28A. Obstructive sleep apnoea syndrome: Difference between revisions

Latest revision as of 10:46, 24 November 2023

Obstructive sleep apnoea (OSA) (sometimes called obstructive sleep apnoea syndrome) is characterised by repetitive episodes of sleep apnoea or hypopnea (respiratory arrest lasting > 10 seconds during sleep) due to upper airway obstruction occurring during sleep. It results in reductions in blood oxygen saturation. The hypoxaemia triggers the sympathetic nervous system, briefly arousing the person from sleep.

It’s a highly prevalent but likely very underdiagnosed condition. It’s a risk factor for cardiovascular disease, motor vehicle accidents, and mortality. It mostly affects elderly overweight people, however it may also affect children.

Central sleep apnoea is related but not the same and much less common.

Risk factors

Obesity, especially around the neck
Male gender
Old age
Tonsillar hypertrophy (especially in children)
Certain anatomical variations in the upper airways

Pathomechanism

Apnoea occurs because of upper airway obstruction, usually because the pharyngeal muscles have a low muscle tone, causing them to collapse and close the oropharynx. The resulting hypoxaemia and hypercapnia cause:

Pulmonary vasoconstriction -> pulmonary hypertension
Sympathetic activation -> secondary hypertension
Respiratory acidosis

Clinical features

Excessive daytime sleepiness is a major presenting complaint in many cases. The patient may also complain of headache, impaired cognitive function, and depression. The partner may report loud snoring, or interruptions in breathing while sleeping.

Diagnosis and evaluation

Secondary hypertension is a common finding.

Polysomnography is required for diagnosis. During polysomnography, the following parameters are measured:

Air flow through the mouth and nose
Work of breathing (movement of thorax and abdomen)
Oxymetry
EEG
EMG
Electrooculography

By measuring air flow and work of breathing, the machine can detect apnoea/hypopnoea episodes. Hypoxaemia, arousal events on EEG, increased pulse pressure, and interruption of sleep phases are also typical findings.

The diagnosis is basd on the apnoea-hypopnoea index (AHI), which is the number of apnoea/hypopnoea events divided by the number of hours of sleep, as well as the oxygen desaturation index (ODI), which is the number of episodes of oxygen desaturation per hour during sleep.

An AHI >5 gives the diagnosis of OSA. The higher the AHI, the more severe the condition.

Respiratory polygraphy is a less invasive method of evaluating OSA, but polysomnography is the gold standard.

Treatment

Treatment involves avoiding risk factors, especially lowering weight, and treating underlying causes if present.

There exist oral appliances which keep the upper airway open during sleep.

In severe cases, nocturnal CPAP may be used to hold the oropharynx open during night. However, sleeping with CPAP is uncomfortable and thus the compliance is only moderate.

@@ Line 1: / Line 1: @@
-Obstructive sleep apnoea (OSA) is characterised by repetitive episodes of apnoea or hypopnea lasting > 10 seconds. These episodes are caused by upper airway obstruction occurring during sleep, and result in reductions in blood oxygen saturation. The hypoxaemia triggers the sympathetic nervous system, briefly arousing the person from sleep.
+{{:Obstructive sleep apnoea}}
-Central sleep apnoea is related but not the same. In central sleep apnoea, there is no obstruction but the respiratory centre stops for short periods of time during the night.
-It’s a highly prevalent but likely very underdiagnosed condition. It’s a risk factor for cardiovascular disease, motor vehicle accidents, and mortality. It mostly affects elderly overweight people, however it may also affect children.
-== Risk factors ==
-* Obesity
-* Male gender
-* Old age
-* Tonsillar hypertrophy (especially in children)
-* Certain anatomical variations in the upper airways
-== Pathomechanism ==
-Apnoea occurs because of upper airway obstruction, usually because the pharyngeal muscles have a low muscle tone, causing them to collapse and close the oropharynx. The resulting hypoxaemia and hypercapnia cause:
-* Pulmonary vasoconstriction -> pulmonary hypertension
-* Sympathetic activation -> secondary hypertension
-* Respiratory acidosis
-== Clinical features ==
-Excessive daytime sleepiness is a major presenting complaint in many cases. The patient may also complain of headache, impaired cognitive function, and depression. The partner may report loud snoring, or interruptions in breathing while sleeping.
-== Diagnosis and evaluation ==
-Secondary hypertension is a common finding.
-Polysomnography is required for diagnosis. During polysomnography, the following parameters are measured:
-* Air flow through the mouth and nose
-* Work of breathing (movement of thorax and abdomen)
-* Oxymetry
-* EEG
-* EMG
-* Electrooculography
-By measuring air flow and work of breathing, the machine can detect apnoea/hypopnoea episodes. Hypoxaemia, arousal events on EEG, increased pulse pressure, and interruption of sleep phases are also typical findings.
-The diagnosis is basd on the apnoea-hypopnoea index (AHI), which is the number of apnoea/hypopnoea events divided by the number of hours of sleep, as well as the oxygen desaturation index (ODI), which is the number of episodes of oxygen desaturation per hour during sleep.
-An AHI >5 gives the diagnosis of OSA. The higher the AHI, the more severe the condition.
-Respiratory polygraphy is a less invasive method of evaluating OSA, but polysomnography is the gold standard.
-== Treatment ==
-Treatment involves avoiding risk factors, especially lowering weight, and treating underlying causes if present.
-There exist oral appliances which keep the upper airway open during sleep.
-In severe cases, nocturnal CPAP may be used to hold the oropharynx open during night. However, sleeping with CPAP is uncomfortable and thus the compliance is only moderate.
 [[Category:Neurology 2]]