Clinical Evidence Handbook

A Publication of BMJ Publishing Group

Sleep Apnea

Am Fam Physician. 2010 Jan 15;81(2):195-196.

This clinical content conforms to AAFP criteria for evidence-based continuing medical education (EB CME). See CME Quiz on page 115.

Sleep apnea is the popular term for obstructive sleep apnea-hypopnea syndrome (OSAHS), which is abnormal breathing during sleep that causes recurrent arousals, sleep fragmentation, daytime sleepiness, and nocturnal hypoxemia.

  • Apnea may be central, in which there is cessation of inspiratory effort, or obstructive, in which inspiratory efforts continue but are ineffective because of upper airway obstruction.

  • OSAHS affects up to 4 percent of men and 2 percent of women in the United States, with obesity being a major determinant.

In persons with severe OSAHS, nasal continuous positive airway pressure (CPAP) has been shown to reduce daytime sleepiness compared with control treatments.

  • Although effective, it can be difficult getting patients to comply with the prescribed CPAP regimen. Compliance seems no better with variations of CPAP, such as automatically titrated CPAP, bilevel positive airway pressure, patient-titrated CPAP, or CPAP plus humidification. We do not know whether educational or psychological interventions may improve compliance with CPAP.

Oral appliances that produce anterior advancement of the mandible seem to be effective in improving sleep-disordered breathing in persons with severe or non-severe OSAHS.

  • Oral appliances are probably not as effective as CPAP, and we do not know how well they work in the long term.

We found no sufficient evidence judging the effectiveness of weight loss on severe or nonsevere OSAHS, although there is consensus that advice about weight reduction is an important component of management of OSAHS.

Nasal CPAP also seems beneficial in persons with nonsevere OSAHS.

  • Nasal CPAP is less acceptable in persons with nonsevere OSAHS, and we do not know whether measures aimed at improving compliance effectively increase its use.

Clinical Questions

What are the effects of treatment for severe OSAHS?

Beneficial

Nasal CPAP

Likely to be beneficial

Oral appliances

Unknown effectiveness

Measures aimed at improving compliance with nasal CPAP

Weight loss

What are the effects of treatment for nonsevere OSAHS?

Likely to be beneficial

Nasal CPAP

Oral appliances (more effective than no treatment, control appliance, or placebo, but less effective than nasal CPAP at improving symptoms including sleep-disordered breathing)

Unknown effectiveness

Measures aimed at improving compliance with nasal CPAP

Weight loss


CPAP = continuos positive airway pressure; OSAHS = obstructive sleep apnea-hypopnea syndrome.

Clinical Questions

View Table

Clinical Questions

What are the effects of treatment for severe OSAHS?

Beneficial

Nasal CPAP

Likely to be beneficial

Oral appliances

Unknown effectiveness

Measures aimed at improving compliance with nasal CPAP

Weight loss

What are the effects of treatment for nonsevere OSAHS?

Likely to be beneficial

Nasal CPAP

Oral appliances (more effective than no treatment, control appliance, or placebo, but less effective than nasal CPAP at improving symptoms including sleep-disordered breathing)

Unknown effectiveness

Measures aimed at improving compliance with nasal CPAP

Weight loss


CPAP = continuos positive airway pressure; OSAHS = obstructive sleep apnea-hypopnea syndrome.

Definition

Sleep apnea is the popular term for OSAHS, which is abnormal breathing during sleep that causes recurrent arousals, sleep fragmentation, and nocturnal hypoxemia. The syndrome includes daytime sleepiness, impaired vigilance and cognitive functioning, and reduced quality of life. Apnea is the absence of airflow at the nose and mouth for at least 10 seconds, and hypopnea is a major reduction (i.e., greater than 50 percent) in airflow for at least 10 seconds. Apneas may be central, in which there is cessation of inspiratory effort, or obstructive, in which inspiratory efforts continue, but are ineffective because of upper airway obstruction. The diagnosis of OSAHS is made when a patient with daytime symptoms has significant obstructive sleep-disordered breathing revealed by polysomnography (study of sleep state, breathing, and oxygenation) or by more limited studies (e.g., measurement of oxygen saturation overnight).

Criteria for the diagnosis of significant sleep-disordered breathing have not been rigorously assessed, but have been set by consensus and convention. Diagnostic criteria have variable sensitivity and specificity. For example, an apnea-hypopnea index (AHI) of fewer than five episodes of apnea or hypopnea per hour of sleep is considered normal. However, persons with upper airway resistance syndrome have an index below five episodes per hour, and many healthy older persons have an index greater than five episodes per hour. In an effort to achieve international consensus, new criteria have been proposed and are becoming more widely used.

The severity of OSAHS can be classified by the severity of two factors: daytime sleepiness and AHI. Severe OSAHS is defined as severe sleep-disordered breathing (i.e., AHI greater than 30 episodes per hour) plus symptoms of excessive daytime sleepiness (e.g., Epworth Sleepiness Scale score of greater than 10; Multiple Sleep Latency Test result of less than five minutes). Central sleep apnea and sleep-associated hypoventilation syndromes are not covered in this review.

Incidence and Prevalence

The Wisconsin Sleep Cohort Study (n = greater than 1,000 participants; mean age = 47 years) in North America found prevalence rates for an AHI of more than five episodes per hour of 24 percent in men and 9 percent in women, and for OSAHS with an index greater than five episodes per hour plus excessive sleepiness of 4 percent in men and 2 percent in women. There are international differences in the occurrence of OSAHS, of which obesity is considered to be an important determinant. Ethnic differences in prevalence have also been found after adjustment for other risk factors. Little is known about the incidence in resource-poor countries.

Etiology and Risk Factors

The site of upper airway obstruction in OSAHS is around the level of the tongue, soft palate, or epiglottis. Disorders that predispose to narrowing of the upper airway or reduction in its stability (e.g., obesity, certain craniofacial abnormalities, vocal cord abnormalities, enlarged tonsils, enlarged tongue) have been associated with an increased risk of OSAHS. It has been estimated that a 1 kg per m2 increase in body mass index (3.2 kg [7.1 lbs] for a person 1.8 m [70.9 in] tall) leads to a 30 percent increase (95% confidence interval, 13 to 50 percent) in the relative risk of developing abnormal sleep-disordered breathing (AHI of five or more episodes per hour) over a period of four years. Other strong associated risk factors include increasing age and sex (male-to-female ratio is 2:1). Weaker associations include menopause, family history, smoking, and nighttime nasal congestion.

Prognosis

The long-term prognosis of persons with untreated severe OSAHS is poor quality of life, likelihood of motor vehicle collisions, hypertension, and possibly cardiovascular disease (CVD) and premature mortality. Unfortunately, the prognosis of treated OSAHS is unclear. The limitations in the evidence include bias in the selection of participants, short duration of follow-up, and variation in the measurement of confounders (e.g., smoking, alcohol use, other cardiovascular risk factors).

Treatment is widespread, making it difficult to find evidence on prognosis for untreated OSAHS. Observational studies support a causal association between OSAHS and systemic hypertension, which increases with the severity of OSAHS (odds ratio = 1.21 for nonsevere OSAHS to 3.07 for severe OSAHS). OSAHS increases the risk of motor vehicle collisions three- to sevenfold. It is associated with increased risk of premature mortality, CVD, and impaired neurocognitive functioning.

Author disclosure: Nothing to disclose.


search date: May 2008.

Adapted with permission from Hensley M, Ray C. Sleep apnoea. Clin Evid Handbook. June 2009:572–573. Please visit http://www.clinicalevidence.bmj.com for full text and references.

This is one in a series of chapters excerpted from the Clinical Evidence Handbook, published by the BMJ Publishing Group, London, U.K. The medical information contained herein is the most accurate available at the date of publication. More updated and comprehensive information on this topic may be available in future print editions of the Clinical Evidence Handbook, as well as online at http://www.clinicalevidence.bmj.com (subscription required). Those who receive a complimentary print copy of the Clinical Evidence Handbook from United Health Foundation can gain complimentary online access by registering on the Web site using the ISBN number of their book.

A collection of Clinical Evidence Handbook published in AFP is available at http://www.aafp.org/afp/bmj.


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