74
CHAPTER

OBSTRUCTIVE SLEEP APNOEA:
MEDICAL MANAGEMENT
Dev Banerjee

Introduction ............................................................................... 1061
Epidemiology, risk factors and associated medical conditions .... 1061
Symptoms, clinical examination and assessment of
excessive daytime sleepiness .................................................... 1062
The diagnosis of obstructive sleep apnoea .................................1063

Treatment – continuous positive airway pressure .......................1066
Alternative strategies to CPAP ...................................................1068
Follow-up and legal issues.........................................................1068
References ................................................................................ 1069

SEARCH STRATEGY
Data in this chapter may be updated by a Medline search using the keywords: obstructive sleep apn(o)ea, excessive daytime sleepiness,
continuous positive airway pressure, polysomnography and road traffic accidents.

INTRODUCTION
Obstructive sleep apnoea (OSA) can be regarded as a condition characterized by repetitive upper airway obstruction
leading to sleep fragmentation, cardiovascular stimulation
and oxygen desaturation during sleep. These together lead
to symptoms such as snoring, unrefreshing sleep, excessive
daytime sleepiness (EDS) and the increased risk of cardiovascular disease, hypertension, insulin resistance and
road traffic accidents. Any individual with time may oscillate within a spectrum of sleep disordered breathing, from
intermittent simple snoring, to chronic heavy snoring, to
upper airway resistance syndrome (UARS), to mild OSA,
to moderate OSA, to severe OSA or to obesity hypoventilation syndrome (OHS). OSA is characterized by complete
breath-holds (apnoeas) and partial breath-holds (hypopnoeas) – scientific physiological descriptions are presented
in Chapter 73, Physiology of sleep and sleep disorders.
With the present obesity epidemic, ear, nose and throat
(ENT), hypertension, obesity, diabetes and sleep specialists are witnessing a large increase in the prevalence of
OSA in their practice. This chapter describes the medical management of OSA, especially associated comorbidities, diagnosis and continuous positive airway pressure
(CPAP), all relevant to the work environment of ENT
specialists. Mandibular devices are not discussed in this
chapter and are described in Chapter 75, The surgical
management of snoring.

EPIDEMIOLOGY, RISK FACTORS AND
ASSOCIATED MEDICAL CONDITIONS
Earlier studies of the prevalence of OSA in society
(Wisconsin Sleep Cohort Study) estimated that 4% of
men and 2% of women had OSA with sleepiness,1 also
known as obstructive sleep apnoea hypopnoea syndrome
(OSAHS). However, since then, the prevalence of obesity has been increasing in all age groups. In the UK, it is
estimated that 26% of adults are obese (body mass index
(BMI) ≥ 30 kg / m 2). 2 Further analysis of the epidemiology
of OSA has suggested the prevalence of OSAHS is around
5% in a given population, 3 and it is likely this will increase
with time. The exact incidence of OSA without EDS is
unclear, as this population is less likely to seek medical
input in the primary care setting. The prevalence differences between men and women are intriguing and the
exact reason why OSA is more common and more severe in
men is not fully understood. Men generally have a higher
prevalence of OSA than women but the effects of menopause, pregnancy and the presence of polycystic ovarian
syndrome have been shown to increase the risk of OSA in
women.4 Various mechanisms may exist, including body
fat distribution, cranio-facial differences, and the role of
female hormones, over and beyond simply BMI. 5 There
is increasing evidence that ethnic differences do exist and
people of oriental Chinese origin have a greater risk of

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developing OSA at a lower level of obesity compared to
European Caucasians. Cranio-facial differences may
explain this phenomenon.6 There is little information,
however, on the prevalence of sleep disordered breathing
in the South Asian population in the UK compared to the
indigenous population in South Asia.
Obesity is recognized as an important risk factor for
OSA. The prevalence of OSA rises with obesity7 and it
is estimated that up to 75% of those with a BMI above
40 kg / m 2 have OSA.8 The exact relationship between
obesity and OSA is not well understood, however, and is
probably multifactorial. Factors including BMI, neck soft
tissue mass, parapharyngeal and lingual adipose deposition, and body fat distribution all play a role. Any weight
gain is not necessarily wholly adipose and an increase in
soft tissue mass around the airway may be more crucial.
Other factors such as pharyngeal muscle tone and the biophysical compliance relationship between airway patency
and critical closing pressure remain unresolved.
OSA is associated with cardiovascular disease9–11
and clinicians treating and dealing with patients with
OSA are increasingly involved in modifying cardiovascular risk in their practice. OSA is associated with an
increased risk of hypertension, as shown in population
studies. There is growing evidence that treating OSA will
decrease blood pressure, and even modest falls in blood
pressure may translate into significant modification of
cardiovascular risk. Associated comorbidities such as obesity, diabetes and smoking history may cloud any direct
causal relationship between OSA and cardiovascular disease and further larger longitudinal studies assessing the
impact of CPAP therapy on cardiovascular outcomes, particularly coronary artery disease, are warranted.12
The term metabolic syndrome has been increasingly
used and described in relation to OSA.13 Metabolic
syndrome encompasses a cluster of features related to
obesity, diabetes and hypertension. These include waist
circumference, triglyceride and glucose levels, and hypertension. There is an increased incidence of metabolic
syndrome in patients with OSA.14 With increasing evidence that OSA is associated with insulin resistance and
diabetes mellitus,15–17 it is becoming more apparent that
OSA may play an important role in metabolic syndrome
and diabetes mellitus.

SYMPTOMS, CLINICAL EXAMINATION
AND ASSESSMENT OF EXCESSIVE
DAYTIME SLEEPINESS
Symptoms associated with OSA are shown in Box 74.1.
Clinical assessment of OSA entails a detailed history,
ideally with the partner present during the consultation.
The partner may be able to describe the breath-holding,
associated gasping, and movement arousals (associated
with the apnoeas and hypopnoeas) and may possibly display a raised level of anxiety. Many couples may express
marital strife and hence it is prudent for the clinician consider their issues with compassion. Even if the patient with

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BOX 74.1 Symptoms of obstructive sleep apnoea (OSA)
•
•
•
•
•
•
•
•
•
•

Snoring
Fatigue
Witnessed breath-holds
Gasping and choking
Excessive daytime sleepiness
Fragmented sleep
Unrefreshing sleep
Reduced alertness
Mood changes
Nocturia

possible OSA is banished to the next bedroom, the witnessed apnoeas are still reportable by the pauses in the
audible snoring. Some patients may have had OSA for
many years and therefore become accustomed to their
EDS and hence may underestimate their symptoms. An
appreciation of their sleep patterns is important, as one of
the commonest causes of EDS is sleep deprivation rather
than sleep fragmentation (i.e. OSA).
Some will relay how EDS may affect their working lives,
especially those who work with heavy machinery or drive
professionally. Taking a history of road traffic accidents
(RTAs), therefore, is vital. Individuals with OSA are at a
higher risk of RTAs, with associated costs.18, 19 Although
individuals may not have had an RTA as a result of falling
asleep at the wheel, subtle clues such as drifting across
lanes, clipping the kerb, or a history of being beeped at by
other drivers whilst driving are useful indicators of driving whilst sleepy.
The presence of central obesity is a particularly relevant
physical finding during an OSA consult. A BMI greater
than 28 kg / m 2 should increase the suspicion for OSA.
Neck circumference is a useful measure; above 43 cm may
be predictive. Other examination features of importance
include a detailed nasal and oropharyngeal assessment,
including the Mallampati score, 20 and the presence or
absence of retrognathia, cranio-facial abnormalities and
tonsillar hypertrophy. Information about possible associated medical conditions such as hypertension, diabetes
and dyslipidaemia should always be sought during the
consultation.
Unfortunately, the assessment of history and clinical
findings has been shown to lack sensitivity and specificity
in diagnosing OSA. It is estimated that history and examination can only predict OSAHS in 50% of patients. 21 The
measurement of EDS may be subjective and objective. The
commonest subjective questionnaire used is the Epworth
Sleepiness Scale (ESS; see Table 74.1), named after the
Epworth hospital, Melbourne, Australia.22 A score above
10 (out of 24) may indicate EDS; but the ESS lacks sensitivity and specificity. Therefore, in any individual, the
ESS may not on its own be very useful, but act only as a
guide. It is generally not recommended that clinical decision-making is based purely on the ESS. More recently, the
STOP-Bang questionnaire (Box 74.2) has been developed
as a pre-operative screening tool to identify patients with
undiagnosed OSA, 23 and has been shown to identify moderate to severe cases of OSA in the surgical population. 24

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TABLE 74.1 Epworth Sleepiness Scale (ESS)
Assesses the likelihood of an individual dozing off at the
following situations (score 0 = never, 1 = slight chance,
2 = moderate chance and 3 = high chance of dozing)
Situation

Chance of dozing

Sitting and reading
Watching TV
Sitting inactive in a public place
(e.g a theatre or a meeting)
As a passenger in a car for an hour
without a break
Lying down to rest in the afternoon when
circumstances permit
Sitting and talking to someone
Sitting quietly after a lunch without alcohol
In a car, while stopped for a few minutes in
traffic
TOTAL

BOX 74.2 STOP-Bang questionnaire – answer Yes or No
•
•
•
•
•
•
•
•

Snoring – Do you snore loudly (louder than talking or heard
through closed doors)?
Tired – Do you often feel tired, fatigued, or sleepy during
daytime?
Observed – Has anyone observed you stop breathing during your sleep?
Blood pressure – Do you have or are you being treated for
high blood pressure?
BMI – BMI of more than 35 kg / m2?
Age – Age over 50?
Neck circumference – neck circumference greater than
40 cm?
Gender – Gender male?

High risk of OSA (AHI > 5 / hr): answering yes to three or
more items
Low risk of OSA (AHI < 5 / hr): answering yes to less than
three items

Objective measurements of EDS include the Multiple
Sleep Latency Test (MSLT), which measures how quickly
an individual can fall asleep, and the Maintenance of
Wakefulness Test (MWT), which measures how long an
individual can stay awake. However, such diagnostic tests
can only be measured if full polysomnography facilities,
including EEG, are available, as without EEG, accurate
assessment of wake and sleep cannot be made.

THE DIAGNOSIS OF OBSTRUCTIVE
SLEEP APNOEA
Methods designed to diagnose OSA may include domiciliary single channel (overnight oximetry), domiciliary
multichannel (respiratory and oximetry signals) and inhospital full polysomnography (PSG), which includes measurement of respiratory, oximetry and sleep architecture

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assessment using electroencephalography (EEG), electrooculography (EOG) and electromyography (EMG) parameters. The merits of each tool are discussed below.

74

Overnight oximetry
This method measures variations in oxygen saturation
and pulse rate during sleep. It assumes that when an individual has an apnoea or hypopnoea, the oxygen saturation falls. Once the apnoea or hypopnoea is relieved,
the oxygen desaturation recovers. The falls and rises are
regarded as ‘oxygen dips’. The pulse oximeter is applied
over the end of a digit, which is attached to a wristwatch
computer that the patient wears during the night. This is
where the data are collected. For convenience, the device
can be worn at home. More sophisticated software products provide pulse rate variability (e.g. the number of pulse
rises of over six beats per minute averaged out per hour),
which would reflect autonomic cardiovascular changes
during arousals as a result of apnoeas and hypopnoeas.
However, pulse rate variability can only be analyzed in
the presence of sinus rhythm rather than in patients with
atrial fibrillation.
In the UK, some sleep clinicians use oximetry alone as
a screen for OSA. It is standard practice that a ‘dip’ of
4% oxygen saturation (e.g. from 94% to 90%) is regarded
as more meaningful than a 2% or a 3% dip. An oxygen
desaturation index (ODI) (i.e. the number of times the oxygen saturation falls by 4% averaged out per hour) of more
than 15 per hour may be suggestive of OSA. The presence of other associated features that are measured that
may lean towards a diagnosis of OSA in the presence of a
‘positive’ oximeter result include EDS (ESS > 10), obesity
(BMI > 28 kg / m 2), and the presence of other comorbidities
(e.g. hypertension, coronary artery disease, metabolic syndrome and diabetes mellitus). However, an ODI > 15 per
hour can only be used if the resting saturation of oxygen is
above 90% and there is an absence of obstructive airway
disease. Figures 74.1 and 74.2 show a classic case of repetitive oxygen desaturation during sleep, typical of OSA.
Although studies using overnight oximetry as a screening tool for OSA have shown good specificity and positive
predictive value, this test is associated with poor sensitivity
and negative predictive value. 25 In other words, overnight
oximetry may miss patients with OSA who do not desaturate, but in the presence of a positive result, the oximetry
can be a useful screen. However, an abnormal ODI may
underestimate the true severity of OSA, as demonstrated
in Figures 74.3 and 74.4. Generally it is accepted that
young, less obese patients may not have oxygen desaturations in the presence of apnoeas and hypopnoeas and
therefore will be missed by oximetry. Mechanisms why
some patients desaturate and some do not is unclear but it
may be related to lung volumes, functional residual capacity or central respiratory response to apnoeas (i.e. if an
arousal response to airway obstruction is blunted then the
individual is more likely to hypoventilate and desaturate).
It is recommended that, if the ODI is less than 15 oxygen
desaturations (‘dips’) per hour, but there is the presence
of EDS, obesity or existing comorbidity, then a further

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Section 1: Head and Neck

Sp02
100

Saturation

80

60

40

20

Figure 74.1 A patient with an
oxygen desaturation index (ODI) of
55 4% oxygen dips per hour. The
oximetry trace shows the whole
night data. Minimum oxygen
saturation is approximately 45%.

Hour
1

2

3

4

5

6

7

referral for multichannel assessment of respiration is recommended. It is not advocated that a trial of CPAP be carried out in those where the diagnosis and severity of OSA
s in question following a negative oximeter study.

Home multichannel testing
The advantages of home overnight respiratory monitoring over in-hospital studies are multiple. They include
better patient comfort, cost savings and prevention of
hospital admission, and allow quicker data analysis.
Disadvantages include sensor failure at home and loss of
signal (which may lead to repeat studies). Fewer channels
will inevitably result in less available information. In particular, home monitoring without EEG will not determine
when the patient is asleep during the night. Sleep disordered breathing occurs during sleep, and it may be possible that without an assessment of exact sleep time, home

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Figure 74.2 The same patient as
in Figure 74.1, with a close up of
the oximetry trace demonstrating
oxygen dips. X axis is one hour.
Y axis is 70–100% saturations.
Note the marked repetitive
desaturations of oxygen, typical
of OSA. Occasional dips are
below 70%.

monitoring may underestimate the severity of OSA. Some
home portable kits also include EEG probes to determine
sleep architecture. However, in the UK, multichannel
kits that measure nasal/oral flow via a pressure cannula,
chest and abdominal movements via a pressure transducer
housed in a velcro belt and pulse oximetry, but not EEG
activity, are the most popular. A number of such products
are available on the market. A classic example of repetitive
apnoeas is shown in Figure 74.5. The chest and abdominal belt allows the assessor to determine if the apnoeas
and hypopnoeas are related to respiratory effort (during
the apnoea or hypopnoea, the chest and abdominal signals still display movement) and therefore obstructive in
nature, as opposed to central sleep apnoea (CSA) where
there is no chest or abdominal movement or effort during
apnoeas. In contrast to OSA, the apnoeas seen in CSA
originate from the respiratory drive centre of the brain
and may occur in patients with cerebrovascular disease or

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Sp02
100

1065

Saturation

74

80

Figure 74.3 This patient has an
ODI of 22 4% oxygen dips per
hour, a body mass index (BMI)
of 36 kg / m2 and an ESS score
of 6. The desaturation is not
as marked as the example
in Figure 74.1. The mid page
reading signal to zero is an
artefact.

60

40

20

Hour
1

2

3

4

5

6

7

8
0

10

20

30

40

50

60

Figure 74.4 The same patient as
in Figure 74.3, showing close up
of oxygen dips from Figure 74.3.
X axis is one hour and Y axis is
70–100% oxygen saturations.
Repetitive but intermittent oxygen
desaturations were seen, particularly 2% and 3% dips. The patient
underwent a diagnostic polysomnography showing severe OSA,
apnoea/hypopnoea index of 73
per hour. In this case the overnight
oximetry on its own underestimated the true severity of OSA.

Figure 74.5 A classic example of
OSA with repetitive apnoeas. X axis
is 5 minutes. Top trace is oronasal cannulae flow trace, second
trace is thoracic band, third trace
is abdominal band, fourth trace
is oxygenation and fifth trace is
pulse rate. Note marked desaturations of oxygen with each apnoea,
which recovers once apnoea is
abolished and the pulse variability.
Due to lag time effect, the nadir of
oxygen saturation always follows
the apnoea.

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those who take regular opioids in high doses. One form
of CSA known as Cheyne-Stokes respiration (‘crescendodecrescendo’ chest and abdominal movements) is more
common in patients with heart failure. Therefore oximetry alone would not pick up the origin of apnoeas (i.e.
obstructive vs central), in such patients.
Patients are taught how to attach the necessary equipment, either at home or in the hospital physiology department. The patient then either goes home wearing the
equipment or reattaches it themselves later in the evening.
Following overnight data collection, the equipment is
returned and the data are analyzed. Whilst in most models
data analysis occurs automatically, it is recommended that
the data are scored by a trained clinician or technician
in an attempt to reduce software mismatching of apnoeas
and hypopnoeas.
An apnoea is regarded as a completed cessation of
airflow (more than 90% reduction in nasal airflow/pressure signal amplitude of the pre-event baseline) for at
least 10 seconds, regardless of whether there is an associated oxygen desaturation or arousal. The definition of
hypopnoea varies from centre to centre but it is typically
regarded as a reduction in airflow/pressure signal amplitude by 30% of pre-event baseline or more with a 3% or
more oxygen desaturation, or if the event is associated
with an EEG arousal. These criteria are based on the
updated American Academy of Sleep Medicine (AASM)
guidelines 201226 (these guidelines superseded the 2007
AASM guidelines27). If the airflow signal is missing
(e.g. mouth breathing or displaced oro-nasal cannulae),
amplitude changes in the thoraco and abdominal wall
movement signals can still be used to determine if apnoeas
or hypopnoeas are taking place. As explained above, chest
wall movement – and therefore by inference, respiratory
effort – is measured indirectly as changes in pressure
detected by a pressure transducer worn around the chest
during sleep. The changes in pressure signal are proportional to airflow and any change in signal can be regarded
as a change in airflow.

Overnight polysomnography
The disadvantages of in-hospital overnight PSG compared
with domiciliary multichannel testing have been stated
above. However, home testing is inadequate for a cohort of
more complex OSA patients. For example, some patients
may need further respiratory monitoring such as transcutaneous CO2 testing, particularly if OHS is suspected. In
other cases, such as patients with neuromuscular disorders, in-hospital assessment is warranted as assisted ventilation is required. Tertiary referral sleep centres will see a
variety of sleep disorders where the EEG, EOG and EMG
component of the PSG are essential (e.g. narcolepsy, parasomnias and periodic leg movement syndrome). Prior to
assessment, equipment is arranged by a sleep technician.
The patient stays overnight at the sleep centre and most
have video monitoring during the night as well. In some
centres, the technician observes the signals from a central
computer room during the night. This allows for troubleshooting, such as disconnected leads, but also allows more

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complex assessments, such as trials with assisted ventilators or titration with CPAP machines. Whether the technician stays overnight is dependent on the staffing and
funding in the particular centre. In cases where the PSG
is unattended, if leads do become disconnected, with the
subsequent loss of signal, a repeat PSG may be necessary.

Criteria for the diagnosis of OSA
The number of apnoeas and hypopnoeas averaged out
per hour of sleep is regarded as the apnoea-hypopnoea
index (AHI). Some centres use the term respiratory disturbance index (RDI), which incorporates the number of
apnoeas, hypopnoeas and respiratory effort related arousals (RERA). The latter are diagnosed by EEG arousals
associated with respiratory effort (from intra-oesophageal
pressure measurement) in the absence of apnoeas and
hypopnoeas. However, as intra-oesophageal pressures are
seldom used, the term AHI is more reflective of clinical
practice and is most commonly used. If home respiratory
monitoring testing is carried out, an estimate of the number of hours slept by the individual is necessary. A common mistake is to calculate the total number of apnoeas
and hypopnoeas and then divide this number by the total
number of hours of respiratory recording and not sleep
time.
The severity of OSA has been defined as:
• no evidence of OSA if AHI < 5 apnoeas and hypop-

noeas per hour
• mild OSA if AHI ≥ 5 and < 15 apnoeas and hypopnoeas

per hour
• moderate OSA if AHI ≥ 15 and < 30 apnoeas and

hypopnoeas per hour
• severe OSA if AHI ≥ 30 apnoeas and hypopnoeas per

hour.
It is important to note that these criteria do not take into
account the desaturation index or the length of apnoeas
and hypopnoeas.
When to treat varies from centre to centre. Most centres would not treat mild OSA without EDS and/or
existing comorbidities (i.e. hypertension, cardiovascular
disease, coronary artery disease, diabetes mellitus) with
CPAP. Lifestyle changes, such as weight loss strategies
(particularly if the BMI is greater than 25 kg / m 2), and/or
treatment of any troublesome rhinitis are recommended.
However, if patients have mild OSA with EDS and/or
comorbidities, or moderate to severe OSA with or without
EDS and comorbidities, then a trial with CPAP therapy
may be considered.

TREATMENT – CONTINUOUS
POSITIVE AIRWAY PRESSURE
Continuous positive airway pressure (CPAP) is regarded
as the mainstay of OSA treatment. 28 This technique was
first described in 198129 and since then there have been
immense technological advances driven by industry.

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CPAP machines may provide a constant positive pressure
(‘fixed pressure’) or may vary pressure depending on the
presence of apnoeas. The latter system, delivered by autoCPAP machines, relies on an algorithm set in the machine
mechanics, whereby a reduction of airflow (i.e. apnoea or
hypopnoea) is detected by the machine and as a result the
machine generates the appropriate retrograde flow (and
therefore pressure) to overcome the apnoea or hypopnoea.
For this to work successfully, a closed system between the
machine and the patient has to exist.
Patient preference typically determines which mask
is used but when a nasal mask is chosen, patients must
ensure mouth leaks are minimized. To this end, chin
straps are sometimes used to keep the mouth closed.
Most masks are kept in place by Velcro straps. All masks
must have an expiratory port to prevent re-inhalation
of expired air. All patients are reminded to clean their
masks and strappings regularly, to ensure longevity. The
newer machines are smaller and lighter to allow easy
portability. All new machines have an internal mechanism to allow switching between 220 and 110 volts,
depending on where the user is around the world. The
ease of using CPAP on planes can vary from airline to
airline. 30 The use of an inverter mechanism will allow
CPAP usage driven from a DC battery pack. For those
who suffer from nasal congestion and/or a dry mouth, a
humidifier is recommended.

needs a supervising technologist and a big disadvantage
is that the true severity of OSA may not be determined
during the diagnostic first half of the night. However, an
advantage is that both diagnostic and CPAP titration are
performed on the same night, therefore saving an extra
admission. The CPAP titration technique is carried out by
a technologist from the central computer room, who has
video access to the patient and electronic linkage to the
CPAP machine. The starting pressure is usually around
4 cm H 2O and the pressure is quickly increased until all
apnoeas and hypopnoeas are eliminated. It is the aim to
reach the required pressure to eliminate the majority of
apnoeas and hypopnoeas within an hour, and the rest of
the night is spent fine-tuning and troubleshooting, for
example, mask leaks or the need for supplemental oxygen
in some cases.
Another technique that is increasingly being used is to
send the patient home with an autoCPAP machine. Most
autoCPAP machines will collect data on compliance, leaks
and pressure profile. A trial of between 7 and 14 days may
allow better adjustment to the concept of CPAP rather
than an autoCPAP trial of one night. Generally autoCPAP
machines are more expensive than the fixed pressure
machines and as a result, in the UK, funding from clinical commissioning groups (CCGs) are predominantly for
fixed pressure machines. Many centres set the fixed pressure as determined by the 90th or 95th centile pressure
(i.e. the blowing pressure to eliminate 90% or 95% of
apnoeas and hypopnoeas) as determined by the autoCPAP
data download. CPAP therapy is recommended by the
National Institute for Health and Care Excellence (NICE)
as the treatment of choice for moderate to severe OSA.32
The Scottish Intercollegiate Guidelines Network (SIGN)
has produced useful recommendations on the management of OSAHS in adults.33

Setting up CPAP

Side effects

Centres differ in how a patient with OSA is set up on
CPAP. All centres should have educational programmes
to ensure patients gain a better understanding of their illness, in order to maximize long-term CPAP compliance.
Some centres use group video workshops to achieve this.
CPAP set-up should be carried out by a trained technician
who understands the technology and appreciates where
problems may arise.
Patients differ in the level of pressure necessary to
eliminate the vast majority of their apnoeas and hypopnoeas. The method of determining this opening of airway
pressure differs from centre to centre. Some use a mathematical equation. One example that has shown reasonable
correlation with titration studies is: predicted pressure
(cm H 2O) = (0.16 × BMI) + (0.13 × NC) + (0.04 × AHI) – 5.1
2, where NC is neck circumference (cm).31
Another method of titration of CPAP used in some
centres is to admit a patient for overnight diagnostic
PSG. The severity and diagnosis of OSA is confirmed
by PSG during the first half of the night, then CPAP is
commmenced for the second half of the night. This is
referred to as a ‘split night’ regime. However, the process

Most side effects are related to the nasal/face mask
interface. Claustrophobia can be problematic in some
patients. Trying different face masks, from full face, to
nasal, to an interface that sits on the nostril edge (nasal
pillows) may be one solution. However, with patience,
education and reassurance (an experienced technician
is the key here), most patients are able to alleviate such
claustrophobia issues. Nasal stuffiness is a common
troublesome side effect, although interface technology
has improved greatly recently to reduce this. However,
despite this, nasal stuffiness and coryzal illnesses can
lead to poor compliance in those patients with nasal
masks. Heated humidification is recommended as one
solution. Cold and dry air may provoke mucus production and vasodilation in the nasal mucosa and hence
humidification may potentially address this. Although
nasal corticosteroids and/or corrective surgery for
mucosal thickening and polyps may be considered, most
sleep centre practitioners believe that a full-face mask
may be a simpler solution.
Other side effects, such as skin abrasions and leaks,
are usually related to poorly fitting masks. Leaks can be a

The mode of action can be regarded as a ‘pneumatic
splint’ whereby the air pressure generated via a tube and
mask, through the nasal and/or oral passageway, prevents
collapse of the pharyngeal and palatal walls, and consequently, the airway.

The equipment

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nuisance, especially if they are directed towards the eyes.
The patient has to be educated that a good fit rather than a
tight fit is more likely to be successful in eliminating leaks
without skin and eye trauma.
Air-swallowing and pulmonary barotrauma may also
occur, although the latter is very rare. Air-swallowing and
subsequent gastric distension is more likely if the pressure
delivery exceeds physiological oesophageal sphincter pressure (e.g. above 15 cm H 2O). The obvious remedy is to
reduce the pressure.

Compliance and troubleshooting
Compliance of CPAP usage is dependent on many factors.
It has been reported that by 3 years, up to 12–25% of
patients will have discontinued treatment. 34 Compliance
has been defined arbitrarily in the literature as usage
of CPAP for more than 4 hours for at least 5 nights per
week. The biggest factor that will determine long-term
compliance is the improvement of symptoms soon after
commencing CPAP therapy and the severity of the OSA
suffered by the individual.34 What is unclear, when faced
with an individual about to commence CPAP therapy, is
whether 4 hours for 5 nights per week is enough to reduce
the risk of RTAs or future cardiovascular comorbidity.
It is anticipated that future clinical trial data will determine this but generally all patients are encouraged to use
CPAP for at least 6 hours, 7 nights per week.
It follows that adequate education, follow-up by an
experience technician and motivation of the patient all
influence long-term adherence to CPAP. When CPAP failure does occur, troubleshooting interface issues, addressing side effects and assessing the presence of coexisting
sleep disorders (e.g. shift-work related sleepiness, narcolepsy, psychological illness or drug-induced conditions)
should be considered. This latter point is particularly
important as it is not uncommon for an individual to have
two coexisting sleep disorders.
There have been some suggestions that autoCPAP has
advantages over fixed pressure CPAP, particularly with
respect to comfort, possibly by reducing the average pressure applied throughout the night. However, although this
may be the case, there is no evidence that this improves
compliance or symptoms of EDS compared to fixed pressure CPAP. 35 A recent systematic review of fixed pressure
CPAP vs autoCPAP showed that although there was an
improved compliance by 11 minutes per night (0.18 hours;
95% CI, 0.05 to 0.31 minutes; P = 0.006), and that ESS
score improved by 0.5 (95% CI, −0.81 to −0.15; P = 0.005)
in the autoCPAP group, the clinical importance of these
small margins of improvement remain unknown, despite
being statistically significant. 36 Therefore, as the treatment effects are similar between APAP and fixed CPAP,
the therapy of choice will be dependent on patient preference, the cost, and issues of non-compliance. Until there
are definite cost-benefits shown for autoCPAP over the
fixed pressure CPAP machine, there is no justification to
mass provide autoCPAP machines on the NHS in the UK
at present.

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ALTERNATIVE STRATEGIES TO CPAP
Bilevel positive airway pressure (sometimes known as
BiPAP) devices allow specific and separate pre-set inspiratory and expiratory pressures, for example inspiratory positive airway pressure (IPAP) between 10 cm H 2O
and 20 cm H 2O, and expiratory positive airway pressure
(EPAP) between 5 cm H 2O and 10 cm H 2O. These devices
may improve compliance in some patients who are intolerant to CPAP but should only be used in selective cases.
For those who have CSA, newer devices known as adaptive
servo-ventilator (ASV) have been commonly tried. It is generally recommended that such treatment should be initiated
by specialist sleep centres. Other novel treatments, such as
nasal EPAP devices, are being introduced as alternative
therapies37 but randomized controlled trials comparing
this form of device against CPAP are still awaited.38

FOLLOW-UP AND LEGAL ISSUES
At the time of diagnosis of OSA, in the UK, the individual is recommended to self-inform the Driver and Vehicle
Licensing Authority (DVLA), Swansea, UK, of the diagnosis. However, the DVLA recognizes only the diagnosis of ‘obstructive sleep apnoea syndrome’, defined by the
DVLA as OSA with sleepiness, but there is no indication
of how the sleepiness is qualified or quantified and therefore diagnosis is at the discretion of the diagnosing clinician. The emphasis of responsibility to inform the DVLA
in the UK is placed on the patient with ‘OSA syndrome’
and not the sleep clinician/ENT surgeon and so on. In
reality, many patients do not inform the DVLA, as in
many parts of the country the treatment for OSA (CPAP)
may not be available immediately. All drivers should be
reminded that by law (Road Traffic Act 1998), all drivers
have a duty of care when driving. However, those patients
deemed to be a genuine threat to the public by continuing
to drive whilst sleepy may be considered for notification
by the clinician, despite this potentially breaking rules of
patient confidentiality.
Follow-up CPAP clinics are aimed to determine
compliance, minimize intolerance, improve symptoms
(as shown by reduced sleepiness) and continue to modify
cardiovascular risk factors. Follow-up PSG with CPAP is
not necessary unless other sleep disorders (e.g. periodic leg
movement, insomnia) are suspected. Some centres utilize
a repeat overnight oximetry with CPAP, but an abnormal
tracing may not necessarily differentiate poor compliance
from inadequate treatment pressure. A significant increase
in weight with time may lead to the appearance of snoring with the mask on and an increase in the fixed CPAP
pressure may be necessary. Leaks around the mask may
be caused by the mask components wearing out, but if the
mask is well looked after it should last for up to a year.
CPAP machines that are provided on the NHS must be
electrically serviced and checked by an engineer on an
annual basis by law. The equipment technically belongs to
the centre that provided the machine and therefore it is the

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74: OBSTRUCTIVE SLEEP APNOEA: MEDICAL MANAGEMENT

responsibility of the centre to ensure that it is electrically
safe. During servicing, the engineer will routinely download usage data from the machine and this will provide
useful compliance data. Patients with moderate to severe
OSA who have suboptimal compliance are challenging
to the clinician, and reasons for non-compliance should

1069

be addressed. If a patient refuses treatment with CPAP,
then other solutions (e.g. weight loss, mandibular devices
or even surgery) may be considered. The patient should be
reminded of the issues of driving with OSA without treatment. Clinical psychology approaches, particularly cognitive behavioural therapy, may also be considered.

74

KEY POINTS
• Obstructive sleep apnoea is becoming more and more prevalent in society as more and more individuals become obese.
• A significant proportion of individuals with obstructive sleep
apnoea are however not obese and therefore the clinician should look out for airway anatomical reasons for the
apnoeas.
• Obstructive sleep apnoea is commonly associated with
other comorbidities such as hypertension, cardiac disease,
diabetes mellitus type II and cerebrovascular disease.
• Obstructive sleep apnoea is a common reason for impaired
well-being particularly impaired mood, concentration,
memory, and alertness.

• There is a higher risk of fatigue-related road traffic accidents
in those who have severe obstructive sleep apnoea.

• The clinician looking after an individual with obstructive
sleep apnoea should be aware of the medical (CPAP), dental
(mandibular advancement splint) and surgical (Ear Nose and
Throat) approaches of treatment.
• Services delivering diagnostic and therapeutic patient pathways are more commonly involving a multidisciplinary and
holistic approach.

REFERENCES
1.

Young T, Palta M, Dempsey J, et al. The
occurrence of sleep-disordered breathing
among middle-aged adults. N Eng J Med
1993; 328: 1230–35.
2. The NHS Information Centre, Lifestyles
Statistics. Statistics on obesity, physical
activity and diet: England, 2012. Leeds:
The Health and Social Care Information
Centre; 2012.
3. Young T, Peppard PE, Gottlieb DJ.
Epidemiology of obstructive sleep apnea:
a population health perspective. Am J Resp
Crit Care Med 2002; 165: 1217–39.
4. Ralls FM, Grigg-Damberger M. Roles of
gender, age, race/ethnicity, and residential
socioeconomics in obstructive sleep apnea
syndromes. Curr Opin Pulm Med 2012;
18(6): 568–73.
5. Jordan AS, McEvoy RD. Gender differences in sleep apnea: epidemiology, clinical
presentation and pathogenic mechanisms.
Sleep Med Rev 2003; 7: 377–89.
6. Villaneuva AT, Buchanan PR, Yee BJ,
Grunstein RR. Ethnicity and obstructive
sleep apnea. Sleep Med Rev 2005; 9(6):
419–36.
7. Young T, Peppard PE, Taheri S. Excess
weight and sleep-disordered breathing.
J Appl Physiol 2005; 99: 1592–99.
8. Lopez PP, Stefan B, Schulman CI,
Byers PM. Prevalence of sleep apnea in
morbidly obese patients who presented
for weight loss surgery evaluation: more
evidence for routine screening for obstructive sleep apnea before weight loss surgery.
Am Surg 2008; 74: 834–38.
9. Wolk R, Somers VK. Cardiovascular consequences of obstructive sleep apnea. Clin
Chest Med 2003; 24: 195–205.
10. Robinson GV, Stradling JR, Davies RJ.
Sleep 6: obstructive sleep apnoea/hypopnoea syndrome and hypertension. Thorax
2004; 59: 1089–94.

K17879_Volume III_Book.indb 1069

11. Shahar E, Whitney CW, Redline S, et al.
Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the
Sleep Heart Health Study. Am J Resp Crit
Care Med 2001; 163: 19–25.
12. Monahan K, Redline S. Role of obstructive sleep apnoea in cardiovascular disease.
Curr Opin Cardiol 2011; 26(6): 541–47.
13. Vgontzas AN, Bixler EO, Chrousos GP.
Sleep apnea is a manifestation of the
metabolic syndrome. Sleep Med Rev 2005;
9: 211–24.
14. Coughlin SR, Mawdsley L, Mugarza JA,
et al. Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome. Eur Heart J
2004; 25: 735–41.
15. Ip MS, Lam B, Ng MM, et al. Obstructive
sleep apnea is independently associated
with insulin resistance. Am J Resp Crit
Care Med 2002; 165: 670–76.
16. Punjabi NM, Sorkin JD, Katzel LI, et al.
Sleep-disordered breathing and insulin
resistance in middle-aged and overweight
men. Am J Resp Crit Care Med 2002; 165:
677–82.
17. Wang X, Bi Y, Zhang Q, Pan F. Obstructive
sleep apnoea and the risk of type 2 diabetes: a meta-analysis of prospective cohort
studies. Respirology 2013; 18: 140–46.
18. George CF, Smiley A. Sleep apnea and
automobile crashes. Sleep 1999; 22:
790–95.
19. Findley LJ, Suratt PM. Serious motor
vehicle crashes: the cost of untreated sleep
apnoea. Thorax 2001; 56: 505.
20. Mallampati SR, Gatt SP, Gugino LD, et al.
A clinical sign to predict difficult tracheal
intubation: a prospective study. Can Anaes
Soc J 1985; 32: 429–34.
21. Hoffstein V, Szalai JP. Predictive value of
clinical features in diagnosing obstructive
sleep apnea. Sleep 1993; 16: 118–22.

22. Viner S, Szalai JP, Hoffstein V. Are history
and physical examination a good screening
test for sleep apnea? Ann Int Med 1991;
115: 356–59.
23. Johns MW. A new method for measuring
daytime sleepiness: the Epworth Sleepiness
Scale. Sleep 1991; 14: 540–45.
24. Farney RJ, Walker BS, Farney RM, et al.
The STOP-Bang equivalent model and
prediction of severity of obstructive sleep
apnea: relation to polysomnographic
measurements of the apnea/hypopnea
index. J Clin Sleep Med 2011; 7(5):
459–65.
25. Chung F, Subramanyam R, Liao P, et al.
High STOP-Bang score indicates a high
probability of obstructive sleep apnoea.
Br J Anaes 2012; 108: 768–75.
26. Ryan PJ, Hilton MF, Boldy DA, et al.
Validation of British Thoracic Society
guidelines for the diagnosis of the sleep
apnoea/hypopnoea syndrome: can polysomnography be avoided? Thorax 1995;
50: 972–75.
27. Berry RB, Brooks R, Garnaldo CE, et al.
The AASM manual for the scoring of sleep
and associated events: rules, terminology
and technical specifications, version 2.0.
Darien, Illinois: American Academy of
Sleep Medicine; 2012. Available from:
www.aasmnet.org
28. Iber C, Ancoli-Israel S, Chesson A, et al.
The AASM manual for the scoring of sleep
and associated events: rules, terminology
and technical specifications. 1st ed.
Westchester, Illinois: American Academy of
Sleep Medicine; 2007.
29. Patel SR, White DP, Malhotra A, et al.
Continuous positive airway pressure
therapy for treating sleepiness in a diverse
population with obstructive sleep apnea:
results of a meta-analysis. Arch Intern Med
2003; 163: 565–71.

5/26/18 7:27 AM

1070

Section 1: Head and Neck

30. Sullivan CE, Issa FG, Berthon-Jones M,
Eves L. Reversal of obstructive sleep
apnoea by continuous positive airway
pressure applied through the nares. Lancet
1981; 1(8225): 862–65.
31. Banerjee D, Yee B, Grunstein R. Airline
acceptability of in-flight CPAP machines –
flight, fright, or fight? Sleep 2003; 26(7):
914–15.
32. Oliver Z, Hoffstein V. Predicting effective
continuous positive airway pressure. Chest
2000; 117(4): 1061–64.
33. National Institute for Health and
Clinical Excellence. Continuous positive airway pressure for the treatment
of obstructive sleep apnoea/hypopnoea
syndrome. Technology Appraisals TA139.

K17879_Volume III_Book.indb 1070

London: NICE; 2008. Available from:
https://www.nice.org.uk/guidance/ta139
34. Scottish Intercollegiate Guidelines
Network. Guideline 73: Management
of obstructive sleep apnoea/hypopnoea syndrome in adults: a national
clinical guideline. Edinburgh: Scottish
Intercollegiate Guidelines Network;
2003. Available from: http://www.
lothianrespiratorymcn.scot.nhs.uk/
wp-content/uploads/2010/11/SIGN-73Management-of-Obstructive-Sleep-Apnoea_
Hypopnoea-Syndrome-in-Adults.pdf
35. Engleman HM, Wild MR. Improving
CPAP use by patients with the sleep
apnoea/hypopnoea syndrome (SAHS).
Sleep Med Rev 2003; 7: 81–99.

36. Ayas NT, Patel SR, Malhotra A, et al.
Auto-titrating versus standard continuous
positive airway pressure for the treatment
of obstructive sleep apnea: results of a
meta-analysis. Sleep 2004; 27: 249–53.
37. Ip S, D’Ambrosio C, Patel K, et al.
Auto-titrating versus fixed continuous
positive airway pressure for the treatment
of obstructive sleep apnea: a systematic
review with meta-analyses. Syst Rev 2012;
1(1): 20.
38. Berry RB, Kryger MH, Massie CA. A novel
nasal expiratory positive airway pressure
(EPAP) device for the treatment of obstructive sleep apnea: a randomized controlled
trial. Sleep 2011; 34(4): 479–85.

5/26/18 7:27 AM