AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Obstructive sleep apnea (OSA) occurs in persons of all age groups, across all ethnicities, and of both sexes. OSA is an increasingly prevalent condition in modern society, affecting approximately 5% of the white population. OSA is associated with an increased incidence of pathologic outcomes, particularly stroke, if it is not treated. Therefore, clinicians must know how to diagnose and effectively treat patients with OSA. The combination of clinical evaluation of symptoms and polysomnography (PSG) provides the clinician with data to diagnose and treat patients.

The patient's spouse often urges the patient to seek clinical evaluation because of loud snoring that forces the couple to sleep apart, and the spouse often accompanies the patient to the visit. Because many patients are not aware of their loud snoring, they come reluctantly to the first visit.

For other patients, the absence or cessation of snoring—and not its presence—is the impetus for the visit. The quiet time is when the snorer has apnea, during which the airway is closed. This time varies greatly among patients but can last 10 seconds to 2 minutes. At the end of the apneic period, a release of withheld air leads to sudden noisy reverberations, arousals from sleep, restlessness, and other various perturbations of sleep that interrupt the spouse. Depending on the severity of the apnea, the patient may repeat an apneic episode as soon as one ends. On a typical night, patients may have several hundred apneic events. When PSG confirms these events, patients may be surprised to learn of their occurrence and of the grave risks the events pose to their health.

Historical perspectives

The dramatic nature or course of apnea makes one wonder why so much time elapsed before medical science recognized its importance. In 1965, Gestaut, Tassinari, and Duron in France and Jung and Kuhlo in Germany provided the first accurate clinical descriptions of OSA at nearly the same time.

The first known successful treatment for OSA was tracheostomy, which Elio Lugaresi and coworkers first described in 1970 in Italy. For the next 11-16 years, tracheostomy was the only established beneficial remedy for patients with OSA.

In 1981, Dr Colin Sullivan introduced continuous positive airway pressure (CPAP) as a treatment for OSA. 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).

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.¹

Definition

According to the American Academy of Sleep Medicine (AASM) International Classification of Sleep Disorders: Diagnostic and Coding Manual, Second Edition,² "OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) upper airway [UA] obstruction occurring during sleep. By definition, apneic and hypopneic events last a minimum of 10 seconds." See Media File 2. Hypopneas must be associated with oxygen desaturation of at least 4%, whereas OSA events are not required to be associated with a decrease in oxygen saturation. In central apnea, ventilatory effort is absent and, therefore, airflow ceases (see Media File 3). In mixed apnea, ventilatory effort (central apneic component) is not observed initially, but ventilatory effort (obstructive apnea component) follows (see Media File 2). The focus of this article is OSA.

The following Medscape CME courses may be of interest:

• Patients With Stroke and Obstructive Sleep Apnea at Increased Risk for Early Death
• Obstructive Sleep Apnea Is Risk Factor for Death in Stroke Patients
• Guidelines Issued for Positive Airway Pressure Titrations in Obstructive Sleep Apnea

The following related eMedicine articles may also be of interest:

• Snoring and Obstructive Sleep Apnea, CPAP
• Snoring and Obstructive Sleep Apnea, Physiologic Approach
• Snoring and Obstructive Sleep Apnea, Prosthetic Management
• Snoring and Obstructive Sleep Apnea, Surgery
• Snoring and Obstructive Sleep Apnea, Upper Airway Evaluation

Pathophysiology

Available evidence indicates that pharyngeal collapse is responsible for the recurrent UA obstruction during sleep in patients with OSA. The retropalatal area is the primary, but not only, site of airway narrowing. Airway narrowing occurs in ovoid geometric progression, with narrowing occurring both laterally and anteroposteriorly.

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.³

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.⁴

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

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 Epworth Sleepiness Scale 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.⁵ 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.

The Sleep Heart Health Study⁶ 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 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 apnea-hypopnea index (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.

Cardiovascular comorbidities

Although the data are not conclusive, the increased relative risk of hypertension in patients with SDB persists after the results are adjusted for obesity, male sex, age, and BMI. Data linking SDB and ischemic heart disease are relatively imprecise. Most data are from epidemiologic studies about snoring, which is used as a surrogate for SDB. Results from cross-sectional and longitudinal studies on snoring indicate that cardiovascular disease is more common in people who snore than in those who do not snore.

Pulmonary arterial hypertension, right ventricular dysfunction, and cor pulmonale may occur in patients with lung disease and coexisting OSA. As a decision rule in the care of pulmonary hypertension, OSA must be excluded before primary pulmonary hypertension is diagnosed.

Cardiac arrhythmias, including tachycardia, malignant ventricular arrhythmia, and bradycardia, are described and may occur during apnea. OSA may cause sudden death during sleep.

Reliable data are not available to determine if the overall mortality rate is increased in patients with SDB. OSA likely has an effect on mortality because of its association with an increased risk of cardiovascular and cerebrovascular disease. Some studies demonstrate a reduced lifespan in patients with untreated OSA.

OSA is associated with an increased risk of type 2 diabetes. Whether OSA causes diabetes type 2 or whether it is associated with insulin resistance and diabetes is unclear. Sleep fragmentation and deprivation and hypoxemia are thought to play a role 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 2:1. Differences in RDI are greatest in persons aged 20-45 years, in whom the male-to-female ratio may be as high as 3-4:1. The index sharply increases in both sexes after age 55 years. The male-to-female ratio is not markedly different before puberty and after menopause.

Age

Although SDB can occur in persons of any age, it is most commonly recognized in those aged 50-70 years.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Clinical history and physical examination findings are of paramount importance in the evaluation of a patient with suspected SDB. Management decisions should be made in the context of the complete clinical picture because PSG evidence by itself is insufficient to determine if a patient has clinically significant SDB. Moreover, physical findings alone cannot predict OSA.

• Cardinal symptoms of sleep apnea
  
  
  • Loud, habitual snoring
  • Apneic events witnessed or reported by spouses or significant others
  • Daytime sleepiness
• Predictive value
  
  
  • Disrupted snoring: A history of disruptive snoring has 71% sensitivity in predicting SDB.
  • Disruptive snoring and witnessed apneas: These factors 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 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.
• Other symptoms
  
  
  • Nonrestorative sleep
  • A choking sensation or gasping during the night
  • Morning headaches, probably due to hypercapnia during sleep
  • Insomnia
  • Restless sleep
  • Sore throat or dry mouth in the morning
  • 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 disease (GERD), due to the high negative intrathoracic pressure during apneas

Physical

• Obesity is a risk factor for OSA.
  
  
  • 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 study⁷ showed that the number of people with a BMI greater than 40 has tripled since 2000.
    
  • Patients with obesity hypoventilation syndrome and some patients with OSA may have evidence of pulmonary hypertension and right-sided heart failure.
    
    
• BMI and neck circumference are predictors of OSA.
  
  
  • Neck circumference may correlate with OSA better than BMI. In 1 study, subjects with OSA had necks 4 cm larger than subjects without OSA. In addition, neck circumference 40 cm or larger had a sensitivity of 61% and a specificity of 93% for OSA, regardless of the person's sex.
    
    
  • The airway appears crowded and small.
    
    
• UA abnormalities include severe nasal obstruction, low-hanging soft palate, large (hypertrophied) uvula, enlarged tonsils and/or adenoids, and macroglossia. (See also the eMedicine article Snoring and Obstructive Sleep Apnea, Upper Airway Evaluation.)
  
• Systemic arterial hypertension is present in approximately 50% of patients with OSA.
  
• Craniofacial abnormalities, including malocclusion of the jaws with anterior overjet of the incisor teeth, may be present.
  
• Women with SDB have physical features different from those of men with SDB.
  
  
  • Women may have a high, arched hard palate.
    
  • Women may have BMIs lower than those of men.
    
  • In women, the neck circumference is relatively normal.

Causes

• Obesity
• Structural factors
  
  
  • Structural factors are most likely to be relevant in patients with OSA who are not obese.
  • Craniofacial features more common in patients with SDB than in unaffected individuals include facial elongation, posterior facial compression, reduced posterior and superior air spaces, retrognathia, and inferior displacement of the hyoid.
  • A brachycephalic head appears to be a risk factor for SDB, particularly in white persons. This head form reduces the dimensions of the UA.
  • 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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Loud disruptive snoring
Sleep-related panic attacks
Laryngospasm related to GERD
Dyspnea secondary to pulmonary edema or cardiac disease
Nonobstructive alveolar hypoventilation

Conditions associated with EDS

Residual excessive sleepiness in nasal CPAP-treated OSA and/or hypopnea syndrome
Central sleep apnea
Delayed sleep-phase syndrome
Employment involving work in rotating shifts
Idiopathic hypersomnia
Medical conditions that may interfere with sleep (ie, asthma, chronic obstructive pulmonary disease, congestive heart failure, chronic pain and discomfort)
Medication, drug, and alcohol use
Narcolepsy
Idiopathic hypersomnia
Periodic limb movement disorder
Primary snoring (without other evidence of SDB)
Sleep deprivation (extremely common and must be excluded)
Behaviorally induced insufficient sleep syndrome
Silent apnea (UPPP may correct snoring due to floppy tissue, but airway collapse may persist. Exclude this condition with PSG.)

Other conditions that may be mistaken for OSA

Cheyne-Stokes respiration
Mucopolysaccharide storage diseases
Nocturnal seizures
Paroxysmal nocturnal dyspnea
Obesity hypoventilation syndrome (pickwickian syndrome)
Sleep panic attacks
Sleep-related GERD
Sleep-related laryngospasm
Swallowing disorders (aspiration during sleep)

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Routine laboratory tests usually are not helpful 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 (or another cause of clinically significant pulmonary hypertension) is suspected.

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 in 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 in the initial evaluation of SDB patients is of uncertain benefit and should not be performed unless a specific indication is present.
  
• 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. PSG is indicated for the diagnosis of possible OSA. A minimum duration of 6 hours of PSG evaluation is required for diagnosis. Standard diagnostic PSG may be performed in a health care facility or in the patient's home with a trained technician in attendance.

The 2005 AASM diagnostic criteria and definitions are as follows:

• 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,² 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.

In-laboratory overnight PSG
 
In-laboratory overnight PSG has been the standard method for evaluating SDB for many years. Complete 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).

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

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

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. 

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. Finally, if results of the first PSG are of poor quality, a repeat study is indicated. 

Limited PSG studies
 
A portable monitoring device is being used for limited-channel, in-laboratory diagnostic PSG studies (cardiopulmonary monitoring). ASDA guidelines suggest that limited PSG should include assessments of oronasal airflow, chest-wall respiratory effort, ECG findings, and oxyhemoglobin saturation.

Data from in-laboratory limited PSG are fairly well correlated with results of standard PSG. However, data to compare unattended cardiopulmonary recordings in the home setting with standard PSG findings in the sleep laboratory are limited. The role of unattended PSG studies for diagnosing SDB is uncertain because of a lack of supportive data. Limited PSG studies may be indicated in the following settings:

• Patients with severe symptoms indicative of OSA require limited studies when treatment is urgently needed and when standard PSG is not readily available.
• Patients with established OSA who require follow-up studies should undergo limited PSG.
• Patients who cannot be evaluated in the sleep laboratory should undergo limited PSG.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

Overview

Little evidence supports the treatment of asymptomatic patients with an RDI in the mild range. What makes this finding confusing is the independent association of snoring and morbidity. Patients with mixed apneas should be treated as if they have OSA because OSA can be life threatening and because treatment of OSA commonly abates central sleep apnea. Only health care professionals with adequate training in the evaluation and management of OSA should prescribe therapy for patients with SDB. CPAP therapy should not be prescribed without PSG confirmation of the correct pressure level for CPAP because no standardized pressure value has been established on the basis of age or BMI.

The primary treatment for OSA is positive pressure therapy, and nasal CPAP is the most commonly prescribed type of therapy. Other forms of positive airway pressure include bilevel positive airway pressure (BiPAP) and variable CPAP. Nightly use of CPAP for at least 4 hours is required to produce consistent ameliorative effects. Data show that compliance at 1 month is predictive of compliance at 3 months. Whether patients like CPAP depends on their perception of improvement and not on the severity of their disease, as judged by the clinician.

Variable CPAP (sometimes called auto-CPAP) is administered by using a new device whose niche has yet to be defined. The basis for variable CPAP is that the changes in pressures a patient needs depend on factors such as body position, sleep stages, sleep deprivation, sedative use, and alcohol use, among others.

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.

Application of adequate levels of nasal CPAP during sleep almost always resolves obstructive apnea and/or hypopnea, oxyhemoglobin desaturation, and RERAs from sleep. It also results in adequate sleep continuity.

Effectiveness

CPAP therapy improves daytime hypersomnolence, daytime alertness, and neuropsychiatric functioning. CPAP improves right-sided heart function, left-sided heart function in patients with left ventricular dysfunction, and systemic and pulmonary hypertension. Patients have improved quality of life, and some studies report improved survival rates. The benefits parallel those observed after tracheostomy. CPAP is effective for treating mixed apneas and some central apneas.

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 al⁸ 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 al⁹ and Petelle et al¹⁰ 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

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. 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.

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
• May reduce 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

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Although acetazolamide, medroxyprogesterone, fluoxetine, and protriptyline have been used to treat 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.

Drug Category: CNS stimulants

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

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Outpatient Care

Nasal CPAP therapy   

Many 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

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal 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.