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Review

Obstructive sleep apnoea in adults

Zafar Ahmad Usmani,1,2,3 Ching Li Chai-Coetzer,1,4 Nick A Antic,1,4
R Doug McEvoy1,4,5
1
Adelaide Institute for Sleep ABSTRACT older individuals;4 however, some studies suggest
Health, Repatriation General Obstructive sleep apnoea (OSA) is characterised by that OSA in the elderly may be a condition distinct
Hospital, Adelaide, South
Australia, Australia repetitive closure of the upper airway, repetitive oxygen from that of OSA in middle age.5 OSA is more
2
Discipline of Medicine, desaturations and sleep fragmentation. The prevalence of prevalent in men than in women with an approxi-
University of Adelaide, adult OSA is increasing because of a worldwide increase mate ratio of 2 : 1.However, there is little gender
Adelaide, South Australia, in obesity and the ageing of populations. OSA presents difference after the sixth decade of age.
Australia
3 with a variety of symptoms the most prominent of which Population-based studies have suggested a higher
Department of Respiratory
Medicine, The Queen Elizabeth are snoring and daytime tiredness. Interestingly though, prevalence of OSA amongst African–Americans
Hospital, Adelaide, South a significant proportion of OSA sufferers report little or compared with Caucasians, even after controlling
Australia, Australia
4
no daytime symptoms. OSA has been associated with an for body mass index (BMI).6 7 Asians develop OSA
School of Medicine, Flinders increased risk of cardiovascular disease, cognitive at a mean BMI 2 kg/m2 less than Caucasians. It is
University, Adelaide, South
Australia, Australia abnormalities and mental health problems. Randomised thought that the increased susceptibility to OSA in
5
Discipline of Physiology, controlled trial evidence is awaited to confirm a causal Asians is due to differences in craniofacial and
School of Medical Sciences, relationship between OSA and these various disorders. upper airway anatomy.8
University of Adelaide, The gold standard diagnostic investigation for OSA is During the last two decades, there have been
Adelaide, South Australia,
overnight laboratory-based polysomnography (sleep major advances in the understanding of how recur-
Australia
study), however, ambulatory models of care rent upper airway obstruction occurs during sleep
Correspondence to incorporating screening questionnaires and home sleep in OSA. Obesity is the most important risk factor
Dr Zafar Ahmad Usmani, studies have been recently evaluated and are now being for OSA. An 8-year population-based study with
Department of Respiratory incorporated into routine clinical practice. Patients with 690 subjects found that a 10% weight gain pre-
Medicine, The Queen Elizabeth
Hospital, 4A, TQEH, 28 OSA are very often obese and exhibit a range of dicted a 32% increase in AHI, while a 10% weight
Woodville Road, Woodville comorbidities, such as hypertension, depression and loss predicted a 26% decrease in AHI.9 A narrowed
South, Adelaide, South diabetes. Management, therefore, needs to be based on pharyngeal airway due to increased fat deposition
Australia 5011, Australia; a multidisciplinary and holistic approach which includes in surrounding structures,10 and reduced longitu-
zafar-ahmad.usmani@health.
lifestyle modifications. Continuous positive airway dinal traction on the upper airway due to increased
sa.gov.au
pressure (CPAP) is the first-line therapy for severe OSA. abdominal loading,11 predisposes the airway to col-
Received 25 July 2012 Oral appliances should be considered in patients with lapse at sleep onset when upper airway dilator
Revised 19 September 2012 mild or moderate disease, or in those unable to tolerate muscle tone falls. Other factors that can lead to
Accepted 14 October 2012 CPAP. New, minimally invasive surgical techniques are upper airway narrowing are tonsillar hypertrophy,
Published Online First
17 November 2012 currently being developed to achieve better patient retrognathia and other forms of craniofacial con-
outcomes and reduce surgical morbidity. Successful long- striction. The severity and frequency of obstructive
term management of OSA requires careful patient events during sleep is then determined by a
education, enlistment of the family’s support and the complex interplay of four main factors: (1) the
adoption of self-management and patient goal-setting severity of the underlying anatomic deficiency;
principles. (2) the intrinsic stability/instability of the respira-
tory control system (often referred to as ‘respira-
tory loop gain’); (3) the capacity of the dilator
INTRODUCTION AND BACKGROUND muscles to mount a neuromuscular compensatory
Obstructive sleep apnoea (OSA) is characterised by response to obstruction and (4) the intrinsic sensi-
repetitive, partial or complete closure of the upper tivity of the individual to be aroused from sleep
airway resulting in repeated, reversible blood when obstruction occurs.12 Other factors, such as
oxygen desaturation and sleep fragmentation. In the the surface tension of the upper airway lining fluid,
general population, the prevalence of adult OSA was which may influence airway collapsibility, and
found in the 1990s to be approximately 20% when alcohol and sedating medication, which can sup-
defined as an apnoea hypopnoea index (AHI) press protective reflexes, may also influence the
>5 events/h of sleep.1 The prevalence of ‘OSA syn- severity of OSA.13 14
drome’, a clinical entity defined by an elevated AHI A wide range of clinical manifestations are asso-
in conjunction with daytime sleepiness, was esti- ciated with untreated OSA as shown in box 1.
mated to be 4% in adult men and 2% in adult Snoring (as reported by the bed partner) and
women.2 However, given the recent global trend for excessive daytime sleepiness (EDS) are the most
increasing obesity and ageing of populations, it is common symptoms that lead patients to seek
likely that there has been a substantial increase in medical attention. However, perception and report-
To cite: Usmani ZA, Chai- the prevalence of OSA. A recent Brazilian study, for ing of daytime sleepiness seem to vary greatly
Coetzer CL, Antic NA, et al. example, showed that one-third of people had an among individuals, and subjective tools to measure
Postgrad Med J AHI>5 (with symptoms) or AHI>15.3 Several EDS, such as the Epworth Sleepiness Scale (ESS),
2013;89:148–156. studies have shown a higher prevalence of OSA in do not correlate well with the severity of OSA.15

148 Usmani ZA, et al. Postgrad Med J 2013;89:148–156. doi:10.1136/postgradmedj-2012-131340

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defined as an apnoea. A hypopnoea is a ≥10 s reduction in

Box 1 Common symptoms and signs associated with airflow associated with an EEG arousal or oxyhaemoglobin
obstructive sleep apnoea desaturation. The AHI is the number of apnoeas and hypop-
noeas per hour of sleep, and is the key measure used for quanti-
fying disease severity and for defining disease prevalence in
Daytime symptoms:
normal and clinical populations. Several definitions for hypop-
▸ Sleepiness
noea have been proposed and are in clinical use.24 25 These can
▸ Morning headache
markedly affect the AHI value.25 Thus, care should be taken
▸ Tiredness and fatigue
when comparing research and clinical studies between
▸ Reduced vigilance and executive function
laboratories.
▸ Memory impairment
A growing number of portable sleep monitoring systems are
▸ Depression
being developed for use in a patient’s own home without the
▸ Impotence
need for an attending sleep technician. Many of these exclude
Nocturnal symptoms:
the recording channels used for scoring sleep. In 1994, the task
▸ Snoring
force for the Standards of Practice Committee of the American
▸ Apnoeas observed by the bed partner
Sleep Disorders Association (now the American Academy of
▸ Sudden choking or gasping awakenings/arousals
Sleep Medicine (AASM)) classified the different types of sleep
Common clinical signs:
apnoea evaluation studies into four levels according to the
▸ Obesity which manifests as
number of parameters recorded and the presence or absence of
– Increased neck and/or waist circumference
attending personnel:26
– Oropharynx that is crowded, narrowed or oedematous
Type 1: Standard in-laboratory PSG, performed with an
– Large tongue which sits high in the mouth and obscures
attending sleep technician, with a minimum of seven record-
a view of the oropharynx
ing channels (EEG, EOG, chin EMG, ECG, airflow, respira-
Less common signs
tory effort and oxygen saturation). Additional channels for
▸ Retrognathia
detection of snoring and body position are also usually
▸ Tonsillar hyperplasia or hypertrophy
employed, and video monitoring is sometimes included if a
▸ Coexisting hypertension
parasomnia is suspected.
▸ Peripheral oedema or signs of mild pulmonary hypertension
Type 2: Unattended, comprehensive, portable PSG with a
minimum of seven recording channels as per type 1.
Type 3: Modified portable sleep apnoea testing, with a
minimum of four recording channels (ECG or heart rate,
DIAGNOSIS oxygen saturation, and at least two channels of respiratory
The diagnosis and decisions regarding treatment of OSA require movement or respiratory movement and airflow).
consideration of potential risk factors, severity and impact of Type 4: Continuous recording using one to three recording
patient symptoms, bed partner history, medical comorbidities, channels (usually includes pulse oximetry).
plus the number of sleep-disordered breathing events and sever- In 2007, the Portable Monitoring Task Force of the AASM
ity of oxygen desaturation detected during overnight sleep mon- published clinical guidelines for the use of unattended portable
itoring. A number of screening questionnaires and clinical monitors in the diagnosis of OSA based on a review of the lit-
prediction tools have been developed to help identify patients at erature.27 It was recommended that unattended, portable moni-
high risk for OSA who may benefit from more urgent evaluation toring (recording a minimum of airflow, respiratory effort and
and treatment. Examples of screening tools developed for use in oximetry) could be used as an alternative to PSG for the diagno-
the sleep clinic setting include the Multivariable Apnoea Risk sis of OSA in patients with a high pretest probability of
index16 (based on snorting and gasping, loud snoring, breathing moderate-to-severe OSA and without significant medical
cessation, BMI, age and sex), and the Sleep Apnoea Clinical comorbidities, in conjunction with a comprehensive evaluation
Score17 (SACS) (based on neck circumference, hypertension, by a qualified sleep specialist. It states that portable monitoring
habitual snoring and partner reports of nocturnal choking or devices must allow display of raw data for manual scoring or
gasping). Researchers have also evaluated the role of anatomical editing prior to automated analysis, and should be reviewed by
measures of the upper airway and craniofacial structures in the a sleep specialist. The guidelines also provide recommendations
prediction of OSA risk,18 19 including the use of quantitative regarding the acquisition, analysis and interpretation of data,
analysis of facial photographs.20 OSA screening tools have also and need for appropriate policies and procedures including a
been designed for use outside of the sleep clinic setting. These quality improvement programme to assure reliability and valid-
include the STOP (snoring, daytime tiredness, observed apneas, ity of testing. Based on these recommendations, the Centres for
have or been treated for blood pressure) questionnaire21 which Medicare and Medicaid Services in the USA have approved the
was developed for patients attending surgical preoperative use of a limited home sleep-recording device with at least three
assessment clinics, and the OSA5022 (based on waist circumfer- channels to diagnose OSA for the purposes of reimbursement
ence, snoring, witnessed apnoeas and age ≥50) and Berlin ques- for continuous positive airway pressure (CPAP) treatment.
tionnaires23 which were created for use in the primary care There has been increasing interest in simplified, ambulatory
population. models for diagnosing OSA that combine the use of screening
The current standard for confirmation of a diagnosis of OSA questionnaires and limited sleep monitoring. In a randomised
is laboratory polysomnography (PSG) which includes a compre- controlled trial (RCT) evaluating an ambulatory management
hensive recording of EEG, electro-occulography (EOG) and strategy for OSA, Mulgrew et al.28 applied a simplified diagnos-
chin electromyography (EMG) to identify sleep stages, as well as tic algorithm to identify patients with moderate-severe OSA in a
airflow, respiratory effort, body position, limb movements, ECG sleep clinic population based on an ESS≥10, SACS≥15 and
and oxygen saturation. Cessation of airflow for at least 10 s is oxygen desaturation index ≥15/h on overnight home oximetry,

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followed by auto-adjusting PAP titration to determine a fixed the small OSA treatment-related reductions in blood pressure
treatment pressure for ongoing CPAP therapy. Of the patients was that most patients included in the trials were normotensive.
who scored positively on the diagnostic algorithm and who However, similar results have subsequently been reported in
underwent subsequent PSG, 94% (95% CI 81 to 99%) were RCTs which enrolled newly diagnosed OSA patients with
correctly identified as having an AHI>15/h. In our own untreated hypertension.48 49 At the present time, we can con-
research work, we have evaluated the accuracy of a simplified clude that OSA elevates blood pressure, but the effects appear
diagnostic strategy for OSA in a primary care population con- to be relatively modest. Mild pulmonary artery hypertension
sisting of the OSA50 questionnaire followed by overnight oxim- also appears to be caused by OSA.50
etry.22 We found that the simple two-step model could identify While the sustained effects of OSA on blood pressure appear
moderate-severe OSA with a high degree of accuracy, with a sen- to be quite modest, acute fluctuations in blood pressure at night,
sitivity of 88% and specificity of 82%. In deploying these sim- secondary to the repetitive obstructed breathing events, episodic
plified diagnostic algorithms, it is important to remember that hypoxia and hypercapnia and autonomic instability, are rela-
the pretest probability of disease can have a substantial influence tively large (ie, 10–20 mm Hg). It is possible that these acute
on the post-test probability of disease. Thus, ideally, they should OSA-induced physiological changes combined with the
be validated within the population of intended application increased after-load and stretch placed on the heart during
before use or, as a minimum, the pretest probability of disease obstructed breathing could lead to acute ischaemic events or
estimated and taken into account in the interpretation of results. arrhythmias during sleep, particularly in individuals with pre-
The final test of whether simplified diagnostic algorithms are existing cardiac disease.51 Studies have shown that OSA patients
effective and safe is to determine whether patient outcomes who suffer an acute myocardial infarction, or who die suddenly
using these methods are the same or similar to those used in from cardiac causes, are more likely to do so during the night-
more conventional sleep specialist laboratory-based services. time hours than in the morning after rising, as is usually the
Several recent studies have reported encouraging results using case.52 53 Epidemiological evidence suggests that OSA may be
such methods, finding non-inferior or non-significant differ- an independent risk factor for future strokes, heart failure, atrial
ences for patient outcomes including sleep apnoea symptoms fibrillation, ischaemic heart disease and cardiovascular mortal-
and sleep-related quality of life.28–33 ity.54–58 However, the evidence is not consistent between
studies, with some studies suggesting that only middle-aged
NEUROBEHAVIOURAL, CARDIOVASCULAR AND METABOLIC men, and not older men or women, are at risk.55 56 58
ABNORMALITIES ASSOCIATED WITH OSA Small, short-term RCTs conducted in patients with OSA on
EDS is the cardinal symptom of OSA and is thought to be the CPAP therapy have generally shown inconsistent effects on
main reason for the two–fivefold increased risk of motor vehicle glucose and lipid metabolism.59 However, a recent well-
accidents observed among OSA patients.34 Daytime sleepiness is controlled cross-over RCT of CPAP versus sham CPAP in 75
also a major contributor to the reduced quality of life, mood OSA patients with coexisting metabolic syndrome reported sig-
disturbance, decreased work performance and increased occupa- nificant improvements in HbA1c, low-density lipoprotein and
tional accidents reported by OSA patients. It is important to total cholesterol following OSA treatment.60
remember, however, when assessing patients for snoring and The field is now in need of definitive large-scale RCTs of
possible sleep apnoea, that (1) most subjects identified with OSA treatment that focus on hard cardiovascular outcomes.
OSA in population studies do not report daytime sleepiness35 36 Several trials are currently in progress, including the multi-
and (2) there is an extensive list of causes of self-reported sleepi- national Sleep Apnoea cardioVascular Endpoints study.61
ness apart from OSA37 (eg, depression, lifestyle-related chronic
sleep loss, sedating medication and non-respiratory medical OSA TREATMENT
comorbidities) which can impact on a patient, and may even be A wide range of management options are available for the treat-
the dominant cause of their sleepiness. ment of OSA ranging from conservative measures including life-
There has been a great deal of interest over the last two to style modifications to reduce weight and alcohol consumption,
three decades in the possibility that OSA may lead to hyperten- to CPAP, mandibular advancement splints (MAS) and surgical
sion, diabetes, hyperlipidaemia, stroke, coronary artery disease interventions. Treatment choices are based on the severity of the
and increased mortality.38 Early data from animal experiments patient’s OSA, associated symptoms, comorbidities, occupation
which employed repetitive hypoxia in an attempt to mimic the and patient preferences.
gas exchange disturbance of OSA showed marked systemic
hypertension.39 Similar experiments have shown derangements Conservative treatment and lifestyle modifications
in lipid metabolism, including accelerated atherosclerosis, and Weight loss via dietary modifications and regular exercise should
altered glucose metabolism.40 Thus, it appears biologically be recommended to all patients with OSA (regardless of sever-
plausible, at least, that a patient with OSA might be at increased ity) who are overweight or obese.62 Alcohol has been shown to
risk of cardiovascular and metabolic disease. worsen OSA by suppressing protective neuromuscular and
Early cross-sectional, population studies suggested that OSA arousal reflex responses. Thus, all patients with OSA should be
may be a risk factor for hypertension, independent of other advised to avoid heavy alcohol consumption particularly 4–6 h
known risk factors.41 However, the results from longitudinal prior to bed time. In addition, OSA patients appear to exhibit
studies have been less convincing. Two studies showed that OSA greater decrements in daytime functioning after low-dose
independently predicted incident hypertension,42 43 while two alcohol and partial sleep restriction, than non-OSA subjects.63
other studies did not.44 45 There have been a relatively large They should, therefore, be encouraged to always obtain a full
number of small RCTs of CPAP and mandibular advancement night’s sleep, and to limit their alcohol consumption, particu-
therapy46 for OSA, which have reported the effects on blood larly before undertaking potentially hazardous tasks such as
pressure. Meta-analyses have shown reductions of approxi- driving.
mately 2 mm Hg in both systolic and diastolic blood pressure.47 Supine position-dependent OSA is commonly seen in clinical
A criticism of these earlier studies, and a suggested reason for practice and is found in up to one-third of patients with mild

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and moderate OSA.64 Traditionally, a tennis ball strapped to the

back while sleeping has been used to avoid supine sleep. Box 2
However, studies suggest that long-term compliance with this
technique is poor, limiting its effectiveness.65 66 Newer position
Strategies to maximise continuous positive airway pressure
monitoring and supine alarm devices may be more comfortable
(CPAP) acceptance:
to wear at night. We found in a preliminary study in supine-
▸ Education and provision of written literature at an
predominant OSA patients, that one such technique was highly
appropriate level for the patient
effective in avoiding the supine sleep position and in reducing
▸ Regular weekly phone calls for first few weeks
overnight AHI, although it did not decrease overall snoring
▸ Use of nasal humidification
intensity.67
Strategies to improve suboptimal CPAP adherence
▸ Consideration of cognitive behavioural therapy (CBT) and
Continuous positive airway pressure
desensitisation
CPAP is considered the ‘gold standard’ treatment for OSA. It
▸ Consideration of alternate mask interfaces in case of
was first described by Sullivan et al in 1981.68 CPAP consists of
discomfort or significant leak
a flow generator which delivers air via tubing, and a nasal or
▸ Consideration of a short course of Eszopiclone at CPAP
oral mask to produce a fixed positive pressure in the upper
initiation if no contraindications in patients with high risk on
airway. The PAP splints the upper airway, preventing repeated
non-compliance75
collapse and closure, stabilises overnight oxygen saturation and
reduces sleep fragmentation. Both ‘fixed’ CPAP and auto-
adjusting PAP devices are available. AutoPAP devices automatic-
ally adjust PAP to correct obstructive events and compensate for palatal-lifting devices. A MAS works by advancing the mandible
acute changes in posture or long-term changes in weight. They and has been shown to decrease AHI76 and subjective sleepi-
appear to confer no particular clinical advantage over fixed ness.77 These devices are usually indicated for patients with mild
CPAP devices for long-term treatment except perhaps in patients to moderate OSA who prefer it over CPAP, or who have tried and
who require a high inflating pressure.69 However, a short ambu- failed CPAP therapy. MAS devices are generally less effective in
latory study over several nights using an autoPAP device is a reducing the AHI compared with CPAP, and are generally not
useful alternative to an in-laboratory, overnight, manual titration indicated as a first-line treatment in patients with severe OSA.
to enable a ‘fixed’ CPAP level to be estimated to treat OSA. MAS is contraindicated in some circumstances (box 3).
A systematic meta-analysis of 36 RCTs has shown effective-
ness of CPAP in reducing AHI, symptoms of sleepiness and
improving quality-of-life measures in people with moderate to Surgical interventions
severe OSA.70 The evidence regarding the effect of CPAP on Surgical interventions are generally not indicated as first-line
neuropsychological outcomes has been mixed with some RCTs treatment, and are used only when non-invasive measures have
demonstrating improvement in some outcomes,71 but other been tried and failed or have been rejected by the patient.
studies showing no significant improvement in neurocognitive Surgical interventions can be broadly divided into procedures
functioning.72 aimed at curing OSA via upper airway reconstruction and inter-
ventions to improve CPAP adherence, for instance, improving
CPAP acceptance and adherence nasal patency by septoplasty or polypectomy. Despite progress
A significant proportion of patients with moderate to severe and advancements in surgical techniques for the treatment of
OSA reject CPAP treatment outright when it is offered. Cost OSA, there is still a lack of good quality data with regard to the
may be a barrier in some health systems, but even when this is effectiveness and selection of patients for surgical
not an issue, initial acceptance can be low. Patients’ knowledge interventions.78
and perceptions of the importance of OSA, and the necessity of Uvulopalatopharyngoplasty (UPPP) is the most common OSA
treatment, appear to be the major determinants of whether or surgical procedure. It involves resection of the uvula, redundant
not they accept CPAP therapy. Unfortunately, among those who retrolingual soft tissue, and palatine tonsillar tissue. UPPP, with
initially accept CPAP therapy, long-term compliance is also rela- or without tonsillectomy, has not been shown to reliably cure
tively poor. In one study, only 68% of patients were using CPAP OSA in patients with moderate to severe OSAS.78 An RCT com-
after 5 years.73 Other data suggest that 50% of patients who ini- paring UPPP and conservative management in OSA patients
tiate CPAP discontinue use within the first year, most of them with >50% obstruction at the palatal level showed improve-
within the first month. Initial acceptance and good long-term ment in daytime sleepiness and oxygen desaturations at 1 year,
compliance are obviously vital in order to obtain the desired however, only 38% achieved normality of their oxygen
benefits from CPAP. Many studies have defined acceptable com-
pliance as consisting of at least 4 h of usage for more than 70%
of nights. However, such definitions are arbitrary, and studies
show a dose-response curve across a wide range of CPAP Box 3 Relative contraindications for mandibular
average nightly use for outcomes, such as reduced daytime advancement splints
sleepiness.74 Effort and resources should be dedicated, particu-
larly in the first few weeks of therapy, towards ensuring CPAP ▸ Pre-existing temporo-mandibular joint disease or instability
acceptance and optimal compliance. Some of the strategies to ▸ Insufficient dentition to support device retention, for
increase CPAP compliance and adherence are listed in box 2. instance, less than six teeth in each arch
▸ Severe bruxism
Oral appliance therapy ▸ Patient unable to open the mouth adequately
A MAS is the most common oral appliance used as an alternative ▸ Brisk gag reflex
to CPAP. Other devices include tongue-retaining devices and

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desaturation index at 1 year.79 The surgical complication rate ventilatory support breath-by-breath, according to the patient’s
was 22%. Maxillomandibular advancement (MMA) involves pattern of breathing) may prove, in the long term, to be more
forward-fixing the maxilla and mandible. A meta-analysis which effective. Two international, multicentre RCTs of ASV to treat
included data from several case series suggested MMA to be sleep-disordered breathing in patients with heart failure are cur-
more consistent in reducing AHI compared with the other surgi- rently in progress (SERVE-HF (treatment of sleep disordered
cal techniques, however, a high risk of bias and the heterogen- breathing by adaptive servo-ventilator in heart failure patients),
eity of the studies were limiting factors of this meta-analysis.80 ADVENT-HF (the effect of ASV on survival and frequency of
There are a variety of procedures to reduce or advance the cardiovascular hospital admissions in patients with heart failure
tongue base. Submucosal radiofrequency, or bipolar techniques, and sleep apnea)) Bilevel PAP (BIPAP) with a backup respiratory
are relatively easy, well tolerated and low risk, but only partially rate is also an option for treatment of symptoms and/or respira-
effective for treating sleep apnoea.81 Hypoglossal nerve stimula- tory failure in patients with CSA related to central nervous
tion is a new treatment currently under evaluation which leads system (CNS) suppression (eg, resulting from CNS disease).
to contraction of the genioglossus muscle, tongue protrusion, Complex sleep apnoea refers to a condition in which CSA per-
stiffening of the anterior pharyngeal wall and an increase in sists or emerges following the application of CPAP for OSA,
upper airway diameter. A recent RCT of an implantable hypo- This occurs in approximately 10% of patients with OSA,88 and
glossal nerve stimulation system in 21 patients with moderate to may be a transitory phenomenon that disappears after several
severe OSA who were intolerant of CPAP, showed a success rate weeks of CPAP treatment.89 However, in a small proportion of
(as defined by 50% reduction in AHI with an AHI of <20/h) of patients, it can persist and limit the effectiveness of therapy. In
67% at 6 months.82 This was associated with significant severe cases, a trial of bilevel pressure support with a backup
improvement in ESS. However, studies showing benefit in larger rate should be considered or, alternatively, ASV. Overlap syn-
patient samples, and after longer periods of follow-up, are drome refers to the combination of Chronic Obstructive
required before this therapy can be adopted as part of routine Pulmonary Disease (COPD) and OSA.90 These patients are at
clinical practice. increased risk of hypercapnic respiratory failure and pulmonary
hypertension compared with patients who have OSA or COPD
Other novel therapies currently under evaluation alone,91 and may be at greater risk of COPD exacerbations and
Acetazolamide has been shown to reduce the respiratory loop premature death.92 Management should include a trial of CPAP
gain by approximately 40% in individuals with OSA,83 and, in the case of a suboptimal response or worsening respira-
however, there is insufficient evidence to recommend its clinical tory failure, institution of nocturnal BIPAP with or without sup-
use in patients with OSA at this time. Similarly, eszopiclone has plemental oxygen. Sleep-related hypoventilation can occur in
been shown to improve OSA patients with a low arousal thresh- the absence of OSA if there is severe mechanical impairment to
old,84 but confirmatory studies are needed to confirm its efficacy respiration imposed by morbid obesity or neuromuscular disease
and safety. A disposable nasal one-way valve device designed to and can cause progressive respiratory failure. The reader is
preferentially increase expiratory airway pressure has recently directed to several recent reviews which describe the prevalence,
been shown to reduce AHI and improve subjective sleepiness pathogenesis and clinical management of this group of
when compared with sham treatment in patients with mild to disorders.93 94
severe OSA.85 However, more long-term data on efficacy, adher-
ence and cost-effectiveness is required before its role in the OSA AS A CHRONIC CONDITION AND OSA CHRONIC CARE
routine management of OSA can be determined. MODEL
OSA is a common disorder that meets the characteristics of a
OTHER SLEEP-RELATED BREATHING DISORDERS chronic disease, as it is a disease which is prolonged, does not
A detailed discussion of all the sleep-related breathing disorders resolve spontaneously and is rarely completely cured.95 Thus,
is beyond the scope of this review, however, a brief note about OSA requires ongoing management of residual symptoms, defi-
some of the more relevant conditions which may coexist with cits and comorbidities. Furthermore, many OSA patients have
OSA is worthwhile. Central sleep apnoea (CSA) is characterised modifiable lifestyle factors that contribute to their disease,
by repetitive, complete cessation of airflow and ventilatory which could be improved with interventions. The recent AASM
effort during sleep (compared with OSA, in which ventilatory guideline for OSA shows support for approaching OSA as a
effort persists). CSA may be idiopathic, however, common risk chronic disease requiring long-term multidisciplinary manage-
factors include heart failure (usually associated with Cheyne– ment, and this is an important future direction for the care of
Stokes respiration (CSR,or crescendo-decrescendo breathing), patients with OSA.62
opiate use and stroke). The mainstay of treatment of CSA is There are a number of common comorbidities seen in OSA
control of the underlying or predisposing risk factor. Positive patients. Some contribute independently to one of the common-
pressure-mask therapies have also been used. While the est presenting complaints, EDS, and several have the potential
intention-to-treat analysis of a multicentre RCT of CPAP to influence patient outcomes on CPAP.
therapy for CSR in patients with heart failure was negative with Obesity is an extremely common and important cause of
respect to the primary outcome of mortality,86 CPAP treatment OSA, as mentioned earlier,9 and effective therapies for obesity,
was highly variable in its effect on the sleep-disordered breath- for instance, bariatric surgery, lead to significant improvements
ing, ranging from virtually no effect to complete suppression of in OSA.96 Obesity has also been associated with EDS, independ-
central apnoeas. A posthoc analysis suggested there was clinical ent of OSA.37 Depression is also common among patients with
benefit in the subset of patients in whom central apnoea was OSA, the reported prevalence being between 21% and 41%.97
supressed.86 87 Thus, there is some evidence for the role of Like obesity, depression may contribute to EDS, independent of
CPAP therapy in patients with CSA related to heart failure, but OSA. In a population-based study, Bixler and colleagues found
a newer treatment, adaptive servo-controlled ventilation (ASV), that depression was the most significant risk factor for EDS, fol-
a ‘smart’ form of bilevel positive pressure-mask ventilator lowed by BMI, age, typical sleep duration, diabetes, smoking
support which normalises ventilation by adjusting the level of and finally, OSA.37

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Alcohol intake is an important modifiable risk factor for

OSA. Alcohol, particularly in the last 2 h before bed-time, Main messages
increases the duration and frequency of obstructive episodes,
and worsens OSA. Other common comorbidities in OSA
▸ In the general population, one in every five persons has an
patients are hypertension, cardiovascular disease and type 2 dia-
apnoea-hypopnoea index (AHI)>5/h.
betes mellitus.98 99
▸ Obesity and increased waist circumference are the most
While CPAP is the gold standard treatment for moderate-
important risk factors for obstructive sleep apnoea (OSA).
severe OSA, some residual symptoms and deficits remain even
However, other factors, including craniofacial anatomy,
among those who appear to be optimally treated. We conducted
stability of respiratory control centre, upper airway dilator
a multicentre study of 174 patients treated with CPAP, and
muscle activity are also considered to contribute to the
found that 40% of moderate-severe OSA patients still had an
pathogenesis of OSA.
abnormal ESS score after 3 months of CPAP treatment.74 Very
▸ Various OSA screening tools are increasingly being used to
similar results were reported by Weaver and colleagues in
identify people at high risk of OSA in the population.
2007.100
▸ In-laboratory polysomnography (PSG) is the current standard
This residual EDS may have various aetiologies, such as dis-
for diagnosis of OSA.
ruption to sleep caused by CPAP itself, insufficient use of CPAP,
▸ Home-based PSG can be considered as an alternative in
other sleep disorders not responsive to CPAP, coexistent mood
selected patients with high pretest probability and without
disorders, sedating medications, obesity, advanced age, insuffi-
significant comorbidities, in conjunction with a sleep
cient sleep duration, diabetes, smoking or hypoxic brain injury
specialist review.
from chronic OSA. Depression is a particularly important
▸ Untreated OSA is associated with a modest increase in blood
comorbidity to consider when treating OSA, given the overlap
pressure, and causes mild pulmonary hypertension.
between symptoms and the strong association between the
▸ OSA has been found to be an independent risk factor for
two.37 97 A broader approach to the recognition, diagnosis and
ischaemic heart disease, stroke and overall cardiovascular
management of EDS is warranted, and should be part of
mortality, particularly in middle-aged men. However, there is
chronic condition management in OSA.
a need for good quality treatment intervention studies to see
The Chronic Care model has been accepted as a conceptual
whether OSA treatment can reduce these risks.
framework to reorganise patient care to meet the needs of
▸ OSA should be managed as a chronic condition with a
people with chronic illness, and is ideal for use in a chronic con-
multidisciplinary approach and involvement of the patient,
dition such as OSA.101 The model is comprised of four compo-
their family and relevant health professionals.
nents: (1) ongoing self-management support; (2) delivery system
▸ Continuous positive airway pressure (CPAP) is the first-line
features, such as planned visit schedules and multidisciplinary
therapy for severe OSA. Oral appliance therapy and surgical
collaborative care arrangements; (3) decision supports, such as
interventions can be considered in patients with less severe
guidelines, access to experts and reminder systems and (4) clin-
disease, or in patients who have difficulty tolerating CPAP.
ical information systems which provide timely data about indi-
▸ Treatment and management of coexisting conditions for
vidual patients and populations. The important role of
instance, insomnia and depression is vital for better
self-management support in the chronic care model is justified
outcomes.
by the recognition that patients themselves and their families are
▸ Ongoing follow-up with the aim of education, treatment
the primary caregivers in chronic illness.102
compliance assessment and patient-tailored management
When constructing such a chronic care model, health literacy
are key for successful long-term management of OSA.
must be considered. Health literacy includes the ability to read,
write and understand health-related information, to make sound
health-related decisions, and to navigate life in a way that pro- craniofacial features, respiratory control system stability (loop
motes good health. A recent Australian survey indicated that gain), arousal threshold and upper airway dilator muscle activity.
around 60% of adults lacked the health literacy skills to cope Laboratory-based PSG is the gold standard diagnostic test,
with the demands of modern healthcare, and to make the deci- however, home-based studies could be performed in selected
sions required to manage their health.103 patients with a sleep specialist follow-up. Various models of
In summary, there are many disease management issues for screening and home-based sleep studies have been proposed and
patients with OSA, including: factors known to contribute to are under investigation. CPAP should be considered as first-line
OSA severity and multiple comorbidities, residual daytime treatment in patients with severe OSA, and, moderate OSA with
sleepiness despite CPAP therapy and inadequate CPAP adher- symptoms. Second-line management options include oral appli-
ence. All these disease management issues are ideally addressed ances and surgical interventions. Further research has been
as part of a comprehensive chronic condition management
programme.
It is our view that if Sleep Medicine services focus their thera-
peutic interventions for OSA solely around devices (CPAP, MAS, Current research questions
etc) and do not incorporate chronic disease management pro-
grammes into the care pathways of those with OSA, patient out-
▸ Clearer and more detailed understanding of the various
comes will remain below expectations.
physiologic phenotypes of obstructive sleep apnoea (OSA).
▸ Long-term relationship between OSA and cardiovascular
SUMMARY
risk/morbidity.
Adult OSA is a chronic condition, the prevalence of which is
▸ Association between OSA and neurocognitive outcomes.
increasing with the increasing trend of obesity and ageing. In
▸ Feasibility and effectiveness of various new investigative
addition to obesity, various other anatomical and physiological
treatments for OSA.
factors also play a role in the pathogenesis of OSA, including

Usmani ZA, et al. Postgrad Med J 2013;89:148–156. doi:10.1136/postgradmedj-2012-131340 153

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Review

4. OSA associations and consequences:

Key references A. Drivers with untreated, severe sleep apnoea have a higher
chance of automobile crash compared with other drivers.
B. Untreated OSA has not been to be associated with pul-
▸ Isono S. Obesity and obstructive sleep apnoea: mechanisms
monary hypertension.
for increased collapsibility of the passive pharyngeal airway.
C. OSA may be an independent risk factor for systemic
Respirology 2012;17:32–42.
hypertension.
▸ Iber C, Ancoli-Israel S, Chesson A, et al. The AASM manual
D. OSA may be an independent risk factor for heart failure,
for the scoring of sleep and associated events: rules,
ischaemic heart disease and cardiovascular mortality.
terminology and technical specifications. 1st edn. Medicine
E. Everyone with OSA can expect to feel excessively sleepy
AAoS, editor. Westchester, IL: AmericanAcademy of Sleep
Medicine, 2007. 5. OSA treatment and management:
▸ Somers VK, White DP, Amin R, et al. Sleep apnea and A. CPAP is the second-line treatment for severe OSA.
cardiovascular disease: an American Heart Association/ B. Self-management support is a critical part of chronic care
American College of Cardiology Foundation Scientific model for OSA management.
Statement from the American Heart Association Council for C. Underlying depression should be identified and treated.
High Blood Pressure Research Professional Education D. Alcohol avoidance prior to bed time is usually
Committee, Council on Clinical Cardiology, Stroke Council, recommended.
and Council on Cardiovascular Nursing. J Am Coll Cardiol E. Supine avoidance is ineffective and has no role in the
2008;52:686–717. management of positional OSA.
▸ Giles TL, Lasserson TJ, Smith BJ, et al. Continuous positive
airways pressure for obstructive sleep apnoea in adults. Contributors All the authors have contributed towards the manuscript.
Cochrane Database Syst Rev 2006:CD001106.
Funding None.
▸ Antic NA, Catcheside P, Buchan C, et al. The effect of CPAP
in normalizing daytime sleepiness, quality of life, and Competing interests None.
neurocognitive function in patients with moderate to severe Provenance and peer review Not commissioned; externally peer reviewed.
OSA. Sleep 2011;34:111–19.

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156 Usmani ZA, et al. Postgrad Med J 2013;89:148–156. doi:10.1136/postgradmedj-2012-131340

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Obstructive sleep apnoea in adults

Zafar Ahmad Usmani, Ching Li Chai-Coetzer, Nick A Antic and R Doug

McEvoy

Postgrad Med J 2013 89: 148-156 originally published online November

17, 2012
doi: 10.1136/postgradmedj-2012-131340

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