Obstructive Sleep Apnea (OSA)

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.

• OSA affects 1-2% of children, 2-15% of middle-age adults, and more than 20% of older individuals.
  • 9% of men and 4% of women are thought to have an Apnea-Hypopnea Index (AHI) > 15 (moderate sleep apnea)
• 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.^[1]

Individuals with OSA are at a significantly higher risk for developing obesity, hypertension,^[2] atrial fibrillation and other arrhythmias, heart failure, stroke and transient ischemic attacks (TIAs), coronary heart disease, Type 2 diabetes, and dyslipidemia.^[3] More recent research has also shown a link between OSA and an increased risk for developing dementia.^[4][5]

• Genetic disorders including Marfan syndrome can increase the risk for OSA due to connective tissue laxity.^[6]

• 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.

The STOP-BANG is a screening tool that has been validated for the identification of obstructive sleep apnea.^[7][8] If more than 4 criteria are met, there is a sensitivity of 80% and specificity of 50%.

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.

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.

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.^[9][10]

• 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.^[11]
• 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.^[12]

• Primary snoring and other sleep disorders
• Insomnia disorder
• Panic attacks (nocturnal)
• Attention-deficit/hyperactivity disorder
• Substance/medication-induced insomnia or hypersomnia

On polysomnography, apneic episodes are always worse during REM sleep due to the atonia that occurs from REM.

• 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 interventions include uvulopalatopharyngoplasty, soft palate implants (Pillar Procedure), and hyoid advancement.

• Dental devices called mandibular advancement devices can be used.

• Positional sleep trainers have also been shown to be effective in reducing apnea in patients with positional sleep apnea.^[13][14]

• Weight loss and lifestyle changes can have a significant impact on reducing the severity of symptoms. A 10% reduction in weight can lead to a 26% decrease in the AHI.^[15] Conversely, a 10% increase in weight can lead to a 6-fold increase in the risk of developing a sleep-related breathing disorder.

• Dry mouth upon awakening is a common symptom (~40%) in OSA^[16]
• 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!

• Is it obstructive or central?
• How severe it is?
• Is it REM-related?
• Is it positional?
  • Does your patient sleep on their back or sleep on their side?
• Is it associated with desaturations?
• Are there medical comorbidities?