Clinical Policy Bulletin: Obstructive Sleep Apnea in Adults
Number: 0004
Policy
Aetna considers the diagnosis and treatment of obstructive sleep apnea (OSA) in adults aged 18 and older medically necessary according to the criteria outlined below.
Diagnosis
Aetna considers attended full-channel nocturnal polysomnography (NPSG) (Type I device) performed in a healthcare facility medically necessary for diagnosis in members with symptoms suggestive of obstructive sleep apnea, when attended NPSG is used as part of a comprehensive sleep evaluation, and member has one or more of the following indications for attended NPSG:
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 less than 60 or pCO2 greater than 45),
congestive heart failure (NYHA class III or IV or LVEF less than 45%),
super obesity (BMI greater than 45); or
Member has one or more of 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 score 1 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 use portable 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), if the Apnea Hypopnea Index (AHI) is greater than 15 in first 2 hours of a diagnostic sleep study. An additional full-night CPAP titration NPSG is considered medically necessary only if the AHI is less than or equal to 15 during the first 2 hours of a diagnostic sleep study, or if the split-night study did not allow for the abolishment of the vast majority of obstructive respiratory events (see section III below).
Aetna considers unattended (home) sleep studies using any of the following diagnostic techniques medically necessary for members with symptoms suggestive of OSA (see Appendix B for definition of device types), when the home sleep study is used as part of a comprehensive sleep evaluation:
Sleep monitoring using a Type II device; or
Sleep monitoring using a Type III device, or
Sleep monitoring using a Type IV(A) device, measuring airflow and at least 2 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 Biancamed SleepMinder, SNAP testing with fewer than three channels, and the SleepImage Sleep Quality Screener. Note that the ApneaLink does not meet criteria as a covered 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.
Attended full-channel nocturnal polysomnography (NPSG) (Type I device) performed in a healthcare facility is considered medically necessary for persons diagnosed with obstructive sleep apnea who have any of the following indications for attended NPSG:
To titrate CPAP in persons diagnosed with clinically significant OSA for whom in-laboratory NPSG was medically necessary, but who were unable to undergo a split-night study because they had an insufficient AHI (less than 15) during the first two hours of an attended NPSG; or
To titrate CPAP in persons with clinically significant OSA for whom in-laboratory NPSG was medically necessary, and who underwent a split-night study that did not abolish the vast majority of obstructive respiratory events; or
To monitor results from CPAP in persons with OSA who have persistent 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.
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 NPSG in 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.
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.
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:
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. See CPB 0710 - Actigraphy and Accelerometry; or
Cephalographic X-rays for diagnosis of OSA. Lateral cephalographic X-rays and orthopantograms 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
SleepStrip; 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.
Treatment
Treatment of snoring alone, without significant OSA, is not considered medically necessary.
Continuous Positive Airway Pressure (CPAP)
It is expected that members receive lifestyle advice where applicable (i.e., helping people to lose weight, stop smoking and/or decrease alcohol consumption).
Aetna considers CPAP or autoPAP medically necessary DME for members with a positive facility-based NPSG*, or with a positive home sleep test* including Type II, III, IV(A) or Watch-PAT devices, as defined by either of the following criteria:
Member's apnea-hypopnea index (AHI) or respiratory disturbance index (RDI) is greater than or equal to 15 events/hour with a minimum of 30 events; or
AHI or RDI greater than or equal to 5 and less than 15 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. If the AHI or RDI is calculated based on less than 2 hours of sleep or recording time, the total number of recorded events used to calculate the AHI or RDI (respectively) must be at least the number of events that would have been required in a 2-hour period (i.e., must reach more than 30 events without symptoms or more than 10 events with symptoms). Projections of AHI or RDI based upon shorter testing times and/or fewer events are not acceptable for use in determining whether the member meets medical necessity criteria. In addition, estimates of AHI or RDI should include all stages of sleep. Estimates of AHI or RDI that only count events during periods of REM sleep (and exclude periods of non-REM sleep from the calculation) are not acceptable for use in determining whether the member meets medical necessity criteria.
Notes: For purposes 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.
The apnea-hypopnea index (AHI) is equal to the average number of episodes of apnea and hypopnea per hour of sleepwithout the use of a positive airway pressure device. Sleep time can only be measured in a Type I (facility-based polysomnogram) or Type II sleep study. Thus the AHI is reported only in Tyipe I or Type II sleep studies.
The respiratory disturbance index (RDI) is equal to the episodes of apnea and hypopnea per hour of recording without the use of a positive airway pressure device. The RDI is reported in Type III, Type IV, and other home sleep studies.
Leg movement, snoring, respiratory effort related arousals (RERAs), and other sleep disturbances that may be included by some polysomnographic facilities are not considered to meet the AHI 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 positive airway pressure devices 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 positive airway pressure device.
Aetna considers CPAP experimental and investigational for the treatment of persons 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, or for whom CPAP or AutoPAP is ineffective. Ineffective is defined as documented failure to meet therapeutic goals using CPAP or AutoPAP during the titration portion of a facility-based study or during home use despite optimal therapy (i.e., proper mask selection and fitting and appropriate pressure settings). The records must document that both of the following medical necessity criteria are met:
An appropriate interface for the CPAP and AutoPAP has been properly fit and the member is using it without difficulty; and
The current pressure setting of the CPAP or AutoPAP prevents the member from tolerating the therapy and lower pressure settings of the CPAP or AutoPAP were tried but failed to:
Adequately control the symptoms of OSA; or
Improve sleep quality; or
Reduce the AHI/RDI to acceptable levels.
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 (see CPB 0452 - Noninvasive Positive Pressure Ventilation).
Replacement of positive airway pressure devices is considered medically necessary at the end of their 5-year reasonable useful lifetime (RUL). Replacement of these items is considered medically necessary prior to the end of the 5-year RUL in cases of irreparable damage due to a specific accident or to a natural disaster (e.g., fire, flood).
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 mask is 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.
The following positive airway pressure supplies are considered not medically necessary convenience items:
Positive airway pressure bed pillows
Batteries for positive airway pressure devices
DC adapters for positive airway pressure devices
Note: Aetna follows Medicare DME MAC rules 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. See CPB 452 - Noninvasive Positive Pressure Ventilation. Requests for these devices for non-invasive ventilation of members with lung disease are subject to medical review.
Oral Appliances
Mandibular advancement oral appliances to reduce upper airway collapsibility or tongue retaining devices are considered medically necessary for members who have sleep test results that meets one of the following criteria:
The AHI or RDI is greater than or equal to 15 events per hour with a minimum of 30 events; or
The AHI or RDI is greater than or equal to 5 and less than 15 events per hour with a minimum of 10 events and documentation of:
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 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 1 episode of oxygen desaturation (i.e., oxygen saturation of less than 70 %).
If the AHI is greater than 30 or the RDI is greater than 30 and meets either of the following:
The member is not able to tolerate a positive airway pressure (PAP) device; or
The use of a PAP device is contraindicated.
Oral appliances to reduce upper airway collapsibility are considered experimental and investigational for indications other than OSA. For policy on oral occlusal appliances used to treat temporomandibular joint (TMJ) disorders, see CPB 0028 - Temporomandibular Disorders.
Replacement of oral appliances is considered medically necessary at the end of their 5-year RUL. Replacement of these items is considered medically necessary prior to the end of the 5-year RUL in cases of irreparable damage due to a specific accident or to a natural disaster (e.g., fire, flood).
Note: All follow-up care, including fitting, adjustments, modifications, professional services (not all-inclusive) required during the first 90 days after provision of the oral appliance are considered to be included in the payment for device.
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 or AutoPAP (see above), but who are intolerant to CPAP or AutoPAP. The medical records must document that the member has attempted CPAP or AutoPAP before 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 AutoPAP is 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 AutoPAP because this surgical approach has not been shown to be effective in non-obstructive apnea.
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 AutoPAP or 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.
Somnoplasty and Coblation
Aetna considers radiofrequency ablation of the tongue base, uvula or soft palate (Somnoplasty) or of the nasal passages and soft palate (Coblation) experimental and investigational as a treatment for OSA because there is inadequate scientific evidence to validate the effectiveness of these procedures for this indication. Please see CPB 0592 - Radiofrequency Ablation of Hypertrophied Nasal Turbinates.
The Repose System and the Encore Tongue Base Suspension
Aetna considers the Repose system, a minimally invasive technique involving tongue base suspension, and the Encore tongue base suspension, experimental and investigational. These procedures have been used for treating sleep disordered breathing (SDB) caused by tongue base collapse. No specific criteria exist regarding the diagnosis of tongue base collapse in SDB. Preliminary short-term studies of surgery targeted to alleviate tongue base collapse in SDB have shown subjective improvements in snoring and statistically significant decreases in mean RDI. However, the reported rates of success have been inconsistent among studies, and larger controlled studies with long-term follow-up are necessary to determine whether the Repose system is safe and effective.
Pediatric Obstructive Sleep Apnea Syndrome (OSAS): Tonsillectomy and Adenoidectomy
Aetna considers adult tonsillectomy experimental and investigational for the treatment of adult OSA. Aetna considers adult tonsillectomy medically necessary for members with symptomatic tonsillar hypertrophy. Note: A tonsillectomy is considered an integral component of a uvulopalatopharyngoplasty and is not separately reimbursed.
Jaw Realignment Surgery (i.e., hyoid myotomy and suspension, mandibular osteotomy, genioglossal advancement)
Aetna considers jaw realignment surgery medically necessary for persons who fail other treatment approaches for OSA.
Although jaw realignment surgery may be considered medically necessary on an individual case basis, because of the extent of surgery, these cases may be subject to review by Aetna's Oral and Maxillofacial Surgery Unit to assess medical necessity.
Note: According to the medical literature, persons undergoing jaw realignment surgery must usually also undergo orthodontic therapy to correct changes in occlusion associated with the surgery. Orthodontic therapy (i.e., the placement of orthodontic brackets and wires) is excluded from coverage under standard Aetna medical plans regardless of medical necessity. Please check benefit plan descriptions for details. Benefits for orthodontic therapy may be available under the member's dental plan, if any.
Tracheostomy
Aetna considers tracheostomy medically necessary for those members with the most severe OSA not manageable by other interventions. Requests for tracheostomy for OSA are subject to medical review. Note: Aetna follows Medicare DME MAC rules for the medically necessary quantity of tracheostomy supplies for OSA and other indications.
Cardiac (Atrial) Pacing
Aetna considers cardiac (atrial) pacing for treatment of OSA experimental and investigational because the effectiveness of this procedure for OSA has not been established.
Injection Snoreplasty
Aetna considers injection snoreplasty, injection of a sclerosing agent into the soft palate, experimental and investigational for the treatment of OSA because its effectiveness for this indication has not been established. Treatment of snoring alone, without significant OSA, is not considered medically necessary
Aetna considers cautery-assisted palatal stiffening operation (CAPSO) experimental and investigational for the treatment of OSA because its effectiveness for this indication has not been established.
Pillar™ Palatal Implant System
Aetna considers the Pillar Palatal Implant System (Restore Medical, Inc.) experimental and investigational for the treatment of OSA and all other indications because its effectiveness for this and other indications has not been established.
Flexible Positive Airway Pressure
Aetna considers flexible positive airway pressure (C-Flex, Respironics) experimental and investigational because its effectiveness has not been established.
Transpalatal Advancement Pharyngoplasty
Aetna considers transpalatal advancement pharyngoplasty experimental and investigational for the treatment of OSA because its effectiveness has not been established.
Nasal Surgery
Aetna considers nasal surgery (any technique) experimental and investigational for the treatment of OSA because its effectiveness has not been established.
The Advance System
Aetna considers the Advance System (an adjustable tongue-advancement device) experimental and investigational for the treatment of OSA because its effectiveness has not been established.
Tongue Base Reduction Surgery
Aetna considers tongue base reduction surgery experimental and investigational for the treatment of OSA because its effectiveness has not been established.
Partial Glossectomy
Aetna considers partial glossectomy experimental and investigational for the treatment of OSA because its effectiveness has not been established.
The Provent Sleep Apnea Therapy
Aetna considers the Provent sleep apnea therapy experimental and investigational for the treatment of OSA because its effectiveness has not been established.
The Zzoma Positional Device
Aetna considers the Zzoma positional device not medically necessary because it has not been proven to be superior to other interventions to keep a person in a non-supine position.
Nasal Dilators
Aetna considers nasal dilators experimental and investigational for the treatment of OSA because their effectiveness has not been established.
Apnea-Triggered Muscle Stimulation
Aetna considers apnea-triggered muscle stimulation experimental and investigational for the treatment of OSA because its effectiveness has not been established.
The Winx Therapy System/Oral Pressure Therapy
Aetna considers the Winx therapy system/oral pressure therapy experimental and investigational for the treatment of OSA because of insufficient evidence in the peer-reviewed published medical literature of its effectiveness and safety.
Airway obstruction during sleep is a commonly recognized problem, which may be associated with significant morbidity. Various diagnostic studies and treatment approaches are employed in managing this condition.
Data from the history and physical examination have been shown to be sensitive but not specific for diagnosing obstructive sleep apnea (OSA). According to available guidelines (ICSI, 2006), the following signs and symptoms may suggest significant risk for OSA: reported apneas by sleep partner; awakening with choking; intense snoring; severe daytime sleepiness, especially with impairment of driving; male gender and post-menopausal females; obesity (body mass index [BMI] greater than or equal to 30); large neck circumference; and hypertension.
Diagnostic tests for OSA can be classified into 4 types. The most comprehensive type is Type I: attended, or in-facility polysomnography (PSG). There are 3 categories of portable monitors (used in both attended and unattended settings). Type II monitors have a minimum of 7 channels (e.g., electroencephalogram (EEG), electrooculogram (EOG), electromyogram (EMG), electrocardiogram (ECG), heart rate, airflow, respiratory effort, oxygen saturation). Type III monitors have a minimum of 4 monitored channels including ventilation or airflow (at least 2 channels of respiratory movement or respiratory movement and airflow), heart rate or ECG, and oxygen saturation. Type IV are all other monitors that fail to fulfill criteria for type III monitors. These are split into 2 subgroups: those assessing 3 or more bioparameters (i.e., most newer monitors fall here) and those assessing 1 or 2 bioparameters (i.e., the original ASDA level IV category) (see Appendix B).
There is no "gold standard" for the diagnosis of OSA in adults. NPSG performed in a sleep laboratory (Type I) is a definitive diagnostic tool to confirm the presence and severity of upper airway obstruction. According to current guidelines, a minimum 6-hour NPSG is preferred, which allows for the assessment of variability related to sleep stage and position with respect to the frequency of obstructive respiratory events and the occurrence of other types of nocturnal events such as periodic limb movements.
According to the available literature, NPSG performed in a sleep laboratory should include EEG, EOG, EMG, oronasal airflow, chest wall effort, body position, snore microphone, ECG, and oxyhemoglobin saturation. However, diagnostic NPSG may be performed in a healthcare facility, or for appropriate cases, in the patient's home. The use of unattended home sleep monitoring using a Type II, III, or IV device, may identify AHI suggestive of OSAHS. A technology assessment by the Agency for Healthcare Research and Quality (AHRQ) on Home Diagnosis of Obstructive Sleep Apnea-Hypopnea Syndrome (2007) commissioned by the Centers for Medicare & Medicaid Services (CMS), reported the following: Type II monitors identify AHI suggestive of obstructive sleep apnea-hypopnea syndrome (OSAHA) with high positive ratios (greater than 10) and low negative likelihood ratios (less than 0.1) both when the portable monitors were studied in the sleep laboratory and at home. Type III monitors may have the ability to predict AHI suggestive of OSAHA with high positive likelihood ratios and low negative likelihood ratios for various AHI cut-offs in laboratory-based PSG, especially when manual scoring is used. The ability of type III monitors to predict AHI suggestive of OSAHS appears to be better in studies conducted in sleep laboratories compared to studies in the home setting. Some studies of type IV devices also showed high positive likelihood ratios and low negative likelihood ratios, at least for selected sensitivity and specificity pairs from ROC curve analyses. Similarly to type III devices, the ability of type IV devices to predict AHI suggestive of OSAHS appears to be better in studies conducted in sleep laboratories.
A Decision Memorandum from the Centers for Medicare & Medicaid Services (CMS, 2009) concluded that there is sufficient evidence to support the use of devices that measure 3 or more channels that include actigraphy, oximetry, and peripheral arterial tone (e.g., Watch-PAT 100, Itamar Medical, Inc.) to aid the diagnosis of OSA in persons who have signs and symptoms indicative of OSA if performed unattended in or out of a sleep lab facility or attended in a sleep lab facility. An assessment by the California Technology Assessment Forum (Tice, 2009) found sufficient evidence to support the use of the Watch-PAT device for diagnosis of OSA.
Clinical guidelines on the use of unattended home (portable) monitoring devices for the diagnosis of obstructive sleep apnea in adults, from the American Academy of Sleep Medicine (Collop, et al., 2007) for the diagnosis of OSA should be performed only in conjunction with a comprehensive sleep evaluation. The guidelines state that unattended sleep studies are not appropriate for the diagnosis of OSA in patients with significant comorbid medical conditions that may degrade the accuracy of unattended sleep studies, including moderate to severe pulmonary disease, neuromuscular disease, or congestive heart failure. The guidelines note that unattended sleep studies are not appropriate for the diagnostic evaluation of OSA in patients suspected of having other sleep disorders. The guidelines state that unattended sleep studies are not appropriate for general screening of asymptomatic populations.
According to the AASM guidelines (Collop, et al., 2007), unattended sleep studies may be indicated for the diagnosis of OSA in patients for whom in-laboratory NPSG is not possible by virtue of immobility, safety, or critical illness. Unattended sleep studies may be indicated to monitor the response to non-CPAP treatments for obstructive sleep apnea, including oral appliances, upper airway surgery, and weight loss. The guidelines note that in laboratory NPSG may be indicated in cases where unattended sleep studies are technically inadequate or fail to establish the diagnosis of OSA in patients with a high pretest probability.
According to the American Sleep Disorders Association (ASDA) (1997), split-night study NPSG is indicated for patients with an AHI greater than 40 events/hour during the first 2 hours of a diagnostic NPSG. Split-night studies may also be considered for patients with an AHI of 20 to 40 events/hour, based on clinical observations, such as the occurrence of obstructive respiratory events with a prolonged duration or in association with severe oxygen desaturation. Split-night studies require the recording and analysis of the same parameters as a standard diagnostic NPSG. Accepted guidelines provide that the diagnostic portion of a split-night study should be at least 2 hours duration. A minimum of 3 hours sleep is preferred to adequately titrate CPAP after this treatment is initiated.
Following a standard diagnostic NPSG, the available literature indicates that OSA patients should receive CPAP titration to specify the lowest CPAP level, which abolishes obstructive apneas, hypopneas, respiratory-effort related arousals, and snoring in all sleep positions and sleep stages. On occasion, an additional full-night CPAP titration NPSG may also be required following split-night study if the split-night NPSG did not allow for the abolishment of the vast majority of obstructive respiratory events or prescribed CPAP treatment does not control clinical symptoms. Alternatively, persons diagnosed with portable monitoring may be prescribed an auto-titrating positive airway pressure device (AutoPAP) that does not require attended titration.
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) evaluated 11 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 with OSA 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 with Durable 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 %. Fujita is 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 the 2 palatal arches (Fujita et al, 1985). For a detailed discussion of the UPPP technique and its variants see the review by Koopmann and 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. All 3 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 a 3- to 6-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 for 2 to 3 weeks following surgery, and a soft diet is necessary for a total of 6 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 90 subjects 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 or OSA 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 Pillar Palatal 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, ESS scores 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 of individuals 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 et al (2008) examined the effectiveness of adjustable tongue advancement for the treatment of OSA. A total of 10 patients (mean age of 44 years) with moderate-to-severe OSA, i.e., an AHI between 15 and 50, with CPAP intolerance were included in this prospective, non-randomized, multi-center study to evaluate the feasibility, safety, and effectiveness of this novel procedure, which consists 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 than 32, 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]). Following implantation of the device, 42 patients (mean age of 50 years, BMI 28) noted improvement at 6 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], all p < 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 day 1 and resolved by day 5. Post-titration pain scores were mild (less than 2). 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 researchers addressed 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 treating OSA 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 30 men 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). Standard PSG 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 over 1 day, and thus did 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 repeat PSG with the prescribed device at the end of the 30-day trial. Subjects (n = 34; aged 27 to 67 years) with a baseline AHI greater than or equal to 5 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 AHI greater than 10 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 is needed 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 (AHI greater than 5); 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 exhibited similar 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 notification due to its 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 for 2 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 still unclear. 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".
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.
The SleepStrip is an instrument used for screening of OSA. It incorporates signal detection, acquisition, as well as display in a disposable package. The device is placed on the upper lip at bed-time and adjusted until respiration is detected, as indicated by a flashing light. Two nasal thermistors and 1 oral thermistor produce flow signals that are processed within the SleepStrip’s microprocessor. The 5 possible results are as follows: “0” (no apneas); “1” (mild sleep apnea, comparable to sleep laboratory AHI between 15 and 24); “2” (moderate sleep apnea, comparable to sleep laboratory AHI between 25 and 39); “3” (severe sleep apnea, comparable to sleep laboratory AHI of greater than 40); and “E” (error in measurement).
In a prospective, non-randomized double-blinded single cohort study, Pang et al (2006) examined the role of a portable screening device (SleepStrip) in the diagnosis of OSA. Patients with suspected OSA scheduled for an attended over-night Level I PSG and who consented to participate in the study wore the SleepStrip device at home the night after the PSG. The AHI determined by PSG was compared with the results of the SleepStrip recording. A total of 37 patients with a mean age of 52.1 +/- 12.2 years and mean body mass index of 35.7 +/- 5.2 participated in the study. The overall agreement between the AHI and the SleepStrip results using Cohen's Kappa value was 0.139 (p = 0.19). The sensitivity and specificity of the SleepStrip for diagnosing severe OSA when the AHI was greater than 40 were 33.3 % and 95 % (p = 0.05). When the AHI was greater than 25, the SleepStrip sensitivity and specificity were 43.8 % and 81.3 % (p = 0.26). The sensitivity and specificity of the SleepStrip for diagnosing OSA in patients with an AHI greater than 15 were 54.6 % and 70 %, respectively (p = 0.26). The authors concluded that SleepStrip has a low correlation with the AHI as measured by PSG; they stated that further studies are needed before this device can be recommended as a screening tool for the diagnosis of OSA.
In a prospective, non-randomized, double-blinded single cohort study, Ozmen et al (2011) examined the reliability of SleepStrip as a screening test in OSA syndrome. A total of 72 patients (50 males, 22 females; mean age of 51.4 +/- 11.1 years; range of 20 to 74 years) with OSA syndrome were included in this study between May 2008 and February 2009. Patients who underwent an attended over-night PSG and consented to participate in the study were asked to use SleepStrip device within the week following PSG recording. The AHI was compared with the SleepStrip score (Sscore). The mean BMI of patients was 31.1 +/- 4.3. Both AHI and Sscore were obtained in 64 patients. There was a strong correlation between Sscore and AHI (r = 0.76, p < 0.001). The sensitivity and specificity of the SleepStrip were 94.4 % and 93.5 % when used to diagnose cases with AHI = or > 40. The sensitivity and specificity of the SleepStrip was reduced to 80 % and 87.2 % when AHI threshold was chosen as equal or greater than 25 and 83.3 % and 76. 5 % for AHI equal tor greater than 15, respectively. The authors concluded that there is a strong correlation between SleepStrip and AHI. SleepStrip was found to be effective in diagnosing severe OSAS with AHI equal or greater than 40, however, its diagnostic capability was reduced in patients with lower AHI's who constitute the main target of screening.
The Encore tongue base suspension received FDA 510(k) clearance and is intended to be used for anterior advancement of the tongue base by means of a bone screw threaded with suture. It is indicated for the treatment of mild or moderate OSA and/or snoring. http://www.accessdata.fda.gov/cdrh_docs/pdf11/K111179.pdf. However, there is currently insufficient evidence to support its use.
On behalf of the European Respiratory Society task force on non-CPAP therapies in sleep apnea, Randerath et al (2011) stated that “Evidence supports the use of mandibular advancement devices in mild-to-moderate OSAS. Maxillomandibular osteotomy seems to be as efficient as continuous positive airway pressure (CPAP) in patients who refuse conservative treatment. Distraction osteogenesis is usefully applied in congenital micrognathia or midface 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 apnoea triggered muscle stimulation cannot be recommended as effective treatments of OSAS at the moment. Nasal surgery, radiofrequency tonsil reduction, tongue base surgery, uvulopalatal flap, laser midline glossectomy, tongue suspension and genioglossus advancement cannot 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. Multilevel surgery is only a salvage procedure for OSA patients”.
The Winx therapy system/oral pressure therapy (OPT) is a light, oral vacuum delivered by a quiet console through a slim tube connected to a soft, flexible mouth-piece. The mouthpiece and vacuum work together to gently pull the soft palate forward and stabilize the tongue, increasing the size of the airway and allowing for natural breathing to occur during sleep. Farid-Moayer, et al. (2012) conducted a proof-of-concept study that suggested that OPT can produce clinically relevant relief of OSA in certain subjects who are readily identified by PSG during trial use of the noninvasive system. In this single-center, proof-of-concept, single-treatment-night study, subjects with OSA underwent a baseline PSG study followed by PSG during use of an OPT system. Fifty-four men and 17 women, aged 53.2 ± 11.5 years (mean ± SD) had a baseline apnea-hypopnea index (AHI) greater than 5 events per hour. The authors reported that OPT was generally well tolerated with no serious adverse events. The authors found that OPT significantly decreased AHI from 34.4 ± 28.9 events per hour (mean ± SD) at baseline to 20.7 ± 23.3 (p < 0.001). Treatment produced an AHI less than 10 in 48% of the subjects. The authors stated that OPT significantly improved oxygen desaturation index (p < 0.001) and increased the percentage of the night with oxygen saturation of 90% or greater (p = 0.028). Stage-N1 sleep shifts, total sleep-stage shifts, awakenings and the percentage of sleep time spent in N1 sleep were significantly reduced with treatment. Additional studies of longer duration and larger numbers of patients are necessary, as are studies comparing results of OPT with CPAP as current standard of care.
Appendix
Table 1: 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 circumstances 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.
Table 2: Monitoring Devices
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 (e.g., EOG, peripheral arterial tonometry (PAT), snoring, actigraphy, pulse oximetry)
Type IV(B):
Continuous single- or dual-bioparameter recording
Minimum of 1 parameter (e.g., overnight oximetry) and does not meet criteria for Types I to III or Type IV(A) device.
Tubing with integrated heating element for use with positive airway pressure device
1 per 3 months
Combination oral/nasal mask, used with continuous positive airway pressure, each
1 per 3 months
Oral cushion for combination oral/nasal mask, replacement only
2 per 1 month
Nasal pillows for combination oral/nasal mask
2 per 1 month
Full face mask used with positive airway pressure device
1 per 3 months
Full face mask interface, replacement for full face mask
1 per 1 month
Cushion for use on nasal mask interface
2 per 1 month
Pillow for use on nasal cannula type interface
2 per 1 month
Nasal interface (mask or cannula type, used with positive aiway pressure
1 per 3 months
Headgear used with positive airway pressure device
1 per 6 months
Chinstrap used with positive airway pressure device
1 per 6 months
Tubing used with positive airway pressure device
1 per 3 months
Filter, disposable, used with positive airway pressure devcie
2 per 1 month
Filter, nondisposable, used with positive airway pressure device
1 per 6 months
Water chamber for humidifier, used with positie airway pressure
1 per 6 months
CPT Codes / HCPCS Codes / ICD-9 Codes
Diagnosis:
CPT codes covered if selection criteria are met:
70350
70355
95800
95801
95806
95807
95808
95810
95811
95951
CPT codes not covered for indications listed in the CPB:
70100
70110
70240
70332
76101
76102
76536
78300
92520
94760 - 94762
95803
Other CPT codes related to the CPB:
95805
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
S8262
Mandibular orthopedic repositioning device, each
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
HCPCS codes covered if selection criteria are met:
A4604
Tubing with integrated heating element for use with positive airway pressure device [4 per 12 months]
A7027
Combination oral/nasal mask, used with continuous positive airway pressure device, each [4 per 12 months]
A7028
Oral cushion for combination oral/nasal mask, replacement only, each [24 per 12 months]
A7029
Nasal pillows for combination oral/nasal mask, replacement only, pair [24 per 12 months]
A7030
Full face mask used with positive airway pressure device, each [4 per 12 months]
A7031
Face mask interface, replacement for full face mask, each [12 per 12 months]
A7032
Cushion for use on nasal mask interface, replacement only, each [24 per 12 months]
A7033
Pillow for use on nasal cannula type interface, replacement only, pair [24 per 12 months]
A7034
Nasal interface (mask or cannula type) used with positive airway pressure device, with or without head strap [4 per 12 months]
A7035
Headgear used with positive airway pressure device [2 per 12 months]
A7036
Chinstrap used with positive airway pressure device [2 per 12 months]
A7037
Tubing used with positive airway pressure device [4 per 12 months]
A7038
Filter, disposable, used with positive airway pressure device [24 per 12 months]
A7039
Filter, non-disposable, used with positive airway pressure device [2 per 12 months]
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 [2 per 12 months]
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 or AutoPAP, or for whom CPAP or AutoPAP is ineffective]
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]:
CPT codes not covered for indications listed in the CPB:
42950
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
42950
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
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
41130
41135
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
The above policy is based on the following references:
U.S. Department of Health and Human Services, Centers for Medicare & Medicaid Services (CMS). Continuous positive airway pressure (CPAP). Medicare Coverage Issues Manual §60-17. Baltimore, MD: CMS; 2002.
Fujita S, Conway WA, Zorick FJ. Evaluation of the effectiveness of uvulopalatopharyngoplasty. Laryngoscope. 1985;95:70-75.
Riley, RW, Powell NB, Guilleminault C. Maxillary mandibular and hyoid advancement for treatment of obstructive sleep apnea. A review of 40 patients. J Oral Maxillofac Surg. 1990;48:20-26.
Riley RW, Powell NB, Guilleminault C. Inferior sagittal osteotomy of the mandible with hyoid myomotomy suspension: A new procedure for obstructive sleep apnea. Otolaryngol Head Neck Surg. 1986;84:589.
Riley RW, Powell NB, Guilleminault C. Inferior mandibular osteotomy and hyoid myotomy suspension for obstructive sleep apnea. A review of 55 patients. J Oral Maxillofacial Surg. 1989;47:159-164.
American Sleep Disorders Association, Standards of Practice Committee, Polysomnography Task Force. Practice parameters for the indications for polysomnography and related procedures. Sleep. 1997;20(6):406-422.
American Sleep Disorders Association, Standards of Practice Committee. Practice parameter for the use of portable recording of the assessment of obstructive sleep apnea. Sleep. 1994;17(4):372-377.
American Sleep Disorders Association, Standards of Practice Committee. Practice parameters for the use of laser-assisted uvulopalatoplasty: An American Sleep Disorders Association Report. Sleep. 1994;17(8):744-748.
Thorpy MJ. The clinical use of the multiple sleep latency test. Standards of Practice Committee of the American Sleep Disorders Association Report. Sleep. 1992;15(3):268-276.
American Sleep Disorders Association. Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances. Sleep. 1995;18(6):511-513.
Hillberg RE, Johnson DC. Current concepts: Noninvasive ventilation. N Engl J Med. 1997;337(24):1746-1752.
Schmidt-Nowara W, Lowe A, Wiegand L, et al. Oral appliances for the treatment of snoring and obstructive sleep apnea: An American Sleep Disorders Association Review. Sleep. 1995;18(6):501-510.
Wright J, Johns R, Watt I, et al. Health effects of obstructive sleep apnea and the effectiveness of continuous positive airways pressure: A systematic review of the research evidence. BMJ. 1997;314(7084):851-860.
Loube DI, Gay PC, Strohl KP, et al. Indications for positive airway pressure treatment of adult obstructive sleep apnea patients: A consensus statement. Chest. 1999;115(3):863-866.
Agency for Healthcare Policy and Research (AHCPR). Systematic review of the literature regarding the diagnosis of sleep apnea. Evidence Report/Technology Assessment No. 1. AHCPR Publication No. 99-E002. Bethesda, MD: AHCPR; December 1998.
Coleman J. Sleep studies. Current techniques and future trends. Otolaryngol Clin North Am. 1999;32(2):195-210.
Olson LG, Ambrogetti A, Gyulay SG. Prediction of sleep-disordered breathing by unattended overnight oximetry. J Sleep Res. 1999;8(1):51-55.
Epstein LJ, Dorlac GR. Cost-effectiveness analysis of nocturnal oximetry as a method of screening for sleep apnea-hypopnea syndrome. Chest. 1998;113(1):97-103.
Lacassagne L, Didier A, Murris-Espin M, et al. Role of nocturnal oximetry in screening for sleep apnea syndrome in pulmonary medicine. Study of 329 patients. Rev Mal Respir. 1997;14(3):201-207.
Chesson AL Jr, Ferber RA, Fry JM, et al. The indications for polysomnography and related procedures. Sleep. 1997;20(6):423-487.
McNicholas WT. Clinical diagnosis and assessment of obstructive sleep apnoea syndrome. Monaldi Arch Chest Dis. 1997;52(1):37-42.
Levy P, Pepin JL, Deschaux-Blanc C, et al. Accuracy of oximetry for detection of respiratory disturbances in sleep apnea syndrome. Chest. 1996;109(2):395-399.
Ryan PJ, Hilton MF, Boldy DA, et al. Validation of British Thoracic Society guidelines for the diagnosis of the sleep apnoea/hypopnoea syndrome: Can polysomnography be avoided? Thorax. 1995;50(9):972-975.
Series F, Marc I, Cormier Y, et al. Utility of nocturnal home oximetry for case finding in patients with suspected sleep apnea hypopnea syndrome. Ann Intern Med. 1993;119:449-453.
Stoohs R, Guilleminault C. MESAM 4: An ambulatory device for the detection of patients at risk for obstructive sleep apnea. Chest. 1992;101(5):1221-1227.
Fibbi A, Presta A, Fasciolo G. The REPOSE system. Acta Otorhinolaryngol Ital. 1999;19(1):21-25.
Coleman J, Bick PA. Suspension sutures for the treatment of obstructive sleep apnea and snoring. Otolaryngol Clin North Am. 1999;32(2):277-285.
Troell RJ, Riley RW, Powell NB, et al. Surgical management of the hypopharyngeal airway in sleep disordered breathing. Otolaryngol Clin North Am. 1998;31(6):979-1012.
Teschler H, Stampa JW, Farhat AA, et al. Comparison of the efficacy of BiPAP-S/T and the VPAP-S/T ventilators in patients with stable chronic respiratory insufficiency. Pneumologie. 1998;52(6):305-310.
Schulz R, Mahmoudi S, Hattar K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy. Am J Respir Crit Care Med. 2000;162(2 Pt 1):566-570.
Bloch KE, Iseli A, Zhang JN, et al. A randomized, controlled crossover trial of two oral appliances for sleep apnea treatment. Am J Respir Crit Care Med. 2000;162(1):246-251.
Series F. Accuracy of an unattended home CPAP titration in the treatment of obstructive sleep apnea. Am J Respir Crit Care Med. 2000;162(1):94-97.
Tun Y, Hida W, Okabe S, et al. Effects of nasal continuous positive airway pressure on awake ventilatory responses to hypoxia and hypercapnia in patients with obstructive sleep apnea. Tohoku J Exp Med. 2000;190(2):157-168.
Kingshott RN, Vennelle M, Hoy CJ, et al. Predictors of improvements in daytime function outcomes with CPAP therapy. Am J Respir Crit Care Med. 2000;161(3 Pt 1):866-871.
Findley L, Smith C, Hooper J, et al. Treatment with nasal CPAP decreases automobile accidents in patients with sleep apnea. Am J Respir Crit Care Med. 2000;161(3 Pt 1):857-859.
Fletcher EC, Stich J, Yang KL. Unattended home diagnosis and treatment of obstructive sleep apnea without polysomnography. Arch Fam Med. 2000;9(2):168-174.
Javaheri S. Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure. Circulation. 2000;101(4):392-397.
Woodson BT, Derowe A, Hawke M, et al. Pharyngeal suspension suture with repose bone screw for obstructive sleep apnea. Otolaryngol Head Neck Surg. 2000;122(3):395-401.
DeRowe A, Gunther E, Fibbi A, et al. Tongue-base suspension with a soft tissue-to-bone anchor for obstructive sleep apnea: Preliminary clinical results of a new minimally invasive technique. Otolaryngol Head Neck Surg. 2000;122(1):100-103.
U.S. Department of Health and Human Services, National Institutes of Health (NIH), National Heart, Lung and Blood Institute (NHLBI). Sleep apnea: Is your patient at risk? NIH Pub. No. 95-3803. Bethesda, MD: NIH; September 1995. Available at: http://www.nhlbi.nih.gov/health/prof/sleep/slpaprsk.pdf. Accessed January 18, 2002.
Sher AE. Update on upper airway surgery for obstructive sleep apnea. Curr Opin Pulm Med. 1995;1(6):504-511.
Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep. 1996;19(2):156-177.
Morgan CE, Johnson K. Snoring/obstructive sleep apnea, surgery. eMedicine J 2001;2(9). Available at: http://www.emedicine.com/ent/topic370.htm. Accessed January 18, 2002.
American Sleep Disorders Association. Practice parameters for the treatment of obstructive sleep apnea in adults: The efficacy of surgical modifications of the upper airway. Report of the American Sleep Disorders Association. Sleep. 1996;19:152-155.
Sundaram S, Bridgman SA, Lim J, Lasserson TJ. Surgery for obstructive sleep apnoea. Cochrane Database Syst Rev. 2005;(4): CD001004..
Garrigue S, Bordier P, Jais P, et al. Benefit of atrial pacing in sleep apnea syndrome. N Engl J Med. 2002;346(6):404-412.
Gottlieb DJ. Cardiac pacing - a novel therapy for sleep apnea? N Engl J Med. 2002;346(6):444-445.
Brietzke SE, Mair EA. Injection snoreplasty: How to treat snoring without all the pain and expense. Otolaryngol Head Neck Surg. 2001;125(5):579-580.
Brown LK. Back to basics: If it's dry, wet it. The case for humidification of nasal continuous positive airway pressure air. Chest. 2000;117(3):617-169.
Hayes MJ, McGregor FB, Roberts DN, et al. Continuous nasal positive airway pressure (nasal CPAP) with a mouth leak: Effect on nasal mucosal blood flux and nasal geometry. Thorax. 1995;50(11):1179-1182.
Massie CA, Hart RW, Peralez K, Richards GN. Effects of humidification on nasal symptoms and compliance in sleep apnea patients using continuous positive airway pressure. Chest. 1999;116(2):403-408.
Rakotonanahary D, Pelletier-Fleury N, Gagnadoux F, Fleury B. Predictive factors for the need for additional humidification during nasal continuous positive airway pressure therapy. Chest. 2001;119(2):460-465.
OPAP Inc. Oral Pressure Appliance [website]. Capitola, CA: OPAP; October 31, 2001. Available at: http://www.opap.com. Accessed May 31, 2002.
OPAP Inc. Product labeling for OPAP Oral Pressure Appliance. Capitola, CA: OPAP; revised January 28, 2000. Available at: http://www.opap.com/fda_insert.htm. Accessed May 31, 2002.
Littner M, Kushida CA, Hartse K, et al. Practice parameters for the use of laser-assisted uvulopalatoplasty: An update for 2000. Sleep. 2001;24(5):603-619.
Masood A, Phillips B. Radiofrequency ablation for sleep-disordered breathing. Curr Opin Pulm Med. 2001;7(6):404-406.
Pazos G, Mair EA. Complications of radiofrequency ablation in the treatment of sleep-disordered breathing. Otolaryngol Head Neck Surg. 2001;125(5):462-467.
Guilleminault C, Chervin R, Palombini L, et al. Radiofrequency (pacing and thermic effects) in the treatment of sleep-disordered breathing. Sleep. 2000;23 Suppl 4:S182-S186.
Powell NB, Riley RW, Guilleminault C. Radiofrequency tongue base reduction in sleep-disordered breathing: A pilot study. Otolaryngol Head Neck Surg. 1999;120(5):656-664.
Powell NB, Riley RW, Troell RJ, et al. Radiofrequency volumetric reduction of the tongue. A porcine pilot study for the treatment of obstructive sleep apnea syndrome. Chest. 1997;111(5):1348-1355.
Haniffa M, Lasserson TJ, Smith I. Interventions to improve compliance with continuous positive airway pressure for obstructive sleep apnoea. Cochrane Database Syst Rev. 2004;(4):CD003531.
Nino-Murcia G, McCann CC, Bliwise DL, et al. Compliance and side effects in sleep apnea patients treated with nasal continuous positive airway pressure. Western J Med. 1989;150(2):165-169.
Waldhorn RE, Herrick TW, Nguyen MC, et al. Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea. Chest. 1990;97(1):33-38.
Rolfe I, Olson LG, Saunders NA. Long-term acceptance of continuous airway pressure in obstructive sleep apnea. Am Rev Respir Dis. 1991;144(5):1130-1133.
Hoffstein V, Viner S, Mateika S, Conway J. Treatment of obstructive sleep apnea with nasal continuous airway pressure: Patient compliance, perception of benefits and side effects. Am Rev Respir Dis. 1992;145(4 Pt 1):841-845.
Krieger J. Long-term compliance with nasal continuous positive airway pressure (CPAP) in obstructive sleep apnea patients and nonapneic snorers. Sleep. 1992;15(6):S42-S46.
Pepin JL, Krieger J, Rodenstein D, et al. Effective compliance during the first 3 months of continuous positive airway pressure treatment. A European prospective study of 121 patients. Am J Respir Crit Care Med. 1999;160(4):1124-1129.
Guilleminault C, Stoohs R, Clerk A, et al. A cause of daytime sleepiness. The upper airway resistance syndrome. Chest. 1993;104(3):781-787.
Chesson AL Jr, Ferber RA, Fry JM, et al. The indications for polysomnography and related procedures. Sleep. 1997;20(6):424-487.
Guilleminault C, Khramtsov A. Upper airway resistance syndrome in children: A clinical review. Semin Pediatr Neurol. 2001;8(4):207-215.
Becker HF, Jerrentrup A, Ploch T, et al. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation. 2003;107(1):68-73.
Blumen MB, Dahan S, Fleury B, et al. Radiofrequency ablation for the treatment of mild to moderate obstructive sleep apnea. Laryngoscope. 2002;112(11):2086-2092.
Stuck BA, Maurer JT, Verse T, Hormann K. Tongue base reduction with temperature-controlled radiofrequency volumetric tissue reduction for treatment of obstructive sleep apnea syndrome. Acta Otolaryngol. 2002;122(5):531-536.
Stuck BA, Maurer JT, Hormann K. Tongue base reduction with radiofrequency tissue ablation: Preliminary results after two treatment sessions. Sleep Breath. 2000;4(4):155-162.
Brown DJ, Kerr P, Kryger M. Radiofrequency tissue reduction of the palate in patients with moderate sleep-disordered breathing. J Otolaryngol. 2001;30(4):193-198.
Terris DJ, Chen V. Occult mucosal injuries with radiofrequency ablation of the palate. Otolaryngol Head Neck Surg. 2001;125(5):468-472.
Pazos G, Mair EA. Complications of radiofrequency ablation in the treatment of sleep-disordered breathing. Otolaryngol Head Neck Surg. 2001;125(5):462-467.
Back L, Palomaki M, Piilonen A, Ylikoski J. Sleep-disordered breathing: Radiofrequency thermal ablation is a promising new treatment possibility. Laryngoscope. 2001;111(3):464-471.
Blumen MB, Dahan S, Wagner I, et al. Radiofrequency versus LAUP for the treatment of snoring. Otolaryngol Head Neck Surg. 2002;126(1):67-73.
Woodson BT, Nelson L, Mickelson S, et al. A multi-institutional study of radiofrequency volumetric tissue reduction for OSAS. Otolaryngol Head Neck Surg. 2001;125(4):303-311.
Nelson LM. Combined temperature-controlled radiofrequency tongue reduction and UPPP in apnea surgery. Ear Nose Throat J. 2001;80(9):640-644.
Boudewyns A, Van De Heyning P. Temperature-controlled radiofrequency tissue volume reduction of the soft palate (somnoplasty) in the treatment of habitual snoring: Results of a European multicenter trial. Acta Otolaryngol. 2000;120(8):981-985.
Woodson BT, Steward DL, Weaver EM, et al. A randomized trial of temperature-controlled radiofrequency, continuous positive airway pressure, and placebo for obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg. 2003;128(6):848-861.
Wassmuth Z, Mair E, Loube D, Leonard D. Cautery-assisted palatal stiffening operation for the treatment of obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg. 2000;123(1 Pt 1):55-60.
Mair EA, Day RH. Cautery-assisted palatal stiffening operation. Otolaryngol Head Neck Surg. 2000;122(4):547-556.
American Academy of Pediatrics. Clinical practice guideline: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109(4):704-712.
American Academy of Sleep Medicine, Standards of Practice Committee. Practice parameters for the use of auto-titrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea. Sleep. 2002;25(2):143-147.
Littner M, Kushida CA, Anderson WM, et al. Practice parameters for the role of actigraphy in the study of sleep and circadian rhythms: An update for 2002. Sleep. 2003;26(3):337-341.
Meoli AL, Rosen CL, Kristo D, et al. Nonprescription treatments of snoring or obstructive sleep apnea: An evaluation of products with limited scientific evidence. Sleep. 2003;26(5):619-624.
Chesson AL, Jr, Berry RB, Pack A. Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. American Academy of Sleep Medicine. Sleep. 2003;26(7):907-913.
Littner M, Hirshkowitz M, Kramer M, et al. Practice parameters for using polysomnography to evaluate insomnia: An update. American Academy of Sleep Medicine. Published September 2003. Available at: http://www.aasmnet.org/practiceparameters.asp. Accessed January 6, 2004.
Alberta Heritage Foundation for Medical Research (AHFMR). Radiofrequency ablation of excess tongue tissue. Emerging Technology Report. Edmonton, AB: AHFMR; 1999.
Alberta Heritage Foundation for Medical Research (AHFMR). Somnoplasty system. Emerging Technology Report. Edmonton, AB: AHFMR; 2000.
Alberta Heritage Foundation for Medical Research (AHFMR). RF tonsillar ablation. Emerging Technology Report. Edmonton, AB: AHFMR; 2000.
Shneerson J, Wright J. Lifestyle modification for obstructive sleep apnoea. Cochrane Database Syst Rev. 2001;(1):CD002875.
Hailey D, Jacobs P, Mayers I, Mensinkai S. Auto-titrating nasal continuous positive airway pressure systems in the management of obstructive sleep apnea. Technology Report 39. Ottawa, ON: Canadian Coordinating Office for Health Technology Assessment (CCOHTA); September 2003.
Berry RB, Parish JM, Hartse KM. The use of auto-titrating continuous positive airway pressure for treatment of adult obstructive sleep apnea. Sleep. 2002;25(2):148-173.
Patel SR, White DP, Malhotra A, et al. Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive apnea. Arch Internal Med. 2003;163:565-571.
Agency for Healthcare Research and Quality (AHRQ), Technology Assessment Program. Effectiveness of portable monitoring devices for diagnosing obstructive sleep apnea: Update of a systematic review. Technology Assessment. Final Report. Prepared by RTI International for AHRQ. Rockville, MD: AHRQ: September 1, 2004. Available at: https://www.cms.hhs.gov/mcd/viewtrackingsheet.asp?id=110. Accessed September 9, 2004.
Marcoux M. Home sleep diagnostics fall short of facility-based testing in MCAC's eyes. Health News Daily. 2004;16(190):1-2.
Restore Medical, Inc. Simple, effective treatment for sleep apnea and snoring. Announcing a breakthrough treatment for sleep-related breathing disorders-the Pillar® Procedure from Restore Medical [website]. St. Paul, MN: Restore Medical; 2004. Available at: http://www.restoremedical.com. Accessed December 21, 2004.
U.S. Food and Drug Administration (FDA), Center for Devices and Radiologic Health (CDRH). Pillar™ Palatal Implant System. 510(k) no. K040417. Rockville, MD: FDA; July 28, 2004.
National Institute for Clinical Excellence (NICE). Radiofrequency ablation of the soft palate for snoring. Interventional Procedure Guidance No.124 . London, UK: NICE; May 2005.
Center for Medicare and Medicaid Services (CMS). Decision memo for continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea (OSA) (CAG-00093R). Medicare Coverage Database. Baltimore, MD: CMS; April 4, 2005.
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.
Tice JA. Portable devices for home testing for obstructive sleep apnea. Technology Assessment. San Francisco, CA: California Technology Assessment Forum (CTAF); June 15, 2005. Available at: http://ctaf.org/ass/viewfull.ctaf?id=54588264130. Accessed January 9, 2006.
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.
Kuhnel TS, Schurr C, Wagner B, Geisler P. Morphological changes of the posterior airway space after tongue base suspension. Laryngoscope. 2005;115(3):475-480.
Littner MR, Kushida C, Wise M, et al. Practice parameters for clinical use of the multiple sleep latency test and the maintenance of wakefulness test. Sleep. 2005;28(1):113-121.
Luthje L, Unterberg-Buchwald C, Dajani D, et al. Atrial overdrive pacing in patients with sleep apnea with implanted pacemaker. Am J Respir Crit Care Med. 2005;172(1):118-122.
Pepin JL, Defaye P, Garrigue S, Overdrive atrial pacing does not improve obstructive sleep apnoea syndrome. Eur Respir J. 2005;25(2):343-347.
Simantirakis EN, Schiza SE, Chrysostomakis SI, et al. Atrial overdrive pacing for the obstructive sleep apnea-hypopnea syndrome. N Engl J Med. 2005;353(24):2568-2577.
Kushida CA, Morgenthaler TI, Littner MR, et al.; American Academy of Sleep Medicine. Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances: An update for 2005. Sleep. 2006;29(2):240-243.
Friedman M, Vidyasagar R, Bliznikas D, Joseph NJ. Patient selection and efficacy of Pillar implant technique for treatment of snoring and obstructive sleep apnea/hypopnea syndrome. Otolaryngol Head Neck Surg. 2006;134(2):187-196.
Krahn AD, Yee R, Erickson MK, et al. Physiologic pacing in patients with obstructive sleep apnea: A prospective, randomized crossover trial. J Am Coll Cardiol. 2006;47(2):379-383
Institute for Clinical Systems Improvement (ICSI). Diagnosis and treatment of obstructive sleep apnea. Health Care Guideline. 4th ed. Bloomington, MN: ISCI; March 2006. Available at: http://www.icsi.org/knowledge/detail.asp?catID=29&itemID=891. Accessed May 22, 2006.
Javaheri S. Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure. Circulation. 2000;101(4):392-397.
Wassmuth Z, Mair E, Loube D, Leonard D. Cautery-assisted palatal stiffening operation for the treatment of obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg. 2000;123(1 Pt 1):55-60.
Heinzer R, Gaudreau H, Décary A, et al. Slow-wave activity in sleep apnea patients before and after continuous positive airway pressure treatment. Contribution to daytime sleepiness. Chest. 2001;119(6):1807-1813.
Ferguson K. Oral appliance therapy for obstructive sleep apnea: Finally evidence you can sink your teeth into. Am J Respir Crit Care Med. 2001;163(6):1294-1295.
Smith I, Lasserson TJ, Wright J. Drug therapy for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006;(2):CD003002.
Brietzke SE, Gallagher D. The effectiveness of tonsillectomy and adenoidectomy in the treatment of pediatric obstructive sleep apnea/hypopnea syndrome: A meta-analysis. Otolaryngol Head Neck Surg. 2006;134(6):979-984.
Giles TL, Lasserson TJ, Smith BH, et al. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006;3:CD001106.
Kushida CA, Littner MR, Hirshkowitz M, et al; American Academy of Sleep Medicine. Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breathing disorders. Sleep. 2006;29(3):375-380.
Morgenthaler TI, Kapen S, Lee-Chiong T, et al; Standards of Practice Committee, American Academy of Sleep Medicine. Practice parameters for the medical therapy of obstructive sleep apnea. Sleep. 2006;29(8):1031-1035.
Mundy L, Sullivan T, Merlin T, et al.; Horizon Scanning Unit, Adelaide Health Technology Assessment, University of Adelaide. The Pillar procedure: For the treatment of obstructive sleep apnoea and snoring. Horizon Scanning Report. Canberra, ACT: HealthPACT Secretariat, Department of Health and Ageing, Australian Government; September 2006. Available at: http://www.health.adelaide.edu.au/publichealth/research/horizon_scanning.html. Accessed January 29, 2007.
Canadian Agency for Drugs and Technologies in Health (CADTH). Obstructive sleep apnea: A palatable treatment option? Issues in Emerging health Technologies, Issue 97. Ottawa, ON: CADTH; January 2007. Available at: http://www.cadth.ca/media/pdf/E0008_obstructive-sleep-apnea_cetap_e.pdf. Accessed January 31, 2007.
Danish Centre for Evaluation and Health Technology Assessment (DACEHTA). Diagnosis and treatment of obstructive sleep apnoea - a health technology assessment. Danish Health Technology Assessment -- grant funded projects. Copenhagen, Denmark; DACEHTA; 2006;6(5).
Hawke M, Kwok P. Acute inflammatory edema of the uvula (uvulitis) as a cause of respiratory distress: A case report. J Otolaryngol. 1987;16(3):188-190.
Waeckerle JF, Smith HA, McNabney WK. Hereditary angioneurotic edema treated by partial uvulectomy. JACEP. 1976;5(6):446-448.
Dawodu ST. Swallowing disorders. eMedicine Physicial Medicine & Rehabilitation Topic 152. Omaha, NE: eMedicine.com; updated January 26, 2007.
Aloia MS, Stanchina M, Arnedt JT, et al. Treatment adherence and outcomes in flexible vs. standard continuous positive airway pressure therapy. Chest. 2005;127(6):2085-2093.
Nilius G, Happel A, Domanski U, Ruhle KH. Pressure-relief continuous positive airway pressure vs constant continuous positive airway pressure: A comparison of efficacy and compliance. Chest. 2006;130(4):1018-1024.
Swedish Council on Technology Assessment in Healthcare (SBU). Obstructive sleep apnoea syndrome - Report of a joint Nordic project. A systematic literature review. SBU Report 184E. Stockholm, Sweden: SBU; 2007.
Pang KP, Terris DJ. Modified cautery-assisted palatal stiffening operation: New method for treating snoring and mild obstructive sleep apnea. Otolaryngol Head Neck Surg. 2007;136(5):823-826.
Nordgård S, Hein G, Stene BK, et al. One-year results: Palatal implants for the treatment of obstructive sleep apnea. Otolaryngol Head Neck Surg. 2007;136(5):818-822.
Walker RP, Levine HL, Hopp ML, Greene D. Extended follow-up of palatal implants for OSA treatment. Otolaryngol Head Neck Surg. 2007;137(5):822-827.
Chihorek AM, Abou-Khalil B, Malow BA. Obstructive sleep apnea is associated with seizure occurrence in older adults with epilepsy. Neurology. 2007;69(19):1823-1827.
U.S. Department of Health and Human Services, Centers for Medicare and Medicaid Services (CMS). Decision memo for continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea (OSA) (CAG-0093R2). Medicare Coverage Database. Baltimore, MD: CMS; March 13, 2008.
Ghegan MD, Angelos PC, Stonebraker AC, et al. Laboratory versus portable sleep studies: A meta-analysis.Laryngoscope. 2006;116(6):859-864.
Trikalinos TA, Ip S, Raman G, et al. Home diagnosis of obstructive sleep apnea-hypopnea syndrome. Technology Assessment. Prepared for AHRQ by the Tufts-New England Medical Center Evidence-based Practice Center. Rockville, MD: Agency for Healthcare Research and Quality (AHRQ); August 8, 2007. Available at: http://www.cms.hhs.gov/determinationprocess/downloads/id48TA.pdf. Accessed December 21, 2007.
Trikalinos TA, Lau J. Obstructive sleep apnea-hypopnea syndrome: Modeling different diagnostic strategies. Technology Assessment. Prepared for AHRQ by the Tufts-New England Medical Center Evidence-based Practice Center. Rockvill, MD: Agency for Healthcare Research and Quality (AHRQ); December 4, 2007. Available at: http://www.cms.hhs.gov/determinationprocess/downloads/id50TA.pdf. Accessed January 14, 2008.
Ontario Ministry of Health and Long-Term Care, Medical Advisory Secretariat (MAS). Polysomnography in adults with obstructive sleep apnea. Health Technology Policy Assessment. Toronto, ON: MAS; June 2006.
Chai CL, Pathinathan A, Smith B. Continuous positive airway pressure delivery interfaces for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;(4):CD005308.
National Institute for Health and Clinical Excellence (NICE). Continuous positive airway pressure for the treatment of obstructive sleep apnoea/hypopnoea syndrome. Technology Appraisal Guidance 139. London, UK: NICE; March 26, 2008.
National Institute for Health and Clinical Excellence (NICE). Soft palate implants for simple snoring. Interventional Procedure Guidance 240. London, UK: NICE; November 2007.
National Institute for Health and Clinical Excellence (NICE). Soft palate implants for obstructive sleep apnoea syndrome. Interventional Procedure Guidance 241. London, UK: NICE; November 2007.
Teschler H, Dohring J, Wang YM, et al. Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. Am J Respir Crit Care Med. 2001;164(4):614-619.
Littner M, Hirshkowitz M, Davila D., et al.; Standard of Practice Committee of the American Academy of Sleep Medicine (AASM). Practice parameters for the use of auto-titrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. Sleep. 2002;25(2):143-147.
Pepperell JC, Maskell NA, Jones DR, et al. A randomized controlled trial of adaptive ventilation for Cheyne-Stokes breathing in heart failure. Am J Respir Crit Care Med. 2003;168(9):1109-1114.
Töpfer V, El-Sebai M, Wessendorf TE, et al. [Adaptive servoventilation: Effect on Cheyne-Stokes-Respiration and on quality of life]. Pneumologie. 2004;58(1):28-32.
Kasai T, Narui K, Dohi T, et al. First experience of using new adaptive servo-ventilation device for Cheyne-Stokes respiration with central sleep apnea among Japanese patients with congestive heart failure: Report of 4 clinical cases. Circ J. 2006;70(9):1148-1154.
Pepin JL, Chouri-Pontarollo N, Tamisier R, et al. Cheyne-Stokes respiration with central sleep apnoea in chronic heart failure: Proposals for a diagnostic and therapeutic strategy. Sleep Med Rev. 2006;10(1):33-47.
Zhang XL, Yin KS, Li XL, et al. Efficacy of adaptive servoventilation in patients with congestive heart failure and Cheyne-Stokes respiration. Chin Med J (Engl). 2006;119(8):622-627.
Szollosi I, O'Driscoll DM, Dayer MJ, et al. Adaptive servo-ventilation and deadspace: Effects on central sleep apnoea. J Sleep Res. 2006;15(2):199-205.
Banno K, Okamura K, Kryger MH. Adaptive servo-ventilation in patients with idiopathic Cheyne-Stokes breathing. J Clin Sleep Med. 2006;2(2):181-186.
Morrell MJ, Meadows GE, Hastings P, et al. The effects of adaptive servo ventilation on cerebral vascular reactivity in patients with congestive heart failure and sleep-disordered breathing. Sleep. 2007;30(5):648-653.
Morgenthaler TI, Gay PC, Gordon N, et al. Adaptive servoventilation versus noninvasive positive pressure ventilation for central, mixed, and complex sleep apnea syndromes. Sleep. 2007;30(4):468-475.
Hastings PC, Vazir A, Meadows GE, et al. Adaptive servo-ventilation in heart failure patients with sleep apnea: A real world study. Int J Cardiol. 2010;139(1):17-24.
Morgenthaler TI, Aurora RN, Brown T, et al.; Standards of Practice Committee of the American Academy of Sleep Medicine (AASM). Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome: An update for 2007. Sleep. 2008;31(1):141-147.
Woodson BT. Transpalatal advancement pharyngoplasty outcomes compared with uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg. 2005;133(2):211-217.
Kohler M, Bloch KE, Stradling JR. The role of the nose in the pathogenesis of obstructive sleep apnoea and snoring. Eur Respir J. 2007;30(6):1208-1215.
Randerath W, Bauer M, Blau A, et al; Taskforce der Arbeitsgruppe Apnoe der DGSM. Are there alternative therapeutical options other than CPAP in the treatment of the obstructive sleep apnea syndrome? Pneumologie. 2007;61(7):458-466.
Australian Safety and Efficacy Register of New Interventional Procedures -Surgical (ASERNIP-S). Rapid Review - Upper airway surgery for the treatment of adult obstructive sleep apnoea. ASERNIP-S Report No. 67. Stepney, SA: Australian Safety and Efficacy Register of New Interventional Procedures -Surgical (ASERNIP-S); 2008.
Steward DL, Huntley TC, Woodson BT, Surdulescu V. Palate implants for obstructive sleep apnea: Multi-institution, randomized, placebo-controlled study. Otolaryngol Head Neck Surg. 2008;139(4):506-510.
Koutsourelakis I, Georgoulopoulos G, Perraki E, et al. Randomised trial of nasal surgery for fixed nasal obstruction in obstructive sleep apnoea. Eur Respir J. 2008;31(1):110-117.
Lin HC, Friedman M, Chang HW, Gurpinar B. The efficacy of multilevel surgery of the upper airway in adults with obstructive sleep apnea/hypopnea syndrome. Laryngoscope. 2008;118(5):902-908.
Centers for Medicare & Medicaid Services (CMS). Decision memo for sleep testing for obstructive sleep apnea (OSA) (CAG-00405N). Medicare Coverge Database. Baltimore, MD: CMS; March 3, 2009.
Tice JA. Portable devices in home testing for obstructive sleep apnea. A Technology Assessment. San Francisco, CA: California Technology Assessment Forum (CTAF); 2009.
Smith I, Nadig V, Lasserson TJ. Educational, supportive and behavioural interventions to improve usage of continuous positive airway pressure machines for adults with obstructive sleep apnoea. Cochrane Database Syst Rev. 2009;(2): CD007736.
Smith I, Lasserson TJ. Pressure modification for improving usage of continuous positive airway pressure machines in adults with obstructive sleep apnoea. Cochrane Database Syst Rev. 2009;(4):CD003531.
NHIC, Corp. Respiratory assist devices. Local Coverage Determination (LCD) No. L11504. Durable Medical Equipment Medicare Administrative Carrier (DME MAC) Jurisdiction A. Hingham, MA: NHIC; revised March 13, 2008.
McDaid C, Griffin S, Weatherly H, et al. Continuous positive airway pressure devices for the treatment of obstructive sleep apnoea-hypopnoea syndrome: A systematic review and economic analysis. Health Technol Assess. 2009;13(4): 1-142.
Vanderveken OM, Devolder A, Marklund M, et al. Comparison of a custom-made and a thermoplastic oral appliance for the treatment of mild sleep apnea. Am J Respir Crit Care Med. 2008;178(2):197-202.
Ferguson KA, Cartwright R, Rogers R, et al. Oral appliances for snoring and obstructive sleep apnea: A review. Sleep. 2006;29(2):244-262.
Gotsopoulos H, Chen C, Qian J, Cistulli PA. Oral appliance therapy improves symptoms in obstructive sleep apnea: A randomized, controlled trial. Am J Respir Crit Care Med. 2002;166(5):743-748.
Henke K, Frantz DE, Kuna ST. An oral elastic mandibular advancement device for obstructive sleep apnea. Am J Respir Crit Care Med. 2000;161:420-425.
Thomas AJ, Chavoya M, Terris DJ. Preliminary findings from a prospective, randomized trial of two tongue-base surgeries for sleep-disordered breathing. Otolaryngol Head Neck Surg. 2003;129(5):539-546.
Hamans E, Boudewyns A, Stuck BA, et al. Adjustable tongue advancement for obstructive sleep apnea: A pilot study. Ann Otol Rhinol Laryngol. 2008;117(11):815-823.
Malow BA, Foldvary-Schaefer N, Vaughn BV, et al. Treating obstructive sleep apnea in adults with epilepsy: A randomized pilot trial. Neurology. 2008;71(8):572-577.
Ramachandran SK, Josephs LA. A meta-analysis of clinical screening tests for obstructive sleep apnea. Anesthesiology. 2009;110(4):928-939.
Canadian Agency for Drugs and Technologies in Health (CADTH). Portable monitoring devices for diagnosis of obstructive sleep apnea at home: Review of accuracy, cost-effectiveness, guidelines, and coverage in Canada. Ottawa, ON: CADTH; December 2009. Available at: http://www.cadth.ca/index.php/en/hta/reports-publications/search/publication/950. Accessed January 7, 2010.
Colrain IM, Brooks S, Black J. A pilot evaluation of a nasal expiratory resistance device for the treatment of obstructive sleep apnea. J Clin Sleep Med. 2008;4(5):426-433.
Rosenthal L, Massie CA, Dolan DC, et al. A multicenter, prospective study of a novel nasal EPAP device in the treatment of obstructive sleep apnea: Efficacy and 30-day adherence. J Clin Sleep Med. 2009;5(6):532-537.
Fernández-Julián E, Muñoz N, Achiques MT, et al. Randomized study comparing two tongue base surgeries for moderate to severe obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg. 2009;140(6):917-923.
Woodson BT, Steward DL, Mickelson S, et al. Multicenter study of a novel adjustable tongue-advancement device for obstructive sleep apnea. Otolaryngol Head Neck Surg. 2010;143(4):585-590.
Aurora RN, Casey KR, Kristo D, et al. Practice parameters for the surgical modifications of the upper airway for obstructive sleep apnea in adults. Sleep. 2010;33(10):1409-1413.
Martinho FL, Zonato AI, Bittencourt LR, Soares MC. Obese obstructive sleep apnea patients with tonsil hypertrophy submitted to tonsillectomy. Brazil J Med Biol Res. 2006;39(8):1137-1142.
Verse T, Kroker BA, Pirsig W, Brosch S. Tonsillectomy as a treatment of obstructive sleep apnea in adults with tonsillar hypertrophy. Laryngoscope. 2000;110(9):1556-1559.
Skinner MA, Kingshott RN, Filsell S, et al. Efficacy of the 'tennis ball technique' versus nCPAP in the management of position-dependent obstructive sleep apnea syndrome. Respirology. 2008;13(5):708-715.
Epstein LJ, Kristo D, Strollo PJ Jr, et al; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009;5(3):263-276.
Lee JB, Park YH, Hong JH, et al. Determining optimal sleep position in patients with positional sleep-disordered breathing using response surface analysis. J Sleep Res. 2009;18(1):26-35.
Permut I, Montserrat D, Wissam C, et al. Comparison of positional therapy to CPAP in patients with positional obstructive sleep apnea. J Clin Sleep Med. 2010;6(3):238-243.
U.S. Food and Drug Administration (FDA). Zzoma Positional Sleeper. 510(k) No. K100160. Rockville, MD: FDA; May 11, 2010.
Collop NA, Anderson WM, Boehlecke B, et al.; Portable Monitoring Task Force of the American Academy of Sleep Medicine. Clinical guidelines for the use of unattended portable monitors in the diagnosis of obstructive sleep apnea in adult patients. Portable Monitoring Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med 2007;3(7):737-747.
Valbuza JS, de Oliveira MM, Conti CF, et al. Methods for increasing upper airway muscle tonus in treating obstructive sleep apnea: Systematic review. Sleep Breath. 2010;14(4):299-305.
Gillespie MB, Wylie PE, Lee-Chiong T, Rapoport DM. Effect of palatal implants on continuous positive airway pressure and compliance. Otolaryngol Head Neck Surg. 2011;144(2):230-236.
Randerath WJ, Verbraecken J, Andreas S, et al; European Respiratory Society task force on non-CPAP therapies in sleep apnoea. Non-CPAP therapies in obstructive sleep apnoea. Eur Respir J. 2011;37(5):1000-1028. Available at: http://www.ers-education.org/media/2011/pdf/156487.pdf. Accessed January 3, 2012.
Walsh JK, Griffin KS, Forst EH, et al. A convenient expiratory positive airway pressure nasal device for the treatment of sleep apnea in patients non-adherent with continuous positive airway pressure. Sleep Med. 2011;12(2):147-152.
Berry RB, Kryger MH, Massie CA. A novel nasal expiratory positive airway pressure (EPAP) device for the treatment of obstructive sleep apnea: A randomized controlled trial. Sleep. 2011;34(4):479–485.
Patel AV, Hwang D, Masdeu MJ, et al. Predictors of response to a nasal expiratory resistor device and its potential mechanisms of action for treatment of obstructive sleep apnea. J Clin Sleep Med. 2011;7(1):13-22.
Kryger MH, Berry RB, Massie CA. Long-term use of a nasal expiratory positive airway pressure (EPAP) device as a treatment for obstructive sleep apnea (OSA). J Clin Sleep Med. 2011;7(5):449-453.
Pang KP, Dillard TA, Blanchard AR, et al. A comparison of polysomnography and the SleepStrip in the diagnosis of OSA. Otolaryngol Head Neck Surg. 2006;135(2):265-268.
Ozmen OA, Tüzemen G, Kasapoğlu F, et al. The reliability of SleepStrip as a screening test in obstructive sleep apnea syndrome. Kulak Burun Bogaz Ihtis Derg. 2011;21(1):15-19.
Randerath WJ, Verbraecken J, Andreas S, et al; European Respiratory Society task force on non-CPAP therapies in sleep apnoea. Non-CPAP therapies in obstructive sleep apnoea. Eur Respir J. 2011;37(5):1000-1028.
Farid-Moayer M, Siegel LC, Black J. A feasability evaluation of oral pressure therapy for the treatment of obstructive sleep apnea. Ther Adv Respir Dis. 2012 Nov 26. [Epub ahead of print]
Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.
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