Sleep Disorders Scott Brown

176
Physiology of sleep and sleep disorders

JOHN FLEETHAM
Introduction
Sleep and respiration
Sleep disorders
Key points
2305
2306
2307
2311
Best clinical practice

Deficiencies in current knowledge and areas for future
research
References
2311
2311
2311
SEARCH STRATEGY
The data in this chapter are supported by a Medline search using the key words sleep, respiration, obstructive sleep
apnoea/hypopnoea syndrome, nonrespiratory sleep disorder and focussing on pathogenesis.
INTRODUCTION
This chapter summarizes the current knowledge concerning sleep and its impact on normal respiration. It reviews
in detail the pathogenesis of obstructive sleep apnoea/
hypopnoea syndrome. The pathogenesis and clinical
aspects of nonrespiratory sleep disorders such as narcolepsy, periodic limb movement disorder (PLMD) and
idiopathic hypersomnia are also briefly discussed.
Sleep is a temporary state of unconsciousness that can
be interrupted by external stimuli. It is not a uniform
state, but is organized into a cyclic pattern of sequential stages. The stage of sleep is defined by a combination
of electroencephalographic (EEG), electromyographic
(EMG) and electro-oculographic criteria. Two separate
phases of sleep are generally recognized: quiet or nonrapid eye movement sleep (non-REM) and active or
rapid eye movement sleep (REM). During non-REM
sleep, the EEG waves progressively slow down and increase
in amplitude. Non-REM is divided into four stages,
representing progressively deeper stages of sleep. In
stages 1 and 2 the EEG voltage is low and the frequency
is mixed. In stages 3 and 4 the EEG voltage is high and
the frequency slow, and consequently, these two stages are
often referred to as slow wave sleep (SWS). Stage 2 sleep is
the predominant sleep stage and usually accounts for

about half of an adults sleep. During REM sleep the EEG
is desynchronized with low voltage and high frequency.
REM sleep has been characterized into two patterns, tonic
REM associated with muscle tone depression and phasic
REM associated with periods of rapid eye movements and
twitching movements of the face and limbs. Most dreams
happen during REM sleep and there is also increased
autonomic activity with marked fluctuations in blood
pressure, heart rate and respiratory rate. Increasing age,
alcohol and other sedatives all tend to decrease REM sleep.
A typical sleep usually starts with stages 1 and 2 of nonREM sleep which often alternate with wakefulness prior to
entering the deeper SWS. REM sleep occurs for the first
time approximately 90 minutes after the onset of sleep and
then recurs between four and six times during a nights
sleep. REM sleep accounts for 25 percent of the total sleep
time and as sleep progresses the REM periods become
longer and the non-REM periods shorter. Arousals are
brief neurological awakenings and are a normal feature of
sleep. They may be either cortical or subcortical and the
sleeping individual is usually not aware of them. They may
happen either spontaneously or in response to various
external stimuli, such as sound or internal stimuli, such as
periodic leg movements or sleep apnoea. [**/*]
2306 ] PART 16 THE UPPER AIRWAY

The physiological basis of sleep is poorly understood
but appears to depend on the interaction between the
intrinsic sleep drive, ultradian REM sleep rhythm, adaptive
sleep drive and circadian rhythm.1 The intrinsic sleep drive
increases with the time spent awake and decreases as soon
as sleep occurs. The ultradian REM sleep rhythm has a
90-minute cycle during both wakefulness and sleep and is
independent of the intrinsic drive. The adaptive sleep drive
is influenced by a variety of behavioural responses to the
environment, and reflex responses to sensory stimulation
by factors such as light, noise, temperature, exercise and
food. Sleep, temperature and hormone secretion all have
circadian rhythms with a 2425 hour cycle, which can be
influenced by external factors. These circadian rhythms
are controlled by the suprachiasmatic nuclei in the
hypothalamus, which respond to changes in light
stimulation. The sleep circadian rhythm keeps the sleep/
wake cycle in sequence with environment time but is not
responsible for sleep onset. Cerebral cortical activity
determines when sleep or wakefulness take place but does
not initiate sleep. The reticular activating system in the
brain stem promotes wakefulness when it is active and
permits sleep when it is inactive. It controls the intrinsic
sleep drive and the reflex component of the adaptive
sleep drive. The neurochemistry of sleep and wakefulness
is complex and poorly understood. The primary neurotransmitters involved in the control of sleep and wakefulness are amines, amino acids and peptides. These
neurotransmitters play a major role in the intrinsic sleep
drive and reticular activating system activity. Melatonin
is an important neurotransmitter that is released by the
pineal gland in response to darkness. It promotes sleep and
acts on the suprachiasmatic nuclei to change circadian
rhythms and reduce body temperature. [**/*]
The majority of adults sleep seven to eight hours a

night, but approximately 10 percent sleep less than five
hours and 2 percent sleep more than ten hours. The
optimal sleep duration is eight to nine hours a night
and although many individuals appear to function on less
sleep there is increasing evidence that this is associated
with impaired daytime performance. Sleep pattern
changes with age. Total sleep time is around 16 hours in
full-term infants and 50 percent of this is REM sleep.
There is a progressive decrease in total sleep time with
increasing age and a reduction in the proportion of REM
sleep to 25 percent by middle age. The elderly are more
prone to daytime naps but the total amount of sleep each
24 hours is often similar to younger individuals. Poor
sleep hygiene is the commonest cause of impaired sleep
and a consistent sleep and waking time are important for
good sleep quality. Shift work and time zone changes are
common reasons for an irregular sleep/wake schedule.
Depression and anxiety frequently cause difficulty in
initiating or maintaining sleep. Medical conditions, such
as backache or nocturia, and medications can also reduce
sleep duration and quality. Sleep may also be impaired
because of a bed partners sleep disorder such as sleep
apnoea or periodic limb movement disorder. [**/*]
SLEEP AND RESPIRATION

Sleep has a variety of normal physiological effects on both
the upper and lower respiratory systems (Figure 176.1).
These effects usually have no adverse impact in normal
subjects but may cause a respiratory sleep disorder in
individuals with a narrow upper airway or underlying
respiratory or neuromuscular disease. Normal respiration
Sleep
Cortical
stimulation
Chemical
drive to
breathe
Intercostal
muscle
activity
Upper airway
dilating
muscle activity
Lung volume
Upper airway
narrowing/
collapse
V/Q mismatching
Hypoventilation +/
Hypoxaemia
Hypercapnia
Figure 176.1 The effect of sleep on respiration.
Lower
airway
resistance
Chapter 176 Physiology of sleep and sleep disorders
is regulated by the respiratory centre which has both

afferent input and efferent output. Respiratory rhythmicity originates from the respiratory centre that is in the
medulla. The respiratory centre receives afferent impulses
from central chemoreceptors sensitive to changes in pH,
peripheral chemoreceptors sensitive to changes in PO2
and pH and mechanoreceptors in the airway, lungs
and chest wall. The respiratory centre is also influenced
by input from the cerebral cortex and other brainstem
centres. The cerebral cortex is only irregularly active
during REM sleep and inactive in non-REM sleep so
the respiratory centre is largely under reflex control
during sleep.2 Sleep is associated with reduced chemical
and mechanical drives to breathe and these changes are
most marked during REM sleep. [**/*]
The respiratory efferent output is via the phrenic
nerve nucleus and other motor nuclei to the spinal cord,
peripheral nerves and respiratory muscles. Respiration
in the supine position is principally dependent on the
diaphragm. During non-REM sleep, diaphragmatic
activity remains unchanged and there is an increase in
intercostal muscle activity. This results in expansion of
the ribcage and an increase in diaphragmatic efficiency.
Intercostal muscle activity is decreased and diaphragmatic
activity is increased during REM sleep.3 The loss of
intercostal muscle activity while normal diaphragmatic
activity continues during REM sleep causes a reduction in
lung compliance with an associated decrease in lung
volume and exacerbation of ventilation and perfusion
mismatching. It also results in an increase in the
abdominal contribution to breathing during REM sleep.
Minute ventilation is maintained in response to a
mechanical load during wakefulness. This ventilatory
compensation to mechanical respiratory loads is lost
during sleep, which also contributes to a reduction in
ventilation.
These normal physiological changes during sleep result
in hypoventilation which may be associated with mild
hypercapnia and hypoxaemia. Metabolic rate is also
reduced during sleep by 1025 percent, secondary to
motor activity inhibition and a decrease in body
temperature.4 In normal subjects, the degree of hypoventilation during sleep is greater than the decrease in
metabolic rate and arterial PCO2 increases by approximately 0.5 kPa. Arterial PO2 decreases by 0.52.0 kPa
during sleep because of hypoventilation and increased
ventilation and perfusion inequality. Hypoventilation
during non-REM sleep is largely due to a reduction in
tidal volume,5 whereas the changes in tidal volume and
respiratory frequency are more variable in REM sleep.
The hypocapnic apnoeic threshold is more sensitive
during sleep. Hypocapnia following periods of hyperventilation during sleep is a major cause of central apnoea.
It may also contribute to the development of obstructive apnoea by reducing upper airway dilating muscle
activity. Respiratory-related arousals can occur secondary
to a wide variety of stimuli including hypoxaemia,
] 2307
hypercapnia, coughing and swallowing. The arousal

threshold for respiratory-related stimuli increases during
sleep and is highest in REM sleep. [**/*]
Upper airway muscle activity normally decreases
during sleep with an associated increase in upper airway
resistance, which predisposes to partial upper airway
obstruction.6 Snoring is the low frequency sound
produced by vibration of the upper airway walls during
partial upper airway obstruction. These vibrations usually
take place in the soft palate, but in approximately
30 percent of nonapnoeic snorers they may also be
present at other sites including the tonsils, epiglottis
and the base of the tongue.7 Theoretical modelling has
shown that at critical inspiratory flow rates, the upper
airway becomes unstable with repetitive partial airway
collapse, which generates the sound of snoring.8 The
critical inspiratory flow rate, which causes snoring, is
dependent on upper airway size, shape, compliance and
resistance. Normal individuals also have a circadian
variation in lower airway resistance with mild nocturnal
brochoconstriction. Peak expiratory flow rates during the
night decrease by 8 percent in normal subjects and up to
50 percent in patients with asthma. [**/*]
SLEEP DISORDERS
Sleep disorders are very common and up to 20 percent of
the adult population have some form of sleep disorder. At
least 90 different sleep disorders have been described, and
these are defined in the widely used International
Classification of Sleep Disorders produced by the American
Sleep Disorder Association.9 Sleep disorder medicine
is the subject of several large textbooks,1, 10 and is often
practiced in speciality clinics. Sleep disorders can be
grouped into respiratory and nonrespiratory disorders.
Respiratory sleep disorders

Respiratory sleep disorders are composed of four distinct
syndromes:
1.
2.
3.
4.
obstructive sleep apnoea/hypopnoea (OSAH);

central sleep apnoea/hypopnoea;
Cheyne-Stokes breathing;
sleep hypoventilation.
Each syndrome has a definition, symptoms, associated

features and a differential diagnosis.11 This review will
only discuss OSAH, as this is the condition seen most
commonly by otolaryngologists. OSAH is characterized
by recurrent episodes of partial or complete upper airway
obstruction during sleep which are usually terminated
by an arousal. It is important to understand both the
pathogenesis of the upper airway obstruction and the
mechanism of apnoea termination. The hypoventilation
associated with the upper airway obstruction causes

hypercapnia and hypoxaemia with their related sequelae.
The severity of the hypercapnia and hypoxaemia is
determined by the duration of the hypoventilation and
the baseline arterial PCO2 and PO2 prior to the upper
airway obstruction. The recurrent arousals result in sleep
fragmentation and the symptoms of sleep deprivation
such as excessive daytime sleepiness. The site of the upper
airway obstruction is either in the velopharynx behind the
soft palate, the oropharynx behind the tongue or some
combination of both sites (Figure 176.2).
PATHOGENESIS
The patency of the upper airway is determined by its

compliance and the balance of forces across it
(Figure 176.3).12 The upper airway is more prone to
collapse if there is upper airway narrowing, decreased
intraluminal pressure or if either its compliance or the
extraluminal pressure are increased. The upper airway
dilator muscles are normally activated during inspiration,
Tongue
Soft palate
(a)
Hypopharynx
Oropharynx
Nasopharynx
(b)
Figure 176.2 Upper airway: (a) awake and (b) asleep.
Collapse
Patency
Dilating muscle activity
Large upper airway
which reduces intraluminal pressure, and consequently

decreases the tendency to upper airway collapse. The
upper airway collapses when the force generated by these
muscles is exceeded by the negative airway pressure
produced by the inspiratory muscle activity. Measurement of the critical pressure (Pcrit) required to collapse
the upper airway has been performed in humans undergoing general anaesthesia and complete neuromuscular
paralysis.13 Patients with OSAH had a positive Pcrit,
with the airway collapsing at atmospheric pressure, and
required positive pressure to relieve the obstruction,
whereas normal control subjects required a negative
pressure to collapse the upper airway. [**/*]
Abnormalities in both upper airway size and muscle
activity appear to contribute to the pathogenesis of
OSAH. The majority of patients with OSAH have no
specific upper airway abnormality. However, a range of
different imaging techniques including cephalometry,
computed tomography, magnetic resonance imaging,
nasopharyngoscopy and acoustic reflection have demonstrated narrow upper airways in both awake and asleep
patients with OSAH compared with control subjects.14
Upper airway size is determined by a variety of factors.
Obesity is a major risk factor for OSAH, and upper body
obesity results in fat deposition around the airway and
in the related soft tissues. Gender is an important risk
factor for OSAH and sex hormones influence upper
body obesity. This is probably why OSAH is less common
in premenopausal women than postmenopausal women
or men. Increasing age is associated with narrower
and possibly more collapsible upper airways.15 Finally,
individual variations in mandibular, tongue and soft
palate size and position contribute to upper airway size.
These individual variations have both endogenous and
exogenous causes. They are, in part, genetically determined, and up to 40 percent of the variability of OSAH
may be explained by familial factors.16 It has also been
suggested that adenotonsillar hypertrophy during childhood may cause abnormal craniofacial development
which results in a narrow adult upper airway. [**/*]
There are a large number of upper airway dilating
muscles which include muscles that influence hyoid
position (e.g. geniohyoid), tongue position (e.g. genioglossus) and palate position (e.g. tensor palatini).17 The
geniohyoid and genioglossus are two of the upper airway
dilating muscles that have phasic inspiratory activity
during inspiration which is maintained during non-REM
Upper
airway
Decreased intraluminal pressure

Increased extraluminal pressure
Increased compliance
Figure 176.3 Factors influencing upper airway

patency.
sleep. They stiffen the upper airway and oppose the

negative airway pressure generated by contraction of
the diaphragm. In contrast, the tensor palatini has predominantly tonic activity which decreases during nonREM sleep. This decrease in tonic muscle activity, which
becomes even more marked during REM sleep, is
the primary cause of the increase in upper airway
resistance observed in normal sleep. The upper airway
dilating muscles are activated by negative airway pressure
stimulating nasal and laryngeal receptors.18 Upper airway
dilating muscle activity is impaired by recurrent hypoxia
similar to that seen in patients with OSAH.19 Progesterone increases upper airway dilating muscle activity which
may help protect women from developing OSAH.20 The
relative importance of upper airway dilating muscle
activity is dependent on upper airway size. Minimal
upper airway dilating muscle activity is required to
maintain a large upper airway patent whereas considerable muscle activity may be necessary to maintain the
patency of a small upper airway. The upper airway
muscles of patients with OSAH are hypertrophic21 and
contract more powerfully during wakefulness compared
with normal subjects.22 This is probably to compensate
for the narrow upper airway present in these patients.
This neuromuscular compensation probably develops in
response to upper airway negative pressure stimulation
and may be impaired in some patients with OSAH. There
also may be a delay between the upper airway muscle
activity and diaphragmatic activity during inspiration
in some patients with OSAH, which would result in a
negative intraluminal pressure while the upper airway
dilating muscles are relatively inactive.23 Serotonin is
thought to be an important mediator of upper airway
dilating muscle activity and is reduced during sleep in
patients with OSAH. [**/*]
Additional nonmuscular factors may also play a
role in the pathogenesis of OSAH. Sleep position
contributes to upper airway collapse. In the supine
position, posterior displacement of the tongue and
mandible occurs secondary to the loss of upper airway
tone and the effect of gravity. This is more marked in
REM sleep when upper airway muscle hypotonicity is
greatest. Upper airway size is smaller at low lung volumes.
This is especially relevant in supine obese subjects
who have low end expiratory lung volumes because
of the effect of abdominal weight on diaphragmatic
movement.24 Upper airway shape may also influence
upper airway collapsibility. Patients with OSAH have a
more oval upper airway, which may impair upper airway
dilator muscle function. This upper airway shape may
be an important factor in the pathogenesis of OSAH or
may occur secondary to fat deposition in the lateral
walls of the airway. Chronic vascular over perfusion may
also contribute to upper airway oedema. Changes in
upper airway mucosal adhesiveness and tracheal traction
have also been proposed as contributing to the pathogenesis of OSAH. [**/*]
] 2309
There are a variety of factors which help to continue the upper airway collapse in OSAH once it has
developed. Magnetic resonance imaging14 and histological studies25 have demonstrated that patients with
OSAH develop upper airway oedema secondary to the
mechanical trauma associated with snoring and recurrent
upper airway obstruction. This upper airway oedema
then further reduces the upper airway size and tends to
perpetuate the upper airway obstruction. Animal studies
have shown that upper airway muscle damage may
occur in OSAH in response to the increased workload.26
This muscle damage is consistent with overuse myopathy
and may impair the ability to dilate the upper airway.
Finally, the chronic sleep deprivation associated with
OSAH may also impair upper airway dilating muscle
activity.27 [**/*]
Apnoea termination is associated by a brief cortical
or subcortical arousal. Upper airway muscle activity
increases at the time of the arousal, which results in relief
of the upper airway obstruction. This is usually associated
with a loud snort and a short period of compensatory
hyperventilation. Resumption of sleep then causes a
loss of upper airway muscle activity and recurrence of
upper airway obstruction. Hypoxaemia, hypercapnia,
increased respiratory effort and negative airway pressure
have all been proposed as the arousal stimulus.28 A variety
of studies has been performed which appear to confirm that respiratory arousal happens in each individual
at a relatively fixed respiratory effort irrespective of
the respiratory stimulus. Hypoxaemia and hypercapnia
may cause arousal by increasing respiratory effort or
by a direct stimulation between the respiratory centre
and the reticular activating system. The arousal threshold
is higher during REM sleep and this is responsible
for the longer apnoea duration during REM sleep.
Arousals result in increased sympathetic activity with
vasoconstriction, tachycardia and increased systemic
blood pressure. [**/*]
In summary, the primary cause of OSAH is a narrow
upper airway. Increased upper airway dilator muscle
activity compensates for the narrow upper airway during
wakefulness. Sleep onset is associated with decreased
upper airway muscle activity, which then results in upper
airway collapse and hypoventilation. Hypoventilation
causes hypercapnia and hypoxaemia which stimulate
increased respiratory effort. At a certain arousal threshold
the patient awakens. This results in a resumption
of normal upper airway muscle activity and relief
of the upper airway obstruction. Ventilation resumes
with correction of the hypercapnia and hypoxaemia. The
patient then returns to sleep and the cycle starts
again. The hypoventilation and sleep fragmentation
associated with this sleep/wake cycle are responsible for
the symptoms and long-term consequences of OSAH
(Figure 176.4). The clinical aspects of snoring and
sleep apnoea are discussed in Chapter 177, Obstructive
sleep apnoea: medical management.
Sleep
onset
Upper
airway
collapse
Apnoea/
Hypopnoea
Hypoventilation
Hypoxaemia
Hypercapnia
Arousal
Catecholamines
Pulmonary
hypertension
Sleep fragmentation
Systemic
Daytime sleepiness,
hypertension impaired cognitive function
and quality of life
Nonrespiratory sleep disorders

The majority of patients presenting to otolaryngologists
complain of snoring or have a suspected respiratory sleep
disorder. However, many patients will also present with
excessive daytime sleepiness and may have a nonrespiratory sleep disorder. Excessive daytime sleepiness has a
broad differential diagnosis. It should not be assumed that
a sleepy patient with loud snoring always has OSAH, and
all physicians dealing with patients who snore or who have
suspected OSAH should be aware of the different causes of
excessive daytime sleepiness. In addition to lack of sleep
and medications, these include narcolepsy, periodic limb
movement disorder and idiopathic hypersomnia. Excessive daytime sleepiness requires investigation which, in
addition to clinical assessment, may include completion of
a sleep diary, subjective and objective tests of sleepiness
and polysomnography.
NARCOLEPSY
Narcolepsy is primarily a disorder of REM sleep in which

REM sleep intrudes into non-REM sleep and wakefulness.29 It is associated with human leukocyte antigen
(HLA) types DR2 and DQ1.30 These HLA types do not
necessarily result in narcolepsy as they are present in up to
35 percent of the normal population. HLA testing has no
positive predictive value but has an excellent negative
predictive value. A patient without the HLA phenotype
DRB1*1501-DQB1*0602 is very unlikely to have narcolepsy. The combination of a genetic predisposition and
abnormal neurochemical status is the probable cause
of narcolepsy. The association of narcolepsy with certain
HLA types has led to the speculation that it may have
an autoimmune basis with destruction of hypocretinproducing cells. There is impaired hypocretin production
in the majority of patients with narcolepsy and this may
be the neurochemical basis of narcolepsy. It affects men
and women equally and occurs in approximately one in
2000 of the population. It is a familial condition and up
to 10 percent of patients may have a relative with
narcolepsy. It may present during childhood and almost
always presents before the age of 40 years. It characteristically presents with excessive daytime sleepiness, hypnagogic hallucinations (dreams shortly before sleep), sleep
Figure 176.4 Consequences of OSAH syndrome.
paralysis (inability to move shortly before sleep) and

cataplexy (sudden loss of awake voluntary muscle tone
after emotion), although some of these features are often
absent.31 The diagnosis is usually made clinically based on
the characteristic combination of symptoms. This may be
more difficult in the approximately 10 percent of patients
in whom cataplexy is absent or atypical. A polysomnogram often demonstrates sleep-onset REM (REM sleep
within 20 minutes of onset of sleep). A multiple sleep
latency test may be more helpful and usually reveals a
sleep latency of less than eight minutes with sleep-onset
REM in at least two of the four to five tests. [**/*]
PERIODIC LIMB MOVEMENT DISORDER
Restless leg syndrome (RLS) and PLMD are separate

conditions, but frequently coexist and probably have a
similar aetiology. RLS occurs during wakefulness and is
characterized by abnormal sensation and both voluntary
and involuntary movements in the legs. PLMD takes place
during sleep and is defined polygraphically as periodic
activation of the flexor muscles of the lower limb. The
muscles usually affected are the toe or ankle flexors. More
rarely, the knee, hip and arm flexors are involved. The
muscle usually studied is the anterior tibialis and the
activation should be between 0.5 and 5 seconds and happen
in a series of at least five activations separated by between 5
and 90 seconds. PLMD is diagnosed if at least five
activations take place per hour of sleep. The limb
movements may or may not be associated with arousals.
PLMDs are believed to be caused by a central oscillator
which overcomes the motor inhibition during sleep. They
are more common in stages 1 or 2 of non-REM sleep when
motor inhibition is less pronounced. RLS is associated with
low iron levels but does not appear to improve with iron
therapy. PLMD usually presents with excessive daytime
sleepiness, difficulty initiating sleep and frequent nocturnal
awakenings.32 They are frequently not associated with sleep
disruption or excessive daytime sleepiness, so should not
always be considered to be pathological.33 [**/*]
IDIOPATHIC HYPERSOMNIA
Idiopathic hypersomnia is generally considered to refer to

a heterogeneous group of patients with objectively
confirmed excessive daytime sleepiness in whom all

other diagnoses have been excluded. A more limited
definition refers to patients with excessive daytime
sleepiness that usually presents between the ages of 15
and 30 years and is frequently associated with difficulty
awakening, unrefreshing daytime naps and a positive
family history.34 This occurs in approximately one in
25,000 of the population. No abnormal neurochemical
activity has been determined for this condition and it
is believed to be caused by an increase in the intensity
of the homeostatic control of sleep. As this is a diagnosis
of exclusion, completion of a sleep diary, subjective and
objective tests of sleepiness and polysomnography are
mandatory. [**/*]
] 2311
Deficiencies in current knowledge and

areas for future research
$
$
$
$
The neurochemistry of sleep and wakefulness is

poorly understood.
The physiological changes that cause upper airway
collapse during sleep requires additional study.
The stimulus for respiratory-related arousals remains
largely unexplained.
The long-term consequences of OSAH syndrome need
further research.
REFERENCES
KEY POINTS
! Sleep is a temporary state of unconsciousness that can be interrupted by external
stimuli.
! Sleep has a variety of normal physiological
effects on both the upper and lower
respiratory systems.
! Respiratory sleep disorders are composed of
four distinct syndromes: OSAH, central sleep
apnoea/hypopnoea, Cheyne-Stokes breathing
and sleep hypoventilation.
! OSAH syndrome is characterized by recurrent
episodes of partial or complete upper airway
obstruction during sleep which are usually
terminated by an arousal.
! Abnormalities in both upper airway size and
muscle activity appear to contribute to the
pathogenesis of OSAH syndrome.
! Excessive daytime sleepiness has a broad
differential diagnosis.
! Narcolepsy is primarily a disorder of REM
sleep in which REM sleep intrudes into nonREM sleep and wakefulness.
! PLMD usually presents with excessive
daytime sleepiness, difficulty initiating sleep
and frequent nocturnal awakenings.
!
!
[ It should not be assumed that a sleepy patient with

loud snoring always has OSAH syndrome.
[ Excessive daytime sleepiness requires investigation

that may include completion of a sleep diary,
subjective and objective tests of sleepiness and
polysomnography.
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controls (a neuromuscular compensatory mechanism).
Journal of Clinical Investigation. 1992; 89: 15719.
23. Hudgel D, Harasick T. Fluctuation in timing of upper
airway and chest wall inspiratory muscle activity in
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34.
obstructive sleep apnea. Journal of Applied Physiology.

1990; 69: 44350.
Hoffstein V, Zamel N, Phillipson EA. Lung volume
dependence of pharyngeal cross-sectional area in patients
with obstructive sleep apnea. American Review of
Respiratory Disease. 1984; 130: 1758.
Anastassov GE, Trieger N. Edema in the upper airway in
patients with obstructive sleep apnea syndrome. Oral
Surgery, Oral Medicine, Oral Pathology, Oral Radiology,
and Endodontics. 1998; 86: 6447.
Petrof BJ, Pack AI, Kelly AM, Eby J, Hendricks JC.
Pharyngeal myopathy of loaded upper airway in dogs with
sleep apnea. Journal of Applied Physiology. 1994; 76:
174652.
Leiter JC, Knuth S, Bartlett D. The effect of sleep
deprivation on activity of the genioglossus muscle.
American Review of Respiratory Disease. 1985; 132:
12425.
Gleeson K, Zwillich C, White D. The influence of increasing
ventilatory effort on arousal from sleep. American Review
of Respiratory Disease. 1990; 142: 295300.
Aldrich MS. The clinical spectrum of narcolepsy and
idiopathic hypersomnia. Neurology. 1996; 46: 393401.
Rogers AE, Meeehan J, Guilleminault C, Grumet FC,
Mignot E. HLA DR15 (DR2) and DQB1*0602 typing studies
in 188 narcoleptic patients with cataplexy. Neurology.
1997; 48: 15506.
Parkes JD, Chen SY, Clift SJ, Dahlitz MJ, Dunn G. The
clinical diagnosis of the narcoleptic syndrome. Journal of
Sleep Research. 1998; 7: 4152.
Coleman RM, Pollack C, Weitzman ED. Periodic movements
in sleep (nocturnal myoclonus): relation to sleepwake
disorders. Annals of Neurology. 1980; 8: 41621.
Nicolas A, Lesperance P, Montplaisir J. Is excessive daytime
sleepiness with periodic leg movements during sleep a
specific diagnostic category? European Neurology. 1998;
40: 226.
Bassetti C, Aldrich MS. Idiopathic hypersomnia: a series of
42 patients. Brain. 1997; 120: 142335.
177
Obstructive sleep apnoea: medical management
DEV BANERJEE
Introduction
The spectrum of sleep-disordered breathing
Epidemiology, risk factors and associated medical
conditions
Symptoms, clinical examination and assessment of
excessive daytime sleepiness
The diagnosis of obstructive sleep apnoea
Treatment
2313
2313
2314
2315
2315
2320
Follow-up and legal issues

Conclusions
Key points
research
References
2322
2322
2322
2322
2323
2323
SEARCH STRATEGY
The data in this chapter are supported by a Medline and PubMed search of peer-reviewed articles. Key words used include
obstructive sleep apn(o)ea, obesity, coronary artery disease, cerebrovascular disease, diabetes mellitus, polysomnography
and continuous positive airway pressure.
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.
Together, these lead to symptoms such as snoring,
unrefreshing sleep, excessive daytime sleepiness (EDS),
and the increased risk of cardiovascular disease, hypertension, insulin resistance, cerebrovascular disease and road
traffic accidents. With the current growth of obesity, ear,
nose and throat (ENT), hypertension, obesity, diabetes as
well as sleep clinicians are witnessing a large increase in
the prevalence of OSA in their practices. This chapter
describes the medical management of OSA, especially
continuous positive airway pressure (CPAP), relevant to
the work environment of ENT specialists. Mandibular
devices are not discussed in this chapter. Readers are
recommended to refer to a recent review of such devices
in OSA.1 Pharmacotherapy for EDS, including the role of
wakefulness-promoting drugs in OSA, is reviewed elsewhere.2
THE SPECTRUM OF SLEEP-DISORDERED

BREATHING
Any individual may oscillate within a spectrum of sleepdisordered 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 definitions will follow in this
chapter. Upper airway resistance syndrome applies to
individuals with increased inspiratory efforts (as identified by oesophageal pressure measurements) with frequent arousals, as measured from electroencephalography
(EEG), during diagnostic overnight polysomnography

(PSG) but without overt apnoeas and hypopnoeas. The
fragmented sleep results in increased subjective and
objective daytime sleepiness. Few clinical centres measure
respiratory effort using oesophageal probes and therefore
UARS is probably an underdiagnosed condition. However, overnight noninvasive respiratory monitoring for
apnoeas and hypopnoeas is easier, in practice, and
diagnosing OSA is relatively straightforward. It is
standard practice to regard EDS in the presence of OSA
as obstructive sleep apnoea/hypopnoea syndrome
(OSAHS). Obesity hypoventilation syndrome describes
daytime respiratory failure in the presence of obesity
(body mass index (BMI) 430 kg/m2) in the absence of
airways obstruction from respiratory spirometry.3 The
exact definition of daytime respiratory failure in OHS
varies from centre to centre but our sleep centre regards
this as a PaCO2 46.0 kPa (45 mmHg) and PaO2 o9.3 kPa
(70 mmHg). Not all obese subjects with OSA will develop
OHS but some subjects with mild, moderate or severe
OSA may develop it. The exact mechanism is not totally
clear but it is probably a combination of reduced lung
volumes as a result of a restrictive spirometry, upper
airway obstruction (i.e. OSA) and abnormal central
ventilatory responses to CO2.4
EPIDEMIOLOGY, RISK FACTORS AND

ASSOCIATED MEDICAL CONDITIONS
Earlier studies of the prevalence of OSA in society
(Wisconsin Sleep Cohort Study) estimated that 4 percent
of men and 2 percent of women had OSAHS.5 However,
since then, the prevalence of obesity has increased in all
age groups. A more recent analysis of the epidemiology of
OSA has suggested the prevalence of OSAHS is approximately 5 percent in a given population,6 but it is likely
that 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 difference in prevalence between men and women is
intriguing and the exact reason for why OSA is more
common and more severe in men is not fully understood.
Various mechanisms may exist including body fat
distribution, craniofacial differences and the role of
female hormones, over and beyond simply BMI.7 There
is increasing evidence that ethnic differences exist, and
subjects of Chinese origin have a greater risk of
developing OSA at a lower level of obesity compared
with Caucasian subjects. Craniofacial differences may
explain this phenomenon.8 There is little information,
however, on the prevalence of OSA in the South Asian
population in the UK compared with the indigenous
population in South Asia.
Obesity is recognized as an important risk factor for
OSA. The exact relationship between obesity and OSA is
not well understood, 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 unsolved.
Obstructive sleep apnoea is associated with cardiovascular disease,9, 10, 11 and clinicians treating and dealing
with subjects with OSA are becoming more and more
involved in modifying cardiovascular risk in their
practice. As shown in population studies, OSA is
associated with an increased risk of hypertension. In the
Sleep Heart Health Study,12 conducted in over 6000
people aged between 40 and 97, the odds ratio for
hypertension in patients with severe OSA after adjusting
for BMI was 1.37 (95 percent confidence interval
1.031.83; p = 0.005). There is growing evidence that
CPAP treatment will decrease blood pressure, and even
modest falls in blood pressure may translate into
significant modification of cardiovascular risk. Associated
co-morbidities 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.
There is growing evidence that sleep apnoea is also
associated with cerebrovascular disease,13 with the recognition that some subjects with strokes also have sleep apnoea.
It is possible that sleep apnoea may become an important
modifiable risk factor for cerebrovascular disease. In a
cross-sectional analysis, subjects with moderate-to-severe
OSA had increased odds for stroke (odds ratio, 4.33; 95
percent confidence interval 1.3214.24; p = 0.02) compared
with those without OSA after adjustment for known
confounding factors.14 In the four-year follow-up data, the
odds ratio for having a stroke was raised but not significant
after adjusting for age and BMI (3.08; 95 percent
confidence interval, 0.7412.81; p = 0.12).
The term metabolic syndrome has been increasingly
used and described in relation to OSA.15 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 subjects with OSA.16 With increasing
evidence that OSA is associated with insulin resistance,17, 18 it is becoming more apparent that OSA will
play an important role in metabolic syndrome. In a crosssectional and longitudinal analysis performed in 1387
participants of the Wisconsin Sleep Cohort, up to 15
percent of those with moderate-to-severe sleep apnoea
had diabetes mellitus (defined as an abnormal fasting
sugar or diabetes diagnosed previously by their physician).19 The odds ratio for having diabetes mellitus with
moderate-to-severe OSA versus those with no OSA was
Chapter 177 Obstructive sleep apnoea: medical management
2.30 (95 percent confidence interval 1.284.11; p = 0.005)

after adjustment for age, sex and body habitus. [***/**]
SYMPTOMS, CLINICAL EXAMINATION AND

ASSESSMENT OF EXCESSIVE DAYTIME
SLEEPINESS
The symptoms associated with OSA are:
!
!
!
!
!
!
!
!
!
!
snoring;
fatigue;
witnessed breath-holds;
gasping and choking;
EDS;
fragmented sleep;
unrefreshing sleep;
reduced alertness;
mood changes;
nocturia.
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, movement arousals (associated with
the apnoeas), and may possibly display a raised level of
anxiety. Many couples may express marital strife and
hence it is prudent for the clinician to regard their issues
with compassion. Even if the subject with possible OSA is
banished to the next bedroom, the witnessed apnoeas are
still present by the pauses in the audible snoring. Some
patients may have had OSA for many years and therefore
have become accustomed to their EDS and consequently
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). Shift work-related sleepiness is
also a well-recognized phenomenon and may coexist with
OSA.
Some will relate how EDS may affect their working
lives, especially those who work with heavy machinery or
drive buses, lorries and trains. A history of road traffic
accidents, therefore, is vital as individuals with OSA are at
higher risk of them, at considerable cost.20, 21 Although
individuals may not have had crashes as a result of falling
asleep at the wheel, subtle clues such as drifting across
lanes, clipping the kerb or a history of being honked at by
other drivers, are part of the detailed history assessment.
A physical finding that is particularly relevant during
an OSA consultation is the presence of central obesity. A
BMI greater than 28 kg/m2 should increase the suspicion
for OSA. Neck circumference is a useful measure; above
43 cm (17 inches) may be predictive. Other important
examination features include a detailed nasal and
oropharyngeal assessment including the Mallampati
score,22 the presence or absence of retrognathia, craniofacial abnormalities and tonsillar hypertrophy. Associated
medical conditions such as hypertension, diabetes and
] 2315
hypertriglyceridaemia should always be looked for during

the consultation.
Unfortunately, the assessment of history and clinical
findings have been shown to lack sensitivity and
specificity in diagnosing OSA. It is estimated that history
and examination can only predict OSAHS in 50 percent
of patients,23 and that the male sex, snoring and BMI were
found to be useful predictors of OSAHS.24 The measurement of EDS may be subjective and objective. The
commonest subjective questionnaire used is the Epworth
Sleepiness Scale (ESS), named after the Epworth hospital,
Victoria, Australia (see Table 177.1).25 A score above 10
(out of 24) may indicate EDS but the ESS lacks sensitivity
and specificity, therefore, in an individual, the ESS may
not on its own be very useful, but only a guide. This
author does not recommend clinical decisions based
purely on the ESS. Objective measurements of EDS
include the multiple sleep latency test, which measures
how quickly an individual can fall asleep, and the
maintenance of wakefulness test, which measures how
long an individual can stay awake. However, such
diagnostic tests can only be measured if full PSG,
including EEG, are available. [**]
THE DIAGNOSIS OF OBSTRUCTIVE SLEEP

APNOEA
As the sensitivity and specificity of clinical examination to
diagnose OSA in the clinic setting is poor, other tools are
necessary. These can best be described as domiciliary
single channel (overnight oximetry), domiciliary multichannel (respiratory and oximetry signals) and inhospital full PSG, which includes measurement of
respiratory, oximetry and sleep architecture assessment
using EEG, electrooculography (EOG) and electromyelography (EMG). The merits of each tool are discussed next.
Table 177.1 The Epworth Sleepiness Scale assesses the
likelihood of an individual dozing off in the following situations.
Activity
Score
Sitting and reading

Watching television
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
Score: 0 = never; 1 = slight chance; 2 = moderate chance; 3 = high chance
of dozing. Adapted from Ref. 22., with permission from the Associated
Professional Sleep Societies, LLC.
Overnight oximetry
This device measures oxygen saturation and provides
pulse rate data. 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 gadget is sited at the end of the digit,
with a wristwatch device that the patient wears during
the night. This is where the data are collected. The device
can be worn at home. Some software products provide
pulse rate variability (e.g. the number of pulse rises of
over six beats per minute averaged per hour) which 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 subjects 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
percent oxygen saturation, for example from 94 to 90
percent, is regarded as more meaningful than a 2 or 3
percent dip. An oxygen desaturation index (ODI) (i.e. the
number of times the oxygen saturation falls by 4 percent
averaged out per hour) of over 15 per hour may be
suggestive of OSA. The presence of other associated
features that may tend towards a diagnosis of OSA
include ESS 410, obesity (BMI 428 kg/m2) and comorbidities, for example hypertension, coronary artery
disease, metabolic syndrome and diabetes mellitus.
However, an ODI 415 per hour can only be used if the
resting saturation of oxygen is above 90 percent and there
is an absence of obstructive airway disease. Figures 177.1
and 177.2 show a classic case of repetitive oxygen
desaturation, typical of OSA.
Unfortunately, studies using overnight oximetry as a
screening tool for OSA have shown good specificity and
positive predictive value but poor sensitivity and negative
predictive value.26 In other words, overnight oximetry
may miss subjects with OSA who do not desaturate, but
in the presence of a positive result oximetry can be a
useful screen. However, an abnormal ODI may underestimate the true severity of OSA, as demonstrated in
Spo2
100
Figures 177.3 and 177.4. In general, it is accepted that

young, less obese subjects may not have oxygen
desaturations in the presence of apnoeas and hypopnoeas
and therefore will not be identified by oximetry. The
reasons why some patients desaturate and some do not
are unclear but 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). If the ODI is less than
15 per hour but there is the presence of EDS, obesity or
existing co-morbidity, then the author would recommend
those clinicians who use oximetry to screen for OSA to
refer further to clinicians where multichannel assessment
of respiration is available. The author would not advocate
a trial of CPAP in those patients where the diagnosis and
severity of OSA is in question due to a negative oximetry
study. [Grade B/C/D]
Home multichannel testing

The advantages of home, overnight respiratory monitoring over in-hospital studies are multiple and include
better patient comfort, cost savings, prevention of
hospital admission and speed of analysis data. Disadvantages include sensor failure at home and loss of signal
(which may lead to repeat studies). Fewer signal channels
will mean less information is available. However, 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
monitoring may underestimate the severity of OSA. Some
home, portable kits also include EEG probes to determine
sleep architecture. However, in the UK, the multichannel
kit that utilizes nasal/oral flow (by use of pressure
cannulae), chest and abdominal movements (by use of a
Velcro belt) and pulse oximetry (end of the digit), are
most popular (see Figure 177.5). A classic example of
repetitive apnoeas is demonstrated in Figure 177.6. The
chest and abdominal belts allow the assessor to determine
Saturation
80
60
40
20
Figure 177.1 A subject with an ODI of 55 4 percent oxygen dips per hour. This trace shows the whole nights data. Minimum oxygen
saturation is approximately 45 percent.
Hour
] 2317
Start time + Date. 22.41.00 06/09/2003

Y-axis from 70% to 100%
Figure 177.2 The same patient as in Figure 177.1, showing the oxygen dips in detail. X-axis is one hour. Y-axis is 70100 percent
saturations. Note the marked repetitive desaturations of oxygen, typical of OSA. There are occasional dips below 70 percent.
Spo2
100
Saturation
80
60
40
20
Figure 177.3 This subject has an ODI of 22 4 percent oxygen dips per hour, BMI is 36 kg/m2 and ESS score is 6, and not as marked as
the example in Figure 177.1. The mid-reading signal to zero is an artefact.
whether 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 where there is no chest or abdominal
movement (no effort) during apnoeas. As the name
describes, central sleep apnoea originates from the central
respiratory drive centre of the brain and occurs
occasionally in subjects with cerebrovascular disease.
One form of central sleep apnoea known as CheyneStokes respiration (crescendodecrescendo chest and
abdominal movements) is more common in patients with
heart failure, and thus oximetry alone would not identify
the origin of the apnoeas (i.e. obstructive versus central)
in such patients.
Patients are taught how to apply the gadgets, either at

home or in the hospital physiology department. The
patient either goes home already set up or they prepare
themselves later in the evening. The portable kit is
returned the next day and the data are analyzed. The kits
allow automated analysis of the data, but the author
recommends that a trained clinician or technician scores
the data, thus avoiding the possibility of the software
incorrectly scoring apnoeas and hypopnoeas.
An apnoea is regarded as a completed cessation of
airflow for at least ten seconds regardless of whether there
is an associated oxygen desaturation or arousal. The
definition of hypopnoeas (partial breath-holds) varies
from centre to centre but the author regards them as a
reduction in airflow (amplitude of signal) of between 50
Hour
Start time + Date: 23:13:00 05/10/2005

Y-axis from 70% to 100%
8
0
10
20
30
40
50
60
Figure 177.4 Shows close up of oxygen dips from Figure 177.3. X-axis is one hour and Y-axis is 70100 percent oxygen saturations.
Repetitive but intermittent oxygen desaturations were seen, particularly 2 and 3 percent dips. The patient underwent a diagnostic PSG
showing severe OSA, apnoea/hypopnoea index of 73 per hour. Therefore, in this case, the overnight oximetry on its own underestimated
the true severity of OSA.
and 90 percent (with or without a 3 percent or more

oxygen desaturation and/or EEG arousal) or a reduction
in airflow of less than 50 percent, which must be
accompanied with a 3 percent or more oxygen desaturation and/or EEG arousal. If the airflow signal is missing
due to mouth breathing or displaced oronasal cannula,
amplitude changes in the thoracic and abdominal wall
movement signals can be used to determine whether
apnoeas or hypopnoeas are taking place (see Figure
177.6). It must be pointed out that the respiratory kit
actually measures change in pressure rather than strictly
changes in flow within the oronasal cannulae, and a
pressure transducer detects this. The changes in pressure
signal are proportional to airflow and any change in signal
can be regarded as a change in airflow. [Grade D]
Overnight polysomnography
The disadvantages of in-hospital overnight PSG compared with domiciliary multichannel testing have been
stated above. However, there are some patients whose
assessment is more complex than straightforward OSA
and they may need further respiratory monitoring, such
as transcutaneous CO2 testing, particularly if OHS is
suspected. Other patients, such as those with neuromuscular disorders, may need in-hospital assessment,
especially if assisted ventilation is considered. Tertiary

sleep centres will experience a variety of sleep disorders
where the EEG, EOG and EMG component of the PSG is
essential, for example narcolepsy, parasomnias, periodic
leg movement syndrome, etc. A sleep technician will
prepare the individual in the evening. The patient stays
overnight at a sleep centre, most of which have video
monitoring throughout the night. In some centres the
technician observes the signals from a central computer
room during the night. This allows for any troubleshooting, such as disconnected leads, but also allows more
complex assessments, for example trials with assisted
ventilators or titration with CPAP machines. In some
centres, whether the technician stays overnight is
dependent on staffing and funding. In cases where the
PSG is unattended, should leads become disconnected
with a subsequent loss of signal, a repeat may be
necessary. [Grade D]
Which test should be used?

The issue of whether a PSG should be regarded as the
gold standard is highly debated in the sleep medicine
fraternity. The Standards of Practice Committee of the
American Academy of Sleep Medicine have indicated that
PSG should be the investigation of choice to diagnose
] 2319
sleep-disordered breathing.27 However, other centres

hotly debate this and, in reality, not all ENT clinicians
will have access to tertiary centre PSG facilities.28 Local
availability of services as well as health resources and
funding will determine the route of the diagnostic
procedure. The author recommends that if oximetry
alone is used to screen for OSA, then borderline or
uncertain cases should be referred for more detailed
respiratory monitoring. The key to accurate diagnosis and
management is adequate training in assessing sleepdisordered breathing with expertise in sleep physiology
analysis so that the clinician is aware of the limitations of
each diagnostic procedure. [Grade D]
Criteria for the diagnosis of obstructive sleep

apnoea
Figure 177.5 The author demonstrating a home respiratory

monitoring kit, including oronasal cannulae, thoracic and
abdominal bands, and finger oximetry probe. The kit can be
programmed to switch on and off at set times.
The number of apnoeas and hypopnoeas averaged per

hour of sleep is regarded as the apnoea/hypopnoea index
(AHI). Some centres use the term respiratory disturbance
index, which incorporates the number of apnoeas,
hypopnoeas and respiratory effort-related arousals. The
latter are diagnosed by EEG arousals associated with
respiratory effort (from intraoesophageal pressure measurement) in the absence of apnoeas and hypopnoeas.
However, as intraoesophageal pressures are seldom used,
the term AHI is more reflective of clinical practice and is
popularly 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
2
100
95
90
SpO2 85
80
75
70
110
100
90
BPM 80
70
60
Figure 177.6 A classic example of OSA with repetitive apnoeas. X-axis is five minutes. The top trace is the oronasal cannulae flow,
the second the thoracic band, the third the abdominal band, the fourth trace is oxygenation and the fifth is pulse rate. Note the
marked desaturations of oxygen with each apnoea, which recovers once the apnoea has ended, and because of lag time effect, the
nadir of oxygen saturation always follows the apnoea.

and then divide this number by the total number of hours
of respiratory recording and not sleep time.
The severity of OSA has been arbitrarily defined as:
! no evidence of OSA if the AHI is less than five
apnoeas and hypopnoeas per hour;
! mild OSA if the AHI is five or more and less than 15
apnoeas and hypopnoeas per hour;
! moderate OSA if the AHI is 15 or more and less than
30 apnoeas and hypopnoeas per hour;
! and severe OSA if the AHI is 30 or more apnoeas
and hypopnoeas per hour.
It is important to note that these criteria do not take into
account the desaturation index nor the length of apnoeas
and hypopnoeas.
TREATMENT
When to treat
When to treat varies from centre to centre. Our centre
would not treat mild OSA without EDS and/or existing
co-morbidities (i.e. hypertension, cardiovascular disease,
coronary artery disease, diabetes mellitus) with CPAP.
Lifestyle changes such as weight loss (particularly if the
BMI is greater than 25 g/m2) and/or treatment of any
troublesome rhinitis are recommended. However, if
subjects have mild OSA with EDS and/or co-morbidities,
or moderate-to-severe OSA with or without EDS and comorbidities, then treatment with CPAP therapy would be
considered. [Grade C/D]
How to treat
CONTINUOUS POSITIVE AIRWAY PRESSURE
First described in 1981,29 CPAP is regarded as the

mainstay of OSA treatment,30 and has been of particular
benefit in technological advances. The mode of action can
be regarded as a pneumatic splint, whereby blowing air
via a tube and mask through the nasal and/or oral
passageway, will support the pharyngeal and palatal walls,
preventing collapse of the airway. [****]
The equipment
Continuous positive airway pressure machines provide
either a constant blowing pressure (fixed pressure) or 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
cessation of flow (i.e. apnoea or hypopnoea) is detected
by the machine and results in the machine blowing the
appropriate flow (and therefore pressure) to overcome the
apnoea or hypopnoea. This assumes a closed system
between the machine and the patient (i.e. no leaks). The
autoCPAP may confer more comfort to the patient but no

trials have suggested that clinical outcomes of autoCPAP
are superior to fixed pressure machines.
The masks may essentially be nasal or full face. Patient
preference will determine which mask is chosen, but those
patients choosing a nasal mask must ensure no mouth
leaks occur. Sometimes, chin straps to keep the mouth
closed are used. Most masks are kept in place by Velcro
straps. All masks must have an expiratory port to prevent
reinhalation of expiratory air. All patients are reminded to
clean their masks and strappings regularly to ensure
prolonged longevity. The newer machines are smaller and
lighter to allow portability. All new machines have an
internal mechanism enabling voltage switching between
220 and 110 volts depending on where the user is in the
world. The ease of using CPAP on planes is variable
among different airlines.31 The use of an inverter
mechanism will allow a CPAP machine to be driven from
a DC battery pack. Those who suffer from nasal
congestion can use a humidifier. [Grade D]
Setting up on continuous positive airway pressure
Centres differ in how a subject with OSA is set up on
CPAP. All centres should have comprehensive education
programmes to ensure that patients have a better
understanding of their illness and to guarantee acceptable
long-term CPAP compliance. Some centres undergo
group video workshops. A trained technician who
understands the technology and appreciates where
problems may arise should carry out the CPAP set-up.
Patients differ as to what level of pressure is necessary
to eliminate the vast majority of apnoeas and hypopnoeas. The method of determining this opening of airway
pressure differs from centre to centre. Some use a
mathematical equation and one example that has shown
reasonable correlation with titration studies is predicted
pressure (cm H2O) = (0.16 " BMI) 1 (0.13 " NC) 1
(0.04 " AHI) # 5.12, where NC is neck circumference
(cm).32 Another method of titration is to admit a patient
for overnight diagnostic PSG, and halfway through the
night, when the severity and the diagnosis of OSA have
been confirmed, to commence CPAP for the second half
of the night. This is referred to as a split night. The
process must have a supervising technologist, and a big
disadvantage may be that the true severity of OSA may
not be determined by half a diagnostic night. There is,
however, the bonus 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 technician from the central computer
room, linked up electronically to the subjects bedroom
and CPAP machine. The starting pressure is usually
approximately 4 cm H2O and the pressure is increased
quickly until all apnoeas and hypopnoeas are eliminated.
The majority of centres will reach the required pressure to
eliminate most 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 increasingly used is to send the
subject 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. In general,
autoCPAP machines are more expensive than fixed
pressure machines (450 versus 250) and, as a result,
in the UK, funding from primary care trusts (PCTs) is
predominantly for fixed pressure machines. In our centre,
the set fixed pressure is the 95th centile pressure (i.e. the
blowing pressure to eliminate 95 percent of apnoeas and
hypopnoeas), as determined by the autoCPAP data. The
funding for CPAP machines is variable throughout the
UK, and is usually dependent on the individual PCT. Our
centre, for example, has set up a volume-demand
contract with individual PCTs, however, unfortunately
not all patients that the centre covers will have readily
available funding. Some patients decide to self-fund to
bypass waiting lists. Currently, there are no guidelines on
CPAP therapy as recommended by the National Institute
of Clinical Excellence. However, the Scottish Intercollegiate Guidelines Network has produced useful recommendations on the management of OSAHS in adults.33
[Grade D]
Side effects
Most side effects are related to the nasal/face mask (the
interface). Claustrophobia can be a problem for some
patients, and increasing the choice of mask 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
key here), we manage to alleviate most claustrophobia
issues. Nasal stuffiness is a common troublesome side
effect, and although interface technology has greatly
improved recently, it can lead to poor compliance.
Coryzal illnesses can also lead to poor usage in those
patients with nasal masks. The use of heated humidification is recommended as one solution.34 Cold and dry air
may provoke mucus production and vasodilation in the
nasal mucosa and humidification can potentially address
this. Although nasal corticosteroids and/or corrective
surgery for mucosal thickening and polyps might be
considered, the author believes that a full-face mask may
be a simpler solution.
Other side effects include skin abrasions and leaks and
both are usually related to poorly fitting masks. Leaks can
be a nuisance especially if directed towards the eyes. Illfitting masks can even lead to ulceration of the bridge of
the nose. The patient has to be reminded that a good fit
rather than a tight fit is more likely to be successful in
eliminating leaks without skin and eye trauma. Other
problems include air swallowing and pulmonary barotraumas, although the latter is very rare. Air swallowing
] 2321
may be more likely if the pressure delivery is greater than

physiological oesophageal sphincter pressure. [Grade C/D]
Treatment failure
Despite the intensive support there are patients in whom
treatment has clearly failed, the usual cause being poor
tolerance to CPAP. Treatment failure can therefore lead
to continued symptoms plus a continued risk of comorbidities, particularly cardiovascular, cerebrovascular
diseases and diabetes. The sleep apnoea physician must
convey the risks attached to nontreatment of OSA, in
particular, the relevance of driving safely. Other alternatives, such as weight loss therapy in those who are
overweight should be considered as well as mandibular
devices or other forms of surgery, as discussed elsewhere. The author feels that tracheostomy should be
regarded as a last resort in very exceptional circumstances. [Grade D]
Compliance and troubleshooting
Compliance or CPAP usage is dependent on many factors.
It is expected that by three years 1225 percent of subjects
will have discontinued treatment.35 Compliance to CPAP
has been defined arbitrarily in the literature as use of
CPAP for over four hours for at least five nights per week.
The biggest factors to determine long-term compliance
are the improvement of symptoms after commencing
CPAP therapy and how severe the OSA is in the
individual.35 What is unclear, when faced with an
individual about to commence CPAP therapy, is whether
four hours for five nights per week is enough to reduce
the risk of road traffic accidents or future co-morbidity.
Therefore, at our centre, all patients are encouraged to use
CPAP for at least seven hours, seven nights per week.
Adequate education, close follow-up by an experienced
technician and motivation of the patient will all influence
the long-term use of CPAP, similar to any new treatment
process, such as inhaler therapy in asthma. When CPAP
failure does occur, addressing side effects and the
possibility of coexisting sleep disorders, such as shift
work-related sleepiness, narcolepsy, psychological illness
or drug-induced conditions, should be considered. It is
not uncommon for an individual to have two coexisting
sleep disorders.
It has been suggested that one advantage of autoCPAP
over fixed pressure CPAP is an improvement in long-term
compliance because pressure can be altered as appropriate
to the apnoea severity during the night, and also the
average pressure can be reduced throughout the night.
However, although autoCPAP may increase comfort,
there is no evidence to suggest that compliance or
symptoms of EDS, compared with fixed pressure CPAP,
are improved.36 Until there are definite cost benefits
shown for autoCPAP over the fixed pressure CPAP
machine, there is no justification to provide autoCPAP
machines on the National Health Service (NHS) in the
UK. [Grade A/C/D]
FOLLOW-UP AND LEGAL ISSUES

At the time of diagnosis of OSA, the individual is
recommended to inform the Driver and Vehicle Licensing
Authority (DVLA), Swansea, UK, of the diagnosis. The
DVLA, according to UK law, must be notified of the
diagnosis, and the emphasis to do so is placed on the
subject with OSA and not the sleep clinician. In reality,
many subjects do not inform the DVLA as treatment for
OSA (i.e. CPAP) is not available for up to a year in many
parts of the country. There is little incentive, therefore, for
a patient to notify the DVLA and then be told that,
potentially, their license will be withdrawn for up to one
year until CPAP therapy is established. Improved funding
for CPAP machines on the NHS will improve this
situation. However, those patients deemed to be a genuine
threat to the public by continuing to drive while sleepy
may be considered for notification by the sleep physician,
despite potentially breaking rules of patient confidentiality.
Follow-up CPAP clinics aim to determine compliance,
minimize intolerance, improve symptoms (e.g. reduced
sleepiness) and continue to modify cardiovascular risk
factors. Follow-up PSG with CPAP is not necessary. Some
centres repeat overnight oximetry with CPAP, but an
abnormal tracing may not necessarily differentiate poor
compliance from inadequate treatment pressure. A significant increase in weight over time may lead to snoring
with the mask on and an increase in the fixed CPAP
pressure may be necessary. Mask components wearing out
may cause leaks around the mask, 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 providing the
machine and therefore it is the responsibility of that 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 information. Subjects with moderate-to-severe OSA who have poor
compliance are a challenge to the sleep clinic. Reasons for
noncompliance are addressed but if the subject refuses
treatment with CPAP then other solutions, such as weight
loss, mandibular devices, surgery, etc., may be considered.
The subject should be reminded of the issues of driving
with OSA without treatment. [Grade D]
CONCLUSIONS
Obstructive sleep apnoea is increasing in prevalence and
more patients are presenting to the ENT physician with
snoring and sleep apnoea. Obtaining information, in
particular the symptoms associated with OSA as well as
the presence of EDS and other co-morbidities, should be
routine in the consultation. Diagnostic strategies may
vary between different departments but the fundamental
basis of diagnosis of OSA rests with the demonstration of
cessation of breath using multichannel equipment. The

treatment of sleep apnoea has evolved from only treating
snoring and breath-holding to treating the symptoms and
modifying cardiovascular risks. The role of OSA in road
traffic accidents continues to provoke emotions within
the media, and there is a drive from the sleep apnoea
medical community to raise the profile of sleep apnoea in
UK politics. CPAP remains the mainstay of medical
treatment but emphasis must also be placed on lifestyle
changes such as weight loss strategies.
KEY POINTS
! The incidence of obstructive sleep apnoea will
grow as the prevalence of obesity increases in
all age groups.
! Sleep apnoea is associated with comorbidities such as cardiovascular disease,
diabetes mellitus and cerebrovascular disease.
! Subjects with sleep apnoea are at a higher
risk of road traffic accidents.
! Body mass index and male sex are important
risk factors.
! History and clinical examination is not a
sensitive or specific way of diagnosing sleep
apnoea.
! Further investigation including multichannel
respiratory testing is the key to diagnosis.
! CPAP is the mainstay of treatment in sleep
apnoea.
! The aim to minimize intolerance, improve
symptoms of sleep apnoea and modify
cardiovascular risk factors is essential in all
CPAP clinics.

[ Managing a patient with OSA should not focus only
on the upper airway but consider other comorbidities such as obesity, cardiovascular disease,
diabetes, road traffic safety and social disharmony.
[ Initial investigation for OSA must include some
objective evidence of physiological derangement
suggestive of it, e.g. repetitive oxygen desaturations
and/or airflow cessation with concomitant thorax and
abdomen movement changes.
[ The treatment of choice for moderate-to-severe OSA
is CPAP treatment.
[ To ensure adequate compliance to CPAP early in the
treatment process, troubleshooting by skilled
technicians, i.e. mask fitting, leaks, discomfort and
claustrophobia, is essential.

$
$
$
$
$
13.
Epidemiological studies linking cardiovascular,
cerebrovascular diseases and diabetes with OSA.
The role of pharyngeal airway dimensions and muscle
tone in the development of OSA.
Gender differences in OSA.
The role of obesity in OSA and OHS.
New technologies in medical management of OSA
including CPAP and mandibular devices.
14.
15.
16.
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178
The surgical management of snoring
MARCELLE MACNAMARA
Definitions and epidemiology of adult snoring

Clinical presentation
Preoperative investigations
Indications for surgery
Surgical techniques
Postoperative care
Complications
Short- and long-term outcomes
2325
2326
2326
2329
2329
2332
2332
2332
Nonsurgical treatments of snoring

Conclusions
Key points
research
Acknowledgements
References
2333
2333
2334
2335
2335
2335
2335
SEARCH STRATEGY AND EVIDENCE-BASE

The data in this chapter are supported by a Medline search using the key words adult snoring surgery, snoring
epidemiology, snoring aetiology, snoring clinical presentation, snoring surgery preoperative investigations, sleep
nasendoscopy, snoring imaging, snoring surgery indications, snoring surgery techniques, snoring surgery postoperative
care, snoring surgery complications, snoring surgery outcomes and nonsurgical treatments for snoring. Evidence is based
at levels 2 and 3.
DEFINITIONS AND EPIDEMIOLOGY OF ADULT

SNORING
Simple snoring is defined as snoring without obstructive
apnoeas, frequent arousals or gas exchange abnormalities.
It is generally considered benign, however, there is
growing evidence in children, but not adults, that it is
not as innocuous as is usually believed (see Chapter 85,
Obstructive sleep apnoea in childhood). Snoring is the
low frequency sound produced by vibration of the upper
airway walls during partial upper airway obstruction (see
Chapter 176, Physiology of sleep and sleep disorders).
These vibrations usually occur in the soft palate, but in
approximately 30 percent of nonapnoeic snorers they may
also be present at other sites including the tonsils,
epiglottis and base of the tongue.
Theoretical modelling has shown that at critical
inspiratory flow rates the upper airway becomes unstable,
with repetitive partial airway collapse which generates the

sound of snoring. The critical inspiratory flow rate that
causes snoring is dependent on upper airway size, shape,
compliance and resistance.
Simple snoring is part of the spectrum of sleepdisordered breathing ranging from intermittent snoring,
through obstructive sleep apnoea/hypopnoea syndrome,
to obesity hypoventilation syndrome. Recently, improved
definitions and better monitoring techniques have
allowed clearer clarification of the syndromes within this
spectrum.1
Aggravating factors may include alcohol consumption,2 active and passive smoking,3 obesity,4 reflux,5 male
gender4 and increasing age.4 [***]It is not known whether
persistent paediatric risk factors, such as low socioeconomic status, nasal obstruction, previous tonsil and
adenoid surgery, are relevant in adults. Although mild-tomoderate sleep apnoea is frequently a progressive

condition, there are no studies in the literature which
address this question in simple snorers.
there is a long redundant soft palate with swollen

uvula;
the palatine $ lingual tonsils are enlarged;
the tongue base is prominent;
there is a large floppy epiglottis;
there is bilateral vocal cord palsy or Shy-Drager
syndrome;
there is dental malocclusion and or a large tongue.
CLINICAL PRESENTATION
Before considering a patient for surgery for snoring the
following clinical categories need to be addressed.
History
When taking the patients history the following questions
should be asked.
! Does the patient snore?
! Is the patient or their partner troubled by the snoring
problem?
! How severe is the snoring? Audible if:
in the same room?
in an adjacent room?
downstairs/anywhere in the house?
next-door neighbour?
! Is the snoring positional or does it occur in all sleep
positions?
! For how long has the patient been snoring?
! Are there clinical features suggestive of obstructive
sleep apnoea (OSA):
regular multiple apnoeic episodes most nights?
cerebrovascular complications of OSA such as
stroke, hypertension, myocardial infarct?
endocrine complications or co-morbidity such as
diabetes mellitus or hypothyroidism?
! Are there any aggravating factors:
alcohol, how many units per week?
smoking how many per day? Passive smoking?
current weight and whether this is increasing?
previous tonsil and adenoid surgery as a child?
other upper aerodigestive tract abnormalities?
! Have any conservative treatments been tried, such as
weight loss, mandibular advancement splints (MAS)
or nasal valve dilators?
! Does this patient represent an anaesthetic risk:
is the airway anatomically difficult?
does the patient have cardiovascular, respiratory or
cerebral disease that would significantly increase
risks of anaesthesia?
Examination
The patient should be examined and certain measurements taken.
! Examine the nose, oropharynx, hypopharynx and
larynx to establish whether:
the nasal airway is patent;
the postnasal space is small;
Examination can be carried out easily with a flexible

nasendoscope apart from the oral cavity, which requires
direct inspection. Often, this proves to be normal in the
awake patient, or it may demonstrate relative narrowing
or obstruction at any level. The Mueller manoeuvre does
not satisfactorily predict the level of airway obstruction
during sleep.
! Measure height, weight to calculate body mass index
and collar size.
! Examine the cardiovascular and respiratory system to
establish potential OSA complications.
At initial consultation the Epworth Sleepiness Scale
(Figure 178.1) is usually completed, although this cannot
reliably distinguish between patients with simple snoring
and OSA7 as patients can maximize and minimize their
symptoms. Also, poor sleep quality may be attributable to
microarousals in relation to loud snoring, and the snoring
sound itself may also contribute. A combination of
clinical history, Epworth sleepiness score and body mass
index can be used to screen out nonapnoeic snorers with
a sensitivity of 93 percent and specificity of 60 percent.8
The criteria for defining apnoeic status on clinical
assessment are:
! symptoms of obstructive sleep apnoea/hypopnoea
syndrome;
! nocturnal choking;
! daytime sleepiness;
! witnessed apnoeic events during sleep;
! morning headaches or waking with a sensation of
heavy head with no alcohol consumption the
previous night;
! Epworth sleepiness score Z15;
! body mass index Z28 kg/m2.
PREOPERATIVE INVESTIGATIONS
A number of techniques are used to evaluate patients who
snore. These include:
!
!
!
!
!
!
!
videoendoscopy;
sleep nasendoscopy $ video;
polysomnography;
oesophageal manometry;
cephalometry with Mueller manoeuvre;
fluoroscopy;
three-dimensional computed tomography (CT);
Chapter 178 The surgical management of snoring
] 2327
EPWORTH SLEEPINESS SCALE

How likely are you to doze off or fall asleep in the following situations in contrast to
just feeling tired. Use the following scale to choose the most appropriate number for
each situation:
0 = Would never doze
1 = Slight chance of dozing
2 = Moderate chance of dozing
3 = High chance of dozing
Situation
Chance of dozing
Sitting and reading

Watching television
Sitting inactive in a public place (theatre or meeting)
As a passenger in a car for an hour without a break
Lying down for a rest in the afternoon
Sitting and talking to someone
Sitting quietly after lunch without alcohol
In a car while stopped for five minutes in traffic
! dynamic ultrafast magnetic resonance imaging (MRI);

! acoustic analysis;
! nasal spray test.
These techniques should be used to address four
questions.
1.
2.
3.
4.
Is snoring present and how severe is it?

Can OSA be diagnosed and ruled out?
Can the site(s) of snoring be identified?
Is there relevant co-morbidity?
Is snoring present and how severe is it?

Acoustic analysis of snoring is helpful in determining the
volume and duration of snoring but is only of limited use
in detecting the site of snoring.9 A simple tape recording
made by the patient may be sufficient evidence. It may
also be a useful research tool to evaluate the impact of
various environmental and patient factors on the severity
of snoring.10, 11 [***/**] Using the Glan Clwyd snore box,
a simple device developed for objective measurement of
the loudness and duration of snoring, it has been shown
that the severity and duration of snoring is greater at
home than in hospital, thus making home screening
important.12
Figure 178.1 The Epworth Sleepiness Scale.

Adapted from Ref. 6, with permission from the
Associated Professional Sleep Societies, LLC.
CAN OBSTRUCTIVE SLEEP APNOEA BE DIAGNOSED AND

RULED OUT?
Full polysomnography remains the gold standard and is

discussed in detail in Chapter 177, Obstructive sleep
apnoea: medical management. Various factors including
high cost, length of time and need to perform in a sleep
laboratory have stimulated the development of home
screening machines. None of these devices has sensitivities
or specificities approaching 100 percent therefore significant numbers will be missed. The choice of screening
oximeter may also affect the apnoea hypopnoea index.13
A recent systematic review14 discusses methods of
comparing the results of portable monitoring with
polysomnography. When using portable sleep monitors
for home use, clinicians need to be clear how they plan to
use the information obtained in order to:15
! confirm the diagnosis of suspected sleep apnoea.
! identify patients with a high clinical probability of
disease.
! stratify patients into correct priority for
polysomnography.
In centres in which full polysomnography is not readily
available, a clinical decision algorithm, which incorporates
a clinical prediction rule with the use of portable monitors,
can guide clinicians towards institution of therapy or

further investigations.16 A recent Australian study suggests
that a clinical prediction rule can be used on its own to
prioritize polysomnography without screening sleep/home
studies.17 [***] This was based on five variables: age, sex,
body mass index, snoring and stopping breathing during
sleep, which were found to be significantly associated with
sleep apnoea. Patients who have failed or who have
equivocal home sleep studies, and those with negative
studies but persistent symptoms should have full polysomnography. Intuitively, this approach could reduce
waiting times for polysomnography and delays in diagnosis
but additional evidence for the validity and cost effectiveness of this approach is required. Incomplete or incorrect
diagnosis of the severity of sleep-disordered breathing can
have significant medicolegal implications.17 [**]
CAN THE SITE OF SNORING BE IDENTIFIED?
Both endoscopic and imaging approaches have been used

to answer this question. Endoscopic approaches include
sleep nasendoscopy $ video recording of findings, and
oesophageal pressure monitoring. Imaging approaches
include cephalometry with the Mueller manoeuvre,
fluoroscopy, three-dimensional CT scanning and dynamic
ultrafast MRI.
Sleep nasendoscopy
snorers without sleep apnoea and nonsnorers, and showed

that snoring could be produced at sleep nasendoscopy in
45 percent of nonsnorers but could not be produced in 18
percent of snorers.21 [***] The inability to obtain snoring
in 18 percent of snorers is explained by an inconsistent
sedation technique, i.e. that the relatively narrow propafol
titration window to result in snoring. However, this
argument cannot be applied to the presence of snoring in
nonsnorers unless the histories were not properly
documented. A recent publication comparing sleep
nasendoscopy results in sleep apnoea patients with
nonsnorers showed no snoring or airway collapse at any
level of propafol infusion in the asymptomatic group.22
[***] The distribution of sites of snoring in snorers
without sleep apnoea is shown in Table 178.2. A controlled
study comparing sleep nasendoscopy in nonsnorers,
nonapnoeic snorers and in patients with OSA would be
useful to address this dilemma. Comparison of sleep
nasendoscopy with some form of continuous monitoring
of the site of upper airway obstruction during normal
physiological sleep would help provide reassurance that
sleep nasendoscopy is measuring something of physiological relevance. Video recording of sleep nasendoscopic
findings is helpful for documentation purposes.24
Oesophageal manometry
Oesophageal manometry has been used in conjunction
with screening sleep studies to diagnose apnoeas and
hypopnoeas.25 In addition, it has been used to evaluate the
relationship between reflux and OSA.26 Adaptation of the
manometry devices might allow more precise localization
of sites of upper airway obstruction. This could then be
used as a technique to validate sleep nasendoscopy.
Sleep nasendoscopy, which is the most widely used

technique to evaluate the site of snoring in the UK, was
first described by Croft and Pringle in 1991.18 [**] It
involves sedating the patient with propafol to a level of
sleep sufficient to induce snoring, i.e. a target-controlled
propafol infusion.19 The operator then examines the upper
aerodigestive tract, in the supine position with a nasendoscope, to determine the level(s) of obstruction. Levels of
obstruction can be graded as shown in Table 178.1.20 [**]
This procedure should be carried out with an anaesthetist
present to monitor the propafol infusion, and with cardiac
monitoring as well as full resuscitation facilities. Respiratory stimulants can be used to encourage snoring. Oxygen
saturation should be monitored throughout the procedure
and oxygen administered as appropriate. Only one study
in the literature has compared sleep nasendoscopy in
Ultrafast MRI can be used in awake and asleep patients to

assess the site of upper airway obstruction. Midline sagittal
sections and cross sections at various levels are the most
useful images.27 [**] There are significant differences in
the pattern of dynamic airway motion in patients with
OSA and those with no sleep-disordered breathing.28 [***]
In the awake patient there is very close correlation between
the sites of upper airway narrowing in patients with OSA,
Table 178.1 Sleep nasendoscopy grading.
Table 178.2 Sites of snoring at sleep nasendoscopy in

nonapnoeic snorers.
Grade Obstruction
1
2
3
4
5
6
a
Simple palatal level snoring/palatal flutter

Single level palatal obstruction
Palatal level obstruction with intermittent oropharyngeal
involvement
Sustained multisegmental obstruction
Tongue base level obstruction
Isolated epiglottic involvementa
Authors addition.
Magnetic resonance imaging
Site
Palatal flutter only
Palatal flutter 1 other site
Supraglottic
Tonsil
Tongue base
Tongue base only
Epiglottic
Reprinted with permission from Ref. 23.
Percentage
70
20
10
8
2
8
2
as defined by digitized video endoscopy and MRI,29 but

these data are not available in the asleep patient for OSA
or for either state in the simple snorer without OSA. MRI
is not widely used in the UK for the investigation of
snoring and sleep apnoea because of the high cost and
significant time taken as well as the lack of normative data
for both simple snoring and OSA populations. Also, short
periods of sleep in an MRI machine may not be
representative of normal sleep patterns. A useful research
tool might be to try and quantify the surgical tissue
volume reduction necessary to achieve resolution of
snoring or OSA.
Three-dimensional computed tomography
Three-dimensional CT measurements may be useful to evaluate upper airway patency in patients with sleepdisordered breathing. The retropalatal space is the most
relevant anatomical concept. Modifications of palatal
surgery techniques to increase the lateral dimensions of
this space may help to improve the success rate of this type
of surgery.30
Cephalometry
Cephalometry should be considered in the preoperative
evaluation of patients considered for uvulopalatopharyngoplasty (UPPP)31 and patients in whom treatment
with MAS is contemplated.32
Nasal spray test
This test involves using a topical nasal decongestant on
alternate nights and comparing the severity of snoring
and apnoea. If the decongestant results in improved
symptoms it may be worth treating nasal abnormalities to
help in snoring.33
INDICATIONS FOR SURGERY

Surgery is indicated in the following groups of patients.
! Patients with severe, antisocial snoring:
without OSA;
localized obstruction at one level in the upper
airway, usually at palatal level;
multisegmental obstruction with predominant
obstruction at palatal level.
This usually involves palatal surgery and, although
individual approaches vary, they should involve procedures with minimal morbidity, such as radiofrequency
tissue volume reduction (RFTVR), before considering
laser-assisted uvulopalatoplasty (LAUP) or UPPP.
! Patients with mild-to-moderate sleep apnoea:
with severe antisocial snoring;
failed or inadequate response to continuous
positive airway pressure (CPAP);
localized obstruction at one level in the upper
airway, usually at palatal level.
] 2329
This usually involves palatal surgery and, although

individual approaches vary, they should involve procedures with minimal morbidity, such as RFTVR, before
considering LAUP or, finally, UPPP.
! Patients with moderate-to-severe sleep apnoea:
with severe antisocial snoring;
failed or inadequate response to CPAP;
multisegmental obstruction.
This may involve a combination of procedures on the
palate, tongue base and lateral pharyngeal walls, possibly
with tracheostomy cover in severe cases. The RFTVR
technique may be conveniently applied at multiple levels
but other combinations have also been shown to be
effective. Again, the choice of procedure should be governed
by both prospects of success as well as associated morbidity.
SURGICAL TECHNIQUES
Uvulopalatopharyngoplasty
This technique was first described by Ikematsu in the 1950s
but was popularized by Fugita in 1985 and involves
resecting a strip of soft palate and uvula in combination
with tonsillectomy. The tonsillar pillars are then sutured
together. The effect of this is to stiffen the soft palate by
scarring and to increase the space behind the soft palate to
minimize obstruction. It is performed as a single-stage
procedure, usually under general anaesthetic. It is most
effective for treating patients with severe antisocial snoring
of palatal origin but is also used in the treatment of OSA. It
is associated with significant complications, which are
increasingly regarded as unacceptable. The incidence of
serious nonfatal complications is 1.5 percent and the 30day mortality rate is 0.2 percent.34 Forty-two percent of
patients having UPPP have complaints about their
treatment postoperatively and 14 percent may not be
satisfied with the outcome of their surgery.35 The specific
complications include severe postoperative pain,36 haemorrhage (214 percent), respiratory events such as airway
obstruction due to laryngospasm, postoperative pulmonary oedema and hypoxia (211 percent),37, 38 nasal
regurgitation (13 percent) due to excessive palatal resection, velopharyngeal stenosis,39 dry throat due to loss of
pharyngeal lubricating function of the uvula, excessive
pharyngeal hypersecretion (10 percent), swallowing problems (9 percent), voice changes (7 percent)36, 40, 41 and
taste disturbances. Short-term success rates are quoted as
ranging from 76 to 95 percent in well-selected patient
groups, however, unfortunately, long-term successes fall
dramatically to approximately 45 percent.42 The significant
potential for serious complications and the declining
success rates over time have encouraged surgeons to devise
alternative approaches. Preservation of the uvula eliminates
nasal regurgitation and minimizes pharyngeal dryness,
globus-type symptoms, hypersecretion and swallowing

difficulties. It also appears to improve the outcome of
surgery.43 Eliminating the pharyngoplasty part of the
UPPP operation, i.e. not suturing the tonsillar pillars after
tonsillectomy, can reduce morbidity when there is thought
to be no redundant tissue in the lateral pharyngeal wall.44
Laser-assisted uvulopalatoplasty
Table 178.3 Comparison of somnoplasty device with diathermy.

Feature
Patient part of circuit (kHZ)
Tissue temperature (1C)
Power (W)
Volts
Somnoplasty
Diathermy
460
6090
210
80
4600
750900
4100
Up to 800
Reprinted with permission from Ref. 51.
This procedure was originally introduced by Kamami in

France, in 1993, as an outpatient procedure under local
anaesthesia. Lignocaine with adrenaline is injected above
the base of the uvula and 1 cm lateral to the midline in the
inferior portion of the soft palate. Bilateral vertical
incisions are made in the soft palate followed by partial
vaporization of the uvula with a CO2 laser. There are
numerous techniques and modifications of this procedure.
Each patient requires between one and five laser
procedures spaced approximately one month apart to
complete treatment. It may also be carried out as a singlestage treatment. The principle behind the operation is to
stiffen the soft palate and thereby minimize snoring due to
palatal flutter. Variations in technique involve the extent
and distribution of palatal laser vaporization, the amount
of uvula removed and whether the tonsils are laser ablated.
Usually, a CO2 laser is used but alternatives include the Nd
Yag laser. Complication rates are generally lower than after
UPPP but depend on the degree of vaporization. Notably,
there are no reports of significant postoperative nasal
regurgitation after LAUP. Globus-type symptoms are more
common after LAUP than UPPP, probably because of the
greater area of insensate palate.45 Pain levels are not
necessarily better than after UPPP and may in fact be
worse, and are probably proportional to the amount of
laser vaporization. Fungal infections of the lasered palatal
mucosa have also been described. Short- and long-term
results are similar to UPPP, in that there is a significant
decline in benefit over time with early success rates of 79
percent and later ones of 55 percent.46 Two randomized
controlled trials of LAUP in the treatment of simple
snoring and mild OSA suggest that it had minimal impact
for either condition when compared with no treatment or
treatment with placebo.47, 48 [***] In a considerable
number of patients the procedure may lead to mild OSA
and worsening in nasal breathing in previously simple
snorers owing to increased palatal fibrosis and contraction
of the velopharyngeal space.49 [***] Laser-assisted uvulopalatoplasty has no significant impact on middle ear
pressures49 or smell and taste.50 [***]
Radiofrequency tissue volume reduction/

thermal ablation
The principle behind this is similar to diathermy, but uses
lower power and lower tissue temperatures with a current
working at a frequency of 460 kHz (Table 178.3). The
device applies thermal injury to specific submucosal sites

in the soft palate resulting in fibrosis of the muscular layer
and volumetric tissue reduction.51
The main advantages of this technique are that it can
be carried out as a day case or outpatient procedure
under local anaesthetic and causes significantly less
postoperative pain and other complications than UPPP
or LAUP for simple snoring. The short-term efficacy
depends on the number of lesions performed and how
often they are repeated. Single- and multilesion groups
showed significant improvement in snoring following
treatment. The multilesion group required fewer treatments than the single-lesion group and was more than
twice as likely to be cured after two treatments. There was
a trend towards improved clinical outcome with increased
number of lesions and total energy per treatment when
patients with one, three and four lesions were compared.
The four-lesion group had the most pronounced
improvement in snoring, the lowest number of treatments required for cure and the greatest number of
patients cured after two treatments. There was minimal
relapse in the multilesion group at 16 months. In
addition, delivery of increased numbers of lesions was
found to be safe and not associated with increased levels
of complications. Pain was significantly greater in the
multilesion group but was considered minimal by
patients and was controlled by the use of nonprescription
analgesics and did not result in unplanned time away
from work.52 [***]
Multilevel, temperature-controlled radiofrequency
therapy of the palate, base of the tongue and tonsils in
adults with OSA was effective in 33 percent of patients.53
Three types of radiofrequency devices have been used
with similar results. These are the Somnus unit,51 Celon
device,53 which has the additional advantages of a bipolar
electrode tip, auto stop application and reduced procedure time, and the Coblator unit.54 The latter has lost
favour because of its larger electrode tip and thus
increased risk of complications. One study specifically
addresses the question of complications reporting a rate
of 2 percent, which includes ulcers of the tongue base or
soft palate, dysphagia necessitating hospital admission,
temporary hypoglossal nerve palsy and an abscess at the
base of tongue.55 Radiofrequency volumetric tissue
reduction in the soft palate has no adverse impact on
voice quality.56
Nasal obstruction and nasal surgery in the

pathogenesis and treatment of snoring and
obstructive sleep apnoea
Clinical reports document nasal obstruction-induced
snoring and OSA57, 58, 59 but the exact role of the nasal
airway in its pathogenesis is unclear. The reduced nasal
cross-sectional area promotes increased nasal resistance to
airflow and promotes inspiratory collapse of both the oroand hypopharynx.60 Controversial data exist regarding the
role of improved nasal breathing in managing OSA. If
nasal obstruction contributes to OSA development,
correction of the obstructed airway should improve
OSA. The first study that objectively investigated the
result of nasal surgery alone on OSA showed no significant
impact on the respiratory disturbance index (RDI) or
lowest oxygen saturation levels but CPAP levels required to
correct OSA were reduced. Patients with mild OSA
showed significant worsening of RDI but lowest oxygen
saturation levels improved in patients with moderate OSA.
In patients with severe OSA neither RDI or lowest oxygen
saturation levels changed but CPAP levels required to
alleviate obstruction after surgery were reduced.61 [**] A
further objective study on the polysomnographic effects of
nasal surgery for snoring and OSA showed a significant
improvement in the RDI, apnoea index and oxygen
saturation index as well as a decrease in duration of
snoring; however, snoring and OSA were only completely
relieved in 19 percent of 21 patients.62 [***] Although
] 2331
both these studies are interesting, a controlled study in

patients with recorded nasal obstruction assigned to either
nasal surgery or no nasal surgery followed by further
objective documentation of the OSA pathway, as in the
above studies, would be more convincing. In the meantime, proper management of nasal obstruction should be
encouraged as part of the overall management plan for
antisocial snoring and OSA.
Occasional procedures for snoring and

obstructive sleep apnoea
Occasional procedures for snoring and OSA are summarized in Table 178.4. Of the various palatal procedures
described, most are pilot studies of new techniques and
most report subjective criteria only. No trials are
compared with more standard techniques and there is
no objective outcome criteria. Owing to their potential
low morbidity, the injection snoroplasty technique66 and
the outpatient uvulopalatal flap68 may be of possible
interest. Palatal implants may be interesting because the
benefit may not decline with time.69
For the tongue base and lateral pharyngeal wall,
radiofrequency ablation appears to be the technique with
the lowest morbidity although, again, there are no
comparative studies. Therapeutic nightly stimulation of
the hypoglossal nerve during sleep in patients with
moderate-to-severe sleep apnoea markedly diminishes
Table 178.4 Occasional procedures for snoring and obstructive sleep apnoea.
Site
Palatal
Lateral pharyngeal wall

Tongue base
Epiglottis
Trachea
Maxillomandibular procedures
Hyoid myotomy and suspension

Maxillomandibular osteotomy and
advancement
Technique
Literature
Z-pharyngoplasty
Vertical full thickness cuts from the upper pole of the tonsil through
soft palate and posterior pillar
Injection snoroplasty
Modified UPPP with extended uvulopalatal flap
Outpatient uvulopalatal flap
Palatal implants
Lateral pharyngoplasty
RFTVR
Laser midline glossectomy and lingualplasty
Tongue suspension suture
Lingual tonsillectomy
RFTVR
Hypoglossal nerve stimulation
Endoscopic epiglottectomy
Temporary tracheostomy
Designed to enlarge and stabilize the retrolingual airway by
advancing the insertion of the genioglossus or geniohyoid
muscle without moving the entire mandible or teeth
Advances the hyoid and epiglottis anteriorly
Aims to move the maxilla and mandible as far forward as possible
63, 64
65
66
67
68
69
70
53
53
71
72, 73
74, 75

apnoea severity without waking patients.71 This might be
better tolerated than an oral appliance, tongue surgery or
CPAP. The Repose tongue base suspension suture provides
another interesting alternative for increasing the dimensions of the retrolingual space with relatively low morbidity
but, again, no comparative studies are available in the
literature.76, 77 Laser midline glossectomy and its modifications, as well as laser lingual tonsillectomy, are rarely
performed because of the relatively high complication rates
(25 percent) that include bleeding, taste change, odynophagia, dysphagia and tongue oedema. Despite this, in
appropriately selected cases, good results can be obtained.78
Only two reports in the literature refer to treating
snoring/OSA due to epiglottic collapse with epiglottectomy, and in total, five cases have been described.72, 73
Two studies report the role of temporary tracheostomy
in the management of OSA.74, 75 Tracheostomy reliably
eliminated all grades of OSA severity in 79 patients and 20
percent were decannulated eventually, but there was a 2.5
percent tracheostomy-related mortality.74 In the other
series of 17 patients who had a tracheostomy for OSA, ten
were carried out in a planned fashion and a further seven
as an emergency. Planned tracheostomies are indicated
for tongue base procedures such as genioglossus advancement or laser midline glossectomy.75 It may also be
appropriate in those rare patients where maxillomandibular procedures are considered appropriate.
POSTOPERATIVE CARE
In most units patients undergoing surgery for snoring or
OSA are admitted for an overnight stay. For UPPP surgery
this is still generally the case, although two recent publications suggest that in selected patients without co-morbidity same day discharge may be appropriate, even when
combined with tonsillectomy and or nasal surgery.79, 80
Laser-assisted uvulopalatoplasty is a staged procedure that
was designed for day-case use. Postoperative pain, which
has usually been the limiting factor in outpatient management, often does not reach its greatest extent until 48 hours
postsurgery. Radiofrequency ablation seems to be associated
with significantly less postoperative pain, making it much
more suitable as an outpatient or day-case procedure.
Perioperative pain and salivation during LAUP under
local anaesthesia are well controlled with a combination
of morphine and scopolamine.81 [***]
Postoperative pain after UPPP and LAUP may be
difficult to control, particularly if performed in conjunction with tonsillectomy.82 Concerns have been raised about
both the use of opioids, because of the risk of sedation and
respiratory depression, particularly in patients with OSA,
and the use of nonsteroidal antiinflammatory drugs, on
account of the risk of bleeding. However, one of them or a
combination of both is required in more than 40 percent
of patients; the total dosage may be minimized by giving it
as a continuous infusion. The need for patient-controlled
intravenous rescue fentanyl analgesia was twice as great

after UPPP than after tonsillectomy alone.82 [***] Pain
after discharge from hospital may remain a significant
problem, requiring oral nonsteroidal and opiate analgesia
in most patients for about 5 days, but in up to one-third of
patients, it may remain a disturbing issue for more than
two weeks.83 [***] Glossopharyngeal nerve block is helpful
after UPPP but not following simple tonsillectomy.84 [***]
Perioperative systemic corticosteroids do not reduce
morbidity following UPPP.85 [***]
COMPLICATIONS
The complications of individual techniques are discussed
under the relevant sections with the incidence of reported
complications varying widely. Table 178.5 lists the range
of complications for all procedures in the literature. Only
one study compares the complications between the three
major palatal procedures, and this confirms the impression that RFTVR is associated with fewer complications
than UPPP and LAUP.36 The numbers in each group are
too small to provide a representative picture of complications associated with each procedure. Palatal surgery for
snoring and OSA is associated with a small but significant
mortality, as shown by a survey of British otolaryngologists.86 Six intra- and postoperative deaths, related to
both bleeding and airway obstruction, were reported by a
total of 371 otolaryngologists. A large multicentre study
comparing complications of the three most frequently
performed procedure would be useful.
SHORT- AND LONG-TERM OUTCOMES

For UPPP early success rates of between 65 and 100
percent87, 88 for management of simple snoring have been
quoted but longer-term studies have shown that these
results deteriorate over time with results at two to five
years being 4560 percent.42 Causes for late deterioration
include increased body mass index and loss of palatal
stiffening owing to resolution of palatal scar tissue. In
patients with OSA only 41 percent showed significant
improvement in objective response criteria.88 A long-term
survival study of 400 snoring patients from Sweden, of
whom 256 had OSA, showed that there was no increase in
mortality compared with controls.89 [**]
The results of LAUP operations are similar to those of
UPPP with success rates from 60 to 90 percent being
quoted in the literature.90, 91, 92 The favourable subjective
and objective results deteriorate over time from 79 to 57
percent in 1218 months, and the procedure can cause
mild OSA in previously nonapnoeic snorers.93 A six-year
follow-up study showed that most of the failure rate
occurs in the first two years but long-term failure is still
evident at 79 months.94 LAUP is only successful in the
management of OSA in 2030 percent of cases.92, 95 [**]
] 2333
Table 178.5 Complications following palatal snoring surgery.

Early
Pain occurs after all procedures but is least severe and of the
shortest duration after RFTVR
Haemorrhage occurs after both UPPP (214%) and LAUP (09%)
but has not been reported for RFTVR
Airway problems have been described after both UPPP and LAUP
but not after RFTVR. For UPPP this includes laryngospasm,
postoperative pulmonary oedema and hypoxia but for LAUP
only delayed OSA development due to palatal stiffening
Temporary palatal incompetence occurs after UPPP in up to 25%
but may be equally frequent after LAUP. It has not been
described after RFTVR. Significant permanent palatal
incompetence has only been described after UPPP
Wound infection can occur after all procedures but is most
common after UPPP. Abscesses at the site of RFTVR probe
insertion have been described
Wound dehiscence only occurs after UPPP. Ulceration at the
RFTVR probe insertion site has been described
Dysphagia due to pain is a significant early problem after UPPP
and LAUP but not RFTVR
Postoperative polysomnography revealed that LAUP may

lead to deterioration of existing apnoea in up to 30 percent
of patients, probably related to velopharyngeal narrowing
and progressive palatal fibrosis by the laser beam.96
Results of RFTVR for simple snoring demonstrate
subjective and objective improvement in 50-85 percent of
patients,97, 98, 99 and are probably slightly worse than
UPPP and LAUP but do not share the high morbidity of
these procedures. Similar to other treatments, results
deteriorate with time and in one series success deteriorated from 72 to 52 percent in an average of 14 months.98
Results for OSA are conflicting, with one report
suggesting benefit in 65 percent of patients100 while
others suggest no benefit.101
Few studies comparing different surgical techniques
exist, but those that do suggest that initial success for laser
surgery is similar to UPPP for simple snoring102 or that
UPPP has a longer sustained benefit than laser surgery.103
One prospective trial compares LAUP with RFTVR but
the numbers recruited are too small to state that LAUP
outcomes are better than RFTVR.104
NONSURGICAL TREATMENTS OF SNORING

Apart from weight loss, cessation of alcohol and smoking,
the only other nonsurgical treatment consists of the MAS,
which by bringing the tongue base forwards increases the
dimensions of the upper airway. A randomized controlled
trial of a MAS versus placebo for simple snoring showed
subjective improvement in snoring frequency and severity in 76 and 84 percent, respectively.105 [***] A recent
Late
Dry throat, excess pharyngeal secretions, dysphagia and taste
disturbances seem to be related to loss of the throatlubricating effect of the uvula in UPPP and LAUP
Smell and taste disturbances have been described after UPPP and
LAUP but not following RFTVR
Globus-type symptoms are most marked after LAUP and appear to
be related to loss of palatal sensation
Voice changes have only been described after UPPP
Velopharyngeal stenosis has been described after both UPPP and

LAUP but not RFTVR
Velopharyngeal fistula has only been described after RFTVR
Temporary hypoglossal nerve palsy has only been described after
RFTVR
study has shown significant objective improvements in

OSA.106 [**] Similar to CPAP, MAS can improve blood
pressure.107 [***] The main advantages of these devices
are the relative simplicity of the treatment, its reversibility
and cost effectiveness, and that it provides a genuine
nonsurgical alternative to patients who cannot tolerate
CPAP or who represent a poor surgical risk.108 Forty
percent of MAS users will develop some minor complications of the jaw, with mouth or tooth pain, and some 26
percent of long-term users may experience painless but
irreversible changes in dental occlusion even with twopiece adjustable devices.109 A longitudinal observational
study of 100 adults with OSA treated with MAS showed
significant craniofacial changes in maxillomandibular
relationships and bony dimensions on lateral cephalometric radiographs. It was postulated that changes in
overbite could be lessened by keeping bite opening to a
minimum.110 A recent cephalometric study111 has shown
that better treatment responses with adjustable MAS can
be obtained in patients who are younger, have a lower
body mass index, a longer maxilla, a smaller oropharynx,
smaller overjet, less erupted maxillary molars and a large
ratio of vertical airway length to cross-sectional area of
the soft palate. Trials comparing MAS with surgical
interventions and CPAP should be performed to assess
the relative efficacy of these treatments.
CONCLUSIONS
In the preoperative assessment of the snoring patient the
main difficulties still arise in the precise localization of the

site of snoring. Sleep nasendoscopy as a technique requires
further validation. Ideally, the site of obstruction should be
assessed during normal physiological sleep and then further
research to develop an appropriate technique is required.
From a surgical point of view the three main palatal
procedures produce fairly similar results that all deteriorate with time. The main factors determining the choice
of operation are the high risk of complications associated
with UPPP and the associated pain with LAUP. Radiofrequency tissue volume reduction seems currently to be
the choice with least morbidity although the results may
be slightly less good and the benefits may decline more
quickly than the other two procedures.
KEY POINTS
! Simple snoring is part of the spectrum of
sleep-disordered breathing ranging from
intermittent snoring, through obstructive
sleep apnoea/hypopnoea syndrome, to obesity
hypoventilation syndrome. Recently,
improved definitions and better monitoring
techniques have allowed for clearer
definitions of the syndromes within this
spectrum.
! In the UK, sleep nasendoscopy is the most
widely used technique to evaluate the site of
snoring. It involves sedating the patient with
propafol sufficient to induce snoring, i.e. a
target-controlled propafol infusion. The
operator then examines the upper
aerodigestive tract, in the supine position
with a nasendoscope, to determine the
level(s) of obstruction.
! MRI is not widely used in the UK for the
investigation of snoring and sleep apnoea
because of the high cost and significant
length of time taken as well as lack of
normative data for both simple snoring and
OSA populations.
! The main indication for surgery for snoring
in the UK is severe antisocial snoring without
OSA and with a single, well-defined site of
obstruction, usually at palatal level.
! The effect of UPPP is to stiffen the soft palate
by scarring and to increase the space behind
the soft palate to minimize obstruction. It is
associated with a significant profile of
complications, which are being increasingly
regarded as unacceptable. The specific
complications include severe postoperative
pain, haemorrhage (214 percent), respiratory
events such as airways obstruction due to
laryngospasm, postoperative pulmonary
oedema and hypoxia (211 percent), nasal
!
!
!
!
!
!
!
regurgitation (13 percent), velopharyngeal

stenosis, dry throat, excessive pharyngeal
hypersecretion (10 percent), swallowing
problems (9 percent), voice changes (7
percent) and taste disturbances.
Complication rates for LAUP are generally
lower than after UPPP but depend on the
degree of vaporization. Notably, there are no
reports of significant postoperative nasal
regurgitation after LAUP. Globus-type
symptoms are more common after LAUP
than UPPP, probably because of the greater
area of insensate palate. Pain levels are not
necessarily better than after UPPP and may
in fact be worse, and are probably
proportional to the amount of laser
vaporization.
The main advantages of RFTVR are that it
can be carried out as a day case or outpatient
procedure under local anaesthetic and causes
significantly less postoperative pain and other
complications than UPPP or LAUP for
simple snoring. The short-term efficacy
depends on the number of lesions performed
and how often they are repeated.
Reduced nasal cross-sectional area promotes
increased nasal resistance to airflow and
promotes inspiratory collapse of both the
oro- and hypopharynx.
Postoperative pain after UPPP and LAUP
may be difficult to control, particularly if
performed in conjunction with tonsillectomy.
Concerns have been raised about both the
use of opioids, because of the risk of sedation
and respiratory depression, particularly in
patients with obstructive sleep apnoea and
the use of nonsteroidal antiinflammatory
drugs, on account of the risk of bleeding.
However, one of them or a combination of
both is required in more than 40 percent of
patients; the total dosage may be minimized
by giving it as a continuous infusion.
RFTVR is associated with fewer
complications than UPPP and LAUP.
Palatal surgery for snoring and OSA is
associated with a small but significant
mortality.
The outcomes of palatal surgery for snoring
are all fairly similar and all deteriorate over
time.
Adjustable MASs are an important
component of the treatment of severe
antisocial snoring and OSA.
With appropriate fitting to minimize bite
opening, pain and changes in dental
occlusion can be avoided.

[ Detailed clinical evaluation of snoring patients by
[
[
history, physical examination, body mass index and

Epworth sleepiness score can be used to screen out
nonapnoeic snorers with a sensitivity of 93 percent
and specificity of 60 percent and thus prioritize
further investigations. [Grade C]
This initial assessment can take place in an ENT or
respiratory medicine clinic but probably should be
carried out to standard protocols to avoid later
duplication or omissions. [Grade D]
Although there are significant concerns about how
relevant the results of sleep nasendoscopy are to real
sleep, it remains the only readily available and costeffective technique to identify the site of snoring and
therefore the decision which site of surgery to offer.
[Grade D]
Standardization of technique is vital in improving
results and the test is best offered in units where the
technique is practiced regularly. [Grade B]
The test should be used until a better alternative is
available. [Grade D]
MRI is not widely used in the UK for the
investigation of snoring and sleep apnoea due to the
high cost and significant time taken as well as lack
of normative data for both simple snoring and OSA
populations. [Grade D]
The main indication for snoring surgery in the UK is
severe antisocial snoring without obstructive sleep
apnoea and with a single well defined site of
obstruction usually at palatal level. [Grade D]
More complex indications should probably be managed
in a multidisciplinary setting of respiratory physicians,
ENT surgeons and sometimes maxillofacial surgeons as
well as appropriate technical support to ensure the full
range of site indications can be managed and
appropriate surgical experience developed. [Grade D]
In view of the significant risk of complications this
procedure should not generally be offered as first line
surgical treatment for simple palatal flutter. [Grade C]
LAUP is a more proportionate procedure for simple
palatal snoring than UPPP but is by no means free of
problems in that success is often associated with
severe postoperative pain. [Grade C]
RFTVR would be the authors current choice for
management of simple palatal snoring but this may
change as techniques evolve. [Grade D]
Despite the lack of controlled studies comparing the
effect of nasal surgery with no nasal surgery on future
management snoring and OSA, proper management of
nasal obstruction including surgery should be offered
early on as part of the comprehensive management of
antisocial snoring and OSA. [Grade D]
Apart from the very rare emergency tracheostomy for
very severe OSA at tongue base level, occasional
] 2335
surgery should be done by surgeons who are part of

multidisciplinary teams and are evaluating their
outcomes carefully. [Grade D]
[ Training for such occasional procedures is currently
not widely available in the UK and is probably
best obtained at larger American centres.
[Grade D]
[ Postoperative pain after UPPP and LAUP may
be difficult to control particularly if
performed in conjunction with tonsillectomy.
[Grade C]
[ Concerns have been raised both about the use of
opioids, because of the risk of sedation and
respiratory depression, particularly in patients with
obstructive sleep apnea and the use of non-steroidal
anti-inflammatory drugs, on account of the risk of
bleeding, but one or a combination of both is
required in more than 40 percent of patients and the
total dosage may be minimized by giving it as a
continuous infusion. [Grade D]

$
$
$
$
$
$
Is simple snoring a progressive condition that

eventually becomes OSA?
A controlled study looking at sleep nasendoscopy in
nonsnorers, nonapnoeic snorers and OSA.
A comparison of sleep nasendoscopy with continous
pharyngeal and oesophageal pressure manometry
during sleep.
National audit of complications of nonpalatal surgery
for snoring and OSA.
Randomized study on outcomes after various surgical
techniques.
Trials of adjustable mandibular advancement splints
against surgery for snoring and OSA.
ACKNOWLEDGEMENTS
The author would like to acknowledge the advice of
David Morgan, Consultant Otolaryngologist at Birmingham Heartlands Hospital, who has a special interest in
snoring surgery.
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176

Physiology of sleep and sleep disorders

Best clinical practice

the predominant sleep stage and usually accounts for

2306 ] PART 16 THE UPPER AIRWAY

The majority of adults sleep seven to eight hours a

SLEEP AND RESPIRATION

Figure 176.1 The effect of sleep on respiration.

Chapter 176 Physiology of sleep and sleep disorders

is regulated by the respiratory centre which has both

hypercapnia, coughing and swallowing. The arousal

Respiratory sleep disorders

obstructive sleep apnoea/hypopnoea (OSAH);

Each syndrome has a definition, symptoms, associated

2308 ] PART 16 THE UPPER AIRWAY

The patency of the upper airway is determined by its

Figure 176.2 Upper airway: (a) awake and (b) asleep.

which reduces intraluminal pressure, and consequently

Decreased intraluminal pressure

Figure 176.3 Factors influencing upper airway

Chapter 176 Physiology of sleep and sleep disorders

sleep. They stiffen the upper airway and oppose the

2310 ] PART 16 THE UPPER AIRWAY

Nonrespiratory sleep disorders

Narcolepsy is primarily a disorder of REM sleep in which

Figure 176.4 Consequences of OSAH syndrome.

paralysis (inability to move shortly before sleep) and

Restless leg syndrome (RLS) and PLMD are separate

Idiopathic hypersomnia is generally considered to refer to

Chapter 176 Physiology of sleep and sleep disorders

confirmed excessive daytime sleepiness in whom all

Deficiencies in current knowledge and

The neurochemistry of sleep and wakefulness is

Best clinical practice

[ It should not be assumed that a sleepy patient with

[ Excessive daytime sleepiness requires investigation

1. Shneerson JM. Handbook of sleep medicine. Oxford:

2312 ] PART 16 THE UPPER AIRWAY

obstructive sleep apnea. Journal of Applied Physiology.

Follow-up and legal issues

wakefulness-promoting drugs in OSA, is reviewed elsewhere.2

THE SPECTRUM OF SLEEP-DISORDERED

2314 ] PART 16 THE UPPER AIRWAY

EPIDEMIOLOGY, RISK FACTORS AND

lingual adipose deposition, and body fat distribution all

Chapter 177 Obstructive sleep apnoea: medical management

2.30 (95 percent confidence interval 1.284.11; p = 0.005)

SYMPTOMS, CLINICAL EXAMINATION AND

Clinical assessment of OSA entails a detailed history,

hypertriglyceridaemia should always be looked for during

THE DIAGNOSIS OF OBSTRUCTIVE SLEEP

Sitting and reading

2316 ] PART 16 THE UPPER AIRWAY

Figures 177.3 and 177.4. In general, it is accepted that

Home multichannel testing

Chapter 177 Obstructive sleep apnoea: medical management

Start time + Date. 22.41.00 06/09/2003

whether the apnoeas and hypopnoeas are related to

Patients are taught how to apply the gadgets, either at

2318 ] PART 16 THE UPPER AIRWAY

Start time + Date: 23:13:00 05/10/2005

and 90 percent (with or without a 3 percent or more

especially if assisted ventilation is considered. Tertiary

Which test should be used?