eMedicine Specialties > Pulmonology > Sleep-Related Disorders

Obstructive Sleep Apnea

Ralph Downey III, PhD, DABSM, FAASM, Associate Professor of Medicine, Pediatrics, and Neurology, Loma University School of Medicine; Adjunct Associate Professor, Department of Psychology, University of California at Riverside; Chief, Sleep Medicine, Loma Linda University Medical Center and the Loma Linda University Children's Hospital
Philip M Gold, MD, Professor of Medicine, Chief of Pulmonary and Critical Care Medicine, Medical Director of Respiratory Care, Loma Linda University Medical Center; Himanshu Wickramasinghe, MD, MBBS, Attending Physician; Pulmonary, Critical Care, and Sleep Medicine; Henry Mayo Newhall Memorial Hospital, Valencia, California

Updated: Jul 30, 2009

Introduction

Background

Obstructive sleep apnea (OSA) is a sleep disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. OSA is a sleep disorder characterized by recurrent episodes of upper airway (UA) collapse during sleep.¹ By definition, apnea episodes last 10 seconds or longer and commonly last 30 seconds or longer. Apnea may occur hundreds of times nightly, 1-2 times per minute in severe OSA patients, and is often accompanied by wide swings in heart rate, precipitous decrease in oxygen saturation, and brief electroencephalogram (EEG) arousals concomitant with stertorous breathing sounds as a bolus of air is exhaled when the airway reopens. This may occur hundreds of times nightly. Obstructive apnea events are most often associated with recurrent sleep arousals and recurrent oxygen desaturation.

Three cardinal symptoms of sleep apnea include snoring, sleepiness, and significant-other report of sleep apnea episodes. This 3 S alliteration is a helpful mnemonic to busy clinicians in assessing patients for OSA. It has proven to be valuable in teaching residents to be sensitive in the identification and appropriate referral of these patients for further study Also helpful is if the patient’s spouse or someone close to him or her can attend the visit because often the sleeper is unaware he or she has OSA, and, in fact, he or she may regard themselves as "a good sleeper" because they "can sleep anytime, anywhere" (eg, waiting in the physician’s, in traffic, in class, at his or her office) Sleepiness is one of the potentially most morbid symptoms of sleep apnea, owing to the accidents that can occur as a result of it.

OSA is a very important diagnosis for physicians to consider because of its strong association with and potential cause of the most debilitating medical conditions, including hypertension, cardiovascular disease, coronary artery disease, insulin-resistance diabetes, depression, and, as mentioned, sleepiness-related accidents, which are discussed in greater detail in Mortality/Morbidity and Medicolegal Pitfalls.

OSA is an increasingly prevalent condition, in both adults and children, in modern society.  Approximately 24% of men and 9% of women have OSA, with and without excessive daytime sleepiness.² The prevalence in children is less certain, but an increasingly large segment of the adolescent population is seen in the author’s sleep center who are often obese and present similar to many of their adult counterparts, with one important exception: they may be sleepy and/or hyperactive. A 2007 study has suggested that approximately 6% of adolescents have weekly sleep-related disordered breathing.³ Also see Obstructive Sleep Apnea Syndrome in eMedicine’s Pediatrics section.

OSA should be diagnosed and treated promptly. OSA can be reversed quickly with the appropriate titration of continuous positive airway pressure (CPAP) devices. CPAP is the standard treatment option for OSA.

A sleep-related disordered breathing (SRDB) continuum has been described and is supported by research.⁴ The SRDB continuum suggests that snoring is the initial presenting symptom, and it increases in severity over time and it increases in association with medical disorders that may serve to exacerbate the disorder, such as obesity. Snoring has a constellation of pathophysiological effects⁵ ; as the disease progresses SRBD patients begin to develop increased UA resistance that results in a new hallmark symptom: sleepiness. Sleepiness is caused by increased arousals from sleep.⁶ This syndrome has been described as the UA resistance syndrome (UARS).

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.

Before OSA with residual daytime sleepiness is considered and treated, it is important to know if the pressure is indeed ideal. The author’s approach is to be able to conclusively demonstrate that CPAP has effectively eliminate snoring, UARS, and OSA in the supine position and in rapid eye movement (REM) sleep, 2 sleep states during which SRDB is worsened. Sometimes, a single-night CPAP titration study is not sufficient to make this conclusion. Data suggest that the author’s sleep center titration under titrates an average of 2 cm water.¹ Based on these data, some may increase the CPAP pressure by 2 cm water. If the empirical increase does not effectively treat the EDS, then a PSG with a CPAP titration in the sleep disorders center is warranted to adjust the pressure while the patient is in the supine position and in REM sleep so that snoring, UARS, and OSA are eliminated.

If these steps have been taken, then performing a multiple sleep latency test (MSLT) is reasonable in order to (1) verify objective daytime sleepiness compared with the subjective sleepiness of the Epworth Sleepiness Scale (ESS), because the correlation is low (r = 0.34) and(2) exclude other sleep disorders known to have hypersomnia as a major presenting symptom (eg, insufficient sleep syndrome, narcolepsy), because insufficient sleep syndrome is the most common cause of hypersomnia and OSA is more common among patients who have narcolepsy (a 30% incidence rate vs 1-4% in the population).

The description of a continuum may have first been described by Elio Lugaresi, an Italian Sleep Specialist, during a 1987 Association for the Psychophysiological Study of Sleep presentation in Copenhagen, Denmark). Dr Lugaresi used the term "heavy snorers disease" to articulate the SRDB continuum. He made the argument that snoring is the beginning of the so-called heavy snorers disease. He presented data showing that the earlier snoring occurred in adult life, the more severe the obstructive apnea would be later, and OSA presented earlier in life.

Historical perspectives

The history of the discovery of sleep apnea is interesting and is the topic of a paper published in 2008.⁷

In literature, Charles Dickens has been credited with one of the first descriptions in print regarding sleep apnea when he wrote of "Sleepy Joe," an obese man who sat in the corner of an English pub asleep. The archetype of a rotund, sleepy man became eponymous with "pickwickian syndrome" by Burwell in 1956.⁸ The prevailing belief at the time was that "pickwickians" had breathing disorders and drowsiness due to "carbon dioxide poisoning."

A number of individuals have played important roles in advancing sleep science to the point that we have come to understand OSA. Detailing the history of OSA is beyond the scope of this article; however, a few highlights are mentioned.

Gestaut, Tassinari, and Duron⁹ in France and Jung and Kuhlo¹⁰ in Germany provided perhaps the most accurate descriptions of OSA at about the same time, in 1965.

The first known successful treatment for OSA was tracheostomy in 1970 by Elio Lugaresi and colleagues at the University of Bologna in Italy. A primary reason a tracheostomy was important to the understanding of OSA is that performing the tracheostomy left little doubt that OSA was due to an obstructed UA, and not due to a dysfunction of the brain’s respiratory centers. The elevated blood pressure in these patients was of grave concern to Dr Lugaresi, and post-tracheostomy the blood pressure dropped substantially. For the next 11-16 years, tracheostomy and weight loss were the only established beneficial remedies for OSA

In 1981, Sullivan et al introduced CPAP as a treatment for OSA.¹¹ It quickly gained worldwide acceptance by 1986, and it replaced tracheostomy as the most useful and desirable treatment. As is often the case in history, it is perplexing how such a simple device introduced so long ago can transform modern medicine in ways not sooner foreseen. CPAP was a tremendous advance for thousands of OSA patients who needed care and for clinicians who would soon solely specialize in sleep medicine.

Around the time when CPAP was introduced, corrective surgery was introduced and would become the forerunner of further developments in the field of sleep medicine. In 1981, Fugita and colleagues introduced uvulopalatopharyngoplasty (UPPP).¹²

Other treatments, including oral appliance (OA) therapy, are also now treatment alternatives for OSA. Future advances in these and other therapies (eg, stimulation of the genioglossus muscle) are exciting. As was the case with CPAP, the simplest procedure, mechanical device, or drug may astound the medical community by providing the next revolution in the treatment of OSA. For a complete and elegant description of the history of sleep medicine, see Principles and Practice of Sleep Medicine.¹³

Definition

According to the American Academy of Sleep Medicine (AASM) International Classification of Sleep Disorders: Diagnostic and Coding Manual, Second Edition,¹⁴ OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) UA obstruction occurring during sleep. By definition, apneic and hypopneic events last a minimum of 10 seconds. At least 5 apnea events must occur per hour of sleep time in association with clinical symptoms, or at least 15 apnea events must occur per hour of sleep time with or without clinical symptoms.

Pathophysiology

Available evidence indicates that pharyngeal collapse is responsible for the recurrent UA obstruction during sleep in patients with OSA.

UA size and shape

During wakefulness, the pharyngeal airway appears to be smaller in patients with OSA compared with healthy subjects. In the absence of craniofacial abnormalities, the soft palate, tongue, parapharyngeal fat pads, and lateral pharyngeal walls are enlarged.

Changes in transmural pressure in the UA

Transmural pressure is the difference between intraluminal pressure and the surrounding tissue pressure. If transmural pressure decreases, the cross-sectional area of the pharynx decreases. If this pressure passes a critical point, pharyngeal closing pressure is reached. OSA occurs when the net forces reach the closing pressure.

Risk factors for OSA

Static factors and dynamic factors increase the risk of OSA. Static factors include surface adhesive forces, neck and jaw posture, tracheal tug, and gravity. Gravitational forces are felt simply by tilting one's head back to where the retroposition of the tongue and soft palate reduce the pharyngeal space. For most patients, OSA worsens in the supine sleeping position.

Dynamic factors include nasal and pharyngeal airway resistance, the Bernoulli effect, and dynamic compliance.

Any anatomic feature that decreases the size of the pharynx increases the likelihood of OSA. One example of this effect is retrognathia. Dr Robin was the first to work on a mandibular-advancement device to help patients with what became known as Pierre Robin syndrome or Robin syndrome. His patients benefitted because protrusion of the mandible increased the cross-sectional area of the pharynx, among other effects.

The Bernoulli effect plays an important dynamic role in OSA pathophysiology. In accordance with this effect, airflow velocity increases at the site of stricture in the airway. As airway velocity increases, pressure on the lateral wall decreases. If the transmural closing pressure is reached, the airway collapses. The Bernoulli effect is exaggerated in areas where the airway is most compliant. Loads on the pharyngeal walls increase compliance and, hence, increase the likelihood of collapse.

This effect helps to partially explain why obese patients, and particularly those with fat deposition in the neck, are most likely to have OSA. Moreover, the cross-sectional area of the airway in patients with OSA is smaller than that of people without OSA; this difference is due to the volume of the soft tissue, including the tongue, lateral pharyngeal walls, soft palate, and parapharyngeal fat pads. In one study, the increased volume of these areas was independent of sex, age, ethnicity, craniofacial size, and fat deposition surrounding the UA.¹⁵

Given these principles, the reasons why the likelihood of OSA is increased among obese patients, why weight loss decreases the risk of OSA, and why physical examination helps in predicting the presence of OSA are understandable. However, the clinical situation is complex because of the interplay of known static and dynamic factors and because of unknown factors. Data do not explain why sex, age, and ethnicity are not evenly distributed across epidemiologic studies of OSA patients. Furthermore, data or physical findings are not helpful for determining with precision who will or will not have OSA and who can or who cannot be cured with UA surgery.

Frequency

United States

Although early investigators estimated the prevalence of sleep-disordered breathing (SDB) to be 2% for middle-aged women and 4% for middle-aged men, more recent research indicates a prevalence of 4% for women and 9% for men.²

The National Commission on Sleep Disorders Research estimated that minimal SDB (respiratory disturbance index [RDI] >5) affects 7-18 million people in the United States and that relatively severe cases (RDI >15) affect 1.8-4 million people. The prevalence increases with age. SDB remains undiagnosed in approximately 92% of affected women and 80% of affected men.

Mortality/Morbidity

In clinical practice, little doubt exists that sleep apnea can affect a person's quality of life in many ways. Sleep apnea is now known to be a public health hazard because of accidents due to sleepiness. Moreover, patients often have hypoxemia with each apneic event, and profound and repetitive hypoxia can affect end organ systems.

Excessive daytime sleepiness

EDS is one of the most common and difficult symptoms clinicians treat in patients with OSA. Patients do not always accurately describe their sleepiness on the ESS compared with objective measures. Nonetheless, EDS is one of the most debilitating symptoms because it reduces quality of life, it impairs daytime performance, and it causes neurocognitive deficits (eg, memory deficits).

Although CPAP quickly reverses EDS in most patients, not all patients use CPAP. Moreover, some patients remain sleepy despite effective CPAP. In these patients, modafinil at 200-400 mg/d can effectively enhance alertness without changing CPAP use.¹⁶ Patients with residual excessive sleepiness despite effective CPAP use are an interesting subgroup of patients. The mechanism of EDS in these patients awaits further study.

Partly because of their EDS, daytime functioning, intellectual capacity, memory, psychomotor vigilance (decreased attention and concentration), and motor coordination are substantially impaired in patients with OSA. Causes include both sleep fragmentation and hypoxemia due to OSA. Whether these causes can be reversed awaits further study.

Patients with OSA have more automobile accidents than people without OSA. Determining which OSA patients are likely to have an accident is unpredictable from the existing data.

Patients with OSA do not perform as well as healthy control subjects during driving simulation tests, but their performance may return to normal after treatment. Therefore, access to effective treatment is a pivotal concern in sleep medicine.

Cardiovascular

A Scientific Statement was published by the American Heart Association and the American College of Cardiology Foundation on August 25, 2008. This expert review examined OSA and cardiovascular disease. The results are paraphrased below.¹⁷

The possible mechanisms through which OSA may lead to cardiovascular disease were examined. OSA patients often have hypoxemia, reoxygenation, sleep arousals, less sleep time than healthy individuals, elevated negative intrathoracic pressure, and, in some individuals, hypercapnia. The commonly accepted contributions of these OSA-related pathophysiological factors may affect sympathetic activation, metabolic dysregulation, left atrial enlargement, endothelial dysfunction, systemic inflammation, and hypercoagulability. These mechanisms can lead to hypertension (both systemic and pulmonary), heart failure, cardiac arrhythmias, renal disease, stroke and myocardial infarction, and sudden death in sleep.

Two of the most significant findings from the Somers et al¹⁷ review are (1) that the data suggest that evaluation and treatment for OSA is not recommended in every patient with cardiac disease, but the threshold for a referral for a PSG study and for treatment of OSA should be low and (2) because OSA affects younger individuals with cardiovascular disease to a greater extent than older individuals with cardiovascular disease, this threshold for OSA evaluation and treatment should be even lower.

Other significant findings from the review are as follows¹⁷ :

• Hypertension: All-cause mortality rates are higher individuals with blunted or absent decrease in nighttime blood pressure. Additionally, CPAP treatment was shown to have moderate and variable effects on blood pressure in OSA patients.¹⁸ Further, antihypertensive drug treatment does not improve OSA; however, clonidine, which is a REM sleep suppressant, may improve OSA by reducing the patient’s percentage of REM sleep because the REM sleep is when OSA is most severe. Finally, ACE inhibitors may worsen OSA because of the adverse effects of cough and rhinopharyngeal inflammation, 2 effects that cease with discontinuation of the drug.
• Heart failure: OSA has not been established as a cause of heart failure, and whether OSA hastens death in patients with heart failure is uncertain. However, a 2007 study examined untreated OSA in patients with heart failure and reported that those with an apnea-hypopnea index (AHI) of greater than 15 had increased mortality compared with those with an AHI of less than 15.¹⁹ Also note that CPAP treatment in patients with OSA and heart failure may reduce mortality,²⁰ but the evidence is less than absolute because no randomized clinical trials have tested the effects.
• Arrhythmias: Patients with severe SDB have a 2- to 4-fold increased risk of experiencing nocturnal complex arrhythmia. Bradyarrhythmia is more common in OSA patients (occurs in approximately 10% of OSA patients), especially in the REM sleep state and when greater than 4% drop in oxygen saturation occurs. Additionally, atrioventricular block and asystole may occur in the absence of conduction disease. Also, premature ventricular contractions much more common in patients with OSA compared with those who do not have OSA (66% vs 0-12%, respectively), and they are most likely to occur during an apnea; however, CPAP treatment reduces the frequency of the premature ventricular contractions (by up to 58% reported in one study).
• Myocardial ischemia and infarction: OSA patients have double the prevalence of coronary artery disease, and an independent association has been shown between OSA and subclinical coronary artery disease, as demonstrated by coronary artery calcification. Further, OSA apparently affects the timing of sudden cardiac death because research shows that greater than 50% of sudden cardiac deaths that occur in OSA patients do so between 10 PM and 6 AM; the more common time for sudden cardiac death is from 6-11 AM. Men with untreated OSA and an AHI of greater than 30 had an increased number of fatal and nonfatal cardiovascular events, but treated OSA patients have a number of events similar to snorers who do not have OSA.

In a study of sleep-disordered breathing and nocturnal cardiac arrhythmias in older men, Mehra et al found that the likelihood of atrial fibrillation or complex ventricular ectopy increased along with the severity of sleep-disordered breathing. In addition, different forms of sleep-disordered breathing were associated with the different types of arrhythmias. Polysomnography in 2911 participants showed that the odds of atrial fibrillation (P = .01) and of complex ventricular ectopy (P <.001) increased with increasing quartiles of the respiratory disturbance index (a major index including all apneas and hypopneas).²¹
 
Central sleep apnea was more strongly associated with atrial fibrillation (odds ratio [OR], 2.69; 95% confidence interval [CI], 1.61-4.47) than with complex ventricular ectopy (OR, 1.27; 95% CI, 0.97-1.66). In contrast, obstructive sleep apnea and hypoxia was associated with complex ventricular ectopy; participants in the highest hypoxia category had an increased odds of complex ventricular ectopy (OR, 1.62; 95% CI, 1.23-2.14) compared with the lowest quartile. The results suggest that different sleep-related stresses may contribute to atrial and ventricular arrhythmogenesis in older men.²¹

Stroke

The Sleep Heart Health Study²² showed the strongest relationship was between OSA and stroke versus any other cardiovascular disease.

Patients with OSA are more likely to have a stroke and die than people without OSA. This correlation persists even if researchers control for the risk factors of age, sex, race, smoking, alcohol consumption, body mass index (BMI), diabetes mellitus, hyperlipidemia, atrial fibrillation, and hypertension. Time-to-event analyses have shown that patients with OSA (who were undergoing weight loss, CPAP, or surgery) have an increased hazard ratio for stroke or death of 1.97 (95% confidence interval, 1.12-3.48; P = .01). The risk of stroke or death was most severe in the quartile of patients with the most severe AHI. The hazard ratio increased to 3.30 (95% confidence interval, 1.74-6.26) when the AHI was greater than 36. This study was not powered sufficiently to determine if OSA treatment affects survival.

OSA is associated with an increased risk of type 2 diabetes. Whether OSA causes type 2 diabetes or whether it is associated with insulin resistance and diabetes is unclear. Use of CPAP can reverse insulin resistance. Sleep fragmentation, sleep deprivation, and hypoxemia (which all occur in OSA) are thought to play independent roles in glucose intolerance. Conflicting results show that reversal of glucose intolerance may occur when OSA is treated.

Race

African American individuals appear to be more predisposed to SDB than white persons. This increased predisposition varies according to age. The odds ratio is greater than 3 in children younger than 13 years and is 1.88 in persons younger than 25 years. In elderly African Americans, the risk is increased 2-fold.
 
Other populations that may be at increased risk include Mexican Americans and Pacific Islanders.

Sex

In adults, the male-to-female ratio is approximately 3:1. In population studies that have examined the incidence of OSA, women were less likely than men to have OSA and were less likely to be diagnosed early in the disease process. Survival rates are lower for women than for men, after an OSA diagnosis has been established by polysomnography, presumably due to the delayed OSA diagnosis.

Age

Aging is an important consideration of risk for OSA. OSA prevalence increases 2-3 times in older persons (>65 y) compared with individuals aged 30-64 years. After age 65 years, no further relative disparity is noted in the incidence of OSA. One explanation for this plateau is the relative increase in mortality in persons older than 65 years; however, data to support this contention, as attractive as it appears, are insufficient.  Scant data are available to help clinicians determine if the clinical management should differ between the age cohorts.

Clinical

History

• Snoring
• Sleepiness
• Spouse or significant other apnea report
• Hypertension
• Nonrestorative sleep (ie, "waking up as tired as when they went to bed")
• A choking sensation or gasping during the night; though in a very low proportion relative to the number of apneas they experience
• Morning headaches
• Patient report of "trouble sleeping"
• Insomnia
• Restless sleep
• Sore throat or dry mouth in the morning

Symptoms

• Cognitive deficits; memory and intellectual impairment
• Decreased vigilance
• Morning confusion
• Personality and mood changes, including depression and anxiety
• Sexual dysfunction, including impotence and decreased libido
• Gastroesophageal reflux

Risk factors

• Male sex
• Age 40-65 years
• Positive family history
• Body habitus
  • Overweight and obese
  • Central body fat distribution
  • Large neck girth (>17 in)
  • Increased Mallampati score (crowded-appearing pharyngeal airway)
  • UA abnormalities, including nasal congestion
  • Craniofacial abnormalities
• Menopause (in women)
• Alcohol use
• Sedative use
• Smoking
• Supine sleep position
• REM sleep state

Predictive value of clinical history and examination

• Predictive value
  • Disruptive snoring: A history of disruptive snoring has 71% sensitivity in predicting SDB.
  • Disruptive snoring and witnessed apneas: These factors taken together have 94% specificity for SDB.
• Questioning patients and others
  • Others: Obtaining a history from someone who has observed the patient's sleep behavior is important. Patients are usually unaware of snoring and/or sleepiness or may minimize these symptoms. Sleepiness may develop insidiously. Patients may be unaware that they are sleepy; that is, they may forget how normal alertness feels.
  • Patients: Question the patient about drowsiness in boring or monotonous situations and about sleepiness while driving.
• Sex-related differences
  • Reporting of symptoms: Women are twice as likely as men to not report snoring and apneas, even after one corrects for the RDI.
  • Presentation: Women commonly present with symptoms atypical of the classic presentation of OSA. Women are more likely than men to report fatigue and are less likely than men to report sleepiness.
  • Diagnosis and referrals: Although the male-to-female ratio for the prevalence of SDB in the general population is approximately 2-3:1, the male-to-female ratio for patients referred to sleep clinics for an evaluation of possible OSA is approximately 10:1. OSA appears to be notably underdiagnosed in females. A high index of suspicion must be maintained when screening females for SDB.
  • Menstruation: In 1 study, 43% of premenopausal women with SDB had menstrual irregularities that disappeared with the treatment of SDB.

Physical

• Obesity
  • Approximately 30% of patients with a BMI greater than 30 have OSA, and 50% of patients with a BMI greater than 40 have OSA.
  • In the United States, 20% of men and 25% of women have a BMI greater than 30.
  • Unfortunately, obesity has become an epidemic in industrialized nations. One study showed that the number of people with a BMI greater than 40 has tripled since 2000.²⁴
  • Patients with obesity hypoventilation syndrome and some patients with OSA may have evidence of pulmonary hypertension and right-sided heart failure.
• Large neck circumference
  • Neck circumference may correlate with OSA better than BMI.
  • In one study, subjects with OSA had a neck circumference 4 cm larger than subjects without OSA. In addition, neck circumference of 40 cm or greater had a sensitivity of 61% and a specificity of 93% for OSA, regardless of the person's sex.
• Abnormal Mallampati score (1-4 scale) 
• Systemic arterial hypertension present in approximately 50% of patients with OSA
• Congestive heart failure
• Pulmonary hypertension
• Stroke
• Metabolic syndrome
• Type 2 diabetes mellitus

Causes

• Structural factors
  • Structural factors related to craniofacial bony anatomy that predispose patients with OSA to pharyngeal collapse during sleep include the following:
    • Genetic variations (facial elongation, posterior facial compression)
    • Retrognathia and micrognathia
    • Mandibular hypoplasia
    • Brachycephalic head form
    • Inferior displacement of the hyoid
    • Pierre Robin syndrome
    • Down syndrome
    • Marfan syndrome
    • Prader-Willi syndrome
    • High, arched palate (particularly in women)
  • Structural factors related to nasal obstruction that predispose patients with OSA to pharyngeal collapse during sleep include polyps, septal deviation, tumors, trauma, and stenosis.
  • Structural factors related to retropalatal obstruction that predispose patients with OSA to pharyngeal collapse during sleep include (1) an elongated, posteriorly placed palate and uvula and (2) tonsil and adenoid hypertrophy (particularly in children).
  • Structural factors related to retroglossal obstruction that predispose patients with OSA to pharyngeal collapse during sleep include macroglossia and tumor.
• Nonstructural risk factors
  • Some nonstructural risk factors include obesity, age, male sex, postmenopausal state, and habitual snoring with daytime somnolence.
  • Familial factors also play a role. Families with a high incidence of OSA are reported. Relatives of patients with SDB have a 2- to 4-fold increased risk of SDB compared with control subjects.
  • Environmental exposures include smoke, environmental irritants or allergens, and alcohol and hypnotic-sedative medications.
  • Both hypothyroidism and acromegaly are associated with macroglossia and increased soft tissue mass in the pharyngeal region. They are associated with an increased risk of SDB. Hypothyroidism is also associated with myopathy that may contribute to UA dysfunction.

Differential Diagnoses

Asthma
Chronic Obstructive Pulmonary Disease
Depression
Hypothyroidism
Obstructive Sleep Apnea-Hypopnea Syndrome
Sleep Disorders

Other Problems to Be Considered

• Nocturnal panic attacks
• Asthma
• Chronic obstructive pulmonary disease
• Laryngospasm due to gastroesophageal reflux (see Gastroesophageal Reflux Disease and the Medscape GERD Resource Center)
• Dyspnea due to pulmonary edema
• Central Sleep Apnea
• Nonobstructive alveolar hypoventilation
• Sleep disorders associated with hypersomnia - Narcolepsy, idiopathic hypersomnia, insufficient sleep syndrome, periodic limb movement disorder
• Depression
• Hypothyroidism

Workup

Laboratory Studies

• Routine laboratory tests usually are not helpful in obstructive sleep apnea (OSA) unless a specific indication is present.
• Consider obtaining a thyrotropin hormone level if clinically indicated, particularly in elderly individuals.
• An arterial blood gas determination should be obtained if obesity hypoventilation syndrome is suspected.
• If clinically indicated, consider PSG using end-tidal carbon dioxide measurements for a continuous measurement of carbon dioxide pressures as a function of OSA and associated sleep states and by position. Data analysis help determine if OSA versus sleep state is an independent or an interacting factor (eg, REM sleep vs non-REM sleep), and data analysis help determine if OSA versus sleeping body position is an independent or an interacting factor (eg, supine sleep position vs lateral decubitus vs semi-Fowler). A single PSG probably will not be definitive to determine, out of all of these variables, a specific variable that may be a singular cause of hypercapnia; however, it is better than a daytime arterial blood gas determination for determining if OSA is a cause of hypercapnia or not.

Imaging Studies

• Modalities available for identifying the site of obstruction include lateral cephalometry, endoscopy, fluoroscopy, CT scanning, MRI, and radiography.
• The accuracy of these methods for identifying the sites of obstruction is not clear. At present, UA imaging is used primarily as a research tool. Routine radiographic imaging of the UA is not performed.
• See Snoring and Obstructive Sleep Apnea, Upper Airway Evaluation for additional details about UA imaging.

Other Tests

Standard diagnostic nocturnal PSG

The AASM has published standards and guidelines for performing PSG (see American Academy of Sleep Medicine). The AASM has the highest standards to which the top-level American sleep disorders centers adhere. Unfortunately, more unaccredited sleep disorders centers exist than accredited sleep disorders centers. Having a patient studied at an AASM-accredited sleep disorders center is important to ensure the highest quality care. AASM-accredited sleep disorders 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. A PSG is necessary to accurately diagnose OSA and to assess treatment benefit.
 
AASM standard SRDB  definitions¹⁴

• Apnea is defined as the cessation of airflow for 10 seconds or longer.
• Hypopnea is defined as a recognizable transient reduction (but not complete cessation) of breathing for 10 seconds or longer, a decrease of greater than 50% in the amplitude of a validated measure of breathing, or a reduction in amplitude of less than 50% associated with oxygen desaturation of 4% or more. An arousal is unnecessary to score a hypopnea.
• Obstructive apneas and hypopneas are typically distinguished from central events by the detection of respiratory efforts during the event.
• The RDI is defined as the number of obstructive apneas, hypopneas, and respiratory event–related arousals (RERAs) per hour. The RDI is preferred over the AHI because it includes flow-limitation events that end with arousals. The RDI is best suited to meet the new AASM diagnostic criteria for OSA, as discussed below.
• An RERA is an event characterized by increasing respiratory effort for 10 seconds or longer leading to an arousal from sleep but one that does not fulfill the criteria for a hypopnea or apnea. The criterion standard to measure RERAs is esophageal manometry, as the AASM recommends. However, esophageal manometry is uncomfortable for patients and impractical to use in most sleep centers.
• A reliable and valid way to measure RERAs is with the use of a nasal cannula and pressure transducer. Results obtained with this transducer are reliable (intraclass correlation of 0.96). With regard to the diagnosis of OSA, this method does not differ from esophageal manometry in a clinically significant manner. With either method, the RDI is greater than 5 and the normal RDI cutoff is greater than 15.
• According to the International Classification of Sleep Disorders: Diagnostic and Coding Manual, Second Edition,¹⁴ at least 1 of the following criteria must apply for OSA to be diagnosed:
  • The patient reports daytime sleepiness, unrefreshing sleep, fatigue, insomnia, and/or unintentional sleep episodes during wakefulness. The patient awakens with breath holding, gasping, or choking. The patient's bed partner reports loud snoring, breathing interruptions, or both during the patient's sleep.
  • PSG shows more than 5 scoreable respiratory events (eg, apneas, hypopneas, RERAs) per hour of sleep and/or evidence of respiratory effort during all or a portion of each respiratory event.
  • PSG shows more than 15 scoreable respiratory events (eg, apneas, hypopneas, RERAs) per hour of sleep and/or evidence of respiratory effort during all or a portion of each respiratory event.
  • Another current sleep disorder, medical or neurologic disorder, medication use, or substance use does not better account for the patient's condition.

Standard PSG-measured  parameters

The  PSG is a multichannel recording of sleep and breathing and usually involves in-laboratory measurement of sleep architecture and EEG arousals, eye movements, chin movements, airflow, respiratory effort, oximetry, ECG tracings, body position, snoring, and leg movements (see Media File 3).

Segment of a nocturnal polysomnogram shows an episode of central apnea. Airflow and respiratory movements have both ceased.

The following PSG findings are characteristic of OSA:

• Apneic episodes occur in the presence of respiratory muscle effort (see Media File 2).
• Apneic episodes lasting 10 seconds or longer are considered clinically significant. Apneic episodes are usually approximately 20-40 seconds and rarely last several minutes. 
• 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. Mixed apneas are a combination of central sleep apnea and OSA in a single apneic episode (see Media File 2).
• Sleep disruption due to arousals is usually seen at the termination of an episode of apnea.

Segment of a nocturnal polysomnogram shows an episode of mixed apnea. The initial portion of the apnea is central in origin, with cessation of both airflow and respiratory movements. The latter part of the apnea is obstructive, with an absence of airflow despite the resumption of respiratory movements.

Repeat PSG if symptoms persist despite adequate compliance with prescribed CPAP treatment. PSG can be used to assess response to UA surgical procedures and to assess response to 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 monitoring

Tonelli de Oliveira et al indicate that in-home respiratory monitoring can be used to diagnose obstructive sleep apnea syndrome. They suggest that most previous studies did not use the best standards for evaluating the accuracy of in-home respiratory monitoring. They report on the use of all available comparison methods to evaluate efficacy and further suggest in-home respiratory monitoring is an effective diagnostic tool.²⁵

Treatment

Medical Care

Overview

Board-certified sleep specialists evaluate PSG results and make treatment recommendations for obstructive sleep apnea (OSA) patients.

Summary of treatments

From least invasive and effective to most invasive and effective, treatments can be summarized as follows:

• All patients should be offered nasal CPAP therapy first.
• In patients with mild-to-severe OSA who refuse or reject nasal CPAP therapy, BiPAP therapy should be tried next. If this therapy fails or is rejected, OA therapy should be considered.
• OAs may be considered first-line therapy for patients with mild OSA, particularly if they are unwilling to try nasal CPAP therapy.
• All interventions to improve tolerance of CPAP therapy should be attempted prior to deciding that treatment has failed in a particular patient (see Follow-Up).
• Patients in whom noninvasive medical therapy (eg, positive airway pressure, OAs) fails should be offered surgical options. Patients should be made aware of the success rates for each surgical procedure. They should be informed that they might require more than 1 surgical procedure, some fairly extensive, to cure OSA. Refer patients only to centers that have personnel experienced in these special surgical techniques.

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.

Complications and adverse effects

Pressure- and airflow-related complications include a sensation of suffocation or claustrophobia, difficulty exhaling, inability to sleep, musculoskeletal chest discomfort, aerophagia, and sinus discomfort. Pneumothorax and/or pneumomediastinum (extremely rare), pneumoencephalos (isolated case report), and tympanic membrane rupture (rare) also can occur.

Mask-related problems include skin abrasions, rash, and conjunctivitis (due to air leaks). Nasal problems can include rhinorrhea, nasal congestion, epistaxis, and nasal and/or oral dryness. Other problems include noise and spousal intolerance.

Guidelines for use

Patients with severe SDB (RDI >20-30) should be treated irrespective of their symptoms because of the increased risk of cardiovascular morbidity. Patients with an RDI of 5-20 should be treated if they have symptoms or coexistent cardiovascular disease. Patients with UA resistance syndrome may need CPAP therapy.

CPAP is titrated after the diagnostic portion of a split-night protocol or on a separate night after a diagnostic PSG. Proper titration includes identifying the minimum CPAP level that abolishes obstructive apneas and/or hypopneas, oxyhemoglobin desaturation, RERAs, and snoring in all sleep stages and in all sleep positions. The pressure needed is typically 5-20 cm of water.

BiPAP therapy 

In contrast to CPAP, which delivers a constant pressure during both inspiration and expiration, BiPAP permits independent adjustment of the pressures delivered during inspiration and expiration. The ability to set independent inspiratory positive airway pressure and expiratory positive airway pressure levels lowers mean airway pressures compared with those of CPAP. In a given patient, the expiratory positive airway pressure level that must be applied is lower than the corresponding CPAP level required to maintain airway patency.
 
No studies have conclusively demonstrated improved compliance with BiPAP devices compared with CPAP devices. In patients who cannot tolerate CPAP, a trial of BiPAP is warranted. However, BiPAP is too expensive to be used as first-line therapy, and it has no distinct advantages over CPAP therapy.

OA therapy

OAs for repositioning the mandible were first developed for the treatment of mandibular retrusion (retrognathia). Robin described an appliance, called the Monobloc device, that was used in the treatment of retrognathia. This appliance also affected the patient's airway. Subsequent designs incorporated repositioning or advancement of the mandible.

The first-recognized appliance for the management of snoring- and sleep-related breathing disorders (SRBDs) was the tongue-retaining device (TRD). This was similar to an athletic mouth guard and incorporated a pliable bulb in the front that holds the tongue forward. This bulb prevented the tongue from collapsing back into the airway during sleep.

Later, mandibular repositioners became available. These were designed for mandibular advancement. Early devices were made in one piece and locked the mandible in one position. Newer designs have separate upper and lower parts that are attached to each other and that allow for adjustability and jaw mobility. These repositioners are adjusted to advance the jaw to 60-70% of the maximum protrusion of the jaw.
 
At present, 3 basic designs of OAs are used to treat SRBD: mandibular repositioners, TRDs, and palatal lifting devices. More than 40 OAs are available to manage SRBD and OSAS.
 
OAs are believed to be effective for the following reasons:

• OAs enlarge the UA by moving (pulling) the tongue forward (ie, with a TRD) or by moving the mandible and soft palate anteriorly (ie, with a mandibular repositioner). They open or dilate the airway. Most recent studies have been performed with mandibular repositioners.
• The biomechanical factors responsible for the effectiveness of OAs are not completely understood. Increased tone of UA musculature is thought to be the predominant influence on the caliber and volume of the airway. Key among these muscles is the palatoglossus muscle. When the jaw is opened, the palatoglossus muscle (with other muscles in the pharyngeal airway) influences the airway to improve its caliber and stability.
• OAs thin the lateral pharyngeal walls by exerting traction. According to imaging studies, the size of the lateral pharyngeal fat pads and the thickness of the lateral pharyngeal muscular walls are greater in patients with apnea than in healthy subjects. For OA therapy to be successful, the lateral dimension of the airway is the critical factor.

• Overall, 51% of patients studied achieved an RDI of less than 10 with OA therapy.
• Of patients who had a pretreatment RDI of greater than 20, 39% continued to have an RDI above this level despite OA therapy. At least 1 randomized controlled trial demonstrated that OAs have better success rates in patients with mild OSA (81%) than in those with moderate (60%) or severe (25%) OSA.
• Continuous adjustment or replacement, as needed, improves success rates with OAs in the long term.
• No patient characteristics predicted success with OA therapy.
• No particular OA had any advantages over the others studied.
• Some patients have an increase in AHI with OA treatment. 
• Endpoints assessed in the studies of OAs varied and included an RDI of less than 10, an RDI of less than 20, or a greater than 50% reduction in the AHI. This variation made the comparison of results difficult. Furthermore, many studies did not stratify patients by severity of OSA.
• OAs were more likely to be successful in patients with low BMIs, at a young age, with a small neck circumference, with a short soft palate, or with a small oropharynx and in treating positional OSA, as based on retrospective data analysis.

Subsequent prospective controlled clinical trials to compare OA therapy with nasal CPAP therapy to treat OSA and snoring demonstrated the following results:

• Treatment was successful in 55% of patients using an adjustable mandibular repositioner and in 48% of patients using a nonadjustable mandibular repositioner. Treatment success was defined as a posttreatment RDI of less or equal to 10, with symptomatic relief.
• CPAP therapy was superior to mandibular repositioning in normalizing the RDI, reducing snoring, and improving oxygenation.
• CPAP and adjustable mandibular repositioning equally improved daytime sleepiness.
• Most patients preferred mandibular repositioning therapy to CPAP therapy.

Treatment success with mandibular repositioners (OAs in general) appears to be inversely related to the initial RDI. A growing body of evidence now suggests that the severity of OSA is predictive of the response to OAs. In one study, OAs were more effective than UPPP in the treatment of OSA. OAs may also be useful in managing OSA syndrome if surgery fails.

The use of OAs in clinical practice is limited because of the difficulty in predicting the therapeutic response of individual patients. Tsai et al²⁷ used a remote-controlled device to titrate OA treatment during a single-night sleep study to predict the therapeutic response. In concept, this approach is similar to titrating nasal CPAP during a single-night sleep study. Raphaelson et al²⁸ and Petelle et al²⁹ first demonstrated the titration of mandibular advancement during a sleep study. Petelle et al demonstrated that determining the optimum level of mandibular advancement required for an individual patient during a single-night study is possible. Of note, Tsai et al did not report the same.

Apart from raising the possibility of predicting therapeutic responses in individual patients, this titration approach potentially provides an opportunity to determine the optimum therapeutic dose of mandibular advancement required during a single-night sleep study.

Further work is required in this area because it could greatly affect the use of OAs in SRBD. This research may yield the method required to identify patients who may respond to OAs and to determine the optimum level of advancement required for an individual patient.

The 2005 AASM practice parameters for the treatment of snoring and OSA with OAs include the following recommendations:

• The presence or absence of OSA must be determined before treatment with OAs is started in order to identify patients at risk because of complications of sleep apnea and to provide a baseline to establish the effectiveness of subsequent treatment.
• For patients with OSA, the desired outcome of treatment includes resolution of the clinical signs and symptoms of OSA and normalization of the patient's AHI and oxyhemoglobin saturation.
• Although OA therapy is not as effective as CPAP, OAs are indicated for use in patients with mild-to-moderate OSA who prefer OAs to CPAP, those whose condition does not respond to CPAP, those who are not appropriate candidates for CPAP, and those in whom attempted CPAP or behavioral measures (eg, weight loss, changing sleeping positions) fail.
• Patients with severe OSA should receive an initial trial of nasal CPAP because CPAP is more effective than OA therapy. UA surgery may also supersede the use of OAs in patients for whom these operations are predicted to be highly effective in treating sleep apnea.
• To ensure satisfactory therapeutic benefit from OAs, patients with OSA should undergo PSG or an attended cardiorespiratory (type 3) sleep study with the OA in place after final adjustment of fit is performed.

According to the guidelines listed above, the major role for OA therapy appears to be the treatment of patients with mild-to-moderate OSA who cannot tolerate CPAP (and BiPAP) therapy. These devices are relatively unlikely to benefit patients with severe OSA. Clinicians and patients prefer a titratable device, such as a mandibular repositioner, because it can be adjusted to improve both effectiveness and comfort.

Patients should receive a complete evaluation by a sleep disorders specialist and a dental professional, both of whom should be experienced in OA therapy; their close collaboration is required. Follow-up PSG after final adjustment of the device is recommended to ensure that OSA is treated adequately, particularly in patients with moderate-to-severe OSA. OA devices may resolve snoring without adequately treating OSA.

Complications and/or adverse effects include excessive salivation, dental misalignment with bite change, and tooth movement. Additionally, patients may experience temporomandibular joint pain and/or discomfort. The patient should not have notable discomfort or difficulty when opening the jaw upon awakening in the morning. Finally, patients may object to having an appliance in their mouth throughout the night.

The lack of long-term studies with OA may limit the clinician from choosing it as an option. Insurance payers may not pay for the use of OAs at this time. Check with individual insurance carriers.

Surgical Care

AASM recommendations for surgery

Nasal CPAP is the recommended initial therapy for patients with moderate-to-severe OSA (RDI >20, lowest oxyhemoglobin saturation <85%). Patients with symptomatic mild OSA also may prefer nasal CPAP therapy.

Surgery is indicated in patients who have a specific underlying abnormality that is causing the OSA.

Surgery may be indicated if noninvasive medical therapy (nasal CPAP or OA) fails or is rejected, if the patient desires such therapy, and if he or she is medically stable enough to undergo the procedure. If the patient has OSA that is moderately severe or severe (RDI >40 or lowest oxyhemoglobin saturation <80%), the patient requires perioperative airway protection with either nasal CPAP or a tracheostomy.

Surgery is indicated as initial therapy for patients with mild OSA (RDI <20, lowest oxyhemoglobin saturation >90%) if medical therapy is refused or rejected and if the patients are medically stable enough to undergo the procedure.

Obstruction

Three of 200 adults with OSA have a specific space-occupying lesion that causes an UA obstruction. Although surgical correction of such an abnormality (ie, tonsillectomy) can potentially cure OSA, most adult patients do not have such correctible lesions.

The level of obstruction in patients with SDB is classified into 3 types. Type I is obstruction in only the retropalatal region. Type II is obstruction in both the retropalatal and retrolingual regions. Type III is obstruction in only the retrolingual region.

Surgical procedures

Functional division of the pharynx into retropalatal and oropharyngeal (region posterior to the soft palate) and retrolingual and hypopharyngeal (region posterior to the vertical portion of the tongue) regions has been proposed.

Different surgical procedures have been proposed for patients with different levels of obstruction. UPPP may correct type I obstruction. Genioglossus advancement with hyoid myotomy (GAHM) may correct type III obstruction. Maxillomandibular advancement osteotomy (MMO) may correct obstruction at all levels.

Riley-Powell-Stanford surgical protocol^30,31

Because several sites of obstruction may be responsible, a systematic approach for selecting surgery has been developed. This is the Riley-Powell-Stanford surgical protocol designed in 1988. The protocol has 2 phases. Phase I consists of the UPPP and GAHM procedures, and phase II consists of the more complicated MMO procedure. Patients who are not adequately treated with phase I surgery are offered phase II surgery.

For phase I surgery, perform UPPP for patients with type I obstruction, GAHM for patients with type III obstruction, and simultaneous UPPP and GAHM for patients with type II obstruction. The overall success rate for phase I surgery is approximately 61%, although patients with severe OSA (RDI >60, lowest oxyhemoglobin saturation <70%) have a success rate of only 42%.

Phase II surgery consists of MMO, in which the jaw is advanced anteriorly. With the phased protocol, the success rate has been in excess of 90% for phase II surgery.

Postoperative care and outcomes

In some patients, tracheostomy or CPAP therapy is required in the perioperative period to ensure a safe airway.

The success of these surgical procedures depends on accurate identification of the site of obstruction in the UA. Modalities available for identifying the site of obstruction include lateral cephalometry, endoscopy, fluoroscopy, CT scanning, and MRI. The accuracy of these methods in identifying the sites of obstruction is not clear. Success rates for UPPP are only approximately 50% despite preselection of patients with type I obstruction.

Data regarding surgical therapy for OSA are mainly from case series. The phased protocol of Riley-Powell-Stanford holds promise for achieving cure in patients with OSA, but further data from controlled clinical trials are needed to decide its role in the overall management of OSA.

The success rates quoted are from select centers with surgeons highly skilled in these special procedures. These results cannot be extrapolated to the general population of patients with OSA. All patients undergoing surgery for treatment of OSA should undergo follow-up PSG.

• Pain with swallowing and pain with speech, usually for 1-2 weeks postoperatively
• Hemorrhage (2-4%)
• Swallowing difficulties, particularly regurgitation of food 
• Long-term pharyngeal discomfort
• Disturbance in taste
• Numbness of tongue
• Nasopharyngeal stenosis

Silent apnea may result. UPPP may end snoring but have no notable effect on episodes of sleep-associated obstruction. Patients must undergo postoperative PSG to rule out persistent OSA.

AASM recommendations for UPPP state "The UPPP, with or without tonsillectomy, may be appropriate for patients with narrowing or collapse in the retropalatal region. Good preoperative evaluation does not guarantee surgical success; the effectiveness of the UPPP is variable, and the procedure should be considered when non-surgical treatment options, such as CPAP have been considered."

Two studies showed that UPPP may make OSA worse, as it did in 31% of the patient population studied. Previous UPPP reduces the maximal level of pressure that patients who require CPAP therapy can tolerate. It may also compromise subsequent CPAP therapy by promoting mouth leaking. Uvulopalatopharyngoglossoplasty (UPPPG) is a modified UPPP with limited resection of the base of the tongue in which both the retropalatal and retrolingual regions of the UA are enlarged. 

Maxillomandibular advancement osteotomy

The midface, palate, and mandible are moved forward in this procedure, increasing the space behind the tongue and increasing tension on the genioglossus muscle. This surgery is more extensive than any of the others described. It is usually reserved for patients in whom other treatment modalities fail.

Other surgical options

Laser-assisted uvulopalatoplasty is successful for reducing snoring in 90% of patients, but the success rate in patients with SDB is not clear. It may cause more scarring than UPPP, and it could potentially worsen apnea. Worsened OSA has been observed in the early postoperative period after laser-assisted uvulopalatoplasty. Laser-assisted uvulopalatoplasty is not recommended for the treatment of OSA until further data are available.

Laser midline glossectomy and lingualplasty are performed to enlarge the retrolingual region by using a laser to remove a portion of the posterior aspect of the tongue. The role of these procedures in the management of SDB has yet to be defined.

Nasal surgery includes septoplasty, turbinectomy, and polypectomy and may be useful as an adjunct to other procedures or to improve CPAP compliance. Nasal surgery by itself is rarely effective for the treatment of OSA. 

One study of radiofrequency volumetric reduction of the soft palate in 12 patients demonstrated success in treating snoring, but data regarding adequate treatment of SDB are lacking.³⁴ Data from large controlled studies are required before this technique can be recommended for the treatment of SDB. Radiofrequency volumetric reduction appears to decrease morbidity compared with UPPP, laser-assisted uvulopalatoplasty, and lingualplasty.

Finally, animal studies of radiofrequency volumetric reduction of the tongue have shown volume reduction in tongue tissue after treatment. Results of human studies are pending.

Consultations

Patients should undergo complete evaluation by a sleep disorders specialist and a dental professional, both of whom should be experienced in OA therapy; their close collaboration is required.
 
Interestingly, Antic et al report that compared with physician-directed care, simplified nurse-led care was less costly and did not produce inferior care for the management of moderate-to-severe OSA.³⁵

Diet

Because obesity is a major predictive factor for OSA, weight reduction reduces the risk of OSA. The best data suggest that a 10% reduction in weight leads to a 26% reduction in RDI. Benefits of weight reduction in patients with SDB include the following:

• Decreased RDI
• Lowered blood pressure
• Improved pulmonary function and arterial blood gas values
• Improved sleep structure and snoring
• Possible reduction of optimum CPAP pressure required 

Activity

Patients should restrict their body positions during sleep. SDB is worse in the supine position, and some patients have apnea only in this position. Preventing the patient from assuming the supine position by using devices such as a snore ball (eg, a tennis ball sewed onto the back of the patient's pajamas) or a gravity-activated position monitor may be useful. However, these devices are cumbersome and appear to benefit only those patients with mild OSA. Patients with marked obesity may benefit from sleeping in an upright position. Additionally, the FDA has approved a specially designed pillow (PillowPositive) for the treatment of snoring and mild OSA, which maintains the patient's head and neck position during sleep to optimize UA patency.

Patients should avoid smoking. Smoking increases the risk of snoring and apnea. Smoking cessation appears to decrease the risk. Individuals who smoke are also more likely than those who do not smoke to report problems with going to sleep, maintaining sleep, and daytime somnolence.

Patients should avoid drinking alcohol and using other sedatives known to make apnea worse. Finally, patients should avoid sleep deprivation.

Medication

Although acetazolamide, medroxyprogesterone, fluoxetine, and protriptyline have been used to treat obstructive sleep apnea (OSA), none of these medications is recommended. Modafinil is an FDA-approved medication for use in patients who have residual daytime sleepiness despite optimal use of CPAP. The most improvement has been seen in patients who have taken modafinil at doses of 200-400 mg/d. Armodafinil, the R-enantiomer of modafinil, is also now FDA approved for use in these patients.

CNS stimulants

May be used to promote daytime wakefulness in sleep apnea patients who have residual daytime sleepiness despite optimal use of CPAP. Modafinil and armodafinil are indicated for OSA.

Modafinil (Provigil)

Mechanism of action in wakefulness unknown. Has wake-promoting actions similar to sympathomimetic agents. Indicated as adjunctive treatment to standard therapy for obstructive sleep apnea-hypopnea syndrome.

Dosing

Adult

200 mg PO in morning or prn; may increase to 400 mg/d if needed

Pediatric

<16 years: Not established

Interactions

May decrease levels of cyclosporine or steroidal contraceptives, and, to a lesser degree, theophylline; may increase drug concentration levels of diazepam, propranolol, and phenytoin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor patients closely for signs of misuse or abuse, especially those with a history of drug or stimulant abuse such as with methylphenidate, amphetamine, or cocaine; leukopenia has been reported in pediatric patients

Armodafinil (Nuvigil)

R-enantiomer of modafinil (mixture of R- and S-enantiomers). Elicits wake-promoting actions similar to sympathomimetic agents, although pharmacologic profile is not identical to sympathomimetic amines. In vitro, binds dopamine transporter and inhibits dopamine reuptake. Not a direct- or indirect-acting dopamine receptor agonist. Indicated to improve wakefulness in individuals with excessive sleepiness associated with narcolepsy, obstructive sleep apnea-hypopnea syndrome, or shift-work sleep disorder.

Dosing

Adult

150 mg PO qam; may increase dose, not to exceed 250 mg/d

Pediatric

<17 years: Not established
>17 years: Administer as in adults

Interactions

Weakly induces CYP1A2 and CYP3A; may decrease levels of drugs metabolized by CYP1A2 (eg, theophylline) and CYP3A (eg, cyclosporine, midazolam, triazolam, steroidal contraceptives); may inhibit CYP2C19 activity, thereby increasing serum levels of CYP2C19 substrates (eg, omeprazole, phenytoin, propranolol)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hepatic impairment and decrease dose with severe hepatic impairment; serious rash, including Stevens-Johnson syndrome, has been reported; other serious hypersensitivity reactions include angioedema, anaphylactoid reactions, and multiorgan hypersensitivity reactions; psychiatric adverse events (eg, mania, delusions, hallucinations, suicidal ideation) have been reported with modafinil; may increase blood pressure; monitor patients closely for signs of misuse or abuse, especially those with a history of drug or stimulant abuse (eg, methylphenidate, amphetamine, or cocaine)

Follow-up

Further Outpatient Care

Many obstructive sleep apnea (OSA) patients note an immediate improvement in alertness, concentration, and memory, but achieving maximum improvement in neurocognitive symptoms may take as long as 2 months. Adequate adherence is defined as routine use of CPAP for more than 4.5 hours per night. Follow-up visits should be scheduled at least once after CPAP treatment is first started and at least yearly thereafter. Follow-up evaluation is required to ensure symptomatic improvement, CPAP compliance, and equipment maintenance.

CPAP therapy - Compliance issues

Nasal congestion can be treated with antihistamines and/or topical corticosteroids. Nasal dryness can be treated with topical saline sprays or humidification. If the air generated by the unit is too cold, the patient should use a heated humidifier.

If excessive air leaks through the mouth, patients should use a chin strap to keep their mouths closed or they should try an oronasal mask. Consider consultation with an otolaryngologist to rule out sinus dysfunction. If a poorly fitting mask causes skin breakdown and/or air leaks, patients should try mask of different sizes and/or models; a variety of interfaces are now available.

Patients with claustrophobia may try using nasal pillows or behavioral management. If patients feel a sensation of increased resistance to expiration, use of a CPAP unit with a ramp feature is indicated. This unit permits the patient to fall asleep with little or no pressure applied, and the pressure gradually increases to the set optimal level over a predetermined interval (usually 15-30 min). BiPAP may be used as an alternative. 

OA therapy

Regular follow-up with a dental professional allows for adjustment of the dental appliance. The first adjustment is based on symptoms. Follow-up also helps ensure compliance with therapy and helps identify adverse effects or complications, device deterioration, or maladjustment.

Follow-up PSG after the final adjustment of the OA ensures that OSA is adequately treated. However, PSG should be deferred until an adequate symptomatic response and patient comfort are achieved with adjustments to the appliance.

Follow-up with a sleep disorders specialist ensures that OSA is adequately treated. Regular follow-up is required until patient's symptoms resolve and until PSG shows no evidence of clinically significant SDB. Follow-up also helps in determining if another treatment modality is required because of treatment failure or intolerance.

Close collaboration is required between the sleep disorders specialist and dental professional. Pay attention to compliance, comfort, dental complications, and evidence of recurrent OSA.

Surgery 

Follow-up with a sleep disorders specialist ensures that OSA resolves. Follow-up PSG is essential to determine if OSA has been treated adequately. It should be performed after the surgical site has adequately healed. The most effective timing appears to be 4-6 months after surgery to ensure steady body weight, completion of healing, and stabilization of sleep architecture.

Patient Education

A physician, trained technician, or nurse should train patients receiving CPAP for at least the first month of therapy. This training promotes long-term adherence with treatment. For excellent patient education resources, visit eMedicine's Ear, Nose, and Throat Center and Sleep Disorders Center. In addition, see eMedicine's patient education articles Snoring, Sleep Disorders and Aging, and Insomnia.

Miscellaneous

Medicolegal Pitfalls

The following measures should be undertaken in patients with OSA:  

• Assess the patient's risk for motor vehicle accidents. The patients at highest risk should immediately be warned of the potential risk of driving until effective therapy is started.
• Warn any patient with OSA of the potential dangers of driving while sleepy. Inform the patient of the potential personal and social risk.
• Provide additional counseling depending on other risk factors (eg, occupation).
• Advise patients to not drive until their OSA is treated adequately.
• Provide additional counseling to family members as appropriate, and help patients explore alternatives to driving if they are unaware of their sleepiness or if they are unwilling to acknowledge their increased risk. 
• Diagnose and treat OSA expeditiously.
• Document in writing any warnings, concerns, and/or recommendations given to the patient. This documentation reinforces the importance of the message to the patient and helps reduce the risk of legal liability for medical personnel.
• Routinely plan follow-up to determine the effectiveness of therapy and compliance with therapy. Ascertain whether daytime sleepiness is substantially reduced or eliminated. Continue evaluations at regular intervals until therapy controls the patients' condition.

Assess the risk of driving in any patient with OSA. Criteria that increase this risk are as follows: 

• The patient has had previous motor vehicle accidents.
• The patient has had near-miss incidents while driving.
• The patient has evidence of severe daytime sleepiness or impaired driving performance. 

• With the categorical approach, the clinician is obligated to report patients who have specified medical conditions, such as epilepsy. In these states, the reporting obligation is based on diagnosis alone.
• With the functional approach, the clinician is required to report patients with certain medical conditions only if the clinician believes that a condition impairs the patient's driving ability. 

• In states with permissive reporting mechanisms, the clinician should at a minimum notify the state's department of motor vehicles when a highest-risk patient (ie, a patient with OSA with severe daytime sleepiness and a previous motor vehicle accident or near-miss incident) (1) is unwilling to restrict driving until effective treatment is started, (2) is noncompliant or unwilling to accept treatment, or (3) has an untreatable condition or one that is not amenable to expeditious treatment ( £ 2 mo of diagnosis).
• Increased occupational exposure to driving or increased occupational risk for an accident of substantial importance to the public may be other indications for reporting. Examples of patients in this situation are truck drivers who are transporting hazardous waste and school bus drivers. 
• A diagnosis of OSA without additional risk factors for impaired driving should not be the basis for reporting a patient unless required by state law.

A US Federal Aviation Administration specification letter entitled "Sleep Apnea Evaluation Specifications" states that the complications of OSA present a risk to flying safety and recommends an initial workup, acceptable treatments, and follow-up for pilots being evaluated for OSA.

Multimedia

Media file 1: 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.

Media file 2: Segment of a nocturnal polysomnogram shows an episode of mixed apnea. The initial portion of the apnea is central in origin, with cessation of both airflow and respiratory movements. The latter part of the apnea is obstructive, with an absence of airflow despite the resumption of respiratory movements.

Media file 3: Segment of a nocturnal polysomnogram shows an episode of central apnea. Airflow and respiratory movements have both ceased.

Media file 4: 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.

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Keywords

obstructive sleep apnea, OSA, sleep apnea, apnea, sleep disorder, snoring, sleep-related disorder, sleep disordered breathing, SDB, central apnea, obstructive apnea, mixed apnea, hypopnea, upper airway resistance syndrome, UARS, nasal continuous positive airway pressure, nasal CPAP, CPAP, apnea index, AI respiratory disturbance index, RDI, apnea-hypopnea index, AH, PSG, polysomnography, pickwickian syndrome, excessive daytime sleepiness, EDS, uvulopalatopharyngoplasty, UPPP, respiratory event–related arousal, RERA, oral appliance, OA, bilevel positive airway pressure, BiPAP, sleep-related breathing disorder, SRBD

Contributor Information and Disclosures

Author

Ralph Downey III, PhD, DABSM, FAASM, Associate Professor of Medicine, Pediatrics, and Neurology, Loma University School of Medicine; Adjunct Associate Professor, Department of Psychology, University of California at Riverside; Chief, Sleep Medicine, Loma Linda University Medical Center and the Loma Linda University Children's Hospital
Ralph Downey III, PhD, DABSM, FAASM is a member of the following medical societies: American Academy of Sleep Medicine
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

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.

Medical Editor

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.

Pharmacy Editor

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

Managing Editor

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: Boehringer Ingleheim Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching

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.

Available clinical treatment guidelines include the following:

• Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances: an update for 2005
• Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Obstructive Sleep Apnea.
• Practice parameters for the medical therapy of obstructive sleep apnea
• Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome: an update for 2007
• Practice parameters for the indications for polysomnography and related procedures: an update for 2005

Available clinical trials include the following:

• Minimally Invasive Tongue Suture For Obstructive Sleep Apnea
• Cardiovascular Phenotype Study in Patients With Obstructive Sleep Apnea Syndrome
• Coblation-Tonsillotomy vs Electrocautery-Tonsillectomy for the Treatment of Obstructive Sleep Apnea (OSA) in Children
• Sexual Dysfunction And Hypotestosteronemia In Patients With Obstructive Sleep Apnea Syndrome And Its Effects With CPAP Therapy
• Effects of Continuous Positive Airway Pressure (CPAP) in Patients With Resistant Hypertension and Obstructive Sleep Apnea (OSA)

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