Obstructive sleep apnoea — features, comorbidities, tests, management and prognosis

Definition and epidemiology. Obstructive sleep apnoea (OSA) is the most frequent respiratory sleep disorder and involves repeated episodes of complete (apnoea) or partial (hypopnoea) upper airway obstruction during sleep. It is defined by an apnoea–hypopnoea index (AHI) > 5 per hour of sleep together with excessive daytime sleepiness or neurocognitive/behavioural disturbance not attributable to another cause. Prevalence is 1–4% of general adults but far higher in the elderly — about 50% of older people have an AHI > 5 and 20% have an AHI > 15, compared with 10% of younger people.

Pathogenesis in the older patient. The dominant mechanism is increased upper airway collapsibility with age, due to hormonal change (after the menopause the prevalence in women equalises with men), reduced pharyngeal dilator muscle tone and altered pharyngeal reflexes with increased airway resistance during sleep, and anatomical factors including edentulism and increased fat deposition in the pharyngeal wall. Comorbidities that accumulate with age — stroke, heart failure, hypothyroidism, obesity — further promote sleep-disordered breathing.

Clinical features and the age-related shift. The classical triad is snoring, witnessed apnoeas and excessive daytime sleepiness. However, the proportion of OSA patients who do NOT snore increases after the age of 50, so the classical triad is unreliable in the old. Instead suspect OSA from unrefreshing sleep, nocturia, morning headache, fatigue rather than frank sleepiness, poor concentration, memory impairment, irritability or depression, falls and road traffic accidents. Examination: obesity and increased neck circumference, crowded oropharynx (high Mallampati), retrognathia, nasal obstruction, hypertension.

Associated comorbidities. Cardiovascular — resistant hypertension (especially non-dipping and nocturnal), atrial fibrillation and other arrhythmias, ischaemic heart disease, heart failure, pulmonary hypertension and stroke. Metabolic — obesity, insulin resistance and type 2 diabetes, metabolic syndrome. Neurocognitive — cognitive impairment and dementia, depression, delirium; nocturnal hypoxia carries risks of arrhythmia and of myocardial and cerebral infarction. Other — nocturia, glaucoma, reduced quality of life, and increased perioperative and sedative-related risk.

Investigations. Begin with history from the patient and the bed partner, the Epworth Sleepiness Scale and a screening tool such as STOP-BANG. Confirm with polysomnography, which remains the gold standard; a home sleep apnoea test is acceptable in high-probability uncomplicated patients. Severity by AHI: mild 5–15, moderate 15–30, severe > 30. AASM scoring should include arousal-based scoring of hypopnoeas. Add overnight oximetry, thyroid function, ECG, echocardiography and ABG where obesity hypoventilation or cor pulmonale is suspected.

Management and prognosis. Diet and sleep-hygiene measures, weight reduction, avoidance of alcohol, sedatives and opioids, positional therapy, treatment of nasal obstruction, and optimisation of dentition. CPAP is the treatment of choice and improves sleepiness, quality of life, blood pressure and cognition; adherence in older adults is comparable to younger patients when support is given. Alternatives: mandibular advancement devices for mild–moderate disease or CPAP intolerance, and surgery (uvulopalatopharyngoplasty, hypoglossal nerve stimulation) in selected cases. Prognosis: untreated moderate-to-severe OSA increases cardiovascular events, stroke, cognitive decline, accidents and mortality; treatment reliably improves symptoms, though large trials (SAVE) did not show a reduction in cardiovascular events, largely because of poor CPAP adherence.

SURMOUNT-OSA (NEJM 2024) — in adults with obesity and moderate-to-severe OSA, tirzepatide (a dual GIP/GLP-1 receptor agonist) produced a large reduction in the apnoea–hypopnoea index (roughly 25–29 fewer events per hour versus placebo) with improvements in oxygen saturation, blood pressure and sleep-related quality of life, both with and without background CPAP. This led to the first regulatory approval of a drug for obstructive sleep apnoea (December 2024) and establishes pharmacological weight loss as a disease-modifying treatment for OSA rather than merely an adjunct — though in older adults the risks of sarcopenia, weight loss and gastrointestinal effects require careful weighing.