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Last Updated: 8/5/2014  

Obstructive Sleep Apnea

Diagnosis
  • Ask patients and their sleeping partner and/or family members about symptoms including snoring, apneas, awakenings due to gasping or choking, daytime sleepiness, fatigue, poor concentration, nasal congestion, weight gain, and morning headaches.

  • Obtain a sleep study using formal in-laboratory polysomnography for the most accurate diagnosis of OSA.

  • Use the results of the sleep study to determine the severity of OSA.

    • Define mild OSA as an AHI (or RDI) between 5 and 15. Patients with mild OSA often report sleepiness when they are sedentary and under-stimulated.

    • Define moderate OSA as an AHI (or RDI) between 15 and 30. Patients with moderate OSA often report sleepiness more often throughout the day.

    • Define severe OSA as an AHI (or RDI) more than 30. Patients with severe OSA often have sleepiness that interferes significantly with daily activities.

Therapy
  • Treat the majority of patients with OSA with CPAP.

  • Consider oral appliances for patients who are unable to adhere to CPAP.

  • Consider surgical treatment for appropriate patients.

  • Consider a trial of modafinil for patients with residual excessive daytime sleepiness who have no other identifiable cause for their sleepiness.

Obtain a sleep history to assess the risk of OSA and ask about associated conditions. 
  • Ask patients and their sleeping partners and/or family members about:

    • Snoring

    • Witnessed apneas

    • Awakenings due to gasping or choking

    • Excessive daytime sleepiness

    • Excessive fatigue

    • Poor memory or concentration

    • Nasal congestion

    • Weight gain

    • Morning headaches

    • How many hours the patient sleeps per night (to determine if sleep deprivation is present as a contributing factor)

  • Assess patients for conditions that are associated with OSA:

    • Hypertension

    • Coronary artery disease and myocardial infarction

    • HF

    • Stroke

    • Diabetes

    • Motor vehicle collisions

  • See figure Epworth Sleepiness Scale.

Evidence
  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine on the evaluation, management, and care of patients with OSA recommended that patients at high risk for OSA and commercial drivers be asked about symptoms including snoring, witnessed apneas, nocturia, morning headaches, and poor concentration (1).

  • A 2013 guideline from the American Thoracic Society regarding sleep apnea and driving risk recommended that patients with suspected OSA be asked about recent daytime sleepiness and recent motor vehicle collisions or near-collisions (2).

Rationale
  • The sleep history can help determine which patients may need diagnostic testing for OSA.

Comments
  • Eliciting a history of excessive sleepiness from patients may be challenging, because patients have often accommodated themselves to the symptoms. The Epworth Sleepiness Scale is a commonly used questionnaire for this purpose, although not all patients with OSA report excessive sleepiness as a symptom.

Perform a focused physical exam for signs consistent with OSA. 
  • During physical exam, look for:

    • Obesity (BMI ≥30 kg/m2)

    • Large neck circumference (≥16 inches for women, ≥17 inches for men)

    • BP >140/90 mm Hg

    • Decreased oxygen saturation

    • Nasal congestion or obstruction (septal deviation or polyps)

    • Crowded oropharyngeal airway (including enlarged tonsils, retrognathia, macroglossia, enlarged uvula)

    • Wheezing or crackles

    • Lower extremity edema

    • A loud P2 or an S3

Evidence
  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine on the evaluation, management, and care of patients with OSA recommended physical exam including evaluation for obesity, upper airway narrowing, and exams of the respiratory, cardiac, and neurologic systems (1).

  • In middle-aged adults, a BMI >29 is associated with an 8- to 12-fold increased risk of OSA (3).

  • In a large (n=709) population-based survey in Wisconsin, there was a relationship between the baseline level of OSA (AHI measured at entry into the longitudinal study) and the odds ratio for hypertension (BP >140/90 mm Hg or on antihypertensive medication) at 4-year follow-up. Compared to a reference group with normal breathing, subjects with a greater degree of OSA (baseline AHI >15 respiratory events per hour) showed an odds ratio of 2.89 for the presence of hypertension at 4-year follow-up (4).

  • The Sleep Heart Health Study evaluated the relationship between OSA and heart disease in 6424 adults. Compared to the group with normal breathing, the group with the most severe OSA (AHI >11) showed significant relative odds of 2.38 for heart failure and 1.58 for stroke (5).

Rationale
  • Physical exam findings can identify patients at higher risk for OSA and can show possible consequences of untreated OSA (such as pulmonary hypertension or HF).

  • Obesity is the most common risk factor for OSA in the general adult population, but thinner patients can also have OSA.

  • Hypertension is associated with OSA. Greater severity of OSA is associated with greater risk of hypertension, and this association may explain part of the increased cardiovascular risk due to OSA.

Recommend testing for OSA for appropriate patients. 
  • Recommend testing for patients who have nocturnal symptoms of OSA (such as snoring, witnessed apneas, or awakenings due to gasping or choking) with excessive daytime sleepiness.

  • Consider testing for patients with nocturnal symptoms of OSA who do not report excessive daytime sleepiness, but still have a high clinical likelihood of OSA based on other history and physical exam findings.

  • Consider testing for patients with coexisting illnesses that are associated with OSA (including treatment-refractory hypertension, HF, coronary artery disease, pulmonary hypertension, or history of stroke) who have nocturnal symptoms of OSA but do not report excessive daytime sleepiness.

  • Consider testing for patients who work in high-risk professions (such as commercial truck drivers and airline pilots) who have nocturnal symptoms of OSA but do not report excessive daytime sleepiness.

Evidence
  • A 2014 ACP guideline on the diagnosis of OSA in adults recommended performing polysomnography to diagnose OSA in patients with suspected disease, including those with daytime sleepiness (6).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine on the evaluation, management, and care of patients with OSA included recommendations for testing (1).

Rationale
  • A history consistent with OSA, in conjunction with physical exam findings associated with OSA, helps determine which patients should be referred for further testing.

  • The threshold for consideration of testing for OSA may be lowered by the presence of coexisting illnesses associated with OSA or by the danger of undiagnosed OSA for people in high-risk professions.

Comments
  • Clinical impression of OSA has poor diagnostic accuracy, and no one clinical model is recommended to predict the severity of OSA (7; 8).

Obtain a sleep study using formal in-laboratory polysomnography for the most accurate diagnosis of OSA. 
  • Obtain a formal in-laboratory polysomnogram, with EEG for sleep staging, for the most accurate diagnosis of OSA.

  • Consider in-home testing (known as ‘portable monitoring’) for patients with a high pre-test probability of moderate-to-severe OSA and no significant comorbidities (including moderate-to-severe pulmonary disease, HF, coronary or cerebrovascular disease).

  • Do not use overnight pulse oximetry alone to diagnose OSA.

  • Diagnose OSA in asymptomatic patients with ≥15 obstructive respiratory events per hour.

  • Diagnose OSA in patients with ≥5 obstructive respiratory events per hour who also have symptoms consistent with OSA (including excessive daytime sleepiness, loud snoring, witnessed apneas, awakenings due to gasping or choking).

  • See figures Polysomnogram Tracings of Obstructive Apnea, Polysomnogram Tracings of Obstructive Hypopnea, and Polysomnogram Tracings of Upper-Airway Resistance.

Evidence
  • A 2014 ACP guideline on the diagnosis of OSA in adults recommended performing polysomnography to diagnose OSA in patients with suspected disease. The guideline included a systematic review which assessed the accuracy of other diagnostic tests for OSA. At a cutoff value of an apnea-hypopnea index of 15, type II monitors had sensitivity of 79-100% and specificity of 71-100%, type III monitors had sensitivity of 64-100% and specificity of 41-100%, and type IV monitors with two or more channels had sensitivity of 67-98% and specificity of 50-100% (6).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommended full-night polysomnography or split-night polysomnography for patients with suspected OSA (1).

  • A 2000 systematic review of the diagnosis of OSA found disparate evidence; polysomnography was generally considered to be the gold standard for diagnosis (9).

  • A 2009 retrospective study of patients who received 2 nights of polysomnography evaluated the sensitivity of single-night polysomnography by comparing it to the findings of both nights. Overall, single-night polysomnography had sensitivity of 80% for the diagnosis of OSA over 2 nights (10).

  • The Portable Monitoring Task Force of the American Academy of Sleep Medicine issued guidelines in 2007 for the use of portable monitors (11).

Rationale
  • A formal in-laboratory polysomnogram provides the most accurate diagnosis of OSA and may also include initiation and titration of CPAP therapy.

  • In-home portable monitoring is an alternative to in-laboratory polysomnography for patients with a high pre-test probability of moderate-to-severe OSA and no significant comorbidities.

Comments
  • In-laboratory polysomnography counts the number of apneas (cessation of airflow for 10 or more seconds), the number of hypopneas (decrease in airflow for 10 or more seconds, accompanied by 4% oxygen desaturation), and the number of hours of sleep. The AHI is calculated as (apneas + hypopneas)/hours of sleep. The AHI is also sometimes called the respiratory disturbance index or RDI.

  • The RDI is calculated differently when measured by portable monitoring. Since portable monitoring does not include an EEG, it is not possible to measure actual sleep time. The RDI for portable monitoring is therefore calculated as the number of apneas and hypopneas per total recording time (as opposed to per total sleep time during in-laboratory polysomnography). As a result, the RDI measured during portable monitoring may underestimate the true severity of OSA.

  • The results of portable monitoring must be interpreted by an appropriately trained sleep specialist as part of a comprehensive sleep evaluation.

Determine the severity of OSA. 
  • Use the results of the sleep study to determine the severity of OSA:

    • Define mild OSA as an AHI (or RDI) between 5 and 15. Patients with mild OSA often report sleepiness when they are sedentary and under-stimulated

    • Define moderate OSA as an AHI (or RDI) between 15 and 30. Patients with moderate OSA often report sleepiness more often throughout the day

    • Define severe OSA as an AHI (or RDI) over 30. Patients with severe OSA often have sleepiness that interferes significantly with daily activities

Evidence
  • The 2009 guidelinefrom the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine presented diagnostic criteria for OSA and defined severity as mild (RDI, 5 to <15 per hour), moderate (RDI, 15 to ≤30 per hour), or severe (RDI, >30 per hour) (1).

Rationale
  • The severity of OSA determines which treatment options are indicated (CPAP, oral appliance, and/or upper airway surgery).

Comments
  • The severity of OSA as measured during a sleep study does not always correlate with the level of patient symptoms.

Consider additional laboratory and imaging tests to assess the severity of OSA and its complications. 
  • Obtain CBC to assess for polycythemia in patients with severe OSA accompanied by severe hypoxemia.

  • Obtain TSH, if clinically indicated, to exclude hypothyroidism, particularly in patients with recent weight gain and fatigue.

  • Obtain chest x-ray and ECG if coexisting HF is suspected based on history and/or physical exam.

  • Be aware that ABG testing can assess both Pco2 and Po2 to identify hypercapnia and hypoxemia if obesity hypoventilation syndrome is suspected.

Evidence
  • Consensus.

Rationale
  • Polycythemia may be a complication in severe OSA accompanied by severe hypoxemia.

  • The symptoms of hypothyroidism (weight gain, fatigue, and sleepiness) can mimic the clinical presentation of OSA.

  • HF can be a complication of OSA, which increases the urgency of diagnosing and treating OSA.

  • OSA can be complicated by obesity hypoventilation syndrome, which is characterized by hypercapnia and hypoxemia; daytime, awake ABG is the best initial test in this setting.

Comments
  • These tests are usually normal in patients with OSA.

Consider the broad differential diagnosis of OSA, including other primary sleep disorders and medical conditions or neurologic disorders that disturb sleep. 
  • Consider other sleep disorders with symptoms similar to OSA:

    • Central sleep apnea

    • Upper airway resistance syndrome

    • Periodic limb movements of sleep

    • Narcolepsy

    • Sleep deprivation

  • Consider other medical disorders that may cause sleep-related symptoms:

    • Asthma

    • COPD or restrictive lung disease

    • GERD

    • Allergic rhinitis or sinusitis

    • HF

    • Chronic pain

    • Drug abuse

    • Hypothyroidism

  • Consider neurologic disorders:

    • Stroke

    • Movement disorders

    • Seizure disorders

  • Note that clinical correlation is essential to determine appropriate sleep testing and treatment.

  • See table Differential Diagnosis of OSA.

Evidence
  • Consensus.

Rationale
  • A variety of disorders may have nonspecific sleep-related symptoms.

  • A thorough history and physical exam can help to distinguish these various sleep, medical, and neurologic disorders.

Obtain sleep or pulmonary consultation to confirm the diagnosis of OSA. 
  • Consult a sleep or pulmonary specialist when a patient's history and physical exam suggest the diagnosis of OSA to:

    • Determine the need for sleep testing

    • Identify the appropriate testing method (formal, in-house polysomnography, or portable, in-home testing)

    • Interpret test results

    • Confirm the diagnosis when the presentation or data are not clear

Evidence
  • In 2009, the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine published guidelines on the evaluation, management, and care of patients with OSA (1).

Rationale
  • Sleep and pulmonary specialists have the most experience in evaluating patients with a history and physical exam suggestive of OSA and in ordering and interpreting diagnostic tests to confirm the diagnosis.

Consult an appropriate specialist to optimize treatment of sleep apnea. 
  • Consult a sleep or pulmonary specialist to initiate or optimize CPAP therapy, reemphasize lifestyle changes, or help determine if further referrals to dentistry or ENT surgery are indicated.

  • Consult with a dentist to see if an oral appliance may be an option for appropriate patients.

  • Consult an ENT specialist for a detailed evaluation of surgical treatment options for appropriate patients.

Evidence
  • Consensus.

Rationale
  • Sleep and pulmonary specialists have the most experience with OSA management, particularly initiating and optimizing CPAP treatment.

  • In patients who are unwilling or unable to use CPAP therapy, oral appliances or upper airway surgery are potential treatment options, provided the patient understands the risks, benefits, and possible lower success rates of these treatments compared to CPAP.

Consider nutrition consultation or referral to a bariatric surgeon to help the patient achieve and maintain weight loss. 
  • Emphasize the importance of weight loss for obese patients, and provide nutritional education to support the goal of weight loss.

  • If nutritional education is ineffective, consider specialty consultation for bariatric surgery for weight loss.

Evidence
  • A large (n=690), prospective, population-based study in Wisconsin showed that a 10% weight loss over a 4-year follow-up predicted a 26% decrease in the AHI (12).

  • A 2009 meta-analysis of 12 studies on the effects of surgical weight loss on OSA reported that the mean AHI decreased from 54.7 before surgery to 15.8 after surgery while mean BMI decreased from 55.3 kg/m2 to 37.7 kg/m2. Note that while the drop in AHI was significant, the post-surgery AHI was still indicative of moderately severe OSA requiring treatment (13).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommends considering bariatric surgery as an adjunctive treatment in obese patients (1).

Rationale
  • Weight loss will improve airway patency and therefore may reduce the severity of OSA.

  • Weight loss of at least 10% is more likely to reduce the severity of OSA.

  • For morbidly obese patients (BMI >40 kg/m2) who are unable to lose weight, consultation for bariatric surgery may be an option.

Comments
  • In the small percentage of patients who achieve and maintain significant weight loss, a follow-up sleep study should be done to determine if OSA has resolved or if CPAP settings need to be adjusted.

Hospitalize patients with decompensated obesity hypoventilation syndrome. 
  • If a patient with OSA has hypoxemia while awake in the daytime, perform ABG testing to look for obesity hypoventilation syndrome.

  • Consider hospitalization for urgent institution of ventilatory support if the blood gas shows significant hypercapnia (Paco2 >50) accompanied by acidosis (pH <7.30).

Evidence
  • Patients with hypercapnia (mean Paco2 = 82), respiratory acidosis (mean pH = 7.22), and hypoxemia (mean Pao2 = 45) are more likely to have ‘near miss' death events when compared to patients with more typical OSA (14).

Rationale
  • Patients with obesity hypoventilation syndrome may be at risk for morbidity and mortality if treatment is not instituted promptly.

  • Hospitalization allows for more rapid initiation of ventilatory support treatment, often with a BPAP device.

Recommend lifestyle changes to all patients with OSA. 
  • In patients with OSA, recommend:

    • Weight loss

    • Exercise

    • Avoiding alcohol and sedatives for 3 to 4 hours before bedtime

    • Sleeping in the lateral position

Evidence
  • A 2013 American College of Physicians guideline on the management of OSA in adults recommended weight loss for overweight and obese patients with OSA. In addition, the guideline recommended CPAP as initial therapy for OSA and mandibular advancement devices as an alternative therapy for patients who do not tolerate CPAP (15).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommended positional therapy in select patients (1).

  • A 2011 systematic review summarized the evidence from non-CPAP therapies for OSA and found that weight loss was associated with a trend toward improved symptoms and breathing, and that positional therapy can lead to moderate AHI reductions (16).

  • In a prospective cohort study in Wisconsin, participants who had a 10% weight loss had a 26% reduction in the mean AHI. Conversely, participants with 10% weight gain had a 32% increase in the mean AHI (12).

  • In a 12-week trial of 43 patients with OSA, patients were randomly assigned to an exercise regimen or to a stretching program (control group). Patients in the exercise group performed moderate-intensity aerobic exercise for 4 days a week and resistance training for 2 days a week while patients in the control group met twice weekly to perform low-intensity exercises designed to increase whole-body flexibility. Patients in the exercise group had a significant reduction in the mean AHI, from 32.2 to 24.6, without a significant change in weight. The patients in the stretching group had an increase in the mean AHI, from 24.4 to 28.9 (17).

Rationale
  • Weight loss can increase the size of the airway and can decrease the AHI.

  • Exercise can decrease the AHI even in the absence of significant weight loss.

  • Because alcohol reduces the muscle tone of the airway dilating muscles, avoiding alcohol keeps these muscles more active, thus promoting a more patent airway.

  • Sleeping in the lateral position may help because the airway may be less collapsible in the lateral dimension.

Comments
  • Conservative treatments are often ineffective, because most obese patients are unable to lose weight or to exercise on a consistent basis. For patients with moderate-to-severe OSA, more definitive treatments should also be initiated at the time of diagnosis.

Treat the majority of patients who have OSA with CPAP. 
  • Recognize that CPAP is the first-line treatment for moderate-to-severe OSA and is an option for treatment of mild OSA.

  • In patients who are unable to tolerate regular CPAP, consider BPAP or APAP.

Evidence
  • A 2013 American College of Physicians guideline on the management of OSA in adults recommended weight loss for overweight and obese patients with OSA. In addition, the guideline recommended CPAP as initial therapy for OSA and mandibular advancement devices as an alternative therapy for patients who do not tolerate CPAP (15).

  • A 2013 guideline from the American Thoracic Society regarding sleep apnea and driving risk recommended CPAP therapy for high-risk drivers with OSA (2).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommended CPAP as first-line therapy (1).

  • A 2006 Cochrane review of the effect of CPAP compared to various controls included 36 randomized trials with 1718 participants. CPAP improved objective and subjective sleepiness and quality of life, and lowered blood pressure (18).

  • A double-blind, randomized, placebo-controlled trial showed that CPAP can improve many aspects of the metabolic syndrome. Ninety patients were randomly assigned to therapeutic CPAP or sham CPAP for 3 months, followed by a washout period of 1 month, then crossover to the other intervention for 3 additional months. Compared to sham CPAP, therapeutic CPAP reduced mean systolic and diastolic blood pressure, serum total cholesterol, low-density lipoprotein cholesterol, triglycerides, and glycated hemoglobin (19).

  • A systematic review of motor vehicle collisions in people with OSA reported that 23 out of 27 studies showed a significantly higher risk of motor vehicle crashes for people with OSA compared to people without OSA (median odds ratio of 3.1). Of note, subjective daytime sleepiness was correlated with risk of collision in only 8 out of 15 studies. All 11 studies (including one randomized trial) that examined the effect of CPAP on the risk of collisions showed that treatment with CPAP improved driver performance and decreased crash rates (20).

  • Although no randomized trials have assessed whether CPAP therapy decreases mortality, a number of observational cohort studies have reported decreased mortality in patients who are adherent to CPAP therapy (21; 22; 23; 24; 25).

Rationale
  • CPAP provides a pneumatic splint that prevents collapse of the airway during sleep and is the best studied and most consistently effective therapy for OSA.

  • CPAP can eliminate 90% to 100% of apneic events if used on a nightly basis.

  • CPAP improves self-reported sleepiness, improves quality of life, reduces blood pressure in hypertensive patients, improves some aspects of the metabolic syndrome, and possibly decreases the risk of motor vehicle collisions.

  • Many observational trials suggest that CPAP use decreases mortality, especially for patients with severe OSA.

  • BPAP, which allows for a higher inspiratory pressure and a lower expiratory pressure, is potentially more comfortable for patients who find higher fixed pressure CPAP levels to be uncomfortable. Some patients find APAP devices, which deliver variable amounts of pressure based on airway resistance, to be more tolerable.

Comments
  • Most of the literature has studied CPAP therapy. There is no proven benefit of any one mode of positive airway pressure therapy over the others or that any one mode of positive airway pressure therapy is preferable. Patients and their health care providers should work together to identify the most appropriate positive airway pressure interface (26; 27).

  • Although the term BiPAP is widely used to describe any bi-level positive airway pressure device, the correct term is BPAP. BiPAP is a registered trademark of Philips Respironics which produces a line of BPAP. Many other manufacturers also make BPAP devices.

Consider oral appliances for patients who are unable to adhere to CPAP. 
  • Consider oral appliances for patients with mild-to-moderate OSA who prefer an oral appliance over CPAP.

  • Consider oral appliances for patients who do not respond to or have trouble adhering to CPAP.

  • Recall that the recommended treatment for moderate-to-severe OSA is CPAP.

  • Order a follow-up sleep study to document the efficacy of the oral appliance.

Evidence
  • A 2013 American College of Physicians guideline on the management of OSA in adults recommended weight loss for overweight and obese patients with OSA. In addition, the guideline recommended CPAP as initial therapy for OSA and mandibular advancement devices as an alternative therapy for patients who do not tolerate CPAP (15).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommends oral appliances in patients with mild-to-moderate OSA who do not respond to CPAP or who do not tolerate it (1).

  • A 2006 systematic review of 30 trials that compared oral appliances to CPAP reported that oral appliances were less effective than CPAP in reducing the AHI and were likely equivalent to CPAP in improving subjective and objective sleepiness (28).

  • A 2011 systematic review of 27 randomized trials reported that mandibular advancement devices reduced the AHI and subjective daytime sleepiness and improved quality of life compared to control therapies. CPAP reduced the AHI to a greater degree than mandibular advancement devices while the improvements in symptoms were equal. Patients often preferred a mandibular advancement device over CPAP. There were few studies of tongue retaining devices (16).

Rationale
  • Oral appliances increase upper airway volume and patency by altering the local anatomy and therefore can lower the AHI.

Comments
  • Mandibular advancement devices are anchored to the dental arches and advance the mandible in position with respect to the resting position.

  • Tongue retaining devices use suction to move only the tongue into a forward position.

  • Oral appliances have variable success rates depending on complex factors including BMI, individual anatomy, and the severity of OSA. More studies are needed to compare these treatments with each other and with other treatment options.

Consider surgical treatment for appropriate patients.  
  • Consider surgical treatment as primary therapy for patients with mild-to-moderate OSA who have an obstructing lesion that is thought to be surgically correctable (e.g., enlarged tonsils or craniofacial abnormalities).

  • Consider surgical treatment as a secondary therapy for patients whose OSA is inadequately treated with CPAP or an oral appliance (or who are intolerant of or refuse these therapies).

  • Consider tracheostomy for patients with severe, life-threatening OSA that is not amenable to or has not responded to other therapies.

  • Recall that the recommended treatment for moderate-to-severe OSA is CPAP.

  • Order a follow-up sleep study to document the efficacy of surgical treatment.

Evidence
  • A 2010 meta-analysis of upper airway surgery for the treatment of OSA found few controlled trials. The study found that maxillomandibular advancement was effective in treating patients with severe OSA, uvulopalatopharyngoplasty did not reliably normalize the AHI for patients with moderate-to-severe OSA, and that low-quality studies showed that laser-assisted uvulopalatoplasty did not reliably normalize the AHI for patients with OSA. Subsequent studies actually showed an increase in the AHI after the surgery. The associated Practice Parameter concluded that CPAP or oral appliance therapy should be offered to appropriate patients ahead of maxillomandibular advancement, patients with severe OSA should initially be offered CPAP, and patients with moderate OSA should be offered CPAP or an oral appliance. Laser-assisted uvulopalatoplasty was therefore not recommended to treat OSA (29, 30).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommends surgical therapy as a primary treatment for easily reversible abnormalities, or as secondary treatment in patients with a poor response to CPAP (1).

Rationale
  • Surgery can be effective therapy for OSA if there is a surgically correctible obstructive lesion.

  • Tracheostomy is nearly 100% effective at eliminating apneic events but should be reserved for patients who have severe OSA and in whom other treatment options have failed or are not available.

Comments
  • If surgery is successful, adherence to treatment is no longer an issue.

Do not prescribe drug therapy as primary treatment of OSA. 
  • No drug therapy is currently recommended for the primary treatment of OSA.

Evidence
  • A 2006 Cochrane review evaluated drug therapy for OSA and included 26 randomized, controlled trials of 21 drugs. Small studies of poor quality showed reduction in AHI with fluticasone, mirtazapine, physostigmine and nasal lubricants but results were not consistent (31).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine does not recommend medications as a primary treatment for OSA, and particularly does not recommend SSRIs, protriptyline, methylxanthine derivatives or estrogen therapy. The guideline suggests that topical nasal steroids be considered as adjunctive therapy (1).

Rationale
  • Trials of medications such as SSRIs, protriptyline, methylxanthine derivatives (aminophylline and theophylline) have not shown a consistent or significant improvement in the AHI of patients with OSA.

Treat suspected allergic rhinitis with a trial of an inhaled nasal steroid. 
  • If allergic rhinitis is suspected as the cause of nasal congestion, a 4- to 6-week trial of an inhaled nasal steroid is indicated.

Evidence
  • In a small case series of 13 subjects with an initial AHI ≥10 treated with 4 weeks of an inhaled nasal steroid, the mean AHI was reduced from 30.3 to 23.3 (P≤0.05). The median within subject difference was a decrease in the AHI of 6.5 (32; 33).

  • A 2006 Cochrane review evaluated drug therapy for OSA and included 26 randomized, controlled trials of 21 drugs. Small studies of poor quality showed reduction in AHI with fluticasone, mirtazapine, physostigmine, and nasal lubricants but results were not consistent (31).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine does not recommend medications as a primary treatment for OSA, and particularly does not recommend SSRIs, protriptyline, methylxanthine derivatives, or estrogen therapy. The guideline suggests that topical nasal steroids be considered as adjunctive therapy (1).

Rationale
  • If nasal congestion or obstruction can be effectively treated, OSA symptoms may decrease.

  • Improved nasal patency may also improve the effectiveness and tolerance of CPAP.

Consider a trial of modafinil for patients with residual excessive daytime sleepiness who have no other identifiable cause for their sleepiness. 
  • Consider a trial of modafinil for patients who report persistent sleepiness despite appropriate treatment of OSA and have no other identifiable cause of sleepiness (including poor adherence to CPAP or oral appliance therapy, poorly fitting equipment, insufficient sleep time, or other sleep disorders including periodic limb movement syndrome or narcolepsy).

  • If using modafinil, begin at a dose of 200 mg/d orally.

Evidence
  • A 12-week, multicenter, randomized, double-blind, parallel-group, placebo-controlled trial (sponsored by the makers of modafinil) found modafinil to be a useful adjunctive therapy for patients with OSA who were treated with nasal CPAP but still experienced residual excessive sleepiness (34).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommends modafinil to treat residual excessive daytime sleepiness in patients on appropriate CPAP (1).

Rationale
  • Some patients continue to report daytime sleepiness despite adequate treatment of OSA. Primary treatment should be optimized, possibly including a repeat sleep study.

Comments
  • Since modafinil does not treat the underlying obstructive cause of the symptoms and therefore will not mitigate the potential consequences of OSA, modafinil must be used in conjunction with CPAP or other primary treatments of OSA.

  • Side effects can include headaches, insomnia, serious rash, or psychiatric symptoms.

Provide patients with information about the pathophysiology and symptoms of OSA, its risk factors, its association with serious medical conditions, and the importance of CPAP or other primary therapy. 
  • Tell patients that OSA can disturb sleep, leading to excessive daytime sleepiness and poor memory and concentration.

  • Tell patients that OSA is associated with hypertension, cardiovascular and cerebrovascular disease, and increased overall mortality.

  • Inform patients of the risk of driving while drowsy.

  • Highlight the importance of weight loss for obese patients, exercise, and the avoidance of alcohol and other sedatives before bedtime for all patients.

  • Stress to patients the benefits of therapy (including decreased sleepiness, improved quality of life, reduction in blood pressure for hypertensive patients, and possible decreased mortality).

  • Emphasize the critical importance of adherence to therapy.

Evidence
  • Consensus.

  • In a randomized, controlled trial of 80 patients with OSA, an intensive program of CPAP education and follow-up increased nightly use of the CPAP device from 3.9 hours in the control group, to 5.4 hours in the intensive education group. This program included 3 nights in the sleep lab to accommodate to CPAP and weekly nursing visits at home (35). In a separate VA study of 73 patients, a 2-hour CPAP education session at 6 months improved CPAP meter reading from 5.2 hours per night before the CPAP education to 6.3 hours per night after the intervention (36).

Rationale
  • When patients understand how OSA can cause symptoms and is associated with serious medical conditions, they may become more motivated to adhere to therapy.

Comments
  • Education about CPAP is particularly important during the first few weeks to months of treatment to encourage adherence to therapy.

Follow the patient to assess the patient's degree of daytime sleepiness. 
  • At follow-up, ask the patient if he or she experiences daytime sleepiness and determine if these symptoms are changing or persisting on treatment.

  • If sleepiness is persistent, investigate the possible causes, particularly poor adherence to CPAP or oral appliance therapy, and consider a repeat sleep study to adjust the CPAP pressure and to look for possible coexisting sleep disorders (including periodic limb movement syndrome or narcolepsy).

  • Consider a trial of modafinil if appropriate (see section in Therapy).

Evidence
  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommends modafinil in patients with residual daytime sleepiness (1).

Rationale
  • Persistent or changing symptoms can indicate ineffective treatment, poor adherence to therapy, or the presence of an additional sleep disorder.

Assess and address adherence to CPAP or oral appliance therapy. 
  • Determine how many nights per week and how many hours per night the patient sleeps with the CPAP or oral appliance in place.

  • If the CPAP machine has an hour counter that can be read, record the number of hours that the CPAP machine is on for more objective evidence of adherence to CPAP.

  • Assess and address barriers to adherence.

Evidence
  • Consensus.

Rationale
  • CPAP and oral appliance therapy adherence should be assessed regularly because poor adherence can cause persistent sleepiness and put the patient at risk for the complications of OSA.

  • Assessing adherence can identify barriers to adherence which can then be addressed.

Comments
  • Note that the CPAP machine being turned on does not mean the mask is properly delivering the correct CPAP pressure to the patient.

Perform a follow-up sleep study under appropriate clinical circumstances. 
  • Perform a follow-up sleep study after upper airway surgery or after the initiation of oral appliance therapy to document effectiveness of therapy.

  • Perform a follow-up sleep study if the patient experiences a return of significant symptoms despite appropriate therapy.

  • Perform a follow-up sleep study if the patient loses or gains a significant amount of weight to determine if the patient still needs treatment or if CPAP settings need to be adjusted.

  • Consider a follow-up sleep study for patients with a high clinical suspicion of OSA who have a negative initial sleep study.

Evidence
  • A study of 11 patients with a high clinical likelihood of OSA but with a negative result on an initial overnight polysomnogram found that 6 of the 11 patients had a positive second study with a significant rise in the mean AHI from 3.1 to 19.8. The cause of the negative initial studies was unclear (37).

  • A 2009 guideline from the Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine recommends modafinil in patients with residual daytime sleepiness (1).

Rationale
  • A follow-up sleep study can document effectiveness of therapy and determine if treatment adjustments are needed.

Table Grahic Jump Location
 Differential Diagnosis of OSA

Swipe to view table

DiseaseCharacteristics
OSAObesity or airway obstruction, can be seen in the setting of recent weight gain
Use polysomnography for diagnosis
Central sleep apneaMost commonly seen in patients with HF and CVA. Patients with central apnea have witnessed apneas at night accompanied by daytime sleepiness, which is similar to patients with OSA
Polysomnogram shows an absence of respiratory effort during apnea. The absence of effort distinguishes central from obstructive apnea
UARSMost commonly seen in loud snorers with airway narrowing that is significant enough to cause interruptions in the EEG but is not severe enough to cause an apnea or hypopnea. A formal polysomnogram will have a normal AHI of <5 but will show that the increased respiratory effort is causing frequent EEG interruptions during sleep
While the AHI is normal, the frequent EEG interruptions can still cause the same symptoms as OSA. UARS was previously classified as a separate disorder but is now considered to be a subtype of OSA, and treatment is the same as for OSA
Periodic limb movements of sleepFrequent episodes of leg kicking will be noted by sleeping partner or seen during polysomnogram. This is more commonly seen in patients on dialysis. It is a neurologic disorder of unknown cause
Polysomnogram shows frequent episodes of leg kicking but no evidence of sleep apnea
NarcolepsySevere excessive sleepiness is present, and peak age of onset is 15-25 years. Cataplexy (episodes of muscle weakness in response to emotion) is the most specific symptom
Usually seen in younger, thinner patients, compared to patients with OSA, who tend to be older and heavier. Polysomnogram does not show OSA or periodic limb movements, but multiple sleep latency tests (daytime napping study) show that patients fall asleep quickly and have REM sleep during short naps (38)
Obstructive or restrictive lung diseasePatients usually have daytime symptoms of dyspnea; shortness of breath or cough may disturb sleep
Pulmonary function tests establish the diagnosis and can guide specific therapy
GERDCough or choking may disturb sleep, especially if the patient eats a late dinner. The symptom of acid or burning taste in the throat is a diagnostic marker if present, but may be absent
Clinical symptoms, if present, are helpful, or pH testing may be performed. A successful empiric trial of treatment may confirm the diagnosis
Allergic rhinitis/sinusitisCough and drainage usually occur in the daytime and may disturb sleep
Clinical symptoms of nasal congestion or postnasal drip suggest the diagnosis. Sinus CT can confirm sinusitis
HFDyspnea and cough usually occur in the daytime but may also disturb sleep
Clinical symptoms and exam usually suggest heart disease. Central sleep apnea may be seen in patients with severe HF and indicates a worse prognosis
EpilepsySeizures may occur only at night, with or without motor activity
Neurology consultation and EEG testing are recommended
Sleep deprivation or a short sleep scheduleInadequate sleeping hours can cause daytime sleepiness; naps are usually refreshing, which is not typically seen in patients with OSA
Review of the sleep schedule is essential, and a trial of longer sleep hours is warranted
HypothyroidismPatients likely to have recent weight gain and significant fatigue, and their symptoms don't respond to CPAP therapy
TSH is simple screening test; only 2-3% of patients with OSA have hypothyroidism (39)

AHI = apnea-plus-hypopnea index; CPAP = continuous positive airway pressure; CT = computed tomography; CVA = cerebrovascular accident; EEG = electroencephalogram; GERD = gastroesophageal reflux disease; HF = heart failure; OSA = obstructive sleep apnea; REM = rapid eye movement; TSH = thyrotropin; UARS = upper airway resistance syndrome.

  • Epworth Sleepiness Scale
  • Polysomnogram Tracings of Obstructive Apnea Increasing ventilatory effort is seen in the rib cage, the abdomen, and the level of esophageal pressure (measured with an esophageal balloon), despite lack of oronasal airflow. Arousal on the electroencephalogram (EEG) is associated with increasing ventilatory effort, as indicated by the esophageal pressure. Oxyhemoglobin desaturation follows the termination of apnea. Note that during apnea, the movements of the rib cage and the abdomen (Effort) are in opposite directions (arrows) as a result of attempts to breathe against a closed airway. Once the airway opens in response to arousal, rib-cage and abdominal movements become synchronous. Reprinted with permission from 40. Copyright © 1996 Massachusetts Medical Society. All rights reserved.
  • Polysomnogram Tracings of Obstructive Hypopnea Decreased airflow is associated with increasing ventilatory effort (reflected by the esophageal pressure) and subsequent arousal on the EEG. Rib-cage and abdominal movements are in opposite directions during hypopnea (arrows), reflecting increasingly difficult breathing against a partially closed airway. Rib-cage and abdominal movements become synchronous after arousal produces airway opening. Oxyhemoglobin desaturation follows the termination of hypopnea. Reprinted with permission from 40. Copyright © 1996 Massachusetts Medical Society. All rights reserved.
  • Polysomnogram Tracings of Upper-Airway Resistance Asynchronous movements of the rib cage and abdomen and a substantial decrease in airflow are not seen. Arousal on the EEG is associated with increasing ventilatory effort due to increased airway resistance, as reflected by the esophageal pressure. There is no significant oxyhemoglobin desaturation. Reprinted with permission from 40. Copyright © 1996 Massachusetts Medical Society. All rights reserved.
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Fletcher EC, Shah A, Qian W, Miller CC 3rd. “Near miss” death in obstructive sleep apnea: a critical care syndrome. Crit Care Med. 1991;19:1158-64. (PMID: 1884615)
 
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Kline CE, Crowley EP, Ewing GB, Burch JB, Blair SN, Durstine JL, et al. The effect of exercise training on obstructive sleep apnea and sleep quality: a randomized controlled trial. Sleep. 2011;34:1631-40. (PMID: 22131599)
 
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ABG

arterial blood gas

AHI

apnea-plus-hypopnea index

APAP

automatic positive airway pressure

BMI

body mass index

BP

blood pressure

BPAP

bilevel positive airway pressure

CBC

complete blood (cell) count

COPD

chronic obstructive pulmonary disease

CPAP

continuous positive airway pressure

CT

computed tomography

CVA

cerebrovascular accident

ECG

electrocardiography

EEG

electroencephalogram

ENT

ear, nose, and throat

GERD

gastroesophageal reflux disease

HF

heart failure

OSA

obstructive sleep apnea

Pco2

partial pressure of carbon dioxide

Po2

partial pressure of oxygen

Paco2

arterial partial pressure of carbon dioxide

Pao2

arterial partial pressure of oxygen

RDI

respiratory distrubance index

REM

rapid eye movement

TSH

thyrotropin

UARS

upper airway resistance syndrome

VA

Veterans Administration


Terms
Retrognathia

Retroposition of the mandible, which can cause a more posterior position of the base of the tongue, potentially leading to airway obstruction and sleep apnea


Guidelines

Diagnosis of Obstructive Sleep Apnea in Adults: A Clinical Practice Guideline From the American College of Physicians

Management of Obstructive Sleep Apnea in Adults: A Clinical Practice Guideline From the American College of Physicians

An official American Thoracic Society clinical practice guideline: Sleep apnea, sleepiness, and driving risk in noncommercial drivers.

Clinical Guideline for the Evaluation, Management and Long-term Care of Obstructive Sleep Apnea in Adults

Practice parameters for the surgical modifications of the upper airway for obstructive sleep apnea in adults

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: an update for 2007

Practice parameters for the medical therapy of obstructive sleep apnea

Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults

Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breathing disorders

Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances: an update for 2005

Practice parameters for the surgical modifications of the upper airway for obstructive sleep apnea in adults

Systematic Reviews

The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials

Surgery for obstructive sleep apnoea (Cochrane Review)

Continuous positive airways pressure for obstructive sleep apnoea (Cochrane Review)

Lifestyle modification for obstructive sleep apnoea (Cochrane Review)

Adenotonsillectomy for obstructive sleep apnoea in children (Cochrane Review)

Educational, supportive and behavioural interventions to improve usage of continuous positive airway pressure machines for adults with obstructive sleep apnoea (Cochrane Review)

Oral appliances for obstructive sleep apnoea (Cochrane Review)

Pressure modification for improving usage of continuous positive airway pressure machines in adults with obstructive sleep apnoea (Cochrane Review)

Systematic review and meta-analysis of the literature regarding the diagnosis of sleep apnea

Oral appliances for snoring and obstructive sleep apnea: a review

Effects of surgical weight loss on measures of obstructive sleep apnea: a meta-analysis

Surgical modifications of the upper airway for obstructive sleep apnea in adults: a systematic review and meta-analysis

Practice parameters for the surgical modifications of the upper airway for obstructive sleep apnea in adults

Non-CPAP therapies in obstructive sleep apnoea

Systematic review of motor vehicle crash risk in persons with sleep apnea

Drug therapy for obstructive sleep apnoea in adults (Cochrane Review)

DOI: 10.7326/d351
The information included herein should never be used as a substitute for clinical judgment and does not represent an official position of ACP.
Disclosures:
David Claman, MD has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations. Christopher A. Klipstein, MD University of North Carolina School of Medicine
Chapel Hill, NC
has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations.
Deborah Korenstein, MD, FACP, Editor in Chief, ACP Smart Medicine, has no relationships with any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients. Richard B. Lynn, MD, FACP, Editor, ACP Smart Medicine, has no relationships with any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients.
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