Obstructive Sleep Apnoea

Obstructive Sleep Apnoea (OSA) and its more severe form, Obstructive Sleep Apnoea Hypopnoea Syndrome (OSAHS), occur when the pharyngeal muscles relax excessively during sleep, causing the airway to collapse. This results in an 'apnoea' (cessation of airflow for >10 seconds). The resulting hypoxia and hypercapnia trigger a 'micro-arousal' to restore airway patency, severely disrupting sleep architecture. The prevalence is rising in the UK due to the obesity epidemic. Risk factors include a high Body Mass Index (BMI), large neck circumference (>17 inches in men, >16 inches in women), male gender, and Craniofacial abnormalities (e.g., micrognathia). Chronic OSA is a 'silent killer' associated with hypertension, type 2 diabetes, atrial fibrillation, and a significantly increased risk of motor vehicle accidents. Diagnosis involves scoring systems like the Epworth Sleepiness Scale followed by overnight sleep studies. Management ranges from lifestyle changes to CPAP and, occasionally, surgery.

The patency of the upper airway depends on the balance between negative inspiratory pressure and the activity of pharyngeal dilator muscles (e.g., genioglossus). During sleep, muscle tone naturally decreases. In OSA, anatomical narrowing (fat deposition in the parapharyngeal space, enlarged tonsils) combined with this loss of tone lead to airway collapse. The physiological consequences include intermittent hypoxaemia and sympathetic nervous system activation. This 'oxidative stress' leads to endothelial dysfunction and systemic inflammation, explaining the link to hypertension and atherosclerosis. The chronic sleep fragmentation causes a decrease in REM and deep (slow-wave) sleep, impairing cognitive function and glucose metabolism.

Presenting complaints often come from the partner: loud, disruptive snoring and frightening 'gasping' episodes. The patient themselves usually complains of waking up feeling unrefreshed (non-restorative sleep), morning headaches (due to hypercapnia), and excessive daytime sleepiness (falling asleep during meetings or while driving). Physical signs include high BMI, high Mallampati score (crowded oropharynx), and large tonsils. Evaluation using the Epworth Sleepiness Scale (ESS) is essential; a score >10 indicates significant daytime sleepiness. OSA is a common cause of 'resistant' hypertension and should be screened for in patients not responding to three antihypertensives.

- Bedside: Height, weight (BMI), neck circumference, BP, and Mallampati score. Epworth Sleepiness Scale (ESS).
- Bloods: TFTs (hypothyroidism is a rare but treatable cause) and HbA1c.
- Imaging/Special: Sleep Study (Polysomnography is the gold standard, but 'Home Respiratory Polygraphy' is more common). This measures AHI (events per hour).
- ENT: Nasendoscopy to identify sites of obstruction (e.g., septal deviation, large tonsils).

Conservative: Weight loss (most effective), smoking cessation, and avoiding alcohol/sedatives before bed. Positional therapy (avoiding supine sleep). Medical: CPAP is the first-line treatment for moderate or severe OSAHS; it acts as a 'pneumatic splint' to keep the airway open. Mandibular Advancement Devices (MADs) are an alternative for mild-to-moderate OSA. Surgical: Only if there is a clear anatomical obstruction. Options include Tonsillectomy, Septoplasty, or Uvulopalatopharyngoplasty (UPPP). Safety: Immediate advice to stop driving and notify the DVLA if daytime sleepiness occurs.