Sleep Apnea

 

INTRODUCTION

Background: Sleep apnea occurs during sleep when a cessation of airflow occurs for at least 10 seconds (usually 20-30 s but rarely >2 min). The apneas (absences of breath) are accompanied by snoring, sleep arousals, and hypoxia.

The term sleep apnea describes 2 major sleep-related clinical problems: (1) obstructive sleep apnea (OSA) and (2) central sleep apnea. OSA is caused by upper airway (UA) obstruction at the level of the pharynx. It is the most common form of sleep apnea. Central apnea is the result of impairment in respiratory control of breathing.

Sleep apnea syndrome encompasses a spectrum of sleep-related breathing disorders ranging from simple snoring to severe sleep apnea with associated neurocognitive deficits, residual daytime sleepiness, pauses in breathing, and cardiovascular consequences such as hypertension and stroke. UA resistance syndrome is a condition within this spectrum that is intermediate in severity to these 2 extremes. Patients with UA resistance syndrome have clinical features closely related to OSA, but frank apneas are absent.

Historical perspectives

The term pickwickian syndrome originated with the obese character Joe in Charles Dickens' novel The Posthumous Papers of the Pickwick Club. It often is used incorrectly as a synonym for OSA. Pickwickian syndrome should only be used to describe obesity hypoventilation syndrome.

Gestaut and associates demonstrated the features of sleep apnea in 1965 and suggested that apneas are responsible for sleep disruption and daytime sleepiness. OSA was successfully treated with tracheostomy in 1969. Nasal continuous positive airway pressure (CPAP) therapy was first described in 1981 and provided a noninvasive alternative to tracheostomy for management of OSA. During the same year, a less invasive surgical procedure, uvulopalatopharyngoplasty, was introduced for the treatment of OSA. A surgical protocol for the step-wise management of patients with sleep disordered breathing (SDB) was proposed in 1988 (ie, the Riley-Powell-Stanford surgical protocol). Increased interest in the use of oral appliances for the treatment of SDB has developed over the past decade. Newer and less invasive surgical techniques currently are under evaluation.

Definition

According to the International Classification of Sleep Disorders: Diagnostic and Coding Manual, the description of OSA includes (1) repetitive episodes of UA obstruction during sleep, (2) arterial oxygen desaturation in association with apneas, (3) daytime hypersomnolence, and (4) snoring.

Sleep apnea is defined in adults as a temporary absence or cessation of breathing during sleep for 10 or more seconds. In obstructive apnea, ventilatory effort is present but airflow ceases due to closure of the UA. In central apnea, ventilatory effort is absent and, therefore, airflow ceases. In mixed apnea, ventilatory effort is not observed initially (central apnea component) but ventilatory effort follows (obstructive apnea component).

Partial reductions in inspiratory airflow (hypopneas) also have been identified in patients with SDB. A hypopnea is a decrease in inspiratory flow to 50% of baseline and is associated with desaturation.

Apnea index

The apnea index (AI), which is the total number of apneas during sleep divided by the total number of hours of sleep, is a relative measure of apnea severity. Traditionally, an AI of 5 or more has been used to define the presence of OSA. Many laboratories are reporting the apnea-hypopnea index, also known as the respiratory disturbance index (RDI). This index is derived by dividing the sum of apneas and hypopneas by the total number of hours of sleep.

 

Pathophysiology: The available evidence indicates that pharyngeal collapse is responsible for the recurrent UA obstruction during sleep in OSA. The mechanisms responsible for recurrent UA closure still are not completely understood. The following mechanisms have been implicated in the pathophysiology of OSA:

Upper airway size and shape

Compared to healthy subjects, patients with OSA appear to have a smaller pharyngeal airway during wakefulness. The normal pharyngeal airway has a horizontal configuration (horizontal diameter greater than anteroposterior diameter). These patients have lateral narrowing of the UA due to an anteroposterior configuration. This appears to be an essential factor in the causation of SDB. In patients with OSA, increased recruitment of certain UA muscles is required to maintain UA patency in the awake state. The loss of muscle tone during sleep could precipitate UA obstruction in predisposed individuals. Inspiratory UA narrowing has been noted to be worse during sleep compared to wakefulness.

Changes in transmural pressure in the upper airway

The subatmospheric intrathoracic pressure generated by the thoracic muscles during inspiration is transmitted to the airway, resulting in a reduced (subatmospheric) pressure along the length of the airway. This decrease in intraluminal pressure (with a resultant decrease in transmural pressure) has been considered an essential factor in the causation of UA narrowing/obstruction in OSA.

Evidence exists that extraluminal pressure also may contribute to UA narrowing/obstruction during sleep by reducing the transmural pressure across the UA. The extraluminal pressure at which airway closure occurs in patients with OSA has been termed the critical pressure. During sleep, the pharyngeal airway becomes more hypotonic (thus more compliant) due to the reduced ventilatory motor output. Under these conditions, the UA behaves as a collapsible tube that is subject to the pressures both from within (intraluminal) and from outside (extraluminal). Adipose tissue surrounding the pharyngeal airway and gravitational forces imposed on the UA by structures in the head and neck due to the recumbent posture are examples of extraluminal pressure causing UA collapse.

Upper airway–dilating muscle activity and upper airway compliance

Patients with OSA have increased UA-dilating muscle activity during sleep and wakefulness compared to healthy subjects. Despite this, decreased UA-dilating muscle tone during sleep has been associated with reduced UA size, increased UA compliance, and increased UA resistance in patients with OSA.

Thoracic caudal traction

Thoracic muscle activity during inspiration is thought to exert caudal traction on the UA, resulting in decreased collapsibility of the UA (as evidenced by a significant decrease in critical pressure). A loss of caudal traction forces may contribute to increasing UA collapsibility.

Other factors

Other factors implicated in the pathophysiology of OSA include the following:

 

  • Patients with SDB may have blunted/abnormal UA neuromuscular reflexes that predispose to UA collapse.

     

  • Surface mucosal forces may play an important role in preventing UA opening.

     

  • Changes in vasomotor tone in the UA have been shown to affect UA resistance.

     

  • Alcohol and benzodiazepines have been shown to selectively depress UA muscle activity and may contribute to UA collapsibility.

Summary of pathophysiology

Recurrent UA obstruction during sleep is due to a complex interaction of several anatomical, physiological, and neuromuscular mechanisms. A small and highly compliant pharynx appears to be an essential ingredient. A collapsing transmural pressure is generated by the combination of a subatmospheric intraluminal pressure and a positive extraluminal pressure. UA compliance is increased due to decreased activity of UA-dilating muscle activity and due to the loss of thoracic caudal traction. If obstruction occurs, the mucosal adhesive forces prevent the UA from opening up, thus prolonging the obstruction.

 

Frequency:

  • In the US: Although previous studies estimated the prevalence of SDB to be 2% for middle-aged women and 4% for middle-aged men, recent studies show much higher prevalence, at 4% for women and 9% for men (Young, 1993). The National Commission on Sleep Disorders Research has estimated that minimal SDB (RDI >5) affects 7-18 million people in the United States and that more severe cases (RDI >15) affect 1.8-4 million people. Prevalence increases with age. Approximately 92% of affected women and 80% of affected men remain undiagnosed.

Mortality/Morbidity: Clinically, little doubt exists that sleep apnea can affect 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 apnea, and end-organ systems can be affected by profound and repetitive hypoxia.

  • Excessive daytime sleepiness

    • This is the presenting complaint of most patients. It results in impaired daytime performance and neurocognitive deficits. Hypersomnolence probably results from fragmented sleep, which, in turn, is due to repeated arousals. Sleep continuity helps determine sleep restoration.

    • For optimal alertness, sleep should occur in uninterrupted segments of longer than 10 min. Patients with clinically significant SDB have many arousals, some with more than 500 per night.
  • Performance and neurocognitive deficits

    • Patients with OSA who are subjected to sleep deprivation have significant impairment of daytime functioning, intellectual capacity, memory, and motor coordination. These impairments usually resolve with successful treatment of SDB.

    • Performance on psychomotor vigilance tasks may be impaired, resulting in decreased capacity to maintain attention and concentration. These deficits usually return to baseline following successful treatment of SDB.

    • Mood impairment also may occur; depression and anxiety are common. These usually resolve with treatment of SDB.
  • Motor vehicle accidents

    • According to one study, patients with OSA have a 7-times higher rate of motor vehicle accidents compared with healthy controls.

    • Patients with OSA do not perform as well as healthy controls on driving simulator tests, but performance improves to normal following treatment.


  • Medical comorbidity

    • SDB appears to increase the risk of cardiovascular and cerebrovascular disease.

    • Patients with OSA have an increased risk of hypertension (twice the risk), coronary artery disease (3 times the risk), and cerebrovascular disease (4 times the risk) compared to the general population. Unfortunately, many of the studies investigating the effects of OSA on medical comorbidity were poorly designed.

    • Although the data are not conclusive, the increased relative risk of hypertension in patients with SDB persists after adjusting for obesity, male sex, age, and body mass index. Data linking SDB and ischemic heart disease are less precise. Most data are from epidemiological studies on snoring, used as a surrogate for SDB. Cross-sectional and longitudinal studies on snoring indicate that cardiovascular disease is more common in those who snore versus those who do not snore.

    • Pulmonary arterial hypertension, right ventricular dysfunction, and cor pulmonale usually are observed in patients with OSA who have significant hypoventilation and/or coexisting lung disease and are due to chronic hypoxemia. OSA alone usually is not associated with clinically significant levels of pulmonary arterial hypertension or cor pulmonale. Patients with OSA who have decompensated right ventricular failure should be evaluated for other possible causes of pulmonary hypertension.

    • Cardiac arrhythmias, including tachycardia, malignant ventricular arrhythmia, and bradycardia, have been described and may occur during apneas. OSA may cause sudden death during sleep.

    • Reliable data are not available to determine if the overall mortality in patients with SDB is increased. An impact on mortality is likely because of the increased risk of cardiovascular and cerebrovascular disease. Certain studies demonstrate a reduced lifespan in untreated patients with OSA.

Race:

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

Sex:

  • The male-to-female ratio in adults is approximately 2:1. The RDI differences are greatest in persons aged 20-45 years (male-to-female ratio may be as high as 3-4:1). The index increases sharply in both sexes after age 55 years. The male-to-female ratio is not markedly different prior to puberty and after menopause.
  • Progesterone may play a protective role in premenopausal women. Androgenic patterns of body fat distribution (truncal deposition, including the neck area) predispose to the development of SDB.
  • Sex hormones may have an effect on the neurological control of UA-dilating muscles and ventilation.

Age:

  • Although SDB can occur at any age, clinically it has been recognized most commonly in persons aged 50-70 years.

CLINICAL

History: Clinical history and physical examination 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 polysomnographic evidence by itself is insufficient to determine if a patient has clinically significant SDB. Performing detailed evaluations on all patients in which SDB is suggested is too expensive; therefore, clinical screening of patients is essential.

Clinical screening is necessary to determine if a patient’s symptoms are due to a condition other than OSA also known to produce increased daytime somnolence. Some of these alternative diagnoses obviate the need for standard diagnostic nocturnal polysomnography (PSG), while others are strong indicators for PSG evaluation (eg, narcolepsy, periodic limb movement disorder).

The typical history of a patient with OSA is that of a middle-aged man who is obese and snores loudly, is excessively sleepy, and is reported to stop breathing at night. Snoring is nearly ubiquitous in patients with OSA. Most patients are sleepy due to frequent sleep arousals (brief 3-s interruptions of sleep viewed on electroencephalogram [EEG]). When taking a patient's history, excluding other causes of frequent sleep arousals (eg, periodic limb movement disorder, depression, medical disorders, environmental interferences) is important.

  • The cardinal symptoms of sleep apnea include the 3 Ss, as follows:
    • Snoring (loud, habitual)

       

    • Spousal apnea report/witnessed apneas

       

    • Sleepiness (daytime)
  • A history of disruptive snoring has a 71% sensitivity for predicting SDB. Disruptive snoring and witnessed apneas together have a 94% specificity for SDB.
  • Obtaining a history from someone who has observed the patient's sleep behavior is important. Patients usually are unaware of snoring and/or sleepiness or may minimize these symptoms. Sleepiness may develop insidiously. Patients may be unaware that they are sleepy (ie, they forget how normal alertness feels).
  • Patients should be questioned about drowsiness in boring or monotonous situations and about sleepiness while driving.
  • Women are twice as likely as men to not report snoring and apneas, even after correcting for the RDI.
  • Women commonly present with symptoms that are atypical compared with the classic presentation of OSA. Women are more likely to report fatigue and less likely to report sleepiness than men.
  • 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 evaluation of possible OSA is approximately 10:1. There appears to be significant under-diagnosis of female patients. A high index of suspicion must be maintained when screening female patients for SDB.
  • In one study, 43% of premenopausal women with SDB had menstrual irregularities that disappeared with treatment of SDB.
  • Other symptoms include the following:
    • 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, due to the high negative intrathoracic pressure during apneas

Physical:

  • Obesity often is present, but not all patients are obese. Approximately 18-40% of affected patients are not more than 20% heavier than their ideal body weight.
  • The airway appears crowded and small.
  • UA abnormalities include severe nasal obstruction, low-hanging soft palate, large (hypertrophied) uvula, enlarged tonsils/adenoids, and macroglossia.
  • Large neck circumference (collar size >17.5 in) has been associated with SDB.
  • Systemic arterial hypertension is present in approximately 50% of patients with OSA.
  • Craniofacial abnormalities may be present, including malocclusion of jaws with anterior overjet of incisor teeth.
  • Patients with obesity hypoventilation syndrome (and some patients with OSA) may have evidence of pulmonary hypertension and right heart failure.
  • Women with SDB have different physical examination features than men with SDB. These may include the following:
    • They may have a high, arched hard palate.
    • The body mass index is lower.
    • Their neck circumference is relatively normal.
  • Diagnostic criteria and definitions of the American Sleep Disorders Association (ASDA) are as follows:
    • Apnea is defined as the cessation of airflow of 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% that is associated with either an oxygen desaturation of equal to or greater than 3% or an arousal must be present.

       

    • Obstructive apneas and hypopneas typically are distinguished from central events by the detection of respiratory efforts during the event.

       

    • A respiratory effort–related arousal (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. It is detected with nocturnal esophageal catheter pressure measurement. A pattern of progressively negative esophageal pressures terminating in an arousal is observed.

       

    • The RDI is defined as the number of obstructive apneas, hypopneas, and RERAs per hour averaged over the course of at least 2 hours of sleep, as determined by PSG.
  • The diagnostic criteria for OSA according to the International Classification of Sleep Disorders: Diagnostic and Coding Manual produced by the ASDA are as follows:

     

      A. The patient has a complaint of excessive sleepiness or insomnia. Occasionally, the patient may be unaware of clinical features that are observed by others.

      B. Frequent episodes of obstructed breathing occur during sleep.

      C. Associated features include (1) loud snoring, (2) morning headaches, (3) dry mouth upon awakening, and (4) chest retraction during sleep in young children.

      D. PSG monitoring demonstrates the following:

       

      • More than 5 obstructive apneas greater than 10 seconds in duration per hour of sleep and 1 or more of the following: (1) frequent arousals from sleep associated with the apneas, (2) bradytachycardia, (3) arterial oxygen desaturation in association with apneic episodes

         

      • A multiple sleep latency test that may or may not demonstrate a mean sleep latency of less than 10 minutes

      E. The symptoms can be associated with other medical disorders such as tonsillar enlargement.

      F. Other sleep disorders can be present (eg, periodic limb movement disorder, narcolepsy).

  • Minimum criteria for the diagnosis of OSA are A, B, and C from the above criteria.
    • No strict criteria exist for the classification of OSA into mild, moderate, or severe.
    • An RDI of greater than 20 events per hour may be considered to indicate severe OSA in the context of other variables, such as degree of oxygen desaturation and EEG arousals.

Causes:

  • Obesity
    • Obesity and male sex are the strongest risk factors associated with SDB. As with male sex, obesity also seems to have its maximum impact during middle age.

       

    • Persons with a body mass index of more than 29 kg/m2 may be 8-12 times more likely to develop OSA than individuals who are not obese.

       

    • A body mass index greater than 28 kg/m2 is present in 60-90% of patients with OSA who are evaluated in sleep clinics.

       

    • A neck circumference of greater than 17.5 in (a measurement related to obesity) has been highly correlated with the risk of OSA in more than one study (r = 0.38).

       

    • In individuals who are obese, even mild-to-moderate weight loss (approximately 15%) can significantly improve OSA.
  • Structural factors
    • These factors are more likely to be relevant in patients with OSA who are not obese.
    • Craniofacial features more commonly seen in patients with SDB than unaffected individuals include (1) facial elongation, (2) posterior facial compression, (3) reduced posterior and superior air spaces, (4) retrognathia, and (5) inferior displacement of the hyoid.
    • A brachycephalic head form appears to be a risk factor for SDB, particularly in white persons. It 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, 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 the following:

       

      • Polyps

         

      • Septal deviation

         

      • Tumor

         

      • Trauma

         

      • Stenosis
    • Structural factors related to retropalatal obstruction that predispose patients with OSA to pharyngeal collapse during sleep include the following:

       

      • Elongated, posteriorly placed palate and uvula

         

      • Tonsil and adenoid hypertrophy (particularly in children)
    • Structural factors related to retroglossal obstruction that predispose patients with OSA to pharyngeal collapse during sleep include the following:

       

      • Macroglossia

         

      • Tumor
  • Nonstructural risk factors
    • Some of these 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 have been reported. Relatives of patients with SDB have a 2- to 4-fold increased risk of SDB compared to controls.
    • Environmental exposures include smoking, 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 also is associated with myopathy that could contribute to UA dysfunction.
  • Symptoms of OSA and their pathogenic role
    • Snoring and sleepiness, while being symptoms, also may have a pathogenic role in aggravating apneas.
    • Snoring could result in vibration injury to the UA with resultant irritation, congestion, and increased UA resistance.
    • Sleep deprivation contributes to worsening SDB, probably by interfering with central respiratory control mechanisms.
    • Studies have shown that sleep deprivation can increase the RDI.

DIFFERENTIALS

Asthma
Chronic Obstructive Pulmonary Disease
Depression
Hypothyroidism
Sleep Apnea
Sleeping Disorders


Other Problems to be Considered:

Conditions associated with excessive daytime sleepiness include the following:
Central sleep apnea
Delayed sleep phase syndrome
Employment involving rotating shift work
Idiopathic hypersomnia
Medical conditions that may interfere with sleep (asthma, chronic obstructive pulmonary disease [COPD], congestive heart failure, chronic pain and discomfort)
Medication, drug, and alcohol use
Narcolepsy
Periodic limb movement disorder
Primary snoring (without other evidence of SDB)
Sleep deprivation (extremely common and always should be excluded)
Upper airway resistance syndrome

Other conditions that may be mistaken for OSA include the following:
Cheyne-Stokes respiration
Mucopolysaccharide storage diseases
Nocturnal seizures
Paroxysmal nocturnal dyspnea
Obesity hypoventilation syndrome
Sleep panic attacks
Sleep-related gastroesophageal reflux
Sleep-related laryngospasm
Swallowing disorders (aspiration during sleep)


WORKUP

Lab Studies:

  • Routine laboratory evaluation
    • Routine laboratory tests usually are not helpful unless a specific indication is present.
    • Consider obtaining a thyroid-stimulating 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 significant pulmonary hypertension) is suspected.

Imaging Studies:

  • The modalities available for identifying the site of obstruction include lateral cephalometry, endoscopy, fluoroscopy, CT scan, and MRI.
    • The accuracy of these methods in identifying the site(s) of obstruction is not clear.
    • Currently, UA imaging is used primarily as a research tool.
  • Routine radiographic imaging of the UA in the initial evaluation of SDB is of uncertain benefit currently and should not be performed unless a specific indication is present.
  • UA imaging studies (cephalometrics, MRI, CT scan) should be performed in patients being evaluated for UA and craniofacial surgery. Cephalometrics may be useful in some patients being evaluated for oral appliance therapy.

Other Tests:

  • Standard diagnostic nocturnal polysomnography
    • 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, body position, snoring, and leg movements.
    • The ASDA has published standards and guidelines for performing PSGs. The ASDA recommends the following:

       

      • 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.
    • Data are collected in the laboratory in the presence of a qualified technician (full PSG with attended monitoring); this protocol provides the opportunity for direct observation of 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 have PSG performed during the day, to match their normal sleep-wake cycle.
    • Arousals detected on PSG are important to help evaluate the degree of sleep fragmentation. They may be the only clue to UA resistance syndrome in a patient with daytime hypersomnolence if esophageal pressure monitoring is not performed. Esophageal pressure monitoring is not performed routinely in most laboratories due to 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 Image 2).

         

      • Apneic episodes of longer than 10 seconds in duration are considered clinically significant. Apneic episodes usually are approximately 20-40 seconds in duration, rarely lasting up to several minutes.

         

      • Apneic episodes are more prevalent during REM sleep and, in some patients, may occur exclusively during REM sleep.

         

      • Patients may experience a combination of apneas and hypopneas, or they may experience one or the other exclusively.

         

      • Mixed apneas may occur. Mixed apneas are a combination of central sleep apnea and OSA in a single apnea episode.

         

      • Sleep disruption due to arousals usually is seen at the termination of an apnea.
  • Split-night study PSG
    • In an attempt to reduce costs, the trend has been to perform split-night studies (ie, single-night studies), in which the initial part of the study is used for diagnosis of OSA and the latter part is used for continuous positive airway pressure (CPAP) titration. Recent data suggest that this approach is cost effective.
    • ASDA guidelines for split-night studies include the following:

       

      • Patients with an RDI greater than 40 events per hour during the first 2 hours of a diagnostic PSG receive a split-night study PSG. The final portion of the study is used for CPAP titration.

         

      • Split-night studies may be considered for patients with an RDI of 20-40 events per hour, based on clinical observations, such as the occurrence of obstructive events of prolonged duration or the occurrence of marked oxygen desaturation.

         

      • A minimum of 3 hours of sleep is preferred to adequately titrate CPAP after this treatment is initiated.

         

      • Split-night studies require recording and analysis of the same parameters as a standard diagnostic PSG.

         

      • A single split-night study may not permit adequate titration of CPAP therapy. If treatment does not control symptoms, an additional full-night CPAP titration may be required.
  • Indications for repeat PSG are as follows:
    • Symptoms persist despite adequate compliance with prescribed CPAP treatment.

       

    • PSG can be used to assess response to UA surgical procedures.

       

    • It also can be used to assess response to oral appliance therapy.

       

    • If a significant sustained weight change (>15%) occurs, PSG should be repeated.

       

    • If the first PSG is of poor quality, a repeat is indicated.
  • Unattended polysomnography
    • According to the ASDA polysomnography task force report, unattended portable PSG in the patient's home may be effective for the diagnosis of severe SDB when used by a qualified sleep specialist as part of a comprehensive sleep consultation.
    • Any patient initially tested using unattended portable PSG studies who does not have a satisfactory diagnosis must have easy and automatic access to a comprehensive sleep consultation and additional diagnostic testing. Therefore, a home-testing program dedicated to quality care should either originate from or have some formal affiliation with a comprehensive sleep disorders center so that the continuum of patient care is ensured.
  • Limited polysomnography 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 (1) oronasal airflow, (2) chest wall respiratory effort, (3) ECG, and (4) oxyhemoglobin saturation.
    • In-laboratory limited PSG studies show fairly good correlation with standard PSG, but limited data are available to compare unattended cardiopulmonary recordings in the home setting with standard PSG in the sleep laboratory. The role of unattended PSG studies for the diagnosis of SDB is uncertain at present because of a lack of supportive data. These studies may be indicated for the following:

       

      • Patients with severe symptoms indicative of OSA require limited studies when initiation of treatment is urgent and standard PSG is not readily available.

         

      • Patients with established OSA who require follow-up studies should have limited PSG.

         

      • Patients who are unable to be studied in the sleep laboratory should have limited PSG.

       

    • Limited-channel studies are less accurate than the standard PSG in determining obstructive events, particularly hypopneas. Also, they are not helpful for detecting non-OSA sleep disorders that may coexist with OSA.
  • Evaluation of sleepiness
    • The multiple sleep latency test traditionally has been used to quantify sleepiness in patients with symptoms of daytime hypersomnolence.

       

      • It must be performed on the day following a standard PSG.

         

      • The patient is instructed to attempt sleeping for 20 minutes on each of 4 separate naps, each nap being 2 hours apart.

         

      • The average latency to stage 1 sleep is determined for the 4 naps, and a mean sleep latency of less than 5 minutes is considered abnormal (ie, indicative of pathological sleepiness).

         

      • A mean sleep latency of more than 10 minutes is normal.

         

      • The test is not performed routinely following PSG for the diagnosis of OSA.
    • The Epworth sleepiness scale is a self-administered questionnaire that measures predisposition towards sleep (ie, subjective measure of sleep).

       

      • It may be useful when excessive daytime somnolence complaints are out of proportion to actual OSA findings on PSG.

         

      • This test does not appear to correlate well with the RDI or the multiple sleep latency test. Therefore, its usefulness as a general screening tool for SDB is questionable.

TREATMENT

Medical Care: Little evidence supports the treatment of asymptomatic patients with an RDI that is in the mild range. Patients with mixed apneas should be treated as if they have OSA because OSA is most life-threatening and central sleep apnea abates commonly with OSA treatment. Only health care professionals with adequate training in the evaluation and management of OSA should prescribe therapy for patients with SDB. CPAP should not be prescribed without PSG confirmation of the correct CPAP pressure level because no standardized pressure value exists based on age or body mass index.

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 and variable CPAP. Nightly use of at least 4 hours of CPAP is required to produce consistent ameliorative effects. Data show that compliance at 1 month predicts compliance at 3 months. Whether patients like CPAP depends on their perception of improvement, not on the severity of their disease as judged by the clinician.

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

  • Nonsurgical therapy

     

    • General/behavioral measures such as weight loss and avoidance of alcohol, sedatives, and supine position are elements of nonsurgical treatment.

       

    • Mechanical measures include (1) positive airway pressure therapy with CPAP or bilevel positive airway pressure or (2) oral appliance therapy.

       

    • Pharmacologic therapy is not part of treatment. No clinically useful drug therapy is currently available.

     

  • Nasal CPAP therapy - General considerations

     

    • Initially described in 1981, this is currently the treatment of choice for patients with OSA and UA resistance syndrome.

       

    • Continuous positive pressure is applied to the (UA) with a nasal mask, nasal pillows, or a mask that covers both the nose and mouth (ie, oronasal mask)

       

    • CPAP acts as a pneumatic splint to maintain UA patency during sleep, and it is very effective in the treatment of SDB.

       

    • CPAP consists of a blower unit that produces positive-pressure airflow. This usually is applied at the nose, and the airflow is then directed down through the UA.

       

    • CPAP increases airway caliber in the retropalatal and retroglossal regions. It increases the lateral dimensions of the UA and thins out the lateral pharyngeal walls. The lateral pharyngeal walls are thicker in patients with OSA than in patients without OSA.

       

    • Application of adequate levels of nasal CPAP during sleep almost always results in resolution of (1) obstructive apnea/hypopnea, (2) oxyhemoglobin desaturation, and (3) RERAs from sleep and results in adequate sleep continuity.

     

  • CPAP therapy - Efficacy and compliance

     

    • CPAP therapy improves daytime hypersomnolence, daytime alertness, and neuropsychiatric functioning.

       

    • It improves right heart function, left heart function in patients with left ventricular dysfunction, and systemic and pulmonary hypertension.

       

    • Patients have improvement in their quality of life.

       

    • Some studies report improved survival rates.

       

    • The beneficial effects parallel those observed following tracheostomy.

       

    • CPAP therapy is effective for treating mixed apneas and some central apneas.

       

    • Compliance may be poor. Although an average of 20-40% of patients do not use the prescribed therapy, some sleep disorders centers have achieved greater than 90-95% compliance rates with CPAP therapy. In the authors’ experience, regular, close, and personalized follow-up greatly enhances compliance.

     

  • CPAP therapy - Complications and adverse effects

     

    • Pressure/airflow-related complications include (1) the sensation of suffocation/claustrophobia, (2) difficulty exhaling, (3) the inability to sleep, (4) musculoskeletal chest discomfort, (5) aerophagia, and (6) sinus discomfort. Pneumothorax/pneumomediastinum (extremely rare), pneumoencephalos (isolated case report), and tympanic membrane rupture (very rare) can occur.

       

    • Mask-related problems could include skin abrasions, rash, and conjunctivitis (due to air leak).

       

    • Nasal problems can include (1) rhinorrhea, (2) nasal congestion, (3) epistaxis, and (4) nasal/oral dryness.

       

    • Other problems include noise and spousal intolerance.
  • Nasal CPAP therapy – Guidelines for use
    • Patients with severe SDB (RDI >20-30) should be treated irrespective of symptoms because of the increased risk of cardiovascular morbidity.

       

    • Patients with an RDI of 5-20 should be treated if symptomatic or if coexistent cardiovascular disease is present. Patients with UA resistance syndrome may need CPAP therapy.

       

    • CPAP titration is performed following the diagnostic portion of a split-night protocol or on a separate night following a diagnostic PSG.

       

    • Proper titration includes identifying the minimum CPAP level that abolishes obstructive apneas/hypopneas, oxyhemoglobin desaturation, RERAs, and snoring in all sleep stages and in all sleep positions. Typically, the pressure needed is 5-20 cm water.
  • Bilevel positive airway pressure therapy

     

    • In contrast to CPAP, which delivers a constant pressure during both inspiration and expiration, bilevel positive airway pressure permits independent adjustment of the pressures delivered during inspiration and expiration.

       

    • The ability to set independent inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP) levels results in lower mean airway pressures compared to CPAP.

       

    • In a given patient, the EPAP level that needs to be applied is lower than the corresponding CPAP level that will be required to maintain airway patency.

       

    • No studies have conclusively demonstrated improved compliance with bilevel positive airway pressure devices compared to CPAP therapy.

       

    • A trial is warranted in patients who are unable to tolerate CPAP. However, it is too expensive to be used as first-line therapy and has no distinct advantages over CPAP therapy.
  • Oral appliance therapy
    • The 2 main groups of oral appliances are tongue repositioning devices (TRD) and anterior mandibular positioners (AMP)/mandibular advancing devices.

       

    • Oral appliances are believed to be effective for the following reasons:

       

      • They increase the size of the UA by moving (pulling) the tongue forward (ie, TRD) or by moving the mandible and soft palate anteriorly (ie, AMP).

         

      • Oral appliances cause thinning of 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.

       

    • The biomechanical factors responsible for the efficacy of oral appliances are not completely understood.

       

    • A review of the literature by the ASDA indicates the following summary:

       

      • Overall, 51% of patients studied achieved an RDI of less than 10 per hour with oral appliance therapy.

         

      • Of patients who had a pretreatment RDI greater than 20, 39% continued to have an RDI above this level despite oral appliance therapy.

         

      • No patient characteristics were found that predicted success with oral appliance therapy.

         

      • No particular oral appliance had any advantages over the others studied.

       

    • Subsequent prospective controlled clinical trials comparing oral appliance therapy to nasal CPAP therapy for the treatment of OSA and snoring demonstrated the following:

       

      • Treatment was successful in 55% of patients using an adjustable AMP and in 48% of patients using a nonadjustable AMP. Treatment success was defined as a posttreatment RDI equal to or less than 10 events per hour, with symptomatic relief.

         

      • CPAP therapy was superior to AMP therapy in normalizing the RDI, reducing snoring, and improving oxygenation.

         

      • Daytime sleepiness was improved equally by CPAP and AMP therapy.

         

      • The majority of patients preferred AMP therapy to CPAP therapy.

         

      • Treatment success with AMPs appears to be inversely related to the initial RDI.

       

    • The most recent trial, the largest to date, evaluated the effectiveness of an adjustable mandibular positioning device; no comparison was made to CPAP therapy.

       

      • Treatment with the device was successful in 51% of patients (posttreatment RDI <10/h), 86% of patients continued to use the appliance nightly approximately 1 year after trial commencement, and up to 32% of patients had teeth discomfort with the appliance.

         

      • Six of 21 patients with severe OSA (RDI 50-115/h) were treated successfully with this device (posttreatment RDI <10/h).

       

    • The 1995 ASDA practice parameters for the treatment of snoring and OSA with oral appliances include the following:

       

      • Oral appliances are indicated for use in patients with primary snoring or mild OSA who do not respond to or are not appropriate candidates for treatment with behavioral measures such as weight loss or sleep-position change.

         

      • Patients with moderate-to-severe OSA should have an initial trial of nasal CPAP therapy because greater effectiveness has been shown with this intervention than with the use of oral appliances.

         

      • Oral appliances are indicated for patients with moderate-to-severe OSA who are intolerant of or refuse treatment with nasal CPAP. Oral appliances also are indicated for patients who refuse or are not candidates for tonsillectomy and adenoidectomy, craniofacial operations, or tracheostomy.

       

    • According to the above guidelines, the major role for oral appliance therapy appears to be in patients with mild-to-moderate OSA who are intolerant of CPAP (and bilevel positive airway pressure) therapy. These devices are less likely to benefit patients with severe OSA.

       

      • Clinicians and patients prefer a titratable device such as an AMP because it can be adjusted to improve both efficacy and comfort.

         

      • Patients should have a complete evaluation by a sleep disorders specialist and a dental professional, both of whom should be experienced in oral appliance therapy; close collaboration is required.

         

      • Follow-up PSG after final adjustment of the device is recommended to ensure that OSA has been treated adequately, particularly in patients with moderate-to-severe OSA.

         

      • These devices may abolish snoring without adequately treating OSA.

       

    • Complications and/or adverse effects include the following:

       

      • Excessive salivation has been reported, as has dental misalignment.

         

      • Temporomandibular joint pain/discomfort is possible. The patient should not have significant discomfort or difficulty opening the jaw upon waking in the morning.

         

      • Patients may object to having an appliance in their mouth throughout the night.

Surgical Care: A specific space-occupying lesion causing UA obstruction is found in only 3 of 200 adult patients with OSA. Although surgical correction of such an abnormality (ie, tonsillectomy) could potentially cure OSA, the majority of adult patients do not have such correctible lesions.

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

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

Different surgical procedures have been proposed for patients with different levels of obstruction. Uvulopalatopharyngoplasty (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.

Based on the recognition that several sites of obstruction could 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, which advances the jaw anteriorly. Using the phased protocol, the success rate has been in excess of 90% for phase II surgery.

In some patients, tracheostomy or continuous positive air pressure (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. The modalities available for identifying the site of obstruction include lateral cephalometry, endoscopy, fluoroscopy, CT scan, and MRI. The accuracy of these methods in identifying the site(s) of obstruction is not clear. Success rates for UPPP have been only approximately 50% despite preselection of patients with type I obstruction based on these studies.

Data on 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 have a follow-up PSG.

  • Uvulopalatopharyngoplasty
    • UPPP is the most common surgical procedure performed for adults with OSA and was introduced to the United States by Fujita and colleagues in 1981. It involves removal of the tonsils (if present), uvula, distal margin of the soft palate, and redundant pharyngeal tissue and reshaping of the soft tissues in the lateral pharyngeal walls.

       

    • The surgical success rate is approximately 50% when surgical success is defined as both 50% reduction in RDI/AI and a postoperative RDI of less than 20 (or an AI <10); this is despite preselection of patients with type I obstruction using imaging and endoscopic studies. This highlights the inadequacy of the methods available to identify sites of UA obstruction. The outcome of UPPP is difficult to predict.

       

    • Although the procedure usually is well tolerated and uneventful, complications can include the following:

       

      • Pain upon 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 abolish snoring but have no significant effect on sleep-associated obstructive episodes. It is imperative that patients have a postoperative PSG to rule out persistent OSA.

       

    • The ASDA recommendations for UPPP are as follows: “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.”

       

    • Prior UPPP surgery reduces the maximal level of pressure tolerated by patients requiring CPAP therapy; it also may compromise subsequent CPAP therapy by promoting mouth leaking.

       

    • Uvulopalatopharyngoglossoplasty (UPPPG) is a modified UPPP with limited resection of the base of the tongue, enlarging both the retropalatal and retrolingual regions of the UA.
  • Genioglossus advancement with hyoid myotomy

     

    • The genioglossus muscle is repositioned anteriorly through an inferior mandibular osteotomy (genioglossus advancement). This places the pharyngeal muscles and the base of the tongue on tension and results in airway expansion.

       

    • The hyoid is suspended to the superior edge of the larynx and fixed in this position, adding to the effect of genioglossus advancement.
  • Maxillomandibular advancement osteotomy
    • The midface, palate, and mandible are moved forward in this procedure, increasing the space behind the tongue and also increasing the tension on the genioglossus muscle.

       

    • This surgery is more extensive than any of the others described. It usually is reserved for patients in whom other modalities of treatment fail.
  • Tracheostomy
    • This procedure bypasses the UA and is the most effective surgical procedure for treatment of OSA; it is virtually 100% effective.

       

    • Unfortunately, it is a disfiguring procedure and results in decreased quality of life.

       

    • Tracheostomy is now reserved for patients with very severe OSA in whom other medical and surgical treatment modalities have failed. Tracheostomy also is used for airway protection during UA reconstructive surgery.
  • Other surgery options

     

    • Laser-assisted uvulopalatoplasty: Although successful in reducing snoring in 90% of patients, the success rate in patients with SDB is not clear. It may give rise to more scarring than UPPP and could potentially worsen apnea. Increased OSA severity in the early postoperative period following laser-assisted uvulopalatoplasty has been noted. It is not recommended for treatment of OSA until further data are available.

       

    • Laser midline glossectomy and lingualplasty: These 2 procedures enlarge the retrolingual region by using a laser to remove a portion of the posterior tongue. The role of the procedures in the management of SDB has yet to be defined.

       

    • Nasal surgery: This 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.
  • Radiofrequency volumetric tissue reduction of the soft palate (somnoplasty)

     

    • Recent interest has been generated in this new technique pioneered by Powell and associates that used radiofrequency energy to ablate the soft palate. This procedure has US Food and Drug Administration (FDA) approval for the treatment of snoring and OSA.

       

    • A midline soft palate submucosal scar is created by the use of a needle electrode inserted near the border of the hard palate and directed toward the uvula. Pulses of radiofrequency energy are delivered, resulting in tissue necrosis and needle tract fibrosis over subsequent weeks to months.

       

    • A study in 22 patients with mild SDB demonstrated a reduction in the volume of palatal tissue and improvement in symptoms in all subjects, but no data are available regarding improvement of RDI and oxyhemoglobin saturation.

       

      • Long-term follow-up (12-18 mo) revealed that approximately 41% of patients undergoing radiofrequency volumetric reduction of the soft palate develop recurrence of snoring.

         

      • Evidence showed postsurgical improvement in the severity of esophageal pressure swings, indicating that this treatment may be useful in patients with UA resistance syndrome.

       

    • A more recent study of radiofrequency volumetric reduction of the soft palate (12 patients) again demonstrates success in treating snoring, but data regarding adequate treatment of SDB are lacking. Data from larger controlled studies are required before this technique can be recommended for the treatment of SDB; it appears to be associated with less morbidity than UPPP, laser-assisted uvulopalatoplasty, and lingualplasty.

       

    • Animal studies of radiofrequency volumetric reduction of the tongue have shown volume reduction in tongue tissue after treatment. Results of human studies are pending.
  • The ASDA 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 oral appliance) has failed or has been rejected, provided the patient desires such therapy and 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 has been refused or rejected, provided they are medically stable enough to undergo the procedure.

Consultations:

  • Patients should have a complete evaluation by a sleep disorders specialist and a dental professional, both of whom should be experienced in oral appliance therapy; close collaboration is required.

Diet:

  • Obesity (body mass index >29 kg/m2) is the most important predictor of sleep apnea. In patients who are obese, OSA may be reduced or corrected by weight reduction. In these patients, a 10% reduction in weight has been shown to reduce sleep apnea/hypopnea indices in half.

     

  • Some of the benefits of weight reduction in patients with SDB include the following:
    • Decreased RDI

       

    • Lower blood pressure

       

    • Improvements in pulmonary function and arterial blood gas values

       

    • Improvements in sleep structure and snoring
  • The required optimum CPAP pressure may be reduced with weight loss.
  • One of the most important determinants of relapse of OSA following surgical treatment is weight gain. Although accomplishing and maintaining weight reduction are difficult, the results are extremely beneficial when patients are able to do so.
  • The treatment approach to SDB would not be complete if weight reduction is not addressed in patients who are obese.

Activity:

  • Restriction of body position 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 (a tennis ball sewed onto the pajama back) or a gravity-activated position monitor may be useful, but these devices are cumbersome and appear to benefit only patients with very mild OSA.

       

    • Patients with marked obesity may benefit from sleeping in an upright position.

       

    • More recently, the FDA has approved a specially designed pillow (PillowPositive) for the treatment of snoring and mild OSA. This device maintains head and neck position during sleep to optimize UA patency.
  • Patients should avoid alcohol and other sedatives known to make apnea worse.

     

  • Patients should avoid smoking.
    • Smoking increases the risk of snoring and apnea.
    • Smoking cessation appears to decrease risk.

       

    • Individuals who smoke also are more likely that those who do not smoke to complain of problems going to sleep, problems maintaining sleep, and increased daytime somnolence.
  • Patients should avoid sleep deprivation.

MEDICATION

Although acetazolamide, medroxyprogesterone, fluoxetine, and protriptyline have been used for the treatment OSA, none of these therapies is recommended.

FOLLOW-UP

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 of CPAP therapy.

       

    • Adequate adherence is defined as more than 4.5 hours of CPAP use per night, routinely.

       

    • Follow-up visits should be scheduled at least once following initiation of CPAP treatment 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 unit is too cold, the patient should use a heated humidifier.

       

    • If excessive air leak through mouth occurs, patients should use a chin strap to keep their mouths closed, or, they should try the oronasal mask. Consider consultation with an otolaryngologist to rule out sinus dysfunction.

       

    • If a poorly fitting mask causes skin break down and/or air leaks, patients should try different mask sizes and models; a variety of interfaces are now available.

       

    • For claustrophobia, patients may try 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 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 time interval (usually 15-30 min). Alternatively, bilevel positive pressure may be used.
  • Oral appliance therapy
    • Regular follow-up with a dental professional allows for adjustment of the dental appliance, initially based on symptoms. Follow-up helps ensure compliance with therapy and helps identify adverse effects/complications, device deterioration, or maladjustment.

       

    • Follow-up PSG after the final adjustment of the oral appliance ensures that OSA has been adequately treated. However, PSG should be deferred until adequate symptom response and patient comfort have been achieved with adjustments to the appliance.

       

    • Follow-up with a sleep disorders specialist ensures that OSA has been adequately treated. Regular follow-up is required until patient’s symptoms have resolved and PSG evaluation shows no evidence of significant SDB. It also helps determine if another treatment modality is required, due to 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 has resolved.
    • Follow-up PSG is essential to determine if OSA has been treated adequately. It should be performed once the surgical site has healed adequately. The most effective timing appears to be 4-6 months postoperatively to ensure steady body weight, completion of healing, and stabilization of sleep architecture.

Patient Education:

  • Nasal CPAP therapy: Patients should be trained by a physician, trained technician, or nurse for at least the first month of CPAP therapy. This promotes long-term adherence with treatment.

MISCELLANEOUS

Medical/Legal Pitfalls:

  • The following is a summary of the American Thoracic Society (ATS) guidelines on sleep apnea, sleepiness, and driving risks.
    • Laws regarding impaired drivers, including those with OSA, vary from state to state. In some states, the physician is obligated to report patients under specific conditions (ie, mandatory reporting statute) while other states permit reporting but do not require it (ie, permissive reporting statute).

       

    • Mandatory statutes take 1 of the 2 following approaches:

       

      • Categorical approach: The physician is obligated to report patients who have specified medical conditions, such as epilepsy. In these states, the reporting obligation is based on diagnosis alone.

         

      • Functional approach: The physician is required to report patients with certain medical conditions only if the physician believes that a condition impairs the patient's driving ability.
  • Irrespective of whether statutory reporting is required, physicians may be liable for damages if a patient with OSA injures himself or someone else while driving.

     

  • 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.

       

    • Evidence of severe daytime sleepiness or impaired driving performance is present.
  • The following should be undertaken in patients with OSA:

     

    • Assess the patient's risk for motor vehicle accidents. In patients at highest risk, the physician should immediately warn the patient of the potential risk of driving until effective therapy is instituted.

       

    • Warn any patient with OSA of the potential dangers of driving while sleepy. Inform the patient of the potential personal and social risk.

       

    • Additional counseling is required depending on other risk factors (eg, occupation).

       

    • Advise patients to not drive until their OSA has been treated adequately.

       

    • Additional counseling to family members may be appropriate, and alternatives to driving may need to be explored for those who are unaware of their sleepiness or unwilling to acknowledge their increased risk.

       

    • Patients should be diagnosed and treated expeditiously.

       

    • Document in writing any warnings, concerns, and/or recommendations given to the patient. This reinforces the importance of the message to the patient and helps reduce the risk of legal liability for medical personnel.

       

    • Have a plan of follow-up to determine the effectiveness of therapy and compliance with therapy, on a routine basis. Ascertain that daytime sleepiness has been significantly reduced or eliminated. Evaluations should be continued at regular intervals until therapy has controlled the condition.

     

  • Whether and under what circumstances patients with sleep apnea should be reported to the licensing authority depend on the laws of the state in which the physician practices.
    • Physicians taking care of patients with OSA must be aware of state statutes or regulations regarding reporting of high-risk drivers.

       

    • Each physician is obligated to adhere to the requirements of the law in the specific state of practice, even if those laws do not reflect sound public policy or medical evidence.
  • The ATS guidelines on reporting of patients to the appropriate state authorities are as follows:
    • In states with permissive reporting mechanisms, at a minimum, the physician should notify the state’s department of motor vehicles if a highest-risk patient (ie, OSA with severe daytime sleepiness and a previous motor vehicle accident/near-miss incident) is unwilling to restrict driving until effective treatment has been instituted, is not compliant or unwilling to accept treatment, or has an untreatable condition or one that is not amenable to expeditious treatment (within 2 mo of diagnosis).

       

    • Increased occupational exposure to driving or increased occupational risk for an accident of significant importance to the public (eg, truck drivers transporting hazardous waste, school bus drivers) may be other indications for reporting.
  • According to the ATS guidelines, 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.
    • Categorical reporting may be more appropriate in the context of occupational licenses, but this also is arguable; at a minimum, the threshold for suspicion of increased driving risk due to sleepiness should be lower, given the increased hazard.

       

    • The US Department of Transportation convened a group of respiratory experts at a Conference on Pulmonary/Respiratory Disorders in Commercial Drivers in September of 1990. The report from this group recommends that operators with suspected sleep apnea should not be medically qualified for commercial vehicle operation "until the diagnosis has been eliminated or accurately treated."

       

    • 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.

Special Concerns:

  • Following the rule of least invasive (and effective) to more invasive (and effective), a summary of treatment is as follows:
    • All patients first should be offered nasal CPAP therapy.
    • In patients with mild-to-severe OSA who refuse or reject nasal CPAP therapy, bilevel positive airway pressure should be tried next. If this therapy fails or is rejected/refused, then oral appliance therapy should be considered.
    • Oral appliances 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.
    • Patients in whom noninvasive medical therapy (eg, positive airway pressure, oral appliances) 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 one surgical procedure (some fairly extensive) to cure OSA. Only refer patients to centers that have personnel experienced in these special surgical techniques.