Sleep apnoea/Pickwickian syndrome
Sleep apnoea represents the cessation of airflow at the level of the nostrils and mouth lasting at least 10 seconds, the patient is said to suffer from sleep apnoea if more than 15 such episodes occur in any 1 hour of sleep.
1–2% of the general population.
Risk factors include obesity, smoking, chronic obstructive pulmonary disease and alcohol or other sedatives which exacerbate the problem by causing hypotonia and respiratory depression. Apnoea can be divided into the following:
· Central apnoea when there is depression of the respiratory drive, e.g. opiate overdose.
· Obstructive apnoea when air is unable to pass despite a respiratory effort.
· Mixed central and obstructive apnoea.
Snoring arises because of turbulent airflow around the soft palate with partial obstruction. Critical airway obstruction leads to a decrease in arterial oxygen ‘hypopnoea’ and then occlusion leads to apnoea. There is a reflex increase in respiratory drive, which eventually rouses the patient sufficiently to overcome the obstruction, in the process of which the patients sleep is disturbed, although they do not recall it.
Patients complain of continual tiredness (90%), and may fall asleep during the day. Less than half notice that they have a restless or unrefreshing sleep, and about a third complain of morning headache (due to carbon dioxide retention). Sleeping partners will have noticed loud snoring in 95% and often notice the snore–apnoea–choke– snore cycle. Alcohol and smoking should be enquired about. Classical anatomy is a long soft palate, large neck and excess tissue around the tonsils. Systemic hypertension is common.
Oxygen saturations may fall very low. The pulmonary vasculature responds to hypoxia by vasoconstriction thus there may be pulmonary hypertension. Hypoxia also increases arrhythmias and there is an increased risk of stroke and myocardial infarction. Twenty per cent experience reduced libido and even impotence.
A simple sleep study with overnight pulse oximetry together with a history from sleeping companion may be diagnostic. Many require a full sleep study (polysomnogram), which consists of a pulse oximeter, a tidal volume measurement, oronasal flow and electroencephalography to record sleep and arousal patterns. Polycythaemia (raised haemoglobin and packed cell volume) may occur in advanced cases.
Non-pharmacological treatment includes weight loss, exercise, cessation of smoking and reduced alcohol in-take. Mechanical obstruction due to nasal deformities, polyps or adenoids may be correctable.
1. Continuous positive airway pressure (CPAP) via a nasal mask prevents collapse of the upper airway and is the mainstay of treatment.
2. Surgical treatment may be difficult as patients are often a poor anaesthetic risk.
Uvulopalatopharyngoplasty (UPPP) trimming of the redundant tissues in the soft palate and lateral pharynx is sometimes performed but its benefit in true obstructive sleep apnoea is unproven and it may make future CPAP via a nasal mask impossible.