eMedicine Specialties > Pulmonology > Sleep-Related Disorders

Obstructive Sleep Apnea-Hypopnea Syndrome

Author: James A Rowley, MD, Associate Professor, Fellowship Program Director, Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine
Contributor Information and Disclosures

Updated: Apr 2, 2009

Introduction

Background

Obstructive sleep apnea-hypopnea (OSAH) is characterized by recurrent episodes of upper airway collapse and obstruction during sleep. These episodes of obstruction are associated with recurrent oxyhemoglobin desaturations and arousals from sleep. OSAH associated with excessive daytime sleepiness (EDS) is commonly called obstructive sleep apnea-hypopnea syndrome (OSAHS). Despite being a common disease, OSAHS is underrecognized by most primary care physicians in the United States; an estimated 80% of Americans with OSAHS are not diagnosed.1

Also see eMedicine’s article Obstructive Sleep Apnea and Central Sleep Apnea.

Pathophysiology

Conceptually, the upper airway is a compliant tube and, therefore, is subject to collapse.2 Most patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) demonstrate upper airway obstruction at either the level of the soft palate (ie, nasopharynx) or the level of the tongue (ie, oropharynx). Research indicates that both anatomic and neuromuscular factors are important. Anatomic factors (eg, enlarged tonsils; volume of the tongue, soft tissue, or lateral pharyngeal walls); length of the soft palate; abnormal positioning of the maxilla and mandible) decrease the cross-sectional area of the upper airway and/or increase the pressure surrounding the airway, both of which predispose the airway to collapse.3,4

Upper airway neuromuscular activity, including reflex activity, decreases with sleep, and this decrease may be more pronounced in patients with OSAHS.5,6,7 Reduced ventilatory motor output to upper airway muscles is believed to be the critical initiating event leading to upper airway obstruction; this effect is most pronounced in patients with an upper airway predisposed to collapse for anatomical reasons.

Central breathing instability is a well-established factor contributing to the development of central sleep apnea, particularly in patients with severe congestive heart failure.8,9,10 Evidence also indicates that central breathing instability contributes to the development of OSAHS. First, evidence of upper airway obstruction in the absence of ventilatory motor output (central sleep apnea) has been observed.11 Second, reduction in pharyngeal dilator activity has been associated with periodic breathing12,13,14 and hypocapnia in subjects with evidence of inspiratory flow limitation.15 Third, men have been shown to be more susceptible to the development of central sleep apnea and have a decreased responsiveness to carbon dioxide compared with women,16 a result consistent with the increased prevalence of OSAHS in men compared with women.

Frequency

United States

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a common disease in the United States. Data from the Wisconsin Cohort Study indicate the prevalence of OSAHS in people aged 30-60 years is 9-24% for men and 4-9% for women. The estimated prevalence of OSAHS is 2% for women and 4% for men.17 Similar data have been found in an epidemiologic study from Pennsylvania.18,19

International

The prevalence of OSAHS in non-American populations has only been studied in men and has been found to be as low as 0.3% (England) and as high as 20-25% (Israel and Australia). The prevalence of OSAHS in Australian men is estimated to be 3%.

Mortality/Morbidity

Cardiovascular
The effect of obstructive sleep apnea-hypopnea syndrome (OSAHS) on mortality has been investigated using observational cohort studies. Marin et al20 found that severe untreated OSAHS (apnea-plus-hypopnea index [AHI] >30) is associated with an increased risk of cardiovascular mortality, defined by fatal myocardial infarction or stroke (odds ratio, 2.87). Patients with mild OSAHS or those undergoing treatment with continuous positive airway pressure (CPAP) did not have a significantly increased odds ratio compared with a group of subjects without OSAHS.20 In this study, the authors also found that untreated severe OSAHS is a significant risk factor for the development of cardiovascular morbidity, which included nonfatal myocardial infarction and stroke (odds ratio, 3.17).

Two 2008 population-based studies, one from the United States21 and one from Australia,22 also showed increased all-cause mortality in subjects with moderate-to severe OSAHS. The adjusted hazard ratios in both studies ranged from 3-6.24 for subjects with moderate-to-severe disease compared with no disease.

A 2005 article23 suggests that mortality is associated with compliance with CPAP. In a historical cohort of 871 patients, patients who used CPAP more than 6 hours per night had an increased survival rate (96.4%) at 5 years compared with those who used CPAP 1-6 hours per night (91.3%) and less than 1 hour per night (85.5%). Use for more than 6 hours per night was associated with a significantly decreased odds ratio of 0.1.

Systemic hypertension is observed in 50-70% of patients with OSAHS. Several large cross-sectional studies have demonstrated that OSAHS is a risk factor for developing hypertension, independent of obesity, age, alcohol intake, and smoking.24,25 More recently, subjects in the Wisconsin Cohort Study were prospectively monitored for the development of hypertension. The investigators found a dose-response relationship between the degree of OSAHS and the presence of hypertension 4 years later (odds ratio of 2.03 for an AHI of 5-15 and 2.89 for an AHI >15), independent of confounding variables.26 Several small studies have shown small reductions in diastolic blood pressure after treatment of the OSAHS with nasal CPAP.27,28,29 However, no conclusive study has demonstrated that treating OSAHS with nasal CPAP lowers the blood pressure on a long-term basis.

OSAHS has an association with the metabolic syndrome. The metabolic syndrome is now recognized as an important contributor to the development of atherosclerosis and cardiovascular disease. As defined, a patient with the metabolic syndrome has increased fasting glucose levels, increased blood pressure, lipid abnormalities, and obesity. Evidence of proinflammatory and oxidative stress also exists in these patients. Growing evidence suggests that OSAHS may contribute to the metabolic derangements that characterize the metabolic syndrome.

Potential relationship between obstructive sleep ...

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.

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Potential relationship between obstructive sleep ...

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.

  • Hypertension: The relationship between obstructive sleep apnea and hypertension is outlined above.
  • Insulin resistance: Multiple studies have shown that patients with OSAHS have increased glucose levels and increased insulin resistance.30,31,32 The most recent study, from 2004, was from the Sleep Heart Health Study.32 In this study of 2000 research subjects, the prevalence of diabetic 2-hour glucose tolerance values rose from 9.3% in the group with an AHI less than 5 to 15% in the group with an AHI greater than 15. The odds ratio for having an abnormal glucose tolerance test result was 1.44 (P <.0001) for the group with an AHI greater than 15; insulin resistance was also highest in this group. Correlations were also noted for the degree of oxygen desaturation at night, indicating that the OSAHS may contribute to insulin resistance as a result of the hypoxemia that occurs with the syndrome. However, in the Wisconsin Cohort Study, subjects with OSAHS were no more likely to develop diabetes mellitus than subjects without OSAHS.33
  • Oxidative stress: OSAHS has been associated with increased production of reactive oxygen species34 and other oxidative stress biomarkers.35
  • Proinflammatory stress: OSAHS has been associated with increased levels of several proinflammatory cytokines and markers associated with atherosclerosis. These include C-reactive protein in both adults and adolescents,36,37 interleukin 6,36 interleukin 18,38 and matrix metalloproteinase 9.39 However, at least one large epidemiologic study found no relationship between the severity of OSAHS and C-reactive protein levels.40
  • Vasodilator responses: OSAHS has been associated with decreased production of nitric oxide.41 Several studies have shown impaired vasodilator responses, as measured by either flow-mediated dilatation42 or reactive hyperemic blood flow43 techniques. Impaired flow-mediated dilatation was found to best correlate with the degree of oxygen desaturation in an epidemiologic cohort study.44

Note that for most of these abnormalities associated with the metabolic syndrome, evidence from studies with a small number of subjects suggests that CPAP partially reverses the metabolic abnormality that is the focus of the study. That is, CPAP decreased insulin resistance, decreased lipid peroxidation, and increased vasodilator responses.

A large epidemiologic study (the Sleep Heart Health Study) is currently being conducted to provide more definitive data regarding the relationship between sleep apnea and cardiovascular morbidity. Initial findings from the Sleep Heart Health Study indicate that a relationship exists between severe OSAHS and an increased risk of coronary artery disease, congestive heart failure, and stroke.45 This study is ongoing to determine if the presence of OSAHS is associated with the development of cardiovascular morbidity.

OSAHS has been linked with the development of atherosclerosis. In a study of 36 subjects46 with OSAHS and 16 matched controls, all without comorbidities, subjects with moderate-to-severe OSAHS were found to have increased carotid intima media thickness, increased pulse wave velocity, and increased carotid diameter, all of which are consistent with atherosclerosis. Abnormalities in these parameters were predicted either by the AHI or the degree of nocturnal desaturation. A 2007 follow-up study showed regression of these abnormalities in subjects treated with nasal CPAP.47

Other prospective observational cohort studies have investigated the relationship between OSAHS and stroke. In the Wisconsin Cohort Study, an AHI of greater than 20 was associated with an increased risk of stroke over a 4-year follow-up (odds ratio, 4.31), although the odds ratio lost significance when corrected for age, body mass index (BMI), and sex.48 In a study from Yale, after a mean follow-up of 3.4 years, an AHI of greater than 5 was associated with increased risk of stroke after adjustment for multiple confounders (hazard ratio, 1.97).49

Both of these studies provide evidence that OSAHS is a risk factor for the development of stroke.

A 2005 study found that OSAHS was associated with an increased risk of sudden death between the hours of midnight and 6 am, as compared with the general population (sudden death more common between 6 am and noon).50

Evidence indicates that OSAHS is not an independent risk factor for the development of pulmonary hypertension in the absence of other lung disease, as evidenced by the presence of daytime hypoxemia, hypercapnia, or obstructive airway disease.51

All of the above evidence strongly suggests that OSAHS is an independent risk factor for the development of cardiovascular disease and death. However, at this time, no definitive randomized studies have investigated the effect of CPAP in preventing the potential cardiovascular risks.

Driving

Many studies have identified a relationship between OSAHS and motor vehicle accidents. Patients with OSAHS have been reported to be 2-7 times as likely as control individuals to have a motor vehicle crash; the overall estimated risk was 2.5 in a meta-analysis of 6 studies.52 Many studies indicate that motor vehicle accidents are more common in patients with severe OSAHS (generally, AHI >30),53,54 but this is not a universal finding.55 Despite the elevated risk of crashing, most patients with OSAHS have not had a crash; therefore, determining which patients should have driving restrictions and how much benefit would accrue from these restrictions is not clear.56

The reader is referred to the Medical Legal Pitfalls section for further discussion of OSAHS and driving risk.

Race

The prevalence of sleep apnea in young African Americans (<25 y) appears to be greater than in white Americans.57 Additionally, evidence indicates that the prevalence in older age groups is similar between African Americans and white Americans, but the OSAHS is more severe in African Americans (ie, African Americans have higher AHIs).

Sex

The male-to-female ratio in community-based studies is 2-3:1.17,58 Three large epidemiologic studies have demonstrated that the prevalence of OSAHS in women appears to increase after menopause.24,59,60 In these studies, women on hormone replacement therapy had a prevalence similar to that of premenopausal women. Premenopausal women with OSAHS tend to be more obese than men with the same severity of disease. Thin women with symptoms of OSAHS appear to have an increased frequency of craniofacial abnormalities.

Evidence indicates that women underreport the symptoms of loud snoring and witnessed apneas, leading to underreferral to sleep centers. This may explain the marked male predominance (male-to-female ratio of approximately 8:1) in sleep center–based studies. Additionally, women have lower AHIs than men, even after correcting for other demographic factors such as BMI and neck circumference.61,62,63

Age

The prevalence of OSAHS increases with age,18 with an estimated rate as high as 65% in a community sample of people older than 65 years.64 However, the significance of the incidental finding of OSAHS in elderly persons has been debated (see "Geriatric populations" in Special Concerns).

Clinical

History

Obstructive sleep apnea-hypopnea syndrome (OSAHS) symptoms generally begin insidiously and are often present for years before the patient is referred for evaluation.

  • Nocturnal symptoms
    • Snoring, usually loud, habitual, and bothersome to others
    • Witnessed apneas, which often interrupt the snoring and end with a snort
    • Gasping and choking sensations that arouse the patient from sleep
    • Restless sleep, with patients often experiencing frequent arousals and tossing or turning during the night
  • Daytime symptoms
    • Not feeling refreshed upon awakening
    • Morning headache, dry or sore throat
    • EDS that usually begins during quiet activities (eg, reading, watching television): As the severity worsens, patients begin to feel sleepy during activities that generally require alertness (eg, school, work, driving).
      • EDS is most frequently assessed by a sleep physician using the Epworth Sleepiness Scale (ESS). This questionnaire is used to help determine how frequently the patient is likely to doze off in 8 frequently encountered situations.
      • An ESS score greater than 10 is generally considered sleepy. However, a 2003 study showed that an ESS score of 12 is associated with a greater propensity to fall asleep on the Multiple Sleep Latency Test (MSLT), suggesting that 12 would be a better cutoff.65
      • The ESS score does not correlate well with the primary objective measurement of sleepiness, the MSLT (see Other Tests),66,67 in that a higher ESS score does not mean shorter latencies on the MSLT. However, a higher ESS score does mean a greater likelihood of falling asleep on the MSLT.65,68  
      • The ESS is useful for evaluating responses to treatment; the ESS score should decrease with effective treatment.
    • Daytime fatigue/tiredness: Most patients who do not report EDS do report being fatigued, having a lack of energy, or being tired during the day. In one study of 190 patients with OSAHS, patients were more likely to report lack of energy (62%), fatigue (57%), and tiredness (61%) than sleepiness (47%). When asked to choose their most significant symptom, 40% of patients chose lack of energy, compared with 22% for sleepiness.69
    • Problems with memory, concentration, and cognitive function, particularly executive functioning

Physical

The general physical examination is frequently normal in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS), other than the presence of obesity (defined as a BMI >30 kg/m2), an enlarged neck circumference, and hypertension. Perform an evaluation of the upper airway in all patients, but particularly in nonobese adults with symptoms consistent with OSAHS. The following features have been associated with the presence of OSAHS:

  • Neck circumference: A neck circumference greater than 43 cm (17 in) in men and 37 cm (15 in) in women has been associated with an increased risk of OSAHS.
  • Mallampati score: This score has been used for many years to identify patients at risk for difficult tracheal intubation. The classification (see Media File 2) provides a score of 1-4 based on the anatomic features of the airway seen when the patient opens his or her mouth and protrudes the tongue. A 2006 study showed that for each 1-unit increase in the Mallampati score, the odds ratio of having OSAHS (defined by an AHI >5) increased by 2.5. In addition, the AHI increased by 5 events per hour.70
The Mallampati score has been used for many years...

The Mallampati score has been used for many years to identify patients at risk for difficult tracheal intubation.

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The Mallampati score has been used for many years...

The Mallampati score has been used for many years to identify patients at risk for difficult tracheal intubation.

  • Narrowing of the lateral airway walls, which is an independent predictor of the presence of OSAHS in men but not women
  • Enlarged (ie, "kissing") tonsils (3+ to 4+)
Tonsil grades.

Tonsil grades.

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Tonsil grades.

Tonsil grades.

  • Retrognathia or micrognathia
  • Large degree of overjet
  • High-arched hard palate

Causes

  • Risk factors for sleep apnea
    • Obesity
    • Male sex
    • Age
    • Adenotonsillar hypertrophy, particularly in children and young adults
    • Alcohol use
    • Craniofacial skeletal abnormalities, particularly in nonobese adults and children (see Physical)
    • Family history: Risk increases with each additional close family relative with OSAHS.71
  • Other diseases associated with the development of obstructive sleep apnea-hypopnea syndrome (OSAHS)
    • Hypothyroidism: This has been associated with the development of OSAHS; however, evidence indicates that the prevalence of hypothyroidism in patients with OSAHS is no higher than in the general population, and patients with OSAHS should not be routinely screened for hypothyroidism, except possibly elderly women.
    • Neurologic syndromes such as postpolio syndrome, muscular dystrophies, and autonomic failure syndromes such as Shy-Drager syndrome
    • Stroke: The relationship of OSAHS to cerebrovascular disease is still being determined. Growing evidence indicates that the prevalence of OSAHS is increased in patients who have had a stroke. However, whether OSAHS is a risk factor for stroke or stroke is a risk factor for developing OSAHS remains unclear.
    • Acromegaly

More on Obstructive Sleep Apnea-Hypopnea Syndrome

Overview: Obstructive Sleep Apnea-Hypopnea Syndrome
Differential Diagnoses & Workup: Obstructive Sleep Apnea-Hypopnea Syndrome
Treatment & Medication: Obstructive Sleep Apnea-Hypopnea Syndrome
Follow-up: Obstructive Sleep Apnea-Hypopnea Syndrome
Multimedia: Obstructive Sleep Apnea-Hypopnea Syndrome
References
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Further Reading

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Keywords

obstructive sleep apnea-hypopnea, obstructive sleep apnea-hypopnea syndrome, OSAHS, obstructive sleep apnea, apnea, snore, obesity complication, OSA, obstructive sleep apnea syndrome, OSAS, snoring, apneic sleep, sleep disorder, central sleep apnea, CSA, central breathing instability, continuous positive airway pressure, CPAP, apnea-hypopnea index, apnea-plus-hypopnea index, AHI, sleep-disordered breathing, sleep disordered breathing, uvulopalatopharyngoplasty, UPPP, excessive daytime sleepiness, EDS

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Contributor Information and Disclosures

Author

James A Rowley, MD, Associate 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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO 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.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

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