Identifying obstructive sleep apnea


Airflow disturbances during sleep need to be recognized and evaluated before harm comes to the patients themselves or those around them.

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Sleep Disorders

Identifying obstructive sleep apnea

Identifying obstructive sleep apnea


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Mr. and Ms. W come into your clinic to discuss Ms. W's concern about Mr. W's snoring and gasping at night. Mr. W is a 45-year-old truck driver with a body mass index (BMI) of 35. He does note daytime sleepiness but feels he can open the window while driving to assist in maintaining his alertness. 

How can you evaluate Mr. W for a sleep disorder?

Sleep-related breathing disorders are among the most common diagnoses yet also among the most frequently underdiagnosed health problems. An estimated 50 million to 70 million Americans suffer from a chronic sleep disorder which, over time, can hinder their daily function and adversely affect their physical and emotional health.1

The most common sleep disorder is sleep apnea, in which breathing pauses during sleep, and obstructive sleep apnea (OSA) is the most common type of sleep apnea, with the etiology attributed to collapse of the soft tissue of the upper airway during sleep.

This article will review the prevalence, risk factors, clinical presentation, and tools needed to obtain a proper diagnosis of OSA. Because the information being reviewed is extensive, the treatment of OSA will be the focus of another article brought to you in the near future. 


OSA prevalence and risk factors


Many people experience OSA at some point—for instance, during an upper respiratory infection (URI) with swelling of the tonsils and upper airway. In the absence of URI, OSA prevalence in the general population is 9% among middle-aged men and 3% among women in North America.2

The strongest risk factors for OSA are obesity (BMI ≥ 30) and age older than 65 years.3 Studies have shown that surrogate markers of cardiovascular risk, including sympathetic activation, systemic inflammation, and endothelial dysfunction, are significantly increased in obese patients with OSA versus those without OSA.3

Other risk factors include a history of congestive heart failure (CHF), atrial fibrillation, treatment-refractory hypertension, or pulmonary hypertension.

High-risk driving populations (as commercial truck drivers or pilots) and those being evaluated for bariatric surgery are also at risk for OSA.4 In addition, patients with diabetes or “borderline” diabetes are up to 3 times more likely than the general population to have OSA, as OSA is independently associated with alterations in glucose metabolism.5


Alcohol ingestion can exacerbate OSA. Moderate to high amounts of alcohol consumed in the evening can lead to narrowing of the air passage, causing episodes of apnea even in persons who do not otherwise exhibit symptoms of OSA. Alcohol's general depressant effects can increase the duration of periods of apnea, worsening any preexisting OSA.4

Persons with OSA place a significant burden on the health-care system. For example, an analysis published in 1999 showed that medical expenses were approximately twice as much for patients with OSA than for patients without.6

The public-health consequences of the condition are seen almost daily, often taking the form of driving accidents. Correctly identifying OSA will not only improve quality of life for the patient but also the safety of the public.

Clinical features of OSA


The person suspected of having OSA will often complain of daytime sleepiness, or the bed partner will report that the person snores loudly, experiences nocturnal snorting and gasping, and has episodes of apnea. All patients who are the subjects of such reports should be assessed for OSA.


In OSA, the collapse of the upper airway during sleep impairs ventilation and can result in intermittent hypoxemia and hypercapnia.

The resistance to airflow causes the person to increase his/her work of breathing and gasp for air as a mechanism to reopen the airway, and causes a swing in intrathoracic pressures. The increased work of breathing can also result in disruption of sleep.7

The acute physiologic stress generated by OSA can lead to such significant cardiovascular complications as hypertension, congestive heart failure, cardiac arrhythmias, cardiac ischemia, and cerebrovascular disease. During an apnea period in sleep, carbon dioxide builds up in the bloodstream.

Chemoreceptors in the bloodstream note the high carbon dioxide levels, and the brain is signaled to wake the person sleeping and breathe in air. Breathing normally will restore oxygen levels and the person will fall asleep again. This cycle of obstructed sleep and awakenings can also cause hypoxemia. Sleep-disordered breathing is more frequently associated with oxygen desaturation in obese subjects.8

Upper-airway obstruction during sleep can be attributed to anatomic anomalies of the nasopharyngeal or mandibular areas that cause narrowing, as seen in patients noted to have a retrognathic mandible, often referred to as an overbite.

Additional causes of airway obstruction include decreased pharyngeal muscle tone, which can reduce the cross-sectional area of the upper airway and an insufficient neuromuscular response. In children, OSA may be associated with enlarged tonsils and/or adenoids. 


In patients with neuromuscular weakness, as in myasthenia gravis and muscular dystrophy, daytime sleepiness from OSA can be mistaken as progression of disease. Thus, a thorough assessment for sleepiness and possible OSA in this subset of patients is imperative.

Without proper diagnosis and treatment, these patients may experience fatigue leading to overmedication without effective treatment of the cause of fatigue.9

Screening for OSA


The diagnosis of OSA begins with a thorough sleep history. Patients should be asked about any snoring, daytime somnolence, morning headache, gasping/choking episodes at night, sleep fragmentation, decreased concentration and memory, and nocturia. (Nocturia in OSA is an evoked response due to negative intrathoracic pressure generated by attempts to inspire against a closed or narrow airway. This distends the heart, which secretes atrial natriuretic peptide and stimulates water and sodium excretion.)

In one report the most useful individual finding in patients with OSA was nocturnal choking or gasping, which had a sensitivity of 52% and specificity of 84%10

The clinician's assessment of a patient with possible OSA also should include an evaluation of secondary conditions that may occur as a result of OSA, such as hypertension and related risks for stroke, coronary heart disease, heart failure, metabolic syndrome, and type 2 diabetes.

OSA exacerbates the cardiometabolic risk attributed to obesity and the metabolic syndrome. Recognition and treatment of OSA may decrease the cardiovascular risk in obese patients. 


Recent studies have found an association between chronic obstructive pulmonary disease (COPD) and OSA.11

OSA also is associated with impaired quality of life and impaired cognitive functioning, the latter of which may be evidenced by poor school performance as well as increased risk for vehicular accidents or accidents involving other dangerous equipment.

Screening questionnaires for sleep apnea tend to have a higher sensitivity than specificity, meaning they are more useful for ruling out OSA than for diagnosing it. 


The Epworth Sleepiness Scale (ESS) employs 8 questions to measure a person's general level of daytime sleepiness. The ESS is used to distinguish sleepiness from fatigue, not specifically to wean out OSA. In patients with severe OSA, the ESS was able to identify a subset at high risk for hypertension, coronary heart disease, and cerebrovascular disease.12

STOP-Bang questionnaire: The snoring (S), tiredness (T) during daytime, observed apnea (O), and high blood pressure (P) (STOP) questionnaire is a concise and easy-to-use screening tool that helps identify patients at high risk for OSA.

The STOP questionnaire has been validated as an accurate tool for screening OSA in the presurgical population; the occurrence of perioperative and postoperative complications in persons with undiagnosed OSA, including perioperative airway collapse and postoperative desaturation, has been well recognized and can lead toward significant morbidity.13

Incorporating the factors of BMI (B), age (a), neck size (n), and gender (g) into the STOP questionnaire (STOP-Bang) can further increase the instrument's sensitivity in identifying patients who have moderate-to-severe OSA prior to surgery.14

The Berlin questionnaire consists of 10 items relating to snoring, nonrestorative sleep, sleepiness while driving, apneas during sleep, hypertension, and BMI. The results rank the patient as being at high risk or at low risk of OSA. The Berlin questionnaire has not been found to be useful in the clinic population when compared with the STOP-Bang questionnaire.14

Physical examination


OSA is most common among males aged 18 to 60 years, although menopausal woman also may be at significant risk for the condition.15 On physical exam, conditions that narrow the upper airway, as a crowded pharynx with a low-lying uvula and soft palate, are frequently seen with OSA.

Anesthesiologists assess the oral pharynx for difficulty of intubation with a system called the Mallampati score, which assesses for oropharyngeal crowding. A high Mallampati score (class 3 or 4) is associated with more difficult intubation as well as a higher incidence of sleep apnea.16

Large tonsils, a retrognathic mandible, and/or a neck circumference of more than 17 inches in men or 16 inches in women points toward the need for further investigation to determine the presence of OSA. Signs of pulmonary hypertension or cor pulmonale, such as peripheral edema or jugular venous distention, can coexist when OSA is due to obesity hypoventilation syndrome or is affiliated with hypoxemia.17

Diagnosis

Overnight pulse oximetry. As a diagnostic tool for OSA, pulse oximetry is cost-effective and shows substantial accuracy. Sensitivity and specificity remain controversial, however. Studies have noted the importance of assessing the apnea-hypopnea index (AHI) in addition to oxygen desaturation to significantly increase the oximetry's sensitivity.18

The AHI is defined as the sum of apneas and hypopneas during sleep divided by the sleep time in hours. The American Academy of Sleep Medicine uses AHI to rank OSA as mild (AHI of 5 to 14 breathing pauses per hour), moderate (15 to 29 breathing pauses per hour), or severe (30 or more breathing pauses per hour).

A person with an AHI of 5 to 15 may experience sleepiness during activity requiring little attention, as during reading or watching television; a person with an AHI of 15 to 30 may experience sleepiness during tasks requiring some attention, such as sitting at a meeting or a concert, and a person with an AHI higher than 30 may experience sleepiness in a setting requiring active attention, such as driving or speaking.

Polysomnography. Polysomnography is the gold standard for establishing the presence of OSA. This test measures neurologic (electroencephalographic) and cardiorespiratory parameters during sleep.7 As noted in the American Academy of Sleep Medicine guidelines for the performance of polysomnography,19 sleep stages are recorded by means of an electroencephalogram, an electro-oculogram, and a chin electromyogram.

Heart rhythm is monitored by a single-lead electrocardiogram. Leg movements are recorded by an anterior tibialis electromyogram. Breathing is monitored, including airflow at the nose and mouth (using both a thermal sensor and a nasal pressure transducer), effort of breathing (measured using inductance plethysmography), and oxygen saturation.

Respiratory sensors detect any decrease in ventilation during sleep. These episodes are manifested as a reduction in ventilation of at least 50% resulting in a decrease of arterial saturation of 4% or more due to partial airway obstruction (hypopnea) or complete cessation of airflow with ongoing respiratory effort (apnea).

According to the American Academy of Sleep Medicine, obstructive apneas are defined as a near-complete cessation of airflow for more than 10 seconds, a partial decrease in airflow for more than 10 seconds, or respiratory-effort-related arousal (the effort to breathe actually awakens the person). 


On the polysomnogram, OSA in adults shows more than 15 obstructive apneas per hour of sleep, lasting at least 10 seconds, or more than 5 obstructive apneas per hour of sleep in a patient reporting one of the following:19

  • Frequent arousals from sleep; daytime somnolence; unrefreshing sleep; insomnia

  • Waking up breath-holding, gasping, or choking

  • Observation by bed partner of loud snoring, breathing interruptions, or both

  • Bradytachycardia

  • Arterial oxygen desaturation.


Home sleep testing (HST). Although a person's sleep can be most thoroughly evaluated in an in-lab sleep study, home sleep testing (HST) can be a good alternative for individuals who are housebound or elderly, have a chronic illness, or are unable to take time away for an in-lab study.

HST uses similar respiratory equipment as polysomnography and pulse oximetry. Reported sensitivity of the HST ranges from 86% to 100%, and specificity ranges from 64% to 100%.20

HST keeps the person in his or her natural sleeping environment and is substantially less expensive and more widely available than in-facility polysomnography. However, persons being considered for HST should have the ability to troubleshoot technical problems and place the equipment properly so that the test does not yield inconclusive results or inaccurate readings.

Patients with a high pretest probability of OSA should undergo polysomnography rather than HST, as the latter can have a high false-negative value.

Part 2 of this discussion, focusing on effective treatments for OSA, will appear in an upcoming issue of The Clinical Advisor.

Susan Collazo, RN, MSN, APN-CNP, specializes in thoracic surgery at Northwestern Memorial Hospital in Chicago, with extensive experience in pulmonary medicine and internal medicine. 


References 


  1. National Research Council. Sleep Disorders and Sleep Deprivation: An Unmet Public Health Problem . Washington, D.C.: National Academies Press; 2006. Available at iom.edu/Reports/2006/Sleep-Disorders-and-Sleep-Deprivation-an-unmet-public-health-problem.aspx
  2. Rapid Response Report: Summary with Clinical Appraisal. CPAP treatment for Adults with Obstructive Sleep Apnea: Review of the Clinical and Cost-effectiveness and Guidelines. Canadian Agency for Drugs and Technologies in Health: Ottawa, Ontario, Canada; November 18, 2013. Available at www.cadth.ca/en/publication/4038
  3. Drager LF, Togeiro SM, Polotsky VY, Lorenzi-Filho G. Obstructive sleep apnea: a cardiometabolic risk in obesity and the metabolic syndrome. J Am Coll Cardiol. 2013;62(7):569-576.
  4. Balk EM, Moorthy D, Obadan NO, et al. Diagnosis and Treatment of Obstructive Sleep Apnea in Adults. Comparative Effectiveness Review No. 32. Rockville, Md.: Agency for Healthcare Research and Quality Publication No. 11-EHC052-EF; July 2011. Available at effectivehealthcare.ahrq.gov/index.cfm/search-for-guides-reviews-and-reports/?productid=731&pageaction=displayproduct
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  6. Kapur V, Blough DK, Sandblom RE, et al. The medical cost of undiagnosed sleep apnea. Sleep . 1999;22(6):749-755. Available at journalsleep.org/ViewAbstract.aspx?pid=24161 

  7. Kapur VK. Obstructive sleep apnea: diagnosis, epidemiology, and economics. Respir Care. 2010;55(9):1155-1167.

  8. Ling IT, James AL, Hillman DR. Interrelationships between body mass, oxygen desaturation, and apnea-hypopnea indices in a sleep clinic population. Sleep . 2012;35(1):89–96.
  9. Guilleminault C, PhilipP, Robinson A. Sleep and neuromuscular disease: bilevel positive airway pressure by nasal mask as a treatment for sleep disordered breathing in patients with neuromuscular disease. J Neurol Neurosurg Psychiatry. 1998;65(2):225-232. Available at jnnp.bmj.com/content/65/2/225.long
  10. Myers KA, Mrkobrada M, Simel DL. Does this patient have obstructive sleep apnea?: The Rational Clinical Examination systematic review. JAMA . 2013;310(7):731-741.
  11. Mieczkowski B, Ezzie ME. Update on obstructive sleep apnea and its relation to COPD. Int J Chron Obstruct Pulmon Dis. 2014;9:349-362. 

  12. Feng J, He QY, Zhang XL, Chen BY; Sleep Breath Disorder Group, Society of Respiratory Medicine. Epworth Sleepiness Scale may be an indicator for blood pressure profile and prevalence of coronary artery disease and cerebrovascular disease in patients with obstructive sleep apnea. Sleep Breath. 2012;16 (1):31-40.
  13. Chung F, Subramanyam R, Liao P, et al. High STOP-Bang score indicates a high probability of obstructive sleep apnoea. Br J Anaesth. 2012;108(5):768-775. Available at bja.oxfordjournals.org/content/108/5/768.full.pdf+html?sid=2dc20d67-5b3f-404e-9741-0c06a68c284b
  14. Cowan DC, Allardice G, MacFarlane D, et al. Predicting sleep disordered breathing in outpatients with suspected OSA. BMJ Open. 2014;4(4):e004519. Available at bmjopen.bmj.com/content/4/4/e004519.abstract
  15. Bixler EO, Vgontzas AN, Lin HM, et al. Prevalence of sleep-­disordered breathing in women: effects of gender. Am J Respir Crit Care Med. 2001;163(3 Pt 1):608-613. Available at atsjournals.org/doi/full/10.1164/ajrccm.163.3.9911064#.U-jrwPldVWY
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  17. Minai OA, Ricaurte B, Kaw R, et al. Frequency and impact of pulmonary hypertension in patients with obstructive sleep apnea syndrome. Am J Cardiol. 2009;104(9):1300-1306.
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All electronic documents accessed August 15, 2014. 


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