Obstructive sleep apnea in adults.

Hospital Practice

ISSN: 2154-8331 (Print) 2377-1003 (Online) Journal homepage: http://www.tandfonline.com/loi/ihop20

Obstructive Sleep Apnea in Adults Asad Kabir MD, Sarah Ifteqar MD & Abid Bhat MD To cite this article: Asad Kabir MD, Sarah Ifteqar MD & Abid Bhat MD (2013) Obstructive Sleep Apnea in Adults, Hospital Practice, 41:4, 57-65 To link to this article: http://dx.doi.org/10.3810/hp.2013.10.1081

Published online: 13 Mar 2015.

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Obstructive Sleep Apnea in Adults DOI: 10.3810/hp.2013.10.1081

Downloaded by [University of Lethbridge] at 20:22 05 November 2015

Asad Kabir, MD 1 Sarah Ifteqar, MD 2 Abid Bhat, MD 1 1 Department of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of Missouri at Kansas City School of Medicine, Kansas City, MO; 2 Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS

Abstract: Obstructive sleep apnea (OSA) is the most common sleep-related breathing d isorder characterized by repeated episodes of obstructed (apnea) or reduced (hypopnea) airflow in the upper airway during sleep. Obstructive sleep apnea results in variable arterial oxygen desaturations and arousals leading to sleep fragmentation. Most patients with OSA first come to the attention of a clinician when they complain of daytime sleepiness or when their bed partner reports loud snoring and witnessed episodes. Obstructive sleep apnea is associated with impaired quality of life, cardiovascular disease, metabolic syndrome, and motor vehicle accidents, yet the disorder remains undiagnosed in a significant portion of the population. Overnight polysomnography, whether facility-based or portable, is required for appropriate patient diagnosis. Portable monitoring can be used in patients with a high pre-test probability for moderate-to-severe OSA, who are without significant comorbidities. Management of OSA requires a long-term multidisciplinary approach. Continuous positive airway pressure (CPAP) remains the mainstay of treatment for patients with moderate-to-severe OSA. Oral appliances may be indicated in patients with mild-to-moderate OSA who do not wish to use CPAP. Surgical therapy is generally reserved for selected patients in whom CPAP or oral appliance are not an option. Keywords: obstructive sleep apnea; daytime sleepiness; polysomnogram; continuous positive airway pressure (CPAP)

Introduction

Correspondence: Abid Bhat, MD, Associate Professor, Department of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of Missouri at Kansas City School of Medicine, Truman Medical Center, Hospital Hill, 2301 Holmes St, Kansas City, MO 64108. Tel: 816-404-5032 Fax: 816-404-5014 E-mail: [email protected]

Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder characterized by the recurrent complete or partial collapse of the upper airway during sleep.1 Collapse of the upper airway causes cessation (obstructive apnea) or a significant reduction (obstructive hypopnea) of patient airflow. These respiratory events cause oxyhemoglobin desaturations, hemodynamic changes, and frequent arousals resulting in fragmented sleep and subsequent serious adverse conditions for patients.2 Obstructive sleep apnea is associated with adverse consequences, including daytime hypersomnolence, cardiovascular disease (hypertension, stroke, myocardial infarction, and heart failure), increased insulin resistance, metabolic syndrome, and increased risk of motor vehicle accidents.3 Despite significant advancements in the understanding of the mechanisms and the consequences of OSA, the condition often remains unrecognized and underdiagnosed in patients.4

Definitions

The severity of OSA is calculated based on the number of patient apneas and hypopneas present per hour of sleep, which is referred to as the Apnea and Hypopnea Index (AHI), an index of apnea and hypopnea per hour of sleep. Apnea is defined as a cessation or near cessation of the oronasal airflow for . 10 seconds and hypopnea is defined as a reduction of $ 30% of oronasal airflow from baseline, lasting for $ 10 seconds, accompanied by a $ 3% oxyhemoglobin desaturation from the

© Hospital Practice, Volume 41, Issue 4, October/November 2013, ISSN – 2154-8331 57 ResearchSHARE®: www.research-share.com • Permissions: [email protected] • Reprints: [email protected]

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p re-event baseline or an arousal.5 In contrast, the Centers for Medicare and Medicaid Services (CMS) uses a 4% cutoff for oxyhemoglobin desaturation.6 Based on the AHI, OSA is classified as mild (AHI 5–15), moderate (AHI 16–30), and severe (AHI . 30). The frequency index of 5 events/hour as the minimum threshold value was based on epidemiologic data suggesting that minimal health effects, such as hypertension, sleepiness, and motor vehicle accidents may be observed in patients at an AHI threshold of 5 events per hour.7,8 Apnea can be distinguished as obstructive versus central based on the presence or absence of thoracoabdominal effort. Our discussion is limited to OSA in adults in this review article.

Epidemiology and Risk Fators

In the United States, OSA is a highly prevalent problem. An estimated 24% of US men and 9% of US women have some form of sleep-disordered breathing (AHI . 5). Of those numbers, 4% of males and 2% of females are believed to have OSA associated with excessive daytime sleepiness.9 Obesity is the single most important risk factor for OSA in middle-aged adults. It has been estimated that 58% of the moderate-to-severe cases of OSA can be attributed to a body mass index (BMI) $ 25 kg/m2.10 However, despite the strong relationship with obesity, it is important to remember that not all subjects who are obese suffer from sleep apnea and approximately one-third of patients with OSA are not obese. The prevalence of OSA can be as high as 78% in morbidly obese patients who present for bariatric surgery.11 There is also a graded increase in OSA prevalence with increasing patient BMI, neck circumference, and waist-to-hip ratio.12 Patients with a BMI . 30, neck circumference . 17 cm in men, and . 16 cm in women are at a greater risk for OSA. Research studies have reported that OSA is more common in men than women. The male-to-female ratio is estimated to be approximately 2:1 in the general population.13 It has been suggested that hormonal influences play an important role in the pathogenesis of OSA, as the prevalence is higher in postmenopausal females.14 Postmenopausal women have 3 times the risk of developing OSA compared with premenopausal women despite controlling for age, BMI, and other confounding factors. Craniofacial and upper airway structures also play an important role in the prevalence of OSA, especially in people of Asian descent.15 The frequency of developing OSA increases with patient age, which is not as easily explained as other risk factors, 58

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like obesity.16 However, the severity of OSA seems to plateau after age 65. African Americans are at increased risk for OSA compared with whites, when controlled for weight.17 Increased prevalence can be seen in families and can be attributed to lifestyle, genetic predisposition for obesity, and craniofacial features. Endocrine abnormalities also increase the risk for OSA. For example, OSA is more common in patients with hypothyroidism and acromegaly.18,19 Current smokers are 3 times more likely to have OSA compared with former smokers or nonsmokers.20

Pathophysiology

A number of factors have been identified that contribute to the pathophysiology of OSA. In patients with OSA, the pharynx is narrower and more floppy than in subjects without OSA due to fat deposition in the parapharyngeal fat pads and under the mandible in the submental region. This significantly reduces the upper airway caliber, thereby predisposing to development of complete pharyngeal occlusion during sleep.21 Relative hypotonia is particularly pronounced in REM sleep. Other contributing factors include pharyngeal dilator muscle dysfunction, sex genetics, soft tissue edema (secondary to snoring), and posture of an individual (supine versus lateral). Ventilatory instability (loop gain) also plays a role in OSA. A body system with a high loop gain is intrinsically prone to instability, whereas a body with a low loop gain system tends to be quite stable. Patients with OSA have an elevated loop gain compared with individuals who do not.22

Relationship Between OSA and Other Chronic Health Conditions Hypertension

The presence of OSA has been identified as an independent patient risk factor for the onset of arterial hypertension.23 An animal model showed that repetitive obstruction of the airway during sleep produced sustained hypertension during wakefulness, an effect that was reversed when the obstruction was no longer produced.24 Patients with moderate-tosevere OSA are 3 times more likely to have hypertension compared with people without OSA. Unsuspected OSA may also be noted in 83% of patients with resistant hypertension.25 Although observational studies indicate a causal relationship between OSA and hypertension, the effectiveness of reducing blood pressure by treating OSA is less clear with intervention studies using continuous positive airway pressure (CPAP).26

© Hospital Practice, Volume 41, Issue 4, October/November 2013, ISSN – 2154-8331 ResearchSHARE®: www.research-share.com • Permissions: [email protected] • Reprints: [email protected]

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Obstructive Sleep Apnea in Adults


Coronary Artery Disease

Patients with cardiovascular disease frequently have coexi sting undiagnosed OSA and several cross-sectional studies have supported a strong association between OSA and coronary artery disease.27,28 However, in the cited studies, sleep apnea was assessed after the diagnosis of coronary artery disease was established, thereby limiting the conclusion of an etiologic relationship. Obstructive sleep apnea is believed to induce carotid artery atherosclerosis in patients through repetitive periods of hypoxia leading to increased sympathetic discharge and a release of proinflammatory mediators, including catecholamines, c-reactive protein, and a number of interleukins into the blood stream. Various data suggest that OSA occurs more frequently in patients with heart failure than in patients without this condition. The frequency of OSA in patients with heart failure ranges from 11% to 38%.29,30 Sleep apnea has been reported to occur in # 70% of patients with heart failure who have a left ventricular ejection fraction of , 40%, and in 55% of patients with diastolic heart failure.31,32 Of those patients with heart failure, OSA is present in 27% to 43%, whereas central sleep apnea (CSA) occurs in 28% to 44% of the same patient group. The Sleep Heart Health Study reported that patients with AHI $ 11/hour increased the risk of heart failure 2.38 times, independent of other factors.33

Arrhythmias

Sinus bradycardia, sinus pauses, and sinoatrial blocks are the most frequently observed nocturnal rhythm disturbances in patients with OSA. These bradyarrhythmias are associated with apneic events that likely trigger a reflex increase in vagal tone. Supraventricular tachycardias have also been reported in patients with OSA. Effective treatment of OSA has been shown to result in resolution of these arrhythmias. Clinical studies have also indicated that OSA is strongly associated with atrial fibrillation and patients with untreated OSA run a high risk of recurrence of atrial fibrillation at 1 year after an electrical cardioversion.34

Stroke

Data from clinical cohorts suggest an important link between OSA and stroke. Munoz et al 35 reported that severe sleep apnea (AHI $ 30 events per hour) at baseline was associated with a significantly increased patient risk of developing an ischemic stroke (adjusted hazard ratio 2.52, 95% CI, 1.04–6.01).35 Moreover, in stroke survivors, the occurrence of OSA was a significant predictor of early death.36

Diabetes Mellitus

Diabetes and OSA share several risk factors. Cross-sectional studies reveal that, in the general population, there is an association between sleep apnea and insulin resistance and/ or diabetes, independent of obesity and other confounders.37 Harsch et al38 showed that insulin resistance decreased with CPAP treatment.

Clinical Manifestations

The diagnosis of OSA is based upon the combined assessment of patient clinical features together with the objective demo nstration of sleep-disordered breathing using an appropriate sleep study.38 A detailed clinical assessment forms an integral part of the evaluation procedure for a patient suspected of having OSA (Table 1). Typical presentation is that of an overweight person complaining of loud snoring, witnessed apneas, disturbed unrefreshing sleep, and daytime hypersomnolence. Generally, these symptoms develop over years and progress in association with increases in weight, aging, or transition to menopause. Patients may frequently regard their symptoms as normal variants and/or manifestations of a poor lifestyle. It is advantageous to interview the bed partner who can usually provide important additional information based on direct observation of the patient while asleep.39

Snoring

Snoring is the cardinal complaint of patients with sleep apnea.40 Nevertheless, predictive value is poor owing to high prevalence of snoring in the general population.41 Most people who snore are unaware of their problem until they share a sleeping space with someone else. Periods of silence interrupting loud snoring may reflect either the resumption of normal breathing or pathological apneas. From Table 1. Clinical Features Associated With OSA Patient Symptoms Daytime sleepiness Snoring Witnessed apneas Sleep fragmentation resulting in non-refreshing sleep Nocturia Morning headaches Dry mouth in the morning Mood, memory, and learning problems Patient Signs Obesity Larger neck circumference (men, . 17 in; women, . 16 in) Crowded oropharynx Retrognathia Systemic hypertension, particularly drug-resistant Abbreviation: OSA, obstructive sleep apnea.


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a practical point of view, snoring should be taken seriously if it occurs . 2 nights per week, is loud enough to be audible in other rooms, induces a bed partner to move to a separate room, is associated with witnessed apneas, and/or is associated with other symptoms of OSA, such as excessive daytime sleepiness or neurocognitive impairment.


Witnessed Apneas

of an intrusion of sleep during normally active situations, such as eating or talking. Patients in the early stages may have subtle and easily ignored tendencies to sleep, especially during sedentary activities, such as reading, watching TV, or computer-based activities. Patients may also underestimate the severity of sleepiness, which may reflect a genuine underestimation and/or reluctance to admit the symptom for social or work-related reasons.

Complaint by a bed partner concerning breathing pauses is a common reason for referral to a sleep clinic. Indeed, the bed partners often provide useful information regarding the characteristics and frequency of the patient’s breath pauses during sleep. Patients are often unaware of nocturnal obstructive breathing symptoms and only learn of the nature of these symptoms from a bed partner. Although witnessed apneas are considered a good diagnostic predictor of OSA, they do not predict the severity of the disorder.42,43 Witnessed apneas are also less common in females with OSA.44 Importantly, they should be distinguished from conditions such as bronchial asthma and congestive heart failure.

Patients with OSA often report daytime symptoms such as fatigue, memory impairment, personality changes, morning headaches, automatic behavior, and depression. Patients with OSA and daytime sleepiness also have an increased risk of vehicular accidents.47 Effective treatment with CPAP has been shown to decrease the risk to the same level as that of the rest of the population.48 The increased crash risk in patients with OSA can have medicolegal implications. It is therefore important for practicing physicians to be aware about the relevant laws in their individual state.

Insomnia

Diagnosis of OSA

Most patients with OSA have little difficulty in initiating sleep, and the sleep latency objectively recorded is typically shorter than in patients free from OSA. However, some patients with OSA may complain of insomnia, which most likely reflects their perception of recurrent arousals during sleep.45 Women, in particular, are less likely to report the classic symptoms of witnessed apneas and daytime sleepiness, and may instead present with a chief complaint of insomnia.46

Restless Sleep

Agitation, restlessness, and abnormal body movements are common during episodes of obstructive apnea. Patients themselves may note crumpled bed-sheets, pillows, and comforters in the morning, or their bed partner may complain about being accidentally hit during the night.

Other Nocturnal Symptoms

Nocturia, enuresis, excessive salivation, gastroesophageal reflux, diaphoresis, and impotence are symptoms that may also be reported by patients or their bed partners.

Daytime Symptoms

Excessive Daytime Sleepiness Excessive daytime sleepiness is a chief clinical consequence of OSA. Pathological sleepiness can be easily determined from the medical interview because patients will complain 60

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Other Daytime Symptoms

The diagnosis of OSA is based on the presence of characteristic clinical symptoms and objective evidence of OSA. Physical findings are fairly non-specific and commonly include obesity, crowded upper airways, increased neck circumference (. 17 inches in men, . 16 inches in women), retrognathia, overjet, macroglossia, and BMI $ 30 kg/m2. Various screening tools have been designed to evaluate the risk of OSA, including the Epworth Sleepiness Scale (ESS), STOP-Bang questionnaire, and the Berlin questionnaire.49,50 There is no gold standard, but the easiest and the most practical assessment tool is the ESS.51 It is a questionnaire answered by the patient. The ESS contains 8 questions regarding the occurrence of unintended sleep periods during certain monotonous situations (for example, sitting and reading, watching TV, or lying down in the afternoon) in daily life. The major advantages of the ESS are that it is simple, quick, inexpensive, and has a high test-retest reliability. Drawbacks include a poor correlation with the severity of sleep apnea. A sum score of $ 10 of 24 points may indicate a clinically relevant impaired daytime wakefulness. Importantly, a score , 10 points does not always exclude a relevant impairment of vigilance.

Polysomnography

Polysomnography (PSG) is the most comprehensive and reliable monitoring method for the diagnosis of sleep


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apnea. It involves monitoring of a patient by a qualified sleep technician in a sleep lab while measuring a variety of physiological parameters, including electroencephalogram, electromyogram, electro-oculogram, electrocardiogram, snore microphone, body position, leg movements, oronasal airflow, chest and abdominal efforts, oxyhemoglobin saturation, as well as using video recording of the patient.52 A sleep study is performed during usual sleep hours with 6 hours of video recording optimally needed to establish the diagnosis of OSA. Usually, the patient returns to the laboratory for a follow-up sleep study to establish adequate pressures required to eliminate respiratory events. In cases of severe sleep apnea with significant oxyhemoglobin desaturations, a split-night study is performed in which the initial portion of the study establishes the diagnosis and the latter part estimates the optimal positive pressure required for adequate treatment. A successful split-night study (ie, sleep apnea is resolved) obviates the need for a subsequent titration study, making it more economical and easier for the patient. The inherent drawback includes a limited time available to establish the optimal positive pressure settings. The use of PSG provides a highly specific and sensitive test for patients with a high pre-test probability. However, patients with a low pre-test probability of OSA may have a false-negative rate of 20%.53,54

Home Portable Monitoring

Home portable monitoring (PM) is an alternate diagnostic modality for OSA in select patient populations and involves an in-home, unattended diagnostic study.55 Use of PM differs from PSG mainly in that it measures fewer physiological parameters. Because home monitors cannot determine the actual sleep time, AHI cannot be determined. The resultant index is therefore known as the respiratory disturbance index (RDI), which represents the frequency of apnea and hypopnea per hour of the recorded time. Since the total recorded time often exceeds the actual sleep time of the patient, RDI from portable monitors often under-represents the severity of OSA. Hence, a negative result from a portable monitor does not necessarily rule out the diagnosis of OSA. In 1994, the American Sleep Disorders Association, now the American Academy of Sleep Medicine (AASM) classified sleep testing into 4 types based on the number of signals recorded.56 Type 1 testing is full, attended, in-laboratory PSG. It measures a minimum of 7 signals. Type 2 consists of an equivalent number of channels as type 1, with the singular difference being that the study is not attended by a technician.

Type 3 monitors record a minimum of 4 signals, including ECG or heart rate, oxygen saturation, and at least 2 respiratory channels. Type 4 is made up of only 1 or 2 channels, typically including oxygen saturation or airflow. Although PM is less costly and more convenient for the patient, absence of direct supervision by a sleep technician increases the likelihood of data loss, thereby resulting in poor quality sleep studies. However, portable sleep monitoring can be used in patients with a high pre-test probability of moderate-to-severe sleep apnea, who have no significant comorbidities or concomitant sleep disorders (parasomnia, periodic limb movement disorder). Portable sleep monitoring should not be used in the absence of a comprehensive sleep evaluation by a board-certified sleep professional nor should it be used for OSA screening and diagnosing other sleep disorders.57

Management of OSA

Management of the patient with OSA should be approached as a chronic disease requiring a long-term, multidisciplinary treatment strategy.58 The diagnosis, severity, risk factors, symptoms, and health consequences of untreated OSA should be thoroughly discussed with the patient. A special emphasis should also be placed on discussing the hazards of driving with those patients with untreated sleep apnea and increased daytime somnolence. Patient education should optimally be delivered as part of a multidisciplinary, chronic disease management team, including the sleep physician, the referring provider, and allied health care providers. Management of OSA includes behavioral, medical, and surgical options (in appropriate situations), outlined in detail below.

Behavioral Modifications

Behavioral modifications should be discussed with all patients with identifiable risk factors for OSA. Behavioral modifications include but are not limited to weight loss, alcohol avoidance, and advice on sleep positions. Methods of losing weight and the potential of improvement in the severity of OSA with weight loss should be discussed with all obese patients.59 Appropriate sleeping position (discouraging sleep in the supine position) should be discussed, especially in patients with positional OSA. Patient counseling about sleep hygiene (maintaining a regular sleep-wake schedule) and avoidance of alcohol and sedatives (given their ability to reduce upper airway muscle tone, thereby worsening OSA) is an integral part of the management of the patient with OSA.


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Noninvasive Positive Pressure Therapy

Noninvasive positive airway pressure remains the mainstay in the treatment of patients with OSA and is the first-line therapy in all patients for whom treatment is indicated. The Centers for Medicare and Medicaid Services reimburses noninvasive positive pressure therapy for patients who have an AHI . 15 or those patients with an AHI between 5 and 15 with concurrent increased daytime somnolence, hypertension, stroke, ischemic heart disease, or mood disorders.60 The various modes of positive pressure therapy include CPAP, auto-titrating positive airway pressure, bi-level positive airway pressure, and adaptive servo-ventilation.


Continuous Positive Airway Pressure

The use of CPAP has become the mainstay of treatment for patients with OSA.61 Continuous positive airway pressure is conventionally delivered via a nasal mask at a fixed pressure that remains constant throughout the respiratory cycle. The proposed mechanism of action of CPAP is that it acts as a pneumatic splint maintaining the patency of the upper airway in a dose-dependent fashion. It does not exert its effect by increasing upper airway muscle activity and thus acts only as a treatment and not a cure for patients with OSA.62 In patients with moderate-to-severe sleep apnea, use of CPAP improves sleep quality (decrease in the number of arousals), nocturnal oxygen saturations, daytime alertness, and health care utilization. The literature regarding the beneficial effects of CPAP on hypertension has been inconsistent and variable. It should be noted that most published studies in the field of sleep apnea have significant methodologic limitations including: 1) small sample size; 2) most of the studies were performed on men; 3) different ways of measuring blood pressure or diagnosing and treating OSA; 4) variations in the study design; and 5) different statistical analyses. The result of a meta-analysis by Alajmi et al63 revealed the effects of CPAP were modest and not statistically significant; use of CPAP reduced patient systolic blood pressure (SBP) rate by 1.38 mm Hg and diastolic blood pressure (DBP) rate by 1.52 mm Hg.64 However, in trials of patients with more severe OSA (mean AHI . 30), use of CPAP significantly reduced SBP and DBP by 3.03 mm Hg and 2.03 mm Hg, respectively. The meta-analysis by Haentjens et al26 covered only placebo-controlled randomized studies with data for 24-hour ambulatory blood-pressure monitoring and showed that CPAP intervention significantly decreased patient 24-hour mean BP by 1.69 mm Hg.26 Both meta-analyses concluded that CPAP reduced BP rates in patients, especially in those with a more severe degree of OSA. Some data suggest that 62

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the prevalence of OSA may exceed 80% in patients with refractory hypertension (ie, persistent despite treatment with . 2 medications).63 The Joint National Commission on Hypertension VII has listed sleep apnea as the first among all treatable causes of hypertension. Nonadherence to treatment with CPAP is a significant problem in clinical practice. By CMS rules, adherence is defined as the patient use of a CPAP device for $ 4 hours per night for $ 70% of the nights during any given consecutive 30-day period.65 When patients are asked about their CPAP use, subjective compliance ranges from 65% to 90%. Objective measures of CPAP compliance, however, demonstrate that both new and long-term patients overestimate their CPAP use.66,67 Long-term objective follow-up has shown that approximately 68% of patients with OSA continue to use their CPAP after 5 years. Patients reporting problems during their initial night with CPAP therapy are typically less likely to use CPAP on a regular basis.68 Typical problems that may lead to a reduced compliance with CPAP therapy include claustrophobia, nasal congestion, and poor mask fit, leading to leaks and skin irritation. Several factors can improve CPAP compliance, including airway humidification, proper selection of CPAP interface (nasal mask versus nasal pillows versus full face mask), and prompt and aggressive management of adverse effects related to CPAP use. Full face masks may help patients who are mouth breathers, have chronic nasal congestion, or those who are intolerant to nasal masks. Patient education has also been shown to improve CPAP compliance. Simple interventions, such as weekly phone calls may improve patient compliance, especially when performed in the initial weeks of therapy.69 To continue to receive payment (insurance reimbursement) for CPAP after the initial 3 months of therapy, the patient must be clinically reevaluated between days 31 and 91 during the initial treatment period. Physicians and other health care providers must document evidence of symptom improvement and objective CPAP adherence for patients to continue with CPAP therapy. Patients who fail the initial 12-week trial are eligible to requalify for a CPAP device but must have a face-to-face clinical reevaluation by the treating physician to determine the etiology of the failure to respond to CPAP therapy and the patient must undergo a repeat sleep test in a facility-based setting.

Auto-Titrating Positive Airway Pressure

Auto-titrating positive airway pressure (APAP), using a proprietary algorithm, will automatically increase or decrease the continuous pressure a device provides for the patient on


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the basis of identified respiratory events. The APAP device is particularly useful for patients who require higher pressures in the supine than the nonsupine position. Rather than using a single constant pressure, such devices automatically adjust the continuous pressure to meet the patient’s pressure requirement for any given body position. Another capacity of the APAP device is to identify a fixed, single pressure for subsequent patient treatment with a conventional CPAP device. Use of an APAP device is not currently recommended for patients with heart failure, significant lung disease, obesity-hypoventilation syndrome, or for patients who have undergone upper airway surgeries.70


Bi-Level Positive Airway Pressure

Bi-level positive airway pressure (BPAP) devices deliver two independently adjusted levels of pressure: high pressure during inhalation and a low pressure during exhalation. Although studies have not shown an improvement in patient adherence, select patients seem to tolerate use of BPAP better than CPAP, particularly when high pressures are required.71 The AASM suggests BPAP be used when CPAP pressure exceeds 15 cm water.72 Use of BPAP may also benefit patients with hypoventilation that persists despite CPAP therapy.

Adaptive Servo-Ventilation

Approximately 10% of patients who appear to have OSA during diagnostic testing develop central sleep apnea (CSA) on CPAP titration. This group of patients is said to have complex sleep apnea (treatment-emergent CSA).73 Patients with complex sleep apnea tolerate CPAP poorly because of increased sleep disruptions resulting from CSA events. Adaptive servo-ventilation (ASV) is one of the new versions of positive airway pressure that may be helpful in the treatment of patients with complex sleep apnea.74 Because of its complexities, patients with complex sleep apnea should be referred to a sleep center for further evaluation and treatment.

Other Treatment Options Oral Appliances

Oral appliances (OAs) may improve patient upper airway patency during sleep by enlarging the upper airway and/or decreasing upper airway collapsibility.75 Oral a ppliances are broadly divided into mandibular-advancement devices (protrude the mandible forward) and tongue-retaining devices (hold only the tongue in a forward position). Oral appliances are an alternative treatment option for patients with OSA who are unwilling or unable to comply with CPAP therapy. Use of OAs are indicated in patients with mild-to-moderate OSA

who prefer OAs to CPAP therapy.76 Studies comparing OAs to CPAP therapy have demonstrated that CPAP therapy is superior to OAs in reducing patient BP rates, AHI, and oxygen desaturations, as well as in improving sleep efficiency.77 Patients with significant periodontal disease, temporomandibular disease, or lack of sufficient dentition are not candidates for OA use. Follow-up sleep monitoring is needed to verify the efficacy of OA therapy. Patients using OAs also require long-term medical and dental follow-up care.

Upper Airway Surgery

Surgical treatment of patients with OSA is directed primarily toward the correction of defined anatomic deformities that clearly obstruct the upper airway, such as enlarged adenoids or tonsils, deviated nasal septum, and obstruction of the nasal valve.78 Different surgical procedures have been described, including uvulopalatopharyngoplasty (UPPP), which consists of removal of the tonsils, uvula, and part of the soft palate. Overall, UPPP effectively addressed OSA in only 50% of patient cases.79 Unless rigorous preoperative measurements to identify the patient site of airway obstruction is carried out, the success of UPPP seems to be a chance occurrence.80 Maxillomandibular advancement, which involves moving the patient mandible and maxilla anteriorly, creates more physical space for the tongue and can resolve OSA in some patients. Most studies show a 75% to near 100% success rate in treating patients with sleep apnea using maxillomandibular advancement.81 The procedure is one of the most invasive among those used for OSA treatment and requires a longer convalescence period. Tracheostomy is a definitive surgical treatment for the treatment of patients with sleep apnea. The site of airway occlusion during sleep is bypassed, such that unobstructed breathing can be restored. It is considered as the treatment of last resort, and usually reserved for those patients with severe, life-threatening OSA who are unwilling to use CPAP.

Conclusion

Obstructive sleep apnea is a common medical condition with significant cardiac, metabolic, and neurocognitive consequences. Patients with OSA also have increased utilization of health resources. Despite all the recent advances in the diagnosis and management of patients with OSA, the majority of patients with OSA still remain undiagnosed. Family practitioners and primary care physicians can play an increasing role in promoting awareness of OSA in the community, which will go a long way in promoting early diagnosis and timely therapeutic interventions for affected patients.


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Conflict of Interest Statement

Asad Kabir, MD, Sarah Ifteqar, MD, and Abid Bhat, MD, disclose no conflicts of interest.


References

1. No authors listed. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The report of an American Academy of Sleep Medicine Task Force. Sleep.1999;22(5):667–689. 2. Dyken ME, Yamada T, Glenn CL, Berger HA. Obstructive sleep apnea associated with cerebral hypoxemia and death. Neurology. 2004;62(3):491–493. 3. Pack AI. Advances in sleep-disordered breathing. Am J Resp Crit Care Med. 2006;173(1):7–15. 4. Punjabi NM. The epidemiology of adult obstructive sleep apnea. Proc Am Thorac Soc. 2008;5(2):136–143. 5. Berry RB, Budhiraja R, Gottlieb DJ, et al; American Academy of Sleep Medicine. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2012;8(5):597–619. 6. Iber C, Ancoli-Israel S, Chesson AL Jr, Quan SF; for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events. Rules, Terminology and Technical Specifications. Westchester, IL: American Academy of Sleep Medicine; 2007. 7. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Eng J Med. 2000;342(19):1378–1384. 8. Kim HC, Young T, Matthews CG, Weber SM, Woodward AR, Palta M. Sleep-disordered breathing and neuropsychological deficits. A population-based study. Am J Resp Crit Care Med. 1997;156(6): 1813–1819. 9. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Eng J Med. 1993;328(17):1230–1235. 10. Newman AB, Foster G, Givelber R, Nieto FJ, Redline S, Young T. Progression and regression of sleep-disordered breathing with changes in weight: the Sleep Heart Health Study. Arch Intern Med. 2005;165(20):2408–2413. 11. Lopez PP, Stefan B, Schulman CI, Byers PM. Prevalence of sleep apnea in morbidly obese patients who presented for weight loss surgery evaluation: more evidence for routine screening for obstructive sleep apnea before weight loss surgery. Am Surg. 2008;74(9):834–838. 12. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med. 2002;165(9):1217–1239. 13. Bixler EO, Vgontzas AN, Lin HM, et al. Prevalence of sleep-disordered breathing in women: effects of gender. Am J Resp Crit Care Med. 2001;163(3 Pt 1):608–613. 14. Young T, Finn L, Austin D, Peterson A. Menopausal status and sleepdisordered breathing in the Wisconsin Sleep Cohort Study. Am J Resp Crit Care Med. 2003;167(9):1181–1185. 15. Li KK, Kushida C, Powell NB, Riley RW, Guilleminault C. Obstructive sleep apnea syndrome: A comparison between Far-East Asian and white men. Laryngoscope. 2000;110(10 Pt 1):1689–1693. 16. Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A. Effects of age on sleep apnea in men: I, prevalence and severity. Am J Respir Crit Care Med. 1998;157(1):144–148. 17. Young T, Shahar E, Nieto FJ, et al; Sleep Heart Health Study Research Group. Predictors of sleep-disordered breathing in community-dwelling adults: the Sleep Heart Health Study. Arch Intern Med. 2002;162(8):893–900. 18. Grunstein RR, Sullivan CE. Sleep apnea and hypothyroidism: mechanisms and management. Am J Med. 1988;85(6):775–779. 19. Grunstein RR, Ho KY, Sullivan CE. Sleep apnea in acromegaly. Ann Intern Med. 1991;115(7):527–532.

64

07_Bhat.indd 64

20. Wetter DW, Young TB, Bidwell TR, Badr MS, Palta M. Smoking as a risk factor for sleep-disordered breathing. Arch Intern Med. 1994;154(19):2219–2224. 21. Schellenberg JB, Maislin G, Schwab RJ. Physical finding and the risk for obstructive sleep apnea. The importance of oropharyngeal structures. Am J Respir Crit Care Med. 2000;162(2 Pt 1):740–748. 22. Younes M, Ostrowski M, Thompson W, Leslie C, Shewchuk W. Chemical control stability in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 2001;163(5):1181–1190. 23. Nieto FJ, Young TB, Lind BK, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA. 2000;283(14):1829–1836. 24. Brooks D, Horner RL, Kozar LF, Render-Teixeira CL, Phillipson EA. Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model. J Clin Invest. 1997;99(1):106–109. 25. Logan AG, Perlikowski SM, Mente A, et al. High prevalence of unrecognized sleep apnea in drug resistant hypertension. J Hypertens. 2001;19(12):2271–2277. 26. Haentjens P, Van Meerhaeghe A, Mascariello A, et al. The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a metaanalysis of placebo-controlled randomized trials. Arch Intern Med. 2007;167(8):757–764. 27. Franklin KA, Nilsson JB, Sahlin C, Naslund U. Sleep apnoea and nocturnal angina. Lancet. 1995;345(8957):1085–1087. 28. Mooe T, Rabben T, Wiklund U, Franklin KA, Eriksson P. Sleepdisordered breathing in men with coronary artery disease. Chest. 1996;109(3):659–663. 29. Ceia F, Fonseca C, Mota T, et al; EPICA Investigators. Prevalence of chronic heart failure in Southwest Europe: the EPICA study. Eur J Heart Fail. 2002;4(4):531–539. 30. Hoes W, Mosterd A, Grobbee DE. An epidemic of heart failure? Recent evidence from Europe. Eur Heart J. 1998;19(Suppl L):L2–L9. 31. Chan J, Sanderson J, Chan W, et al. Prevalence of sleep-disordered breathing in diastolic heart failure. Chest. 1997;111(6):1488–1493. 32. Ferrier K, Campbell A, Yee B, et al. Sleep-disordered breathing occurs frequently in stable outpatients with congestive heart failure. Chest. 2005;128(4):2116–2122. 33. Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;163(1):19–25. 34. Kanagala R, Murali NS, Friedman PA, et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589–2594. 35. Munoz R, Duran-Cantolla J, Martinez-Vila E, et al. Severe sleep apnea and risk of ischemic stroke in the elderly. Stroke. 2006;37(6):2317–2321. 36. Sahlin C, Sandberg O, Gustafson Y, et al. Obstructive sleep apnea is a risk factor for death in patients with stroke: a 10-year follow-up. Arch Intern Med. 2008;168(3):297–301. 37. Reichmuth KJ, Austin D, Skatrud JB, Young T. Association of sleep apnea and type II diabetes: a population-based study. Am J Respir Crit Care Med. 2005;172(12):1590–1595. 38. Harsch IA. Schahin SP, Radespiel-Troger M, et al. Continuous positive airway pressure treatment rapidly improves insulin sensitivity in patients with obstructive sleep apnea syndrome. Am J Respir Crit Care Med. 2004;169(2):156–162. 38. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 2nd ed. Darien, IL: American Academy of Sleep Medicine; 2005. 39. Kingshott RN, Sime PJ, Engleman HM, Douglas NJ. Self assessment of daytime sleepiness: patient versus partner. Thorax. 1995;50(9): 994–995. 40. Duran J, Esnaola S, Rubio R, Iztueta A. Obstructive sleep apnea-hypopnea and related clinical features in a population-based sample of subjects aged 30–70 yr. Am J Respir Crit Care Med. 2001;163(3 Pt 1):685–689. 41. Gottlieb DJ, Yao Q, Redline S, Ali T, Mahowald MW. Does snoring predict sleepiness independently of apnea and hypopnea frequency? Am J Respir Crit Care Med. 2000;162(4 Pt 1):1512–1517.


10/11/13 3:12 PM


Obstructive Sleep Apnea in Adults 42. Deegan PC, McNicholas WT. Predictive value of clinical features for the obstructive sleep apnoea syndrome. Eur Respir J. 1996;9(1): 117–124. 43. Hoffstein V, Szalai JP. Predictive value of clinical features in diagnosing obstructive sleep apnea. Sleep. 1993;16(2):118–122. 44. Young T, Hutton R, Finn L, Badr S, Palta M. The gender bias in sleep apnea diagnosis. Are women missed because they have different symptoms? Arch Intern Med. 1996;156(21):2445–2451. 45. Krawkow B, Melendrez D, Ferreira E, et al. Prevalence of insomnia symptoms in patients with sleep-disordered breathing. Chest. 2001;120(6):1923–1929. 46. Shepertycky MR, Banno K, Kryger MH. Differences between men and women in the clinical presentation of patients diagnosed with obstructive sleep apnea syndrome. Sleep. 2005;28(3):309–314. 47. Sassani A, Findley LJ, Kryger M, Goldlust E, George C, Davidson TM. Reducing motor-vehicle collisions, costs, and fatalities by treating obstructive sleep apnea syndrome. Sleep. 2004;27(3):453–458. 48. George CF. Reduction in motor vehicular collisions following treatment of sleep apnoea with nasal CPAP. Thorax. 2001;56(7):508–512. 49. Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991;14(6):540–545. 50. Netzer NC, Stoohs RA, Netzer CM, Clark K, Strohl KP. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med. 1999;131(7):485–491. 51. Sullivan SS, Kushida CA. Multiple sleep latency test and maintenance of wakefulness test. Chest. 2008;134(4):854–861. 52. Practice parameters for the indications for polysomnography and related procedures. Polysomnography Task Force, American Sleep Disorders Association Standards of Practice Committee. Sleep. 1997;20(6):406–422. 53. Ahmadi N, Shapiro GK, Chung SA, Shapiro CM. Clinical diagnosis of sleep apnea based on single night of polysomnography vs. two nights of polysomnography. Sleep Breath. 2009;13(3):221–226. 54. Bittencourt LR, Suchecki D, Tufik S, et al. The variability of the apnoeahypopnoea index. J Sleep Res. 2001;10(3):245–251. 55. Chesson AL Jr, Berry RB, Pack A; American Academy of Sleep Medicine; American Thoracic Society; American College of Chest Physicians. Practice parameters for the use of portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. Sleep. 2003;26(7):907–913. 56. Ferber R, Millman R, Coppola M et al. Portable recording in the assessment of obstructive sleep apnea. ASDA standards of practice. Sleep. 1994;17(4):378–392. 57. Collop NA, Anderson WM, Boehlecke B, et al; Portable Monitoring Task Force of the American Academy of Sleep Medicine. Clinical guidelines for the use of unattended portable monitors in the diagnosis of obstructive sleep apnea in adult patients. Portable Monitoring Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med. 2007;3(7):737–747. 58. Epstein LJ, Kristo D, Strollo PJ, et al; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009;5(3):263–276. 59. Smith PL, Gold AR, Meyers DA, Haponik EF, Bleecker ER. Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med. 1985;103(6; Pt 1):850–855. 60. Department of Health and Human Services. Centers for Medicare & Medicaid Services. Continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea (OSA). www.cms.hhs.gov/Transmittals/ Downloads/R35NCD.pdf. Accessed September 17, 2013. 61. Loube DI, Gay PC, Strohl KP, Pack AI, White DP, Collop NA. Indications for positive airway pressure treatment of adult obstructive sleep apnea patients: a consensus statement. Chest. 1999;115(3):863–866. 62. Strohl K, Redline S. Nasal CPAP therapy, upper airway muscle activation, and obstructive sleep apnea. Am Rev Respir Dis. 1986;134(3): 555–558.

63. Logan A, Tkacova R, Perlikowski S, et al. Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex. Eur Respire J. 2003;21(2):241–247. 64. Alajmi M, Mulgrew AT, Fox J, et al. Impact of continuous positive airway pressure therapy on blood pressure in patients with obstructive sleep apnea hypopnea: a meta-analysis of randomized controlled trials. Lung. 2007;185(2):62–72 65. Center for Medicaid and Medicare. http://www.nationwidemedical.com/ wp-content/uploads/2010/06/LCD-for-Positive-Airway-Pressure-docregion-b.pdf. Accessed June 20, 2013. 66. Kribbs NB, Pack AI, Kline LR, et al. Objective measurement of patterns of nasal CPAP used by patients with obstructive sleep apnea. Am Rev Respir Dis. 1993;147(4):887–895. 67. McArdle N, Devereux G, Heidarnejad H, Engleman HM, Mackay TW, Douglas NJ. Long-term use of CPAP therapy for sleep apnea/hypopnea syndrome. Am J Respir Crit Care Med. 1999;159(4 Pt 1):1108–1114. 68. Lewis K, Seale L, Bartle I, Watkins AJ, Ebden P. Early predictors of CPAP use for the treatment of obstructive sleep apnea. Sleep. 2004; 27(1):134–138. 69. Chervin RD, Theut S, Bassetti C, Aldrich MS. Compliance with nasal CPAP can be improved by simple interventions. Sleep. 1997;20(4):284–289. 70. Morgenthaler TI, Aurora RN, Brown T, et al; Standards of Practice Committee of the AASM; American Academy of Sleep Medicine. Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome: an update for 2007. An American Academy of Sleep Medicine report. Sleep. 2008;31(1):141–147. 71. Gay PC, Herold DL, Olson EJ. A randomized, double-blind clinical trial comparing continuous positive airway pressure with a novel bilevel pressure system for treatment of obstructive sleep apnea syndrome. Sleep. 2003;26(7):864–869. 72. Kushida CA, Chediak A, Berry RB, et al; Positive Airway Pressure Titration Task Force; American Academy of Sleep Medicine. Clinical guidelines for the manual titration of positive airway pressure in patients with obstructive sleep apnea. J Clin Sleep Med. 2008;4(2):157–171. 73. Lehman S, Antic NA, Thompson C, Catcheside PG, Mercer J, McEvoy RD. Central sleep apnea on commencement of continuous positive airway pressure in patients with a primary diagnosis of obstructive sleep apneahypopnea. J Clin Sleep Med. 2007;3(5):462–466. 74. Kuzniar TJ, Pusalaviyasagar S, Gay PC, Morgenthaler TI. Natural course of complex sleep apnea—a retrospective study. Sleep Breath. 2008;12(2):135–139. 75. Ferguson KA, Cartwright R, Roger R, Schmidt-Nowara W. Oral appliances for snoring and obstructive sleep apnea: a review. Sleep. 2006;29(2):244–262. 76. Ferguson KA, Ono T, Lowe AA, al-Majed S, Love LL, Fleetham JA. A short-term controlled trial of an adjustable oral appliance for the treatment of mild to moderate obstructive sleep apnoea. Thorax. 1997;52(4):362–368. 77. Ferguson KA, Ono T, Lowe AA, Keenan SP, Fleetham JA. A randomized crossover study of an oral appliance vs nasal-continuous positive airway pressure in the treatment of mild-moderate obstructive sleep apnea. Chest. 1996;109(5);1269–1275. 78. Li KK. Surgical therapy for adult obstructive sleep apnea. Sleep Med Rev. 2005;9(3):201–209. 79. Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep. 1996;19(2):156–177. 80. Hudgel DW, Harasick T, Katz RL, Witt WJ, Abelson TI. Uvulopalatopharyngoplasty in obstructive apnea. Value of preoperative localization of site of upper airway narrowing during sleep. Am Rev Respir Dis. 1991;143(5 Pt 1):942–946. 81. Prinsell JR. Maxillomandibular advancement surgery for obstructive sleep apnea syndrome. J Am Dent Assoc. 2002;133(11):1489–1497; 1539–1540.


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