Obstructive Sleep Apnea (OSA)
Primer
Obstructive Sleep Apnea (OSA) is a sleeping disorder characterized by multiple episodes of cessation of breathing, lasting at least 10 seconds with desaturations and arousals. OSA also involves episodes of upper (pharyngeal) airway obstruction (apneas and hypopneas) during sleep. Apnea is the complete obstruction of airflow, and hypopnea is a reduction in airflow. It is the most common breathing-related sleep disorder.
Prevalence
OSA affects 1-2% of children, 2-15% of middle-age adults, and more than 20% of older individuals.
Undiagnosed OSA may be very high in elderly individuals.
It is estimated that the majority (80%) of individuals with sleep apnea are not diagnosed.
Since it is strongly associated with obesity, areas with high obesity rates also likely to have high rates of OSA.
Comorbidity
Individuals with OSA are at a significantly higher risk for developing obesity, hypertension, atrial fibrillation and other arrhythmias, heart failure, stroke and transient ischemic attacks (TIAs), coronary heart disease, Type 2 diabetes, and dyslipidemia. More recent research has also shown a link between OSA and an increased risk for developing dementia.
Risk Factors
DSM-5 Diagnostic Criteria
Criterion A
Either item (1) or (2) is present:
Evidence by polysomnography of at least 5
obstructive apneas or hypopneas per 1
hour of sleep and either of the following sleep symptoms:
(A) Nocturnal breathing disturbances: snoring, snorting/gasping, or breathing pauses during sleep. AND/OR
(B) Daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportunities to sleep that is not better explained by another mental disorder (including a sleep disorder) and is not attributable to another medical condition.
Evidence by polysomnography of 15
or more obstructive apneas and/or hypopneas per hour of sleep regardless of accompanying symptoms
Apnea-Hypopnea Index (AHI)
Apnea-Hypopnea Index (AHI)
AHI (events/hours) | Severity |
0-5 | Normal |
5 - 15 | Mild sleep apnea |
15 - 30 | Moderate sleep apnea |
>30 | Severe sleep apnea |
Remember, 5 apneas within an hour are actually considered within normal range (apnea is > 10 seconds)
Specifiers
Severity Specifiers
Specify if:
Mild: Apnea hypopnea index is less than 15.
Moderate: Apnea hypopnea Index is 15-30.
Severe: Apnea hypopnea index is greater than 30.
Signs and Symptoms
Snoring, gasping for air, stopping breathing at night, memory complaints, irritability, depression, morning headaches, sexual problems, restless sleep, and sedation or tiredness during the day.
Screening
The STOP-BANG is a screening tool that has been validated for the identification of obstructive sleep apnea. If more than 4 criteria are met, there is a sensitivity of 80% and specificity of 50%.
Psychometric Scales for Depression
Name | Rater | Description | Download |
STOP-Bang Questionnaire | Patient or Physician | The STOP-BANG questionnaire screens for obstructive sleep apnea (OSA) only, not central sleep apnea. | STOP-BANG Download |
Pathophysiology
Children
There is a peak of OSA in children ages 3-8 years, when the nasopharynx has a relatively larger mass of tonsillar tissue relative to the upper airway. As the airway grows and develops during childhood, there is regression of lymphoid tissue and a corresponding reduction
in the incidence of OSA.
Adults
The major risk factors for obstructive sleep apnea hypopnea are obesity and male gender. As obesity prevalence increases in midlife and females enter menopause, obstructive sleep apnea hypopnea again increases.
Anatomy
Maxillary-mandibular retrognathia or micrognathia, genetic syndromes that reduce upper airway patency (e.g., Down's syndrome, Treacher Collin's syndrome), adenotonsillar hypertrophy (especially in young children), and various endocrine syndromes (e.g., acromegaly) all increase the risk of OSA due to anatomical changes to airway patency. Anatomical studies have shown that Asian men are more likely to develop sleep apnea due to differences in craniofacial anatomy (crowded posterior oropharynx) rather than from obesity.
Physiologic Cycle
In patients with OSA, there is first an initial decrease in the drive to breathe due to decreased sensitivity of the peripheral and central chemoreceptors.
As a result, the airway collapses, causing an apneic event that limits lung gas exchange.
This causes a hypoxic-hypercapnic (low oxygen, high carbon dioxide) state that increases the drive to breathe.
This breathing effort, however, is impeded by the already obstructed airway, which causes further impairment of gas exchange.
Eventually, the hypoxia and hypercapnia become severe enough to produce a breathing effort that is strong enough to terminate the apneic event.
This effort often elicits an arousal that disrupts sleep architecture. This pattern will repeat many times during the night for individuals with OSA.
During the periods of hypercapnia, there is also very strong sympathetic neural activity. This pattern of increased sympathetic activity is thought to be implicated in the development of hypertension in individuals with OSA.
Differential Diagnosis
Primary snoring and other sleep disorders
Insomnia disorder
Panic attacks (nocturnal)
Attention-deficit/hyperactivity disorder
Substance/medication-induced insomnia or hypersomnia
Investigations
Polysomnography
On polysomnography, apneic episodes are always worse during REM sleep due to the atonia that occurs from REM.
Treatment
CPAP
Continuous positive airway pressure (CPAP) therapy is the first line of treatment for moderate to severe sleep apnea. However, patient compliance is a major problem. Most studies have shown that even in adherent patients, the actual usage of CPAP is around 50%.
Surgical
Dental Device
Positional Sleep Trainer
Lifestyle
Clinical Pearls
Dry mouth upon awakening is a common symptom (~40%) in OSA
CPAPs are not a panacea and may not always be prescribed properly!
CPAPs can cause more insomnia if your patients are unable adjust to using a CPAP
Patients are more prone to have REM apnea, because muscle paralysis occurs during REM
The snoring is not what causes apnea – it’s the collapse of the airway that is the problem!
Important Questions to Ask on History
Is it obstructive or central?
How severe it is?
Is it REM-related?
Is it positional?
Is it associated with desaturations?
Are there medical comorbidities?
Resources
4)
Chang, W. P., Liu, M. E., Chang, W. C., Yang, A. C., Ku, Y. C., Pai, J. T., ... & Tsai, S. J. (2013). Sleep apnea and the risk of dementia: a population-based 5-year follow-up study in Taiwan. PloS one, 8(10), e78655.
5)
Emamian, F., Khazaie, H., Tahmasian, M., Leschziner, G. D., Morrell, M. J., Hsiung, G. Y. R., ... & Sepehry, A. A. (2016). The association between obstructive sleep apnea and Alzheimer’s disease: a meta-analysis perspective. Frontiers in aging neuroscience, 8, 78.
6)
Li, M., Quanying, H., Yinna, W., Birong, D., & Jinhan, H. (2014). High prevalence of obstructive sleep apnea in Marfan's syndrome. Chinese medical journal, 127(17), 3150-3155.
8)
Chung, F., Yegneswaran, B., Liao, P., Chung, S. A., Vairavanathan, S., Islam, S., ... & Shapiro, C. M. (2008). Stop questionnairea tool to screen patients for obstructive sleep apnea. Anesthesiology: The Journal of the American Society of Anesthesiologists, 108(5), 812-821.
9)
Lee, R. W., Vasudavan, S., Hui, D. S., Prvan, T., Petocz, P., Darendeliler, M. A., & Cistulli, P. A. (2010). Differences in craniofacial structures and obesity in Caucasian and Chinese patients with obstructive sleep apnea. Sleep, 33(8), 1075-1080.
10)
Li, K. K., Kushida, C., Powell, N. B., Riley, R. W., & Guilleminault, C. (2000). Obstructive sleep apnea syndrome: a comparison between Far‐East Asian and white men. The Laryngoscope, 110(10), 1689-1693.
11)
Cutler, M. J., Hamdan, A. L., Hamdan, M. H., Ramaswamy, K., & Smith, M. L. (2002). Sleep apnea: from the nose to the heart. The Journal of the American Board of Family Practice, 15(2), 128-141.
12)
Cutler, M. J., Hamdan, A. L., Hamdan, M. H., Ramaswamy, K., & Smith, M. L. (2002). Sleep apnea: from the nose to the heart. The Journal of the American Board of Family Practice, 15(2), 128-141.
14)
Benoist, L., de Ruiter, M., de Lange, J., & de Vries, N. (2017). A randomized, controlled trial of positional therapy versus oral appliance therapy for position-dependent sleep apnea. Sleep Medicine, 34, 109-117.
15)
Peppard, P. E., Young, T., Palta, M., Dempsey, J., & Skatrud, J. (2000). Longitudinal study of moderate weight change and sleep-disordered breathing. Jama, 284(23), 3015-3021.