indications listed in the CPB:
E0471	Respiratory assist device, bi-level pressure capability, with back-up rate feature, used with noninvasive interface, e.g., nasal or facial mask (intermittent assist device with continuous positive airway pressure device)
ICD-9 codes covered if selection criteria are met [with AHI 15 or >]:
327.23	Obstructive sleep apnea (adult) (pediatric)
ICD-9 codes covered if selection criteria are met [with OSA and AHI 5-14]:
293.83	Mood disorder in conditions classified elsewhere
296.90 - 296.99	Episodic mood disorders
401.0 - 405.99	Hypertensive disease [documented systolic blood pressure > 140 mmHg and/or diastolic blood pressure > 90 mm Hg]
410.00 - 414.9	Ischemic heart disease
438.0 - 438.9	Late effects of cerebrovascular disease [history of stroke]
780.79	Other malaise and fatigue [excessive daytime sleepiness by Epworth >10 or Multiple Sleep Latency Test (MSLT) <6]
V12.54	Personal history of transient ischemic attack (TIA), and cerebral infarction without residual deficits
V12.59	Personal history of other diseases of circulatory system [history of stroke]
ICD-9 codes covered [for BIPAP, DPAP, VPAP, VPAP Adapt SV, and AutoPAP] if selection criteria are met [for OSA member intolerant of CPAP]:
327.23	Obstructive sleep apnea (adult) (pediatric)
327.24	Idiopathic sleep related nonobstructive alveolar hypoventilation [nocturnal hypoventilation]
327.26	Sleep related hypoventilation/hypoxemia in conditions classified elsewhere [nocturnal hypoventilation]
358.00 - 358.9	Myoneural disorders [restrictive thoracic disorders]
490 - 496	Chronic obstructive pulmonary disease and allied conditions
738.3	Acquired deformity of chest and rib [restrictive thoracic disorders]
754.89	Other congenital musculoskeletal deformities [chest wall] [restrictive thoracic disorders]
ICD-9 codes not covered for indications listed in the CPB:
345.00 - 345.91	Epilepsy and recurrent seizures [for the improvement of seizure control]
780.39	Other convulsions [for the improvement of seizure control]
There is no specific code for Nasal Dilators:
There is no specific code for Apnea-Triggered Muscle Stimulator:
Uvulopalatopharyngoplasty (UPPP):
CPT codes covered if selection criteria are met:
42145	Palatopharyngoplasty (e.g., uvulopalatopharyngoplasty, uvulopharyngoplasty) [for OSA members who meet criteria for CPAP but are intolerant]
ICD-9 codes covered if selection criteria are met [for OSA members who are intolerant of CPAP]:
327.23	Obstructive sleep apnea (adult) (pediatric)
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.09	Organic disorders of initiating and maintaining sleep (organic insomnia)
327.20	Organic sleep apnea, unspecified
327.21	Primary central sleep apnea
327.22	High altitude periodic breathing
327.24	Idiopathic sleep related nonobstructive alveolar hypoventilation
327.25	Congenital central alveolar hypoventilation syndrome
327.26	Sleep related hypoventilation/hypoxemia in conditions classified elsewhere
327.27	Central sleep apnea in conditions classified elsewhere
327.29	Other organic sleep apnea
327.30 - 327.39	Circadian rhythm sleep disorder
780.50 - 780.59	Sleep disturbances
786.03	Apnea
Uvulectomy:
CPT codes covered if selection criteria are met:
42140	Uvulectomy, excision of uvula
Other ICD-9 codes related to the CPB:
782.3	Edema [acute of uvula causing respiratory distress]
786.09	Other dyspnea and respiratory abnormalities [respiratory distress caused by acute edema of the uvula]
Laser Assisted Uvuloplasty (LAUP):
CPT codes not covered for indications listed in the CPB:
42160	Destruction of lesion, palate or uvula (thermal, cryo or chemical)
42890	Limited pharyngectomy
HCPCS codes not covered for indications listed in the CPB:
S2080	Laser-assisted uvulopalatoplasty (LAUP)
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances
Somnoplasty and Coblation or Tongue Base Reduction:
CPT codes not covered for indications listed in the CPB:
30801	Cautery and/or ablation, mucosa of inferior turbinates, unilateral or bilateral, any method; superficial [if used to report somnoplasty or coblation]
30802	intramural [if used to report somnoplasty or coblation]
41530	Submucosal ablation of the tongue base, radiofrequency, one or more sites, per session
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances
786.03	Apnea
786.09	Other dyspnea and respiratory abnormalities
The Repose System or Advance System:
CPT codes not covered for indications listed in the CPB:
41512	Tongue base suspension, permanent suture technique
Tonsillectomy (adult):
CPT codes covered if selection criteria are met:
42821	Tonsillectomy age 12 and over
ICD-9 codes covered if selection criteria are met:
474.10	Hypertrophy of tonsils with adenoids
474.11	Hypertrophy of tonsils alone
ICD-9 codes not covered for indications listed in the CPB:
327.0 - 327.8	Organic sleep disorders (adult)
Zzoma positional device:
HCPCS codes not covered for indications listed in the CPB:
E0190	Positioning cushion/pillow/wedge, any shape or size, includes all components and accessories [Zzoma positional device]
Jaw Realignment Surgery:
CPT codes covered if selection criteria are met:
21198	Osteotomy, mandible, segmental [for OSA members who fail other treatment approaches]
21199	with genioglossus advancement [for OSA members who fail other treatment approaches]
21208	Osteoplasty, facial bones; augmentation (autograft, allograft, or prosthetic implant) [for OSA members who fail other treatment approaches]
21209	reduction [for OSA members who fail other treatment approaches]
21685	Hyoid myotomy and suspension [for OSA members who fail other treatment approaches]
ICD-9 codes covered if selection criteria are met:
327.23	Obstructive sleep apnea (adult) (pediatric)
Other ICD-9 codes related to the CPB:
756.0	Anomalies of skull and face bones
Tracheostomy:
CPT codes covered if selection criteria are met:
31600 - 31601	Tracheostomy
ICD-9 codes covered if selection criteria are met:
327.23	Obstructive sleep apnea (adult) (pediatric) [for members with the most severe OSA not manageable by other interventions]
Cardiac (Atrial) Pacing:
CPT codes not covered for indications listed in the CPB:
33202 - 33249	Pacemaker procedures
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances
786.03	Apnea
786.09	Other dyspnea and respiratory abnormalities
Injection Snoreplasty:
No specific codes
Cautery-Assisted Palatal Stiffening Operation (CAPSO):
CPT codes not covered for indications listed in the CPB:
42950	Pharyngoplasty (plastic or reconstructive operation on pharynx) [if used to report CAPSO]
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances
786.03	Apnea
786.09	Other dyspnea and respiratory abnormalities
Pillar™ Palatal Implant System:
HCPCS codes not covered for indications listed in the CPB:
C9727	Insertion of implants into the soft palate; minimum of three implants
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances [if used to report OSA]
786.03	Apnea
786.09	Other dyspnea and respiratory abnormalities
Transpalatal Advancement Pharyngoplasty:
CPT codes not covered for indications listed in the CPB:
42145	Palatopharyngoplasty (e.g., uvulopalatopharyngoplasty, uvulopharyngoplasty) [if used to report transpalatal advancement pharyngoplasty]
42950	Pharyngoplasty (plastic or reconstructive operation on pharynx) [if used to report transpalatal advancement pharyngoplasty]
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances [if used to report OSA]
786.03	Apnea
786.09	Other dyspnea and respiratory abnormalities
Nasal Surgery:
CPT codes not covered for indications listed in the CPB:
30000 - 30999	Surgery/Respiratory System, nose/nasal
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances [if used to report OSA]
786.03	Apnea
786.09	Other dyspnea and respiratory abnormalities
Partial Glossectomy:
CPT codes not covered for indications listed in the CPB:
41120	Glossectomy; less than one-half tongue
41130	Hemiglossectomy
41135	Partial; with unilateral radical neck dissection
ICD-9 codes not covered for indications listed in the CPB:
327.00 - 327.8	Organic sleep disorders
780.50 - 780.59	Sleep disturbances [if used to report OSA]
786.03	Apnea
786.09	Other dyspnea and respiratory abnormalities
Provent sleep apnea therapy:
No specific codes Medical Clinical Policy Bulletin: Obstructive Sleep Apnea in Adults Number:0004. Update: 10/17/12 This CPB is updated to clarify that SNAP testing using 3 or more channels is considered a medically necessary method of home sleep testing.

The above policy is based on the following references:

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Hailey D, Tran K, Dales R, et al. A review of guidelines for referral of patients to sleep laboratories. Technology Report. Issue 55. Ottawa, ON: Canadian Coordinating Office for Health Technology Assessment (CCOHTA); 2005. Available at: https://www.ccohta.ca/publications/pdf/183_sleeplabs_tr_e.pdf. Accessed January 9, 2006.
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Ayas NT, Patel SR, Malhotra A, et al. Auto-titrating versus standard continuous positive airway pressure for the treatment of obstructive sleep apnea: Results of a meta-analysis. Sleep. 2004;27(2):249-253.
Lim J, Lasserson TJ, Fleetham J, Wright J. Oral appliances for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;(1):CD004435.
Hensley N, Ray C. Sleep apnoea. In: BMJ Clinical Evidence. London, UK: BMJ Publishing Group;May 2008.
Nixon GM, Brouillette RT. Diagnostic techniques for obstructive sleep apnoea: Is polysomnography necessary? Paediatr Respir Rev. 2002;3(1):18-24.
D'Andrea LA. Diagnostic studies in the assessment of pediatric sleep-disordered breathing: Techniques and indications. Pediatr Clin North Am. 2004;51(1):169-186.
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