11/14/24, 10\:53 AM Obstructive Sleep Apnoea

Obstructive Sleep Apnoea

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Obstructive sleep apnoea (OSA)\: sleep disorder with recurrent episodes of upper airway obstruction during sleep, causing
apnoea or hypopnoea.
Prevalence\: 1.5 million in the UK, many undiagnosed.
Aetiology\: Narrow upper airway due to fat deposition or abnormal skeletal features; muscle relaxation during sleep;
inadequate genioglossus muscle responsiveness.
Pathophysiology\: Upper airway collapse → hypoxaemia, hypercapnia → arousal from sleep → airway patency; cycle
repeats multiple times per night.
Risk factors\: Obesity, craniofacial abnormalities, increased soft tissue volume, male sex, Down’s syndrome.
Symptoms\: Excessive daytime somnolence (Epworth sleepiness scale), chronic morning headache, arousal during sleep
with choking/gasping, habitual snoring, restless sleep.
Clinical examination\: Obesity (large neck circumference), craniofacial abnormalities, increased soft tissue volume.
Investigations\: Polysomnography (gold-standard), respiratory polygraphy, overnight pulse oximetry.
Di
sleep hygiene.
Management\:
Conservative\: Weight loss, oral appliances, lateral sleeping position.
Ventilatory\: CPAP (gold-standard for severe OSA).
Medical\: Dopamine reuptake inhibitors (rarely used).
Surgical\: Upper airway surgery, bariatric surgery.
Complications\:
Disease-related\: Cardiovascular disease, diabetes, motor vehicle accidents.
Treatment-related\: CPAP (dry mouth, nasal congestion), surgery (regurgitation, voice change, bleeding).
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Introduction

Obstructive sleep apnoea (OSA) is a sleep disorder that is characterised by recurrent episodes of upper airway obstruction
during sleep, which results in apnoea (temporary cessation of breathing) or hypopnoea (temporary decreases in
breathing).
1
OSA has a prevalence of 1.5 million in the United Kingdom, but it is believed that many more patients remain undiagnosed.
2

Aetiology

A narrow upper airway is more likely to collapse than a wide upper airway.
OSA patients have narrow upper airways, which can be due to fat deposition in the pharyngeal wall/tongue, or abnormal
skeletal features (such as posterior positioning of the mandible).
3
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During sleep, all muscles relax, including the pharyngeal dilator muscles. This increases the risk of upper airway collapse.
4
Furthermore, some OSA patients have inadequate genioglossus muscle responsiveness to airway collapse during sleep.
5
The collapse of the upper airway can cause hypoxaemia and hypercapnia. This is detected by peripheral chemoreceptors,
which stimulate the respiratory control centre in the brainstem and the sympathetic nervous system. This leads to arousal
from sleep and activation of the pharyngeal dilator muscles, resulting in airway patency.
6
If sleep resumes after this brief arousal, then the upper airway can collapse again. This cycle can repeat several hundred
times in a night.
Figure 1. Mechanism of apnoea in OSA.
7

Risk factors

Risk factors for obstructive sleep apnoea include\:
Obesity
Craniofacial abnormalities (such as posterior positioning of the mandible)
Increased soft tissue volume (such as adenotonsillar hypertrophy)
Male sex
Down’s syndrome

Clinical features

History

Typical symptoms of OSA include\:
Excessive daytime somnolence\: this can be quantiEpworth sleepiness scale. Patients often wake up
feeling unrefreshed.
Chronic morning headache\: this could be due to hypercapnia-induced cerebral vasodilation
8
Arousal during sleep with choking/gasping\: this may be observed by the patient’s bed partner
Habitual snoring
Restless sleep
Other important areas to cover in the history include\:
Surgical history\: di
9
Family history of OSA
Occupational history\: patients with excessive sleepiness for >3 months must inform the DVLA. 10
the patient’s occupation involves a lot of driving
This may be pertinent if

Clinical examination

A full respiratory examination should be performed in suspected cases of OSA.
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Typical clinical
Obesity\: leads to large neck circumference
Craniofacial abnormalities (such as posterior positioning of the mandible)
Increased soft tissue volume (such as adenotonsillar hypertrophy)

Di

The presenting complaints of OSA have important di
the features which di
Table 1. Di
Di
Central sleep apnoea
Snoring less common
Obesity less prevalent
Polysomnography\: lack of thoraco-abdominal
e
Periodic limb movement
disorder (previously known
as restless leg syndrome)
Laryngospasm secondary
to gastro-oesophageal
re
Urge to move legs during periods of inactivity
Polysomnography\: no apnoeic episodes
Poor sleep hygiene
More exaggerated choking sensation at night
Burning retrosternal pain
Polysomnography\: no apnoeic episodes
Absence of witnessed apnoeic
episodes/choking at night
Increased risk factors for poor sleep, including
shift work and drug abuse
Polysomnography\: no apnoeic episodes

Investigations

Relevant investigations for OSA include\:
Polysomnography (Figures 2 and 3)\: the gold-standard diagnostic test for OSA. This usually involves a patient being
monitored in a sleep laboratory overnight. Polysomnography evaluates many body functions, including brain activity
(electroencephalogram), muscle activity (electromyogram) and respiratory activity (pulse oximetry and airway
capnography). 11
OSA is diagnosed if the apnoea-hypopnoea index (number of apnoeic/hypnoeic events per hour) is ≥15
per hour, or ≥5 per hour if there are OSA symptoms/cardiovascular comorbidities.
1
Respiratory polygraphy\: this is similar to polysomnography, but does not usually contain an electroencephalogram or
electromyogram. Respiratory polygraphy can be performed at the patient’s home. It is interpreted by a sleep specialist.
4
Overnight pulse oximetry\: this can also be performed at home and can demonstrate apnoeic episodes overnight.
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Figure 2. Polysomnography reading.
12
Figure 3. Polysomnography.
13

Management

Conservative management

Conservative management of OSA includes\:
Weight-loss regimens
Oral appliances (such as mandibular advancement devices and tongue retaining devices) (Figure 4)\: these devices
reduce upper airway collapsibility by widening the upper airway
14
Sleeping in the lateral position\: the upper airway becomes more circular when lying in the lateral position, which reduces
the risk of upper airway collapse
15

Ventilatory management

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Continuous positive airway pressure (CPAP) (Figure 5) is used to hold the upper airway open during sleep. This is the gold-
standard treatment for severe OSA (apnoea-hypopnoea index ≥30 per hour).

Medical management

Dopamine reuptake inhibitors (such as moda
in OSA.

Surgical management

Surgical management of OSA includes\:
Upper airway surgery\: may be indicated if CPAP or oral appliances fail. Options include uvulopalatopharyngoplasty
(resecting tissue in the throat to increase the upper airway size, Figure 6) and tonsillectomy (particularly in patients with
adenotonsillar hypertrophy)
Bariatric surgery
Figure 4. Mandibular advancement device.
16
Figure 5. Continuous Positive Airway Pressure (CPAP).
17
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Figure 6. Examples of uvulopalatopharyngoplasty.
18

Complications

Disease-related complications

Disease-related complications may include\:
Cardiovascular disease (such as hypertension and myocardial infarction)\: mechanisms include increased levels of
oxidative stress and sympathetic nervous system activation
19
Diabetes\: increased sympathetic nervous system activation inhibits the release of hormones that are involved in glucose
metabolism
20
Motor vehicle accidents\: due to daytime somnolence

Treatment-related complications

Treatment-related complications may include\:
Due to CPAP\: dry mouth, nasal congestion, skin irritation
Due to upper airway surgery\: nasopharyngeal regurgitation, voice change, post-operative bleeding

References

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Published in 2015. Available from\: [LINK]
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Gottlieb D and Punjabi N. D i a g n o s i s a n d M a n a g e m e n t o f O b s t r u c t i v e S l e e p A p n o e a \: A R e v i e w . Journal of the American
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BMJ Best Practice. O b s t r u c t i v e S l e e p A p n o e a i n A d u l t s . Published in 2021. Available from\: [LINK]
Gov.uk. E x c e s s i v e s l e e p i n e s s a n d d r i v i n g . Published in 2021. Available from\: [LINK]
Boulos M et al. N o r m a l p o l y s o m n o g r a p h y p a r a m e t e r s i n h e a l t h y a d u l t s \: a s y s t e m a t i c r e v i e w a n d m e t a-a n a l y s i s . The Lancet
Respiratory Medicine. Published in 2019. Available from\: [LINK]
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Marklund M et al. U p d a t e o n o r a l a p p l i a n c e t h e r a p y . European Respiratory Review. Published in 2019. Available from\: [LINK]
Jokic R et al. P o s i t i o n a l t r e a t m e n t v s c o n t i n u o u s p o s i t i v e a i r w a y p r e s s u r e i n p a t i e n t s w i t h p o s i t i o n a l o b s t r u c t i v e s l e e p
a p n o e a s y n d r o m e . Chest. Published in 1999. Available from\: [LINK]
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Myupchar. C o n t i n u o u s P o s i t i v e A i r w a y P r e s s u r e . License\: [CC BY-SA]. Available from\: [LINK]
Drcamachoent. U v u l o p a l a t o p h a r y n g o p l a s t y . License\: [CC BY-SA]. Available from\: [LINK]

Related notes

Tietjens J et al. O b s t r u c t i v e S l e e p A p n o e a i n C a r d i o v a s c u l a r D i s e a s e \: A R e v i e w o f t h e L i t e r a t u r e a n d P r o p o s e d
M u l t i d i s c i p l i n a r y C l i n i c a l M a n a g e m e n t S t r a t e g y . Journal of the American Heart Association. Published in 2018. Asthma
from\: [LINK]
Available
Bronchiectasis
Reutrakul S and Mokhlesi B. O b s t r u c t i v e S l e e p A p n o e a a n d D i a b e t e s . Chest. Published in 2017. Available from\: [LINK]
Chronic Obstructive Pulmonary Disease (COPD)
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Contents

Introduction
Aetiology
Risk factors
Clinical features
Di
Investigations
Management
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