Obstructive Sleep Apnoea

A 45-year-old man presents to his GP with excessive daytime sleepiness. His wife reports that he snores loudly at night, and she has noticed him stop breathing for short periods. He has no other significant medical history.

Pathophysiology

Obstructive Sleep Apnoea (OSA) is characterised by repetitive episodes of complete or partial upper airway obstruction, leading to intermittent hypoxia and hypercapnia. This causes:

• Hypoxic pulmonary vasoconstriction leading to pulmonary hypertension and cor pulmonale
• Sympathetic activation over a prolonged period leading to secondary hypertension
• Respiratory acidosis  leading to renal compensation via HCO₃ retention and decreased chloride reabsorption

These episodes cause micro-arousals, leading to fragmented sleep.

Aetiology

OSA is caused by anatomical narrowing of the upper airway at the level of the pharynx during sleep. This narrowing can be exacerbated by muscle relaxation during sleep, leading to collapse of the airway.

Epidemiology & Risk Factors

OSA affects 20-30% of men and 10-15% of women.

Risk factors include:

• Obesity (BMI > 30kg/m2). Neck size >40cm is the best predictor of OSA.
• Male
• Increasing age
• Smoking
• Alcohol consumption
• Sedative use (e.g. benzodiazepines)
• Craniofacial abnormalities
• Upper airway abnormalities (e.g. adenotonsillar hypertrophy in children)
• Hypothyroidism
• Acromegaly

Clinical Features

Nocturnal features:

• Loud snoring - intermittent and may be punctuated by gasping or choking sounds
• Witnessed apnoeas - cessation of airflow for more than 10 seconds
• Restless sleep

Daytime features:

• Excessive daytime sleepiness, the dominant symptom
• Morning headaches
• Fatigue, poor concentration
• Irritability, mood changes
• Nocturnal polyuria
• Reduced libido, erectile dysfunction

Investigations

• Overnight oximetry - recording oxygen saturation and heart rate throughout the night. Can identify most moderate-to-severe cases of OSA.
• Polysomnography (PSG) is the gold standard for diagnosing OSA. A PSG records multiple physiological parameters, including brain waves (EEG), eye movements (EOG), muscle activity (EMG), heart rhythm (ECG), airflow, respiratory effort and oxygen saturation.

Management

The definitive management for OSA is weight loss. Other lifestyle modifications include avoiding smoking, alcohol, and sedatives. Patients should also avoid sleeping in the supine position.

Continuous positive airway pressure (CPAP) therapy is the mainstay of treatment for moderate to severe OSA. CPAP delivers a continuous flow of air through a nasal mask, acting as a splint to keep the upper airway open. A pressure of 4-20cmH2O is typically used. CPAP effectively reverses daytime symptoms and prevents complications.

In cases of severe OSA with CO2 retention, a period of non-invasive ventilation with positive pressure may be required prior to CPAP.

Pharmacological treatments are generally not recommended for OSA. However, some patients with residual sleepiness despite CPAP therapy may benefit from alerting agents such as modafinil to promote wakefulness.

Surgical options include:

• Tonsillectomy may be considered for patients with enlarged tonsils
• Uvulopalatopharyngoplasty (UPPP) is a procedure that removes excess tissue from the soft palate and uvula
• Mandibular/maxillary advancement surgery is reserved for highly selected cases
• Tracheostomy is rarely indicated

Complications & Prognosis

Untreated OSA can lead to a number of systemic complications:

• Cardiovascular morbidity: Systemic hypertension, pulmonary arterial hypertension, coronary artery disease, arrhythmias, heart failure, polycythaemia, stroke.
• Metabolic disorders: Insulin resistance, type 2 diabetes mellitus.
• Neurocognitive impairment: Daytime sleepiness, fatigue, poor concentration, impaired alertness, increased risk of motor vehicle collisions.
• Sudden death

Effective treatment with CPAP can significantly reduce the risk of these complications and improve quality of life.