Sleep apnoea: no laughing matter

Obstructive sleep apnoea (OSA) is often considered amusing, probably because of its association with snoring and obesity. Although the related ‘Pickwickian’ syndrome was identified in the early 20th century, OSA remained invisible until the development of nocturnal electroencephalographic (EEG) and respiratory monitoring in the mid 1960s, which allowed physicians to identify individual respiratory events. OSA was initially thought to be rare, but epidemiological studies showed it to be a common problem, affecting around 4% of the population1 of whom 80% are not diagnosed. As early studies included only men, OSA was thought to be a uniquely male disease, but more recent population studies have shown that the male:female ratio is about 2–3:1. As the ratio in sleep clinic populations is around 8:1, women are not being identified and referred.2 An important risk factor for OSA is obesity, with over 30% of patients with morbid obesity suffering from severe OSA. Rising obesity rates are likely to increase prevalence. However, OSA is also highly prevalent in patients with diabetes (35%), hypertension (40%), resistant hypertension (70%), and atrial fibrillation (45%).3,4 Family history is important, and patients often report close family members suffering from OSA. OSA is caused by intermittent obstruction of the upper airways during sleep. Airway obstruction is multifactorial, and anatomical problems (such as tonsillar hypertrophy), fatty deposits in the pharynx, and weakness of dilatory muscles in the pharynx all play a role. As the airways narrow, airflow becomes turbulent, leading to snoring. As the airways narrow more, respiratory volume decreases, and respiratory effort increases leading to hypopnoeas. Once the airways close, airflow stops which leads to apnoea. Both …