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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #113: Diabetes and Sleep Apnea Part 3

Feb 20, 2018

OSA pathophysiology

OSA is a very complex disorder, and although obesity and fat deposition around the neck plays an important role, there are many other important players that contribute to the development of this condition.

The human upper airway is a unique multipurpose structure involved in performing a variety of tasks such as speech, swallowing, and the passage of air for breathing [28]. The airway, therefore, is composed of numerous muscles and soft tissue but lacks rigid or bony support [28]. Most notably, it contains a collapsible portion that extends from the hard palate to the larynx, which allows the upper airway to change shape and momentarily for speech and swallowing during wakefulness; but this feature also provides the opportunity for collapse at inopportune times such as during sleep [28]. Several imaging-based studies showed that patients with OSA have a smaller upper airway during wakefulness and anesthesia, resulting in an airway that is more prone to collapse [28]. The upper airway muscles (genioglossus) activity is also increased in OSA patients compared to age- and obesity-matched healthy controls [29], suggesting that these muscles are compensating for an underlying defect in the anatomy of the upper airway in patients with OSA [28]. This muscle hyperactivity is resolved in CPAP-treated patients [30]. Sleep onset is associated with greater reductions in upper airway muscles tone in OSA patients, which explains the occurrence of apnea/hypopnea episodes at sleep onset and during REM sleep [28]. This reduction in upper airway muscle tone during sleep seems to result from a central lack of drive and local inhibitory reflexes that respond to changes in pressure in the upper airways [28]. Several studies have also shown that changes in lung volume affect upper airway muscles activity [28]. Other abnormalities described in OSA include irregularities in ventilatory control and stability, changes in chemosensitivity to CO2, and higher arousal thresholds [28].

OSA clinical features and diagnosis

Good history and examination are still an essential part of the assessment of patients with OSA despite the fact that several reports have shown the limited value of symptoms in predicting OSA (in one report, only one third of patients would have been identified clinically) [31]. Snoring is the most common symptom of OSA and it occurs in 95% of patients [6]. Snoring, however, has a poor predictive value due to the high prevalence of snoring and the fact that many snorers do not have OSA [6]. Nonetheless, lack of snoring almost rules out OSA since only 6% of OSA patients (or their partners) have not reported snoring [6]. Witnessed apneas are another important symptom that is usually reported by the partner. However, witnessed apneas do not correlate with disease severity and up to 6% of the “normal” population could have witnessed apneas without OSA [6]. Other nocturnal symptoms such as choking (which is possibly a “proper” rather than a “micro” arousal to terminate apnea), insomnia, nocturia, and diaphoresis have been reported [6]. Daytime symptoms include excessive daytime sleepiness, fatigue, morning headache, and autonomic symptoms [6].

The gold standard to diagnose OSA is polysomnography that typically includes the recording of 12 channels such as EEG, electro-oculogram (EOG), electromyogram (EMG), oronasal airflow, chest wall effort, abdominal effort, body position, snore microphone, ECG, and oxyhemoglobin saturation [6]. The main problem with polysomnography is that it is time consuming and expensive. Portable home-based respiratory devices are another alternative [6]. The main advantages are that they are less resourceful but they are associated with higher failure/loss of lead rate compared to polysomnography [6]. Pulse oximetry is another good way to diagnose OSA, it cannot, however, differentiate between obstructive and central apneas and it has a wide range of sensitivity (31–98%) and specificity (41–100%). The AASM recommends use of a Type III device as a minimum [6].

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