Obstructive sleep apnea

I. What every physician needs to know.

Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder, characterized by recurrent complete or partial obstruction of the upper airway during sleep. It is typically characterized by fragmented sleep from arousals due to respiratory events and oxygen desaturations and may result in neurocognitive dysfunction, cardiovascular comorbidities, metabolic abnormalities, and even reduced survival.

Age, male gender, and obesity are the major risk factors for OSA in adults. On the other hand, adenotonsillar hypertrophy is the most common risk factor in children, although obesity, especially in adolescents, is playing a growing role in children. In women, menopause triples the prevalence of OSA. Despite the lower prevalence of obesity among Asians than Caucasians, Asians may be at higher risk for OSA due to the certain craniofacial features, such as a low-lying soft palate and steep thyromental plane. In the absence of obesity, certain craniofacial features may predispose to OSA including a wide neck circumference (>40 cm), a high Mallampati score, retrognathia, macroglossia, etc.

The basic pathology involves obstruction resulting from an imbalance between factors that enhance airway patency vs. those that promote collapse. Obstructive respiratory events occur more commonly in the recumbent position due to gravitational effects on the soft palate and tongue as well as during rapid eye movement (REM) sleep due to the associated atonia of the oropharyngeal muscles and accessory respiratory muscles. Oropharyngeal dilator muscle relaxation may be particularly problematic postanesthesia or under the influence of alcohol, benzodiazepines, narcotics, or other sedating substances.

The complete or partial collapse of the airway during sleep results in apneas and hypopneas, respectively, which culminate in arousals and/or oxygen desaturations. The arousals occur mainly from the increased negative inspiratory effort mounted against the increased upper airway resistance and are associated with the release of catecholamines (norepinephrine and epinephrine). Inflammatory markers such as C-reactive protein, tumor necrosis factor, interleukin-6, and vascular cell adhesion protein are elevated in OSA even after controlling for age and BMI. The hypoxia-reoxygenation sequence, catecholamine release, and ongoing inflammatory response lead to cardiovascular disease, metabolic disorders, and increased mortality risk. Community-based population and clinical studies have reported an increase in the prevalence and/or incidence of systemic hypertension, congestive heart failure, myocardial infarction, stroke, arrhythmias, diabetes mellitus, arrhythmias, particularly in moderate-to-severe OSA. The hazard of death is increased 4-fold in patients with moderate-to-severe OSA.

II. Diagnostic Confirmation: Are you sure your patient has Obstructive Sleep Apnea?

Firm diagnostic confirmation requires polysomnographic study. This data is obtained in a sleep laboratory where episodes of apneas, hypopneas, and respiratory effort-related arousals are measured and recorded under direct observation. An apnea is an abnormal respiratory event characterized by a ≥90% reduction in airflow from baseline lasting for at least 10 seconds. A hypopnea are defined by ≥30%–90% reduction in airflow lasting for ≥10 seconds, associated with either a ≥3%-4% drop in the arterial oxygen saturation and/or an arousal. A respiratory effort-related arousal (RERA) is characterized by a shift in the EEG waveform to the alpha, theta, or beta range following a sequence of breathing characterized by a <30% reduction of the airflow from baseline. Obstructive apneas can be distinguished from central apneas during the events based on the persistence of respiratory effort based on inductive plethysmography. Distinguishing obstructive from central hypopneas and RERAs from spontaneous arousals is more difficult and may require the use of an esophageal pressure catheter to more accurately monitor intrathoracic pressure. Esophageal pressure monitoring will reveal a progressively increasing negative intrathoracic effort leading to an arousal in obstructive hypopneas and RERAs, whereas reduced negative inspiratory effort proportional to the airflow will indicate a central hypopnea and spontaneous arousals.

A. History Part I: Pattern Recognition:

“Mr. Smith, a mildly obese, plethoric man with significant face and neck fullness, was dosing – and snoring – in the examination room chair when I entered the room.”

The classic clinical presentation of OSA is that of a middle-aged obese male adult complaining of loud snoring, excessive daytime sleepiness, and awakenings due to gasping or choking at night. Thus there may be a tendency for patients and clinical practitioners to underestimate the likelihood of OSA in younger adults, women, and patients with normal body weight. The history may be better described by the patient’s bed partner, who often is the one complaining of the loud snoring and may also be able to describe apneas, followed by a gasping resumption of breathing. Daytime sleepiness may be associated with an increased incidence of motor vehicle accidents or near-misses. In addition to daytime sleepiness, patients with OSA often report impaired cognitive function, mood disorders, morning headaches, and nocturia.

Obese patients have a high incidence of OSA. Bariatric patients are at very high risk and are usually assumed to have OSA unless they have had a sleep study that confirms they do not. Any patient with a history of respiratory arrest when taking sedating medication or postoperative hypoventilation or desaturations, particularly if the event required intubation or transfer to the ICU, should be considered at risk for OSA. Patients who report a history of stroke, systemic or pulmonary hypertension, nocturnal angina, atrial fibrillation, and diabetes mellitus should be screened for OSA, since all of these comorbidities are strongly linked with moderate-to-severe apneas and hypoxemia.

Screening questionnaires, such as the Berlin Questionnaire and the STOP-BANG Questionnaire, have been validated to assess the risk of OSA. Both questionnaires assign points for items corresponding to risk factors for OSA and predict an OSA diagnosis with sensitivities and specificities approaching 80%. These questionnaires have also been useful in identifying patients at high risk for OSA risks during surgical procedures requiring general anesthesia.

The following questions are asked in the STOP-BANG survey:

S–Snore: Do you snore loud enough to be heard through the door?…….. Yes=1

T–Tired: Do you frequently note daytime sleepiness or fatigue?…………..Yes=1

O–Observed: Has anyone observed you stop breathing while asleep?….. Yes=1

P–Pressure: Do you have high blood pressure?…………………………….. Yes=1

B–BMI: Is the patient’s BMI >35 kg/M²?……………………………………… Yes=1

A–Age greater than 50 years?……………………………………………………. Yes=1

N–Neck: Neck circumference >15.75 inches or 40cm?……………………. Yes=1

G–Gender male?…………………………………………………………………….. Yes=1

SCORE:

5–8: high risk for OSA

3–4: intermediate risk for OSA

0–2: low risk for OSA

The Epworth Scale is another screening tool to help quantitate the degree of subjective daytime sleepiness and can be used longitudinally to monitor response to therapy. This questionnaire asks the patient to estimate the probability they would fall asleep in eight different situations, rendering a score between 0–24. A score of 0–9 is considered normal and a score >9 is abnormal. Generally, the Epworth Scale can be administered as follows:

Scale Rating

0= No inclination to fall asleep

1= Slight to moderate inclination to fall asleep

2= Moderate inclination to fall asleep

3= High inclination to fall asleep

In the following circumstances:

A. Sitting or reading

B. Watching TV

C. Sitting in a public place

D. Sitting in a car for 1 hour

E. Lying down in the afternoon

F. Sitting and talking to people

G. Sitting alone after lunch

H. In a car at a traffic light

Scoring: Total points less than or equal to 9 is within normal limits. Total score >9 is abnormal.

B. History Part 2: Prevalence:

OSA should be considered in all obese patients, particularly those with adiposity of the face and neck. The American Society of Anesthesiologists identified a BMI >35 as an independent risk factor for OSA. Seventy percent of patients presenting for bariatric surgery were diagnosed with sleep disordered breathing.

The prevalence of OSA has increased over the past 2 decades likely due to the increasing prevalence of adult obesity. The Wisconsin Sleep Cohort Study first estimated the prevalence of OSA (based on an AHI ≥5/hr and subjective hypersomnolence) in 1993 to be approximately 4% in men and 2% women. However, the same longitudinal study reported much higher prevalence estimates in 2013, even when using a cut off AHI >15/hr: 10% for men younger than 50 years; 17% for men ≥50 years; 3% for women <50 years; and 9% for women ≥50 years.

C. History Part 3: Competing Diagnoses That Can Mimic Obstructive Sleep Apnea.

OSA should be distinguished from central sleep apnea syndromes, sleep-related hypoventilation, and sleep-related hypoxemia disorders. Central sleep apnea syndromes are characterized on PSG by the absence of respiratory effort accompanying the absence of airflow. Cheyne-Stokes breathing pattern, the most common type of central sleep apnea syndrome, is characterized by a crescendo-decrescendo pattern of breathing resulting from a heightened ventilator chemoresponsiveness and is associated with congestive heart failure and/or cerebrovascular disease. Sleep-related hypoventilation is distinguished from OSA based on the polysomnographic recording of sustained hypercapnia (end-tidal or transcutaneous CO₂ >50 mmHg for at least 10 minutes) due to blunted ventilatory chemoresponsiveness or reduced ventilatory capacity from obesity pulmonary disease, neurologic disorders, or thoracic musculoskeletal conditions. Obesity-hypoventilation syndrome, formerly known as the pickwickian syndrome, a prototype of sleep-related hypoventilation, is characterized by obesity, hypercapnia, and excessive daytime sleepiness. When untreated it can lead to polycythemia, pulmonary hypertension, and even death. Sleep-related hypoxemia disorders can be differentiated from OSA based on the sustained hypoxemia (SaO₂ <89% for ≥5 minutes) during sleep at night, as opposed to the saw-tooth transient dips in oxygen saturation in OSA, in the absence of hypercapnia. Other cardiopulmonary disorders, such as congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), and asthma, may also present with awakenings due to nocturnal dyspnea; however, the dyspnea in OSA is typically brief, lasting only a few seconds after awakening as opposed to several minutes in cardiopulmonary disorders. Other non-respiratory sleep disorders (e.g., restless legs syndrome/periodic limb movement disorder, narcolepsy, may also present with disrupted sleep and excessive daytime sleepiness and should be sought after if OSA is not present on polysomnography.

D. Physical Examination Findings.

Although obesity is a risk factor for OSA, thin patients may also have sleep apnea, so do not assume that a thin patient is immune. Physical examination should always start with the vital signs. The height and weight should be recorded and the BMI, calculated. Patients with certain craniofacial features, such as retrognathia, micrognathia, a small oral cavity, macroglossia, a long uvula, a low-hanging soft palate, a narrow space between tonsillar pillars, and adenotonsillar hypertrophy, reduce oropharyngeal and retropalatal spaces and predispose to OSA. The neck circumference should be measured at the level of the cricothyroid cartilage; a width of at least 16 inches (40 cm) increases the risk for OSA.

A thorough cardiopulmonary examination should be conducted to detect comorbid heart failure or lung disease, which may be associated with other types of sleep-related breathing disorders (e.g., Cheyne-Stokes breathing pattern in CHF or sleep hypoventilation in advanced COPD). Usually, there are no characteristic lung findings in OSA. Although there are no pathognomonic heart findings, cardiac arrhythmias, particularly atrial fibrillation, may be present.

More subtle features of certain endocrine disorders associated with OSA should be sought after. Bradycardia, slow reflexes, weight gain, and deepening of the voice may indicate the presence of hypothyroidism, which is associated with OSA. Acromegaly with the associated increased height, large hands and feet, a prominent jaw, and macroglossia, is associated with a high prevalence of OSA and other respiratory disorders. Women with obesity, acne, hirsutism, and menstrual irregularities may have polycystic ovarian syndrome and a high likelihood of having OSA.

E. What diagnostic tests should be performed?

If the suspicion for OSA has been raised by history or physical examination, the next recommended step is using one of the validated questionnaires to objectively assess risk. Several validated questionnaires are available to evaluate patients at risk for OSA. They include the Berlin Questionnaire, STOP-BANG questionnaire, ASA (American Society of Anesthesiology) checklist and the Epworth scale. The STOP-BANG questionnaire (see section “A” above) has been validated and is simple to implement. Three or more positive responses on the questionnaire correspond to a moderate-high risk of having OSA and less than 3 positive responses correspond to a low risk for OSA.

Associated illnesses that raise the index of suspicion include a history of hypertension, ischemic heart disease, stroke, diabetes and a history of otherwise unexplained pulmonary hypertension.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

The most definitive test is polysomnography performed by a sleep technologist overnight in an accredited sleep laboratory. The sleep study generates data on the frequency of apneas, hypopneas, and RERAs during sleep at night. The following physiologic parameters are monitored during the study: airflow via both nasal pressure transducer and thermistor/thermocouple technologies, oxygen saturation via pulse oximetry, electroencephalogram (EEG), electrooculogram (EOG), electrocardiogram (EKG), thoracic and abdominal respiratory effort via inductive plethysmography or strain gauges, chin (mentalis) and leg (anterior tibial) electromyogram (EMG). Audiovisual recording using a microphone and infrared camera is employed to record snoring and abnormal behaviors during sleep at night. A minimum of 2 hours of sleep, which is the length of a typical sleep cycle, is generally required to make a diagnosis of sleep apnea. Thus if a patient is found to have moderate-to-severe OSA (AHI ≥20/hr) during the first 2 hours of a diagnostic polysomnogram, the sleep study can be “split” and a therapeutic CPAP trial can be conducted during the remaining 3 or more hours of monitoring.

A therapeutic polysomnogram (PSG) can be performed to determine the optimal CPAP level that will eliminate/reduce the obstructive respiratory events. Patients who cannot tolerate higher CPAP levels or those requiring pressure levels beyond 20 cm H₂O can be shifted to a bilevel positive airway pressure (BPAP) mode, which can provide lower positive airway pressure during expiration to eliminate obstructive apneas and a higher inspiratory pressure (up to a maximum of 25-30 cm H₂O) to eliminate hypopneas and RERAs. Nasal pillows, which insert into the nasal vestibule, may be preferred over nasal or full-face masks by patients with claustrophobia. Mouth-breathing patients may not have success with nasal interfaces and may require a full face mask and/or a chin strap.

The diagnosis of obstructive sleep apnea requires the presence of either: (1) Moderate-to-severe OSA (respiratory disturbance index or RDI ≥15/hr) or (2) mild OSA (RDI ≥5 to <15/hr) and the presence of neurocognitive dysfunction (e.g., hypersomnolence, impaired memory, decreased vigilance), insomnia, mood disorder, cardiovascular disease (e.g., systemic hypertension, ischemic heart disease, CHF, stroke, arrhythmia), or diabetes mellitus.

The respiratory disturbance index is calculated by dividing the sum of the number of apneas, hypopneas, and RERAs by the total sleep time. Meanwhile, it is worth noting that the United States Center for Medicare and Medicaid Services only uses the AHI (apneas and hypopneas per hour of sleep) and does not include RERAs in the determination of CPAP reimbursement.

Home sleep apnea testing (HSAT) is fast-becoming the first diagnostic tool in confirming an OSA diagnosis due to its convenience, low cost, and acceptable performance characteristics. HSAT involves recording of at least 3 respiratory parameters: (1) airflow; (2) oxygen saturation; and (3) respiratory effort. HSAT can be performed to diagnose OSA patients suspected of having moderate-to-high clinical probability of the disease, to expedite diagnose in those with immobility or transportation issues due to habitus, medical disability, or critical illness, and to determine response to non-CPAP therapies, such as oral appliance devices and otorhinolaryngologic surgery.

Overnight pulse oximetry is being employed by some clinicians as a screening test for sleep apnea but is not approved for this indication because of its low sensitivity in diagnosing OSA, particularly in mild cases. The overnight pulse oximetry allows for the calculation of the oxygen desaturation index or ODI (the number of oxygen desaturations with a magnitude of ≥4% per hour of monitoring). The ODI correlates very well with the AHI but cannot account for apnea, hypopneas, or RERAs not associated with oxygen desaturations.

Other laboratory tests are usually unnecessary in the diagnosis of OSA. Screening for hypothyroidism is not recommended unless the patient presents with its clinical features, because the prevalence of hypothyroidism is not higher in OSA patients compared with the general population. On the other hand, a subset of OSA patients with severe obesity (BMI >45 kg/m²), elevated serum bicarbonate levels ≥28 mm Eq/L, respiratory neuromuscular weakness, or advanced pulmonary disease may be at risk for sleep-related hypoventilation and require capnography (ET_CO₂ monitoring) during polysomnography and daytime arterial blood gases or pulmonary function testing.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

No specific imaging studies are universally indicated.

Neck soft tissue x-rays (cephalometry) or other imaging may be needed if structural head/neck abnormality is suspected. For instance, some patients with rheumatoid arthritis with temporomandibular joint abnormality or atlantoaxial subluxation may have reduced retropalatal or retrolingual diameters due to severe retrognathia or cervical cord compression on cephalometry and cervical spine imaging, respectively. Imaging studies are usually ordered by the otorhinolaryngologist or maxillofacial surgeon if surgical therapy is contemplated.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Since the diagnosis of OSA can be established by polysomnogram or a home sleep apnea test and most patients are managed with CPAP, laboratory tests and imaging studies are generally unnecessary and should not be ordered routinely.

If it is determined that the patient will need surgery, certain imaging studies will be ordered, but this should be left to the discretion of the attending surgeon.

III. Default Management.

Continuous positive airway pressure therapy (CPAP) is the treatment of choice for OSA in adults because it is >90% effective in ameliorating OSA and is associated with salutary effects on neurocognitive function and cardiovascular disorders. On the other hand, adenotonsillectomy is the treatment of choice in children with OSA although some obese children and adolescents with OSA may still require CPAP after the procedure.

For patients who refuse CPAP or could not tolerate the device, alternative therapies include positional therapy, oral appliance therapy (e.g., mandibular advancing device), oral pressure therapy, nasal expiratory positive airway pressure, hypoglossal nerve stimulator, various otorhinolaryngologic surgeries, and bariatric surgery may be explored. These non-CPAP alternative therapies are generally not as effective as CPAP in normalizing the AHI or RDI and have not been demonstrated to ameliorate the cardiovascular complications of OSA. Meanwhile, a tracheostomy is curative in patients with OSA and may reduce mortality in patients with very severe OSA but it is rarely employed nowadays due to its invasiveness.

A. Immediate management.

All patients with a new diagnosis of OSA require a full explanation of the risk factors, mechanisms, and adverse health consequences of the disease. Overweight or obese patients should be encouraged to pursue a weight loss regimen, which may even necessitate bariatric surgery.

Patients should be cautioned about the use of alcohol, benzodiazepines, and other sedating medications because they can worsen OSA. Patients on sildenafil, a phosphodiesterase-5 inhibitor prescribed for erectile dysfunction or pulmonary arterial hypertension, should be warned about the possibility of increased number of respiratory events and worsening oxygen desaturation with its use. Patients contemplating on receiving testosterone replacement therapy should also be advised about worsening OSA, especially during the first few weeks of treatment attributed to dysregulated control of breathing. When hospitalized, opioid medications should be prescribed judiciously, and naloxone should be readily available to reverse an overdose. Patients undergoing surgical or endoscopic procedures requiring sedation or anesthesia should be cautioned about a higher risk of pulmonary complications, such as difficult intubation, respiratory failure due to upper airway obstruction, and the need for close respiratory monitoring post-sedation.

A subset of patients may have positional OSA, in which respiratory events occur predominantly when they are sleeping in the supine position. These subset of patients whose AHI or RDI decreases by 50% from the supine to the lateral position and whose nonsupine AHI or RDI is less than 10/hr may respond to positional therapy (i.e., sleeping prone or in a lateral position with the use of a positional device). If the cost of commercially available positional devices is prohibitive, creative options such as sewing a pocket containing tennis balls in the back of a snug-fitting shirt and wedge pillows can be tried. Unfortunately, the efficacy of positional therapy in normalizing the AHI is somewhat inferior to CPAP and long-term adherence with positional devices is limited (15%).

For patients with mild-to-moderate OSA, normal to near-normal BMIs, a mandibular advancing device can be effective in reducing the AHI by half in up to 45% on a long-term basis. Use of nasal steroids for chronic rhinitis symptoms reduces the AHI by a few points and facilitates use of nasal CPAP. Patients who use CPAP at home are encouraged to bring and use their devices during hospitalization, although use of CPAP in the hospital setting has not been shown to reduce length of stay or readmission rate except in postoperatively. The rate of CPAP use in the inpatient setting has been reported to be anywhere between 5% and 25%. It is prudent to avoid ordering patient-controlled analgesia (PCA) pumps in patients with known or suspected OSA, because unsupervised self-administration of analgesia can result in unmonitored profound respiratory depression.

If a patient is seen preoperatively and felt to have risk factors for OSA, some precautions should be taken. If the surgery is elective and there is time to perform polysomnography prior to surgery, this should be done. Frequently, the patient is seen just a few days prior to surgery or even a few hours prior to surgery and confirmation of suspected sleep apnea is not possible.

When a patient with OSA has surgery, extra precautions should be observed perioperatively. Patients with confirmed OSA and using CPAP at home, should bring their positive pressure equipment to the hospital and use the device at their usual pressure settings as soon as possible after surgery. The positive pressure equipment should be employed almost continuously while the patient is receiving sedating medications and anytime the patient is sleeping while in the hospital. Surgery and post-operative outcomes are better with the use of a specifically-fitted positive pressure breathing apparatus used at the predetermined pressure setting. Failure to use CPAP in the post-operative period in OSA patient has been associated with increased length of stay and increased risk of pulmonary complications.

Recommendations for patients with suspected OSA include continuous use of a pulse oximeter post-operatively, especially while they are receiving sedating medications. Narcotic analgesics and sedating medications should be used sparingly. Patient controlled anesthesia (PCA pumps) should be avoided when possible. Supplemental oxygen should be continued post-operatively until the patient is consistently maintaining oxygen saturations in the pre-hospital range . Regional anesthesia is preferred to general anesthesia and is better tolerated. Avoid extubation until the patient is fully awake post procedure. If the surgery is a same-day surgery, the patient should be observed for additional time, usually 2 hours off oxygen until he or she is able to maintain pre-hospital oxygen saturations, before discharge.

If the patient is assessed to have a high clinical risk of OSA and outpatient titration of CPAP prior to surgery is not feasible or if the patient develops clinical evidence of hypoventilation/apneas post-operatively, a trial of autotitrating continuous positive airway pressure (APAP) may be useful. The APAP device monitors airflow and adjusts the pressure level to eliminate apneas, airflow limitation, and snoring. APAP therapy has been found to be non-inferior to CPAP by at least one study. If CPAP was used in the hospital in a patient not previously known to have OSA, the patient should be sent for a sleep study at discharge. They also need to be warned about risks of operating hazardous equipment and driving.

Nocturnal CPAP has been shown to improve daytime sleepiness, cognition, occupational functioning, and quality of life. Despite this, adherence with CPAP therapy remains problematic. The rate of CPAP adherence in the outpatient setting has been reported to be around 50%–60%. Patients find the face mask cumbersome. Patients that refuse to use CPAP should be recommended for a mouth appliance trial. Benefits of CPAP therapy often results in resolution of the daytime sleepiness and a return to more normal function. Progress and improvement in symptoms may be followed with an Epworth scale. (Note: Epworth scale is discussed in Section 1.A.)

B. Physical Examination Tips to Guide Management.

Patients who are unable to tolerate CPAP with craniofacial abnormalities may be referred to ENT for evaluation for non-CPAP alternative therapies. Edentulous patients are usually not candidates for mandibular advancing devices and may be difficult to fit with a CPAP mask.

After initiation of CPAP therapy, the patient may demonstrate improvement in daytime sleepiness and fatigue and may be noticeably more alert. For patients being monitored in the hospital, one can anticipate fewer desaturation alarm alerts from the pulse oximeter monitor. After several weeks or months of CPAP therapy, blood pressure has been demonstrated by pooled studies to drop by 2 to 3 mm Hg on average in OSA patients with or without systemic hypertension, and up to 10 mm Hg in patients with hypertension on multiple medications. If the patient is on a cardiac monitor, there may be less dysrhythmia noted. Patients with atrial fibrillation who undergo cardioversion via pharmacologic or nonpharmacologic therapies (e.g., electrocardioversion) have a reduced risk of recurrence of their dysrhythmia.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Once the patient is diagnosed with OSA and successfully started on positive pressure breathing, this treatment is continued indefinitely. Patients who experience a good clinical response to therapy are disinclined to want to stop the treatment.

If a patient has had a significant change in physical status, such as significant weight loss from diet or gastric bypass/banding, then repeat sleep evaluation may be indicated to see if they still require CPAP/BiPAP or need lowering of their pressure settings.

Similarly, patients that have tested negatively for OSA may need repeat testing as they get older, gain weight, or become more symptomatic.

D. Long-term management.

The overall goal is to ameliorate daytime sleepiness and cognitive impairment, prevent the long term sequelae, such as systemic hypertension, pulmonary hypertension, congestive heart failure, acute coronary events, stroke, and even death. In addition to the well-documented relationship between OSA and cardiovascular disease, there are a host of “associated” illnesses, from diabetes to kidney disease. Some of these conditions may be causally related to OSA, but others may more accurately reflect comorbidities with common risk factors.

Positive airway pressure devices such as CPAP, BPAP (bilevel positive airway pressure), APAP (autotitrating positive airway pressure) are used with the appropriate interface (e.g., nasal pillows, nasal mask, full face mask, oronasal mask, total face mask) based on patient preference, as well as other considerations (e.g., claustrophobia, craniofacial configuration, mouth breathing, edentulousness). The most common cause of treatment failure is PAP therapy nonadherence. Factors that may associated with CPAP nonadherence include side effects from using the device (e.g., claustrophobia, pressure intolerance, aerophagia, noise, poor mask fit, discomfort or pressure-sores from the mask), early lack of confidence and long-term motivation in using the device, mild severity of OSA, lack of symptomatic response, claustrophobia, inadequate knowledge about the sequelae of the disease and the benefits of therapy, insomnia, cost concerns, and referral for sleep apnea evaluation by relatives or physician rather than self-referral. By working with the patient and trying a variety of interfaces, an acceptable solution may be reached. PAP device-related technological solutions, such as auto-titrating CPAP, BPAP instead of CPAP, and airway pressure release, have been unsuccessful in enhancing CPAP adherence. If the patient absolutely cannot tolerate positive pressure devices, then non-CPAP therapies should be offered.

Non-CPAP therapies include surgical and nonsurgical methods and are generally less effective than CPAP in ameliorating OSA. Several nonsurgical therapies for OSA have been employed, including lifestyle intervention, oropharyngeal exercises, oral appliances, nasal expiratory positive airway pressure therapy, oral pressure therapy, hypoglossal nerve stimulation, etc. All patients with OSA should be instructed to avoid heavy alcohol use and minimize use of sedating medications, especially benzodiazepines and opioids. Sildenafil for erectile dysfunction has been demonstrated to increase the number of disordered-breathing events and worsen nocturnal oxygen desaturation, Testosterone replacement for male hypogonadism can also worsen OSA, particularly during the first 6 weeks of use. Intensive life intervention (e.g., weight loss via diet and aerobic and isometric exercises) appears to modestly reduce the AHI by a few points and should generally be recommended to patients who are overweight or obese. Myofunctional therapy, which employs exercises that strengthen the oropharyngeal muscles, can also minimally improve the AHI. Oral appliance therapy, particularly mandibular advancing devices (MADs), protrudes the jaw by 50%-75% of its maximum protrusion and enlarges the oropharyngeal space. MADs are more effective in patients with mild-to-moderate OSA, normal or near-normal BMI, and positional (nonsupine) improvement in AHI. MADs have been shown to significantly reduce the AHI by half in 45%-60% of patients long-term.

Nasal expiratory positive airway pressure devices involve the application valves across the nostrils, which allow minimally impeded airflow during inhalation but resistive airflow to achieve a certain level of EPAP during exhalation. Although nasal EPAP therapy has been demonstrated to reduce the AHI, particularly in patients with mild-to-moderate OSA, a later study on patients who have been on CPAP therapy showed worsening of the AHI back to baseline with nasal EPAP therapy. Oral pressure therapy works by creating a vacuum inside the mouth by suctioning air through a port of a device placed inside the mouth during sleep. Oral pressure therapy was found to be partially effective in treating OSA and reduces the AHI by 50% on average in patients who refuse or cannot tolerate CPAP. Hypoglossal nerve stimulation involves subcutaneously implanting a device, which senses the inspiratory activity of the respiratory muscles and then sends a stimulatory impulse to the hypoglossal nerve. Hypoglossal nerve stimulation is associated with a widening of the retropalatal and retrolingual spaces during inspiration, resulting in a reduction of the AHI by 50% on average in CPAP-intolerant OSA patients.

Surgical therapies for OSA involve either otorhinolaryngologic or maxillofacial procedures to address OSA-related craniofacial features or bariatric surgery to treat obesity. Adenotonsillectomy is the treatment of choice for children with OSA, although the growing problem with obesity especially among adolescents may still necessitate the use of CPAP therapy postoperatively. In adults, there are several surgical procedures, which may be performed simultaneously or, more commonly, in a multi-staged approach. The most common adult surgical procedure for OSA is uvulopalatopharyngoplasty (UPPP), which involves the removal of the uvula, the tonsils, and part of the soft palate. Long-term efficacy (defined as reduction of AHI by 50%) of UPPP is approximately 35%. Maxillomandibular advanced involves surgical protrusion of the maxilla and mandible is very effective in treating OSA. Tracheostomy bypasses the sites of upper airway obstruction via the insertion of a tube through the extrathoracic portion of the trachea. Although effective in treating upper airway obstruction and reducing mortality in patients with very severe OSA, the procedure is rarely performed nowadays for this indication.

Medications have been considered for the primary treatment of OSA, but none of them have been found to be consistently effective because they cannot overcome the mechanical obstruction of the upper airway. Rapid eye movement suppressing agents, such as tricyclic antidepressants and selective serotonin receptor antagonists; respiratory stimulants, such as carbonic anhydrase inhibitors, theophylline, and progestins; anticholinergic agents, such as donepezil; weight loss-inducing medications, such as sibutramine, topiramate, and phentermine; and many others have failed to significantly abolish obstructive respiratory events and/or improve daytime symptoms.

On the other hand, for CPAP adherent patients who are still sleepy despite using their device for at least 4 hours nightly on at least 70% of the nights, wake-promoting medications, such as modafinil and armodafinil, may be prescribed to ameliorate hypersomnolence. For patients with chronic rhinitis, nasal steroid therapy may reduce the AHI slightly and promote comfort with nasal CPAP use. Stimulants for hypersomnia and topical or systemic decongestants for chronic rhinitis should be avoided, given their potential cardiovascular side effects. Low flow oxygen supplementation via nasal cannula is not recommended as primary treatment for OSA because the airflow rate cannot overcome the critical upper airway opening pressure in OSA and the increase in oxygen breathing reserve can suppress the hypoxemic respiratory drive and prolong the apneas and hypopneas. High flow oxygen via nasal cannula at rates of 20 L/min has been shown to partially ameliorate OSA and can be used while the patient is in the hospital but may be too costly for domestic use.

E. Common Pitfalls and Side-Effects of Management

Managing patients with OSA post operatively is a challenging task and presents a significant risk of morbidity and even mortality. Post-operative hypoventilation as a result of anesthesia and pain medications is a problem in patients without OSA and a major risk for patients with suspected or known sleep disordered breathing.

Any patient with the diagnosis of OSA and using a positive airway pressure device at home, should bring the device to the hospital when admitted for surgery, or for that matter, any other hospitalization, and it should be used at the home settings immediately post operatively and until the patient no longer requires narcotic analgesics.

Patients with suspicion of OSA, but without a diagnosis, who undergo surgery, are at risk of difficult intubation, post-operative hypoventilation, and/or respiratory arrest. If there is a high index of suspicion based on anesthesia evaluation or the STOP-BANG questionnaire, the patient should be monitored carefully and should have continuous pulse oximetry post operatively, at least while they are receiving sedating analgesia. If possible avoid the supine position; sometimes the patient may be positioned in the lateral decubitus position with good results. Regional anesthesia is considered preferable to general anesthesia.

Avoid sedating medications including benzodiazepines, barbiturates, opiates, alcohol, and antihistamines.

*A caveat: If a sedated patient is repeatedly hypoxic while wearing CPAP, reposition the head and try to achieve extension of the neck. If hypoxia persists, remove the CPAP and check the equipment for any type of obstruction or malfunction.

Suggested Orders for patients suspected to have OSA:

Continuous pulse oximetry with an alarm for O₂ saturation <90% (or below their baseline).
May use supplemental oxygen for low O₂ saturations. Saturation goal depends on comorbidities but is generally ≥90%.
Check arterial blood gases to ensure adequate oxygenation and detect possible hypercapnia/respiratory acidosis.
Elevate head of bed ≥30 degrees.
Avoid oversedation. Hold sedating medications for somnolence.
Early ambulation if possible.
Any patient with prescribed CPAP, the equipment should be used while asleep in bed even during daytime naps at the predetermined pressure settings, or the pressure settings recommended by the respiratory therapist.
Consider switching to BPAP in patients with OSA who are found to be hypoventilating (elevated PCO₂ >50 mmHg) due to sedation or other causes.
Patients who are oversedated and unable to protect their airway and/or who have worsening hypercapnia/respiratory acidosis despite BPAP will require intubation and invasive mechanical ventilation.

IV. Management with Co-Morbidities

Oversedation is a major problem in patients with OSA. Any co-morbid condition that decreases level of consciousness or increases the blood level of sedating medication can be a problem. Monitor patients with liver or kidney disease who are receiving sedating medications that are metabolized by these organs. Also consider drug interactions that may cause an increase in drug bioavailability. Because end stage renal disease is frequently associated with sleep apnea, this relationship should be kept in mind when prescribing sedating medications to patients with renal function impairment.

A. Renal Insufficiency.

Sleep apnea is common in patients with chronic renal failure and patients with OSA have increased sensitivity to sedating medications. Any sedating or analgesic medications that are excreted by the kidney may result in higher blood levels in patients with renal insufficiency and therefore, have an increased effect.

B. Liver Insufficiency.

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) have an increased incidence in patients with OSA. Incidence rate of OSA in patients with biopsy proven NAFLD or NASH was 46%, even when corrected for BMI, diabetes, triglyceride levels and cholesterol. CPAP therapy may reduce hepatocellular inflammation by preventing the oxidative damage from recurrent hypoxia-reoxygenation sequence.

Patients with OSA have increased sensitivity to sedating medications. Any sedating or analgesic medications that are metabolized by the liver may result in higher blood levels in patients with hepatic insufficiency and therefore, have an increased effect. Additionally, if the patient has hepatic encephalopathy, OSA with daytime cognitive impairment may complicate the mental status examination.

C. Systolic and Diastolic Heart Failure

Obstructive sleep apnea increases the risk of systemic hypertension, left ventricular hypertrophy, and diastolic dysfunction. A prospective study of 81 ambulatory men with CHF found 51% positive for >15 hypopneas per hour (AHI = 15). In systolic heart failure, patients may demonstrate both obstructive sleep apnea and central sleep apnea simultaneously. Consequently, patients with heart failure, systolic or diastolic, have a high incidence of OSA and should be monitored carefully for this condition, even if not previously recognized. Furthermore, the severity of nocturnal apneas may be severe, because the patient may also have concomitant central sleep apnea. CPAP has been shown to modestly reduce both systolic and diastolic BP and improve both systolic and diastolic dysfunction.

D. Coronary Artery Disease or Peripheral Vascular Disease

Studies confirm that patients with ischemic heart disease suffer ST depressions and evidence of worsening ischemia during nocturnal hypopneas, particularly in the rebreathing phase when the heart rate increases concomitantly with low oxygen saturations. These effects were ameliorated by the use of CPAP. OSA is felt to be etiologic in the development of ischemic heart disease and also worsening of symptoms of previously diagnosed coronary artery disease.

E. Arrhythmias

Arrhythmias are more prevalent in OSA patients due to the oxygen desaturations and the catecholamine (norepinephrine) surges accompanying the obstructive respiratory events. Arrhythmias associated with OSA can run from premature ventricular contractions to atrial fibrillation, and even fatal ventricular arrhythmia. OSA patients with advanced age, cardiovascular disease, and nocturnal hypoxemia, with or without prolonged Q–T syndrome, are at higher risk for sudden unexpected nocturnal death syndrome.

F. Diabetes or other Endocrine issues.

Moderate-to-severe OSA is associated with a significantly increased incidence of diabetes mellitus, up to 20% after 5 years of the diagnosis. Although CPAP may improve insulin sensitivity, it has not been associated with long-term improvement is glycemic control.

Patients with significant hypoglycemia and concomitant decreased level of consciousness are at increased risk of prolonged apneas with OSA.

Hypothyroid patients may present with many clinical features that overlap with OSA: weight, enlarged tongue, hypersomnolence, fatigue, lethargy, and even hypoventilation. However, the prevalence of hypothyroidism in OSA patients is similar to the general population, so routine screening for hypothyroidism is not recommended. Treatment of hypothyroidism with levothyroxine has been associated with reduction in the AHI.

Cushingoid patients, from endogenous or exogenous steroids, who develop truncal and neck adiposity and weight gain are at increased risk of OSA and should be monitored for this problem.

The prevalence of OSA triples after menopause so night sweats attributed to menopause may also be due to sympathetic surges associated with obstructive respiratory events during sleep. Although postmenopausal women on hormone replacement therapy (HRT) appear to have a similar prevalence of OSA, HRT should not be prescribed solely for the treatment of OSA given the thromboembolic and female neoplastic complications.

Testosterone replacement is increasingly being prescribed for male hypogonadism associated with aging and obesity. Patients with OSA should be warned that testosterone replacement may transiently worsen OSA and should be encouraged to use CPAP while on therapy. Because sildenafil, a phosphodiesterase 5 inhibitor prescribed for erectile dysfunction, can similarly increase the AHI and worsen nocturnal hypoxemia, CPAP use should be encouraged with this class of medications.

G. Malignancy.

Patients with cancer or other chronic pain syndromes who are maintained on sedating pain medication should be monitored for symptoms of OSA. Frailty and weakness that may accompany cancer also increases the risk of hypoventilation.

Treatment for head and neck cancers with chemotherapy or radiation, may result in swelling that may, in turn, predispose to develop obstructive sleep apnea.

There is a reported increased incidence of cancer in patients diagnosed with OSA, although causal relationship has been established.

H. Immunosuppression (HIV, chronic steroids, etc).

OSA is a relatively common diagnosis among HIV patients, most commonly as a result of adenotonsillar hypertrophy. One case report describes a patient with antiretroviral induced lipodystrophy with severe OSA. This patient’s BMI was only 26.1, but his neck circumference was 53 cm.

I. Primary Lung Disease (COPD, Asthma, ILD).

OSA can occur in patients with chronic obstructive pulmonary disease (COPD), sometimes referred to as overlap syndrome. In patients with severe-to-very severe COPD, sustained hypoxemia lasting for at least 5 minutes (sleep hypoxemia disorder) may still occur due to ventilation perfusion mismatch, despite providing adequate PAP levels to eliminate obstructive apneas, hypopneas, and RERAs and will require oxygen entrained via the PAP device to correct nocturnal hypoxemia. Other advanced COPD patients with hypercapnia (P_CO₂) due to concomitant sleep hypoventilation may require BPAP +/- O₂ as well. Similar issues prevail with other lung disorders, because the hypoxia is additive. Concomitant lung disease complicates the management of OSA. Each disease needs to be managed independently.

J. Gastrointestinal or Nutrition Issues.

There is a relationship between OSA and gastroesophageal reflux disease. OSA is more common in patients with GERD. Interestingly, treating GERD can improve sleep apnea and likewise, treating sleep apnea can improve the symptoms of GERD. It is not known if this is a causal relationship or not, but most seem to favor the idea that both diseases have common risk factors and therefore, tend to occur in the same population.

K. Hematologic or Coagulation Issues.

Head and neck lymphadenopathy may predispose patients to obstructive hypoventilation. Pharyngeal and soft palate swelling may result in obstructive apnea. OSA appears to be a hypercoagulable state associated with altered clotting functions and increased incidence of coronary heart disease, stroke, and venous thromboembolism.

L. Rheumatologic Disorders

Patients with rheumatoid arthritis (RA) may develop OSA not only from traditional risk factors (age, obesity, etc.) but also disease-specific mechanisms. Temporomandibular joint destruction can produce retrognathia and oropharyngeal narrowing. Atlantoaxial anterior and superior dislocation due to cervical involvement can cause compression of the cervical spinal cord and impair neurogenic control of ventilation. Mandibular advancement devices/procedures and cervical laminectomy may be considered to correct these sleep apnea-promoting RA sequelae.

M. Dementia and Psychiatric Illness.

Sedating psychoactive medications may prolong the duration of apneas and hypopneas and worsen hypoxia. Weight gain associated with certain psychiatric medications (e.g., mirtazapine) may predispose to OSA.

CPAP therapy may enhance neurocognitive function (e.g., memory, executive function) in older adults and has been associated with corresponding structural volume changes in the brain. CPAP adherence in older patients with mild dementia with OSA is not any worse than that of younger adults.

V. Transitions of Care.

A. Sign-out Considerations While Hospitalized.

When signing out to your colleagues, it’s worth mentioning the following:

Avoid oversedation; avoid PCA. Use sleeping medications with care.
Mention positional apnea, if appropriate.
If patient is using CPAP while sleeping, mention that in the cross-coverage note.
If the patient is having nocturnal symptoms or dysrhythmia, discuss management plan.

B. Anticipated Length of Stay.

Many hospitalized patients have this disorder, but it is rarely the reason for admission. Use of CPAP in hospitalized OSA patients has not been shown to affect length of stay or readmission rates in retrospective studies.

C. When is the Patient Ready for Discharge?

For patients that were not on home oxygen prior to admission, the patient should be able to maintain pre-hospital O₂ saturations for 1-2 hours without supplemental oxygen prior to discharge. If they were on home oxygen, the same rule applies, that is, they should be back to their prior baseline.

Patients with previously known OSA should be sent home on their usual CPAP or BPAP settings, unless significant changes in weight and/or respiratory function prompt adjustments. Patients with suspected but undiagnosed OSA due to known risk factors or detection of apneas and/or oxygen desaturations should be referred for polysomnography to determine the severity of OSA, to rule out concomitant sleep-related hypoventilation/hypoxemia disorder, and to retitrate PAP mode and settings.

D. Arranging for Clinic Follow-up.

The vast majority of patients with uncomplicated OSA can be diagnosed and managed by a primary care physician with appropriate knowledge and training. Patients who hesitate or refuse to undergo a sleep study or domiciliary CPAP therapy should be informed about the clinical features, mechanisms, and adverse health effect of untreated sleep apnea. Scheduling a face-to-face clinic follow-up for a formal sleep evaluation by a clinician will provide the venue for education on OSA and is generally required by most health insurance providers for reimbursing the cost of sleep studies and PAP therapies.

1. When should clinic follow-up be arranged and with whom.

A clinic follow-up for evaluation of sleep apnea should be scheduled as soon as feasible as long as the acute illness causing hospitalization has been treated or at least stabilized. Performing polysomnography when the patient is medically unstable due to decompensated CHF, COPD exacerbation, acute respiratory infection, or other untreated conditions may adversely affect the quality of the sleep study. A clinical evaluation for sleep apnea can be conducted by a primary care provider trained in the management of OSA patients. Patients with OSA complicated by very severe obesity, advanced cardiorespiratory and neurologic diseases, or other nonrespiratory sleep disorders will most likely require the evaluation and management of a sleep specialist and/or a pulmonologist.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

Although not highly sensitive and specific in diagnosing OSA, the continuous pulse oximetry report can help document the severity of oxygen desaturations and determine the urgency for diagnosis and treatment. If an echocardiogram was performed in the hospital, this can also provide evidence for sequelae of long standing hypertension (such as LVH) or evidence of pulmonary hypertension, and should be made available to the primary care doctor. Pulmonary function testing and arterial blood gas measurements may assist in evaluating and treating co-morbid respiratory disorders that can aggravate sleep-related breathing disorders.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

Although ordering a sleep study prior to a clinic visit for sleep apnea evaluation with the hope of facilitating care, scheduling a face-to-face clinic follow-up for a formal sleep apnea evaluation by a clinician prior to a sleep study will provide the venue for educating the patient regarding the clinical features, risk factors, mechanisms and adverse health consequences of OSA. Most health insurance providers generally require this face-to-face clinic visit for reimbursing the cost of sleep studies and PAP therapies.

E. Placement Considerations.

Rarely would a patient require placement for sleep apnea unless the disorder was so severe that patient required constant monitoring or assistance with PAP device use. On the other hand, many, if not most patients being referred for placement will have sleep apnea, risk factors for sleep apnea or other sleep disordered breathing. If the patient uses a positive airway pressure device, it should accompany him/her to the long-term care facility.

F. Prognosis and Patient Counseling.

With good patient adherence to OSA therapy, particularly CPAP, most patients experience significant improvement in quality of life and in symptoms of secondary disease. Counseling is key, because the treatment program requires patient participation for implementation. Weight loss alone may result in resolution of the disorder in some patients.

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.

Outcomes assessment is based on monitoring changes in weight and blood pressure, adherence to therapy (e.g., CPAP use for an average of at least 4 hours for at least 70% of the days), level of daytime sleepiness (i.e., Epworth Sleepiness Scale score), risk of motor vehicle crashes, and sleep-related quality of life (e.g., SF-36 score).

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Providing appropriate patient education and ensuring patient compliance with the planned management program are essential. High-risk OSA patients with moderate-to-severe sleepiness and a recent history of motor vehicle crash or near-miss due to sleepiness, fatigue, or inattention should be advised against driving until treatment adherence and response have been documented. When obtaining a commercial driver’s license, the department of transportation requires screening for sleep apnea and mandates adherence to therapy in patients with moderate-to-severe OSA (AHI ≥20/hr).

VII. What’s the Evidence?

Spurr, KF, Graven, MA, Gilbert, RW. “Prevalence of unspecified sleep apnea and the use of continuous positive airway pressure in hospitalized patients, 2004 National Hospital Discharge Survey”. Sleep & Breathing. vol. 12. 2008. pp. 229-234.

Sorscher, AJ, Caruso, EM. “Frequency of provision of CPAP in the inpatient setting: an observational study: CPAP provision in the inpatient setting”. Sleep & Breathing. vol. 16. 2012. pp. 1147-1150.

Proczko, MA, Stepaniak, PS, de Quelerij, M. “STOP-BANG and the effect on patient outcome and length of hospital stay when patients are not using continuous positive airway pressure”. J Anesth. vol. 28. 2014. pp. 891-897.

Mutter, TC, Chateau, D, Moffatt, M, Ramsey, C, Roos, LL, Kryger, MA. “Matched cohort study of postoperative outcomes in obstructive sleep apnea: could preoperative diagnosis and treatment prevent complications?”. Anesthesiology. vol. 121. 2014. pp. 707-718.

Abdelsattar, ZM, Hendren, S, Wong, SL, Campbell, DA, Ramachandran, SK. “The impact of untreated obstructive sleep apnea on cardiopulmonary complications in general and vascular surgery: a cohort study”. Sleep. vol. 38. 2015. pp. 1205-1210.

Nagappa, M, Mokhlesi, B, Wong, J, Wong, DT, Kaw, R, Chung, F. “The effects of continuous positive airway pressure on postoperative outcomes in obstructive sleep apnea patients undergoing surgery: a systematic review and meta-analysis”. Anesth Analg. vol. 120. 2015. pp. 1013-1023.

Bloom, HG, Ahmed, CA, Ancoli-Israel, S. “Sleep related disorders common in older patients: Strong relationship of sleep disorders and hypertension, depression, cardiovascular disease and cerebrovascular disease”. J Am Geriatrics Society. vol. 57. 2009 May. pp. 761-89.

Hauri, PJ. “The International Classification of Sleep Disorders”. 2005.

“National Patient Safety Goals, (included OSA)”. 2008.

“Obstructive Sleep Apnea and Commercial Motor Vehicle Driver Safety presented to : Federal Motor Carrier Safety Administration”. January 14th, 2008.

Gupta, RM, Parvizi, J, Hanssen, AD, Gay, PC. “Postoperative complications in patients with OSA syndrome undergoing hip or knee replacement: a case-control study”. Mayo Clin Proc. vol. 76. 2001. pp. 897

Gross, JB. “Practice Guidelines for the perioperative management of patients with OSA: A report by the American Society of Anesthesiology task force on perioperative management of patients with OSA”. Anesthesiology. vol. 104. 2006. pp. 1081-93.

Adesanya, AO, Lee, W, Greilish, ND, Joshi, GP. “Chest”. vol. 138. 2010 Dec. pp. 1489-98.

Peled, Nir, Abinader, E, Giora, P. “Nocturnal ischemic events in patients with obstructive heart disease”. JACC. vol. 34. 1999. pp. 1744-1749.

Vasu, TS, Doghramjik, Cavallazzi, R. “Obstructive sleep apnea syndrome and post operative complications: Clinical evaluation of the STOP-BANG Questionnaire”. Arch Otolaryngol Head and Neck Surgery. vol. 136. 2010 Oct. pp. 1020-4.

Chung, F. Anesthesiology. vol. 108. 2008 May. pp. 812-821.

Chung, F. Anesthesiology. vol. 110. 2009 Jan.

Jobin, V, Mayer, P, Bellemare, F. “Predictive value of automated oxygen saturation analysis for the diagnosis and treatment of OSA in a home-based setting”. Thorax. vol. 62. 2007. pp. 422-427.

Greenburg, DL. “Effects of surgical weight loss on measures of OSA: a meta-analysis”. Am J Med. vol. 122. 2009. pp. 535

Eur Respir J. vol. 9. 1996. pp. 634-635.

Stepanski, E, Faber, M, Zorick, F, Basner, R, Roth, T. “Sleep disorders in patients on CAPD”. J Am Soc Nephrol. vol. 6. 1995. pp. 192-7.

Kimmel, PL, Miller, G, Mendelson, WB. “Sleep apnea syndrome in chronic renal disease”. Am J Med. vol. 86. 1989. pp. 308-14.

Sharp, JT, Druz, WS, Souza, VD, Diamond, E. “Effect of metabolic acidosis upon sleep apnea”. Chest. vol. 87. 1996. pp. 619-24.

McNeil, Jane. “Screen sleep disorder patients for GI reflux”. May 1, 2007. pp. 39

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