Obstructive Sleep Apnea Workup

  • Author: Ralph Downey III, PhD; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: May 9, 2012
 

Approach Considerations

Routine laboratory tests usually are not helpful in obstructive sleep apnea (OSA) unless a specific indication is present.

An overnight sleep study, or polysomnography (PSG), is required to diagnose OSA. PSG is a multichannel recording of sleep and breathing and usually involves in-laboratory measurement of sleep architecture and electroencephalographic (EEG) arousals, eye movements, chin movements, airflow, respiratory effort, oximetry, electrocardiographic (ECG) tracings, body position, snoring, and leg movements (see the image below).

MRI rendering of a patient without obstructive sleMRI rendering of a patient without obstructive sleep apnea (OSA) (left panel) and a patient with OSA (right panel).

Sleep specialists differ in their acceptance of home sleep testing and how it should be used. The American Academy of Sleep Medicine (AASM) has guidelines on its use. Over time, portable sleep testing will evolve into a niche of diagnostic testing that will meet a community standard of sleep medical care.

Modalities available for identifying the site of obstruction include lateral cephalometry, endoscopy, fluoroscopy, computed tomography (CT) scanning, magnetic resonance imaging (MRI), and radiography. The accuracy of these methods for identifying the sites of obstruction is not clear. At present, upper airway (UA) imaging is used primarily as a research tool. Routine radiographic imaging of the UA is not performed.

Go to Upper Airway Evaluation in Snoring and Obstructive Sleep Apnea for complete information on this topic.

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Lab Studies

Routine laboratory tests usually are not helpful in OSA in the absence of a specific indication. A thyrotropin test should be performed on any patient with possible OSA who has other signs or symptoms of hypothyroidism, particularly in elderly individuals.

A study by Cintra et al studied 150 subjects (75 patients and 75 control subjects, matched for age and sex). They determined that cysteine levels were higher in patients with OSA compared with control subjects, and levels were reduced after effective OSA treatment.[132] Thus, cysteine may be a potential biomarker of OSA.

Pulmonary function tests (PFTs) are not indicated to make a diagnosis of or treatment plan for OSA alone. The PFT standard indications apply to OSA patients as with any other patient. Comorbid conditions with OSA that may require PFTs are listed in the text.

If clinically indicated, consider PSG using end-tidal carbon dioxide measurements for a continuous measurement of carbon dioxide pressures as a function of obstructive sleep apnea and associated sleep states and by position.

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Polysomnography

A PSG is necessary to accurately diagnose OSA and to assess treatment benefit. Data are collected in the laboratory in the presence of a qualified technician (ie, full PSG with attended monitoring). This protocol provides the opportunity to directly observe a variety of sleep-associated disturbances (eg, apneas, periodic leg movements, seizures, rapid eye movement [REM] behavior disorder). Patients who regularly work night shifts should undergo PSG during the day to match their normal sleep-wake cycle.

AASM standards and guidelines for diagnostic PSG

The AASM has published standards and guidelines for performing PSG (see American Academy of Sleep Medicine).[133] Having a patient studied at an AASM-accredited sleep disorders center is important because such centers adhere to standards that have been established by the AASM. This includes the criterion standard test for sleep disorders: the sleep disorders center PSG.

AASM guidelines for the indications and performance of PSG include the following:

  • Sleep stages are recorded via an EEG, electrooculogram, and chin electromyogram (EMG).
  • Heart rhythm is monitored with a single-lead ECG.
  • Leg movements are recorded via an anterior tibialis EMG.
  • Breathing is monitored, including airflow at the nose and mouth (using both a thermal sensors and a nasal pressure transducer), effort (using inductance plethysmography), and oxygen saturation.
  • The breathing pattern is analyzed for the presence of apneas and hypopneas, determined according to definitions standardized by the AASM (see below).[133]

Obstructive apnea is the cessation of airflow for at least 10 seconds with persistent respiratory effort (see the image below).

Obstructive sleep apnea. Note the absence of flow Obstructive sleep apnea. Note the absence of flow (red arrow) despite paradoxical respiratory effort (green arrow).

Central apnea is the cessation of airflow for at least 10 seconds with no respiratory effort (see the images below).

Central sleep apnea (thick areas). Note the absencCentral sleep apnea (thick areas). Note the absence of both flow and respiratory effort (green double arrows). Comparison of a central apnea (box) and obstructivComparison of a central apnea (box) and obstructive apnea (circle).

Mixed apnea is an apnea that begins as a central apnea and ends as an obstructive apnea (see the image below).

Mixed sleep apnea. Note that the apnea (orange arrMixed sleep apnea. Note that the apnea (orange arrow) begins as a central apnea (effort absent; red double arrow) and ends as an obstructive apnea (effort present; green double arrow). Note the arousal (blue arrow) that terminates the apnea and the desaturation (purple arrow) that follows.

Hypopnea is a 30% or greater decrease in flow lasting at least 10 seconds and associated with a 4% or greater oxyhemoglobin desaturation. An alternative definition is a 50% or greater reduction in flow lasting at least 10 seconds and associated with either a 3% or greater oxyhemoglobin desaturation or an arousal (see the image below).

A 2-minute recording of sleep showing 4 hypopneas A 2-minute recording of sleep showing 4 hypopneas (thick arrows) and associated oxygen desaturations (red arrows). This recording illustrates the recurrent nature of the sleep-disordered breathing observed in many patients.

Respiratory event–related arousal (RERA) is an event in which patients have a series of breaths with increasing respiratory effort or flattening of the nasal pressure waveform leading to an arousal from sleep that does not otherwise meet the criteria for an apnea or hypopnea.

Arousals detected on PSG are important for the evaluation of the degree of sleep fragmentation. They may be the only clue to UA resistance syndrome (UARS) in a patient with daytime hypersomnolence if esophageal pressure is not monitored. Monitoring of esophageal pressure is not routinely performed in most laboratories because of the invasive nature of the procedure.

PSG findings characteristic of OSA

The following PSG findings are characteristic of OSA:

  • Apneic episodes occur in the presence of respiratory muscle effort.
  • Apneic episodes lasting 10 seconds or longer are considered clinically significant.
  • Apneic episodes are most prevalent during REM sleep. In some patients, they may occur exclusively during REM sleep.
  • Patients may have a combination of apneas and hypopneas, or they may have one or the other exclusively.
  • Mixed apneas may occur.
  • Sleep disruption due to arousals is usually seen at the termination of an episode of apnea.

The apnea-hypopnea index (AHI) is derived from the total number of apneas and hypopneas divided by the total sleep time. A normal cutoff for AHI has never been defined in an epidemiological study of healthy people. Most sleep centers use a cutoff of 5-10 episodes per hour. The severity of OSA is arbitrarily defined and differs widely between centers. Recommendations for cutoff levels on AHI include 5-15 episodes per hour for mild, 15-30 episodes per hour for moderate, and more than 30 episodes per hour for severe.

Split-night PSG

Patients with a respiratory disturbance index (RDI) higher than 40 during the first 2 hours of diagnostic PSG should undergo a split-night PSG study. The final portion of the study is used for titrating the continuous positive airway pressure (CPAP) device. Split-night studies may be considered for patients with an RDI of 20-40, as based on clinical observations (eg, prolonged obstructive events, marked oxygen desaturation). A minimum of 3 hours of sleep is preferred to adequately titrate the CPAP device after this treatment is started.

Split-night studies require recording and analysis of the same parameters as those evaluated in standard diagnostic PSG. A single split-night study may not permit adequate titration of CPAP therapy. If treatment does not control symptoms, additional full-night CPAP titration may be required.

Repeat PSG

If symptoms persist despite adequate adherence to prescribed CPAP treatment (see Treatment and Management), PSG should be repeated. PSG can be used to assess response to UA surgical procedures and to assess response to oral appliance (OA) therapy. If sustained weight change of greater than 15% occurs, PSG should be repeated. If results of the first PSG are of poor quality, a repeat study is indicated.

Patients who stop REM sleep–suppressant medications should be restudied, if symptomatic on treatment, because OSA is most prevalent in REM sleep. The OSA that occurs during REM sleep should be examined whenever possible to avoid undertreatment of the OSA or a false-negative diagnosis on a diagnostic study.

Home testing

Considerable debate exists about the validity of portable testing for the diagnosis of OSA compared with a sleep disorders center PSG. The increasingly common use of home testing, especially since the Centers for Medicare and Medicaid Services (CMS) published guidelines for practitioners to receive payment for conducting them. An important part of the guidelines requires that portable testing can only be performed in conjunction with accredited sleep disorders centers. Studies have not proven that portable testing is superior to PSG testing. Cost analysis studies comparing no testing versus in-sleep-center PSG testing showed that in-sleep-center PSG was cost effective. Portable testing was not included in that analysis; however, it stands to reason that if PSG was cost effective compared with no testing, PSG would be cost effective compared with portable testing.

The 3 levels of portable monitors are (1) level 2, a portable monitor with the same parameters as a full attended PSG (includes EEG); (2) level 3, with at least 4 channels, including flow, effort, oximetry and heart rate; and (3) level 4, with fewer than 4 channels, often oximetry with flow or oximetry alone.

level 3 portable monitors have the largest body of supportive evidence for use in diagnosing OSA. In general, level 3 monitors are best used to confirm the diagnosis of OSA rather than to rule it out. In addition, most of the studies using portable monitoring have validated the equipment in the laboratory, not in the home, and have done so in patients with high probability of disease and without significant comorbidities (particularly heart and lung disease).[134, 135]

At least 2 studies have compared an at-home approach to diagnosis and treatment of OSA (home portable monitoring followed by autotitrating CPAP [see below]) to a conventional in-laboratory sleep study. Both studies showed that in carefully selected patients (generally those with a high pretest probability of disease and without comorbidities), patients with a home-based approach had similar clinical outcomes to those patients studied in the laboratory.[136, 137] A study by Kuna et al also reported that functional outcome and treatment adherence in patients evaluated using a home-testing algorithm was not clinically inferior to standard in-laboratory polysomnography.[138]

Chai-Coetzer et al developed a simplified, two-stage model for identifying OSA in primary care. The model used a screening questionnaire followed by home sleep monitoring.[139] The two-stage model was found to be accurate in identifying OSA in primary care and may allow expedited care for patients.

The AASM’s published guidelines on the use of portable monitors recommend that they be used only in patients with a high probability of disease and those without comorbidities (particularly congestive heart failure) and that negative studies be followed by a full, attended study.[140]

It is generally expected that more sleep centers will be adopting home portable monitoring for patients in the future. In theory, a home-based approach to testing will lead to faster diagnosis and treatment for a subset of patients with high probability of disease.

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Multiple Sleep Latency and Maintenance of Wakefulness Tests

The measurement of sleepiness and alertness remains controversial (ie, the multiple sleep latency test [MSLT] for objectively measuring sleepiness and the maintenance of wakefulness test [MWT] for measuring alertness).[141]

The MSLT may follow PSG. It is considered an objective measurement of excessive daytime sleepiness (EDS). The MSLT consists of 4-5 naps of 20-minute duration every 2 hours during the day. The latency to sleep onset for each nap is averaged to determine the daytime sleep latency. Normal daytime sleep latency is greater than 10-15 minutes. OSAHS is generally associated with latencies of less than 10 minutes. It is not uncommon for the MSLT to demonstrate profound daytime sleepiness in OSA patients; mean sleep latency cannot discriminate between patients with OSA and patients with narcolepsy.

Routine use of the MSLT in the evaluation of OSA has significantly decreased because sleep physicians generally treat OSA on basis of the subjective symptoms reported by the patient. The MSLT is generally used to confirm the diagnosis of narcolepsy in patients in whom narcolepsy is a consideration. As opposed to people without narcolepsy, narcoleptic patients have rapid eye movement sleep on at least 2 of the 4-5 naps during the day.

Whether the MWT is a good enough test to measure treatment efficacy is debated. The low correlation between self-reported sleepiness, as typically measured by the Epworth Sleepiness Score (ESS), and objective measures of sleepiness, as measured by the MSLT, continues to present a problem to clinicians and researchers in the determination of how to use these disparate measures in clinical practice and in research.

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Contributor Information and Disclosures
Author

Ralph Downey III, PhD  CEO and President, Dr Downey Sleep, Inc

Ralph Downey III, PhD is a member of the following medical societies: American Academy of Sleep Medicine and Neuroscience Education Institute

Disclosure: Nothing to disclose.

Coauthor(s)

Philip M Gold, MD  Professor of Medicine, Chief of Pulmonary and Critical Care Medicine, Medical Director of Respiratory Care, Loma Linda University Medical Center

Philip M Gold, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Heart Association, American Lung Association, American Medical Association, American Thoracic Society, Association of Subspecialty Professors, California Medical Association, California Thoracic Society, Society of Critical Care Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Glaxo-Smith-Kline Honoraria Speaking and teaching; Covidien Honoraria Speaking and teaching; Boeringer-Ingleheim Honoraria Speaking and teaching

James A Rowley, MD  Professor, Fellowship Program Director, Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine

James A Rowley, MD is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Himanshu Wickramasinghe, MD, MBBS  Attending Physician; Pulmonary, Critical Care, and Sleep Medicine; Henry Mayo Newhall Memorial Hospital, Valencia, California

Himanshu Wickramasinghe, MD, MBBS is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Sat Sharma, MD, FRCPC  Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Daniel R Ouellette, MD, FCCP  Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Gregory Tino, MD  Director of Pulmonary Outpatient Practices, Associate Professor, Department of Medicine, Division of Pulmonary, Allergy, and Critical Care, University of Pennsylvania Medical Center and Hospital

Gregory Tino, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

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Sleep-related disordered breathing continuum ranging from simple snoring to obstructive sleep apnea (OSA). Upper airway resistance syndrome (UARS) occupies an intermediate position between these extremes. Note areas of overlap among the conditions.
In this polysomnogram summary graph, obstructive sleep apnea (OSA) severity and the degree of oxygen desaturation (SpO2%) worsen in rapid eye movement (REM) sleep (the black underlined sections) compared with non-REM sleep. This is often the case in OSA patients, especially in OSA patients with comorbid lung disease.
MRI rendering of a patient without obstructive sleep apnea (OSA) (left panel) and a patient with OSA (right panel).
Top image is 3-dimensional surface renderings of the upper airway demonstrating the effect of progressive increases in continuous positive airway pressure (CPAP) from 0-15 cm of water on upper-airway volume in a patient with upper airway narrowing. CPAP significantly increases airway volume in the retropalatal (RP) and retroglossal (RG) regions. Bottom image is soft tissue images in the same patient in the RP region at analogous levels of CPAP. With increasing CPAP, the upper airway progressively enlarges, particularly in the lateral dimension. Note the progressive thinning of the lateral pharyngeal walls as the level of CPAP increases. Little movement occurs in the parapharyngeal fat pads, the white structures lateral to the airway. The first image in each series depicts the baseline upper airway narrowing present in this patient.
Potential relationship between obstructive sleep apnea-hypopnea syndrome (OSAHS) and the metabolic syndrome. OSAHS has been associated with 3 of the 5 major clinical abnormalities associated with the metabolic syndrome, which is hypertension, insulin resistance, and proinflammatory/oxidative stress. OSAHS may be contributing to and/or modulating the severity of these metabolic abnormalities.
The Mallampati Classification is illustrated. The airway class is based on this visual heuristic.
Tonsil grades.
Obstructive sleep apnea. Note the absence of flow (red arrow) despite paradoxical respiratory effort (green arrow).
Central sleep apnea (thick areas). Note the absence of both flow and respiratory effort (green double arrows).
Comparison of a central apnea (box) and obstructive apnea (circle).
Mixed sleep apnea. Note that the apnea (orange arrow) begins as a central apnea (effort absent; red double arrow) and ends as an obstructive apnea (effort present; green double arrow). Note the arousal (blue arrow) that terminates the apnea and the desaturation (purple arrow) that follows.
A 2-minute recording of sleep showing 4 hypopneas (thick arrows) and associated oxygen desaturations (red arrows). This recording illustrates the recurrent nature of the sleep-disordered breathing observed in many patients.
Effect of nasal continuous positive airway pressure (CPAP) on oxygen saturation in sleep apnea. The upper portion of this figure shows the raw oxygen saturation trace from 1 night of a sleep study. Below the raw trace are vertical lines that indicate the presence of either an apnea or hypopnea. Before CPAP, frequent respiratory events with significant desaturations occurred. During the night, CPAP was applied, resulting in the elimination of the apnea and hypopneas and normalization of the oxygen trace.
Examples of good (upper panel) and poor (lower panel) compliance. In the upper panel, the patient is using continuous positive airway pressure (CPAP) most nights and generally for more than 4 hours (solid black line). In the lower panel, the patient is using CPAP infrequently and, when used, is wearing the CPAP device for less than 4 hours.
Approach to a patient with excessive daytime sleepiness after treatment with nasal continuous positive airway pressure.
 
 
 
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