Before we discuss the epidemiology, let us consider what obstructive sleep apnea (OSA) actually looks like.
Figure 1 shows evidence of snoring on the flow tracing preceding the apneic event during which oxygen saturation progressively falls. In this example, despite a lowered arousal threshold and progressive increases in EMGgg activity throughout the obstructive event, airflow was not able to be restored without an arousal (awakening) (Eckert & Malhotra, 2008). Learn more about the events that lead to OSA in the pathophysiology section.
OSA is the most common type of sleep apnea which occurs in about 10% of the adult population (Young et al., 2002). OSA occurs two to three times more often in older adults and is twice as common in men as in women (Table 1).
Table 1. Incidence of obstructive sleep apnea in adults (Peppard et al., 2013).
Many patients are unaware that their breathing is affected during sleep and it has been estimated that 12–18 million persons in the United States are untreated (Young et al., 2009).
Positional obstructive sleep apnea (POSA) is a distinct subset of OSA. It is a condition in which most of the apneic events occur when a patient lies on their back. POSA can often be avoided by sleeping on one’s side (van Maanen et al., 2014) and there are a number of ways of avoiding sleeping in the supine position, some being more attractive than others.
However, POSA is not simply about avoiding sleeping in a supine position and its prevalence is underestimated. Approximately 56% of patients with OSA are known to suffer from POSA (Oksenburg et al., 1997) and it appears to vary with apnea severity. One study showed that 49.5% of patients with an AHI of 5–15/hour had POSA, whereas for patients with an AHI of 15–30/hour or >30/hour the figures were 19.4% and 6.5%, respectively.
Some patients have exclusive POSA (ePOSA), where their apnea-hypopnea index (AHI) normalises in non-supine positions (Cartwright et al., 1984). In a large population-based study of 1,719 subjects (HypnoLaus), 71% of subjects had OSA. POSA was present in 53% of all subjects and in 75% of OSA subjects. ePOSA was present in 26% of all subjects and in 36% of OSA subjects (Heinzer et al., 2018).
Visit the Sleep and Breathing conference 2019 section where Dr Raphaël Heinzer gives more details about POSA and ePOSA epidemiology and the HypnoLaus study.
OSA is mainly due to an anatomically small pharyngeal airway and so risk factors are conditions that reduce the size of the resting pharynx or increase airway collapsibility (Veasey & Rosen, 2019).
We have already highlighted that gender and age are important risk factors for OSA but there are several other risk factors that should be considered.
Obesity: Although slender people can also develop the disorder, obesity is the most significant risk factor for OSA (Shah & Roux, 2009). Increased adipose tissue around the upper airway (often causing a thick neck) may obstruct breathing or make the airway more prone to collapse during sleep. OSA has been reported in >40 % of patients with a body mass index (BMI) >30 and in 60% of patients with metabolic syndrome (Veasey & Rosen, 2019). Further, moderate to severe obesity is found in between 60 and 90% of people with OSA.
Narrowed airway: This can be associated with obesity, but a narrow airway due to bony structures (micrognathia) or enlarged tonsils or adenoids (particularly in children) can block the airway and lead to sleep apnea.
Menopause: The prevalence of OSA in females rises markedly after menopause- 47% to 67% of postmenopausal women have been found to have OSA. This may be because women tend to gain weight after menopause, but it is not likely to be the only factor (Jehan et al., 2016).
Genetic predisposition: Genetically inherited physical traits like face and skull shape, characteristics of the upper airway muscles, as well as body fat content and distribution can all contribute to sleep apnea.
Use of alcohol, sedatives or tranquilisers: Because these substances relax the muscles in the person’s throat, frequent use can lead to the disorder.
Smoking: Smoking can increase the amount of inflammation and fluid retention in the upper airway and smokers are more likely to develop OSA.
Nasal congestion: Allergies, a deviated septum and other issues that make it difficult to breathe through the nose may increase the risk of sleep apnea.
Medical comorbidity: OSA may contribute to the development of cardiovascular conditions, including hypertension, coronary artery disease, congestive heart failure, arrhythmia and stroke. There is also a high prevalence of sleep apnea in patients with type 2 diabetes.
Obstructive sleep apnea can lead to both short- and long-term health risks if left untreated:
OSA is associated with an increased risk of cardiovascular disease, including hypertension, stroke, coronary artery disease or heart failure, even after adjustment for BMI and other cardiovascular risk factors. OSA is also associated with an increased risk of diabetes and glucose dysregulation (independent of obesity). Patients with untreated OSA have three times more risk of motor vehicle accidents (MVA) than the general population (Veasey & Rosen, 2019). An EU directive has recognised that OSA represents an important risk factor for MVA and adopted new rules on driver licensing for OSA patients (Bonsignore et al., 2016). Untreated OSA is also associated with cognitive impairment and depression (Osman et al., 2018).
Pre-diagnosis, OSA is associated with healthcare costs per person of between 50%–100% more than those for the general population (ELF/ERS, 2019). In the US economic burden of undiagnosed sleep apnea was estimated at $150 billion per year (AASM, 2016). Sleep apnea can also occur in children. The typical child with OSA will snore loudly and may present as hyperactive rather than sleepy. It is not uncommon for children with this condition to be misdiagnosed as having attention deficit hyperactivity disorder (ADHD).
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