REVIEW ARTICLE

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OBSTRUCTIVE SLEEP APNOEA HYPOPNEA SYNDROME – AN OVERVIEW

WHW Mohamad MB ChB (Birm), MRCP (UK); T Ismail MBBS (Glasgow), MRCP (UK), MD (Glasgow)
Faculty of Medicine, Universiti Teknologi MARA (UiTM), Selayang Campus (Wan Haniza Wan Mohamad, Tengku Saifudin Tengku Ismail).

Address for correspondence: Dr Wan Haniza Wan Mohamad, Faculty of Medicine, Universiti Teknologi MARA, Selayang Campus, Jalan Prima 7, 68100 Batu Caves, Selangor DE, Malaysia. Tel: 03-6126 4800 or 016-722 0047, Fax: 03-6126 4888, Email: wanhaniza@hotmail.com. Dr Tengku SaifudinTengku Ismail, Email:  tengkusaifudin@yahoo.co.uk

Conflict of interest and funding: None.

INTRODUCTION

Breathing-related sleep disorder refers to a spectrum of conditions ranging from simple snoring to obesity hypoventilation syndrome. Sleep disorders causing fragmented sleep during the night is known to have a negative impact on physical and psycho-social aspects of life.^1,2 Patients commonly complain of excessive daytime sleepiness (EDS). It is estimated that the prevalence of EDS in the community varies between 0.3-35%.^1,3,4 A recent study reported an EDS prevalence of 15% among the Malaysian population.⁵ Although there are many possible conditions which can explain the symptom, a recent survey shows that the most common diagnosis for EDS is a condition called obstructive sleep apnoea hypopnoea syndrome (OSAHS), accounting for approximately 67% of the diagnosis.⁶ This article aims to provide a comprehensive review of the clinical features and treatment of OSAHS.

The following case is a typical presentation of OSAHS:

Mr M is a 60-year-old retired engineer, who complains of lethargy and excessive sleepiness during the day. He finds that he can easily fall asleep in various situations such as when watching television, reading and after meals. His daytime sleepiness was worse before he retired as he had problems concentrating in meetings. He has had two near misses whilst driving in the past year but has never had an accident. His wife says that he snores loudly when he sleeps. Often, she notices that he chokes or stop breathing during sleep but is unrousable. However, he does get up frequently at night to pass urine. When asked about his sleeping habits, he feels that he slept well but this does not translate to feeling fresh during the morning. He also complained of a headache upon waking up. He is an ex-smoker of five years with a 40 pack year history of smoking. He denies alcohol intake and is otherwise well and independent. Examination revealed a pleasant middle aged gentleman, who was nodding off intermittently during the consultation. His body mass index (BMI) was 34. There was evidence of micrognathia and his collar size was 20 inches. He had a blood pressure (BP) recording of 153/90 mmHg. Cardiovascular, respiratory and abdominal examination was otherwise normal.

What is OSAHS?

OSAHS is a condition which causes intermittent and repeated upper airway narrowing or collapse, usually at multiple levels. This result in partial or total obstruction of the upper respiratory tract, also referred to hypopnea and apnoea, respectively. Once thought to be uncommon, the prevalence of OSAHS in middle-aged men (30-65 years) is estimated to range from 0.3-4%, with most studies quoting a prevalence of 1-2%.^7-9 It is estimated that the prevalence in women is half of that in men.⁸ OSA appears to be more common in the elderly.¹¹

What are the risk factors for developing the condition?

It is well recognized that narrowing of the upper airway, at multiple levels, is responsible for the consequences of OSAHS.¹¹ Increased muscle tone prevents the upper airways from collapsing during wake. The reverse occurs during sleep. When combining collapsibility of the airways, extraluminal pressure exerted from surrounding soft tissue structures and negative intraluminal pressure of the upper airway during inspiration, this results in upper airway collapse during sleep. Obesity can further reduce upper airway caliber causing more severe clinical consequences, compared to non-obese subjects.¹²

Studies show a genetic predisposition of OSAHS. The probability of developing OSAHS is greater in those with a positive family history.¹³ The risk of OSAHS is higher among relatives with the condition, despite adjustments made for well known risk factors.¹⁴ It is postulated to be related to inherited craniofacial abnormalities such as high and narrow hard palate, shorted mandibles, retroposed mandible and maxillae, and longer soft palates. 

Other risk factors outlined in Table 1, should prompt the search for the condition.

Table 1: Risk factors for OSAHS

Cardiac	Atrial fibrillation
	Congestive cardiac failure
	Refractory hypertension
	Nocturnal dysrhythmias
Respiratory	Pulmonary hypertension
Endocrine	Diabetes mellitus type 2
	Obesity
Neurological	Stroke
Others	High risk driving population
	Pre-operative for bariatric surgery

What are the clinical features?

The possibility of OSAHS should be considered in any patients with risk factors and typical clinical features. Collateral history from bed partners, family members or fellow employees are helpful in deriving to a diagnosis, as they will often notice symptoms suggestive of the condition such as falling asleep unintentionally in certain situations, of which the patient may be unaware of. In the case illustration, the history was not only from the patient but the description from his wife was equally important. 

Patients with OSAHS or their bed partners frequently complain of a long history of loud habitual snoring, followed by episodes of gasping and breathing pauses during sleep, resulting in wakefulness. It is not uncommon for patients with OSAHS to report undisturbed sleep when the apnoea or hypopneoa episodes occur during rapid eye movement (REM) sleep stage. In this stage of sleep, there is total muscle paralysis and any disturbances rarely results in awakening. Nevertheless, the outcome is the same regardless of presence of arousal. Repeated sleep disturbances causes chronic sleep fragmentation and EDS.

Other common complaints are unrefreshing sleep, nocturia, reduced libido, impotence, reduced concentration and morning headaches. It is not uncommon to have a history of chronic nasal congestion, hypertension and recent weight gain. Often, patients can also present with insomnia due to frequent arousals and inability to obtain a consolidated sleep.¹⁴ A search for symptoms suggestive of the condition should be enquired as part of routine health examination (Table 2).

Table 2: Routine questions to search for OSAHS

1. Do you snore?

2. Do you suffer from daytime sleepiness?

3. Does the patient have hypertension?

4. Is the patient obese?

5. Is the patient retrognathic?

Examination is helpful. It is mainly directed to look for risk factors for OSAHS. Measurement of neck circumference and BMI are good predictors for OSAHS. However, a normal BMI does not exclude the diagnosis. Patients may have crowded oropharynx and micrognathia. Mallampati classification is a rough classification of tongue size in relevant to the oral cavity (the diagram can be obtained from BMJ 2004;329:955-959). It is generally used by anaesthetists to predict the ease of intubation. Mallampati class III and IV are good predictors of OSAHS.¹⁵ BP and oxygen saturation are equally important as it may have therapeutic implications. It is important to exclude corpulmonale which can complicate long standing untreated OSAHS and other endocrinology abnormalities such as hypothyroidism and acromegaly.³⁰

Are there any screening tools to measure daytime sleepiness?

Epworth sleepiness scale (ESS) is a widely used tool to assess probability of falling asleep in different situation (Table 3). It was first developed by an Australian researcher in 1990. It is currently used widely in clinical practice as a simple rapid assessment of subjective sleepiness. In some centres, it is used to prioritize investigations.

For each question, subjects are required to score between 0 to 3, with scores of 0 equate to ‘unlikely to doze’ and scores of 3 equate to 'high chance of dozing'. The maximum score is 24. A score of nine or less is considered normal. Patients who score more than nine are excessively sleepy and may have underlying OSAHS. In general, a higher score suggest excessive daytime sleepiness but does not confirm the diagnosis. Therefore, such screening tool should be used in conjunction with other mode of assessment.

Table 3: Epworth sleepiness scale

How likely are you to doze off or fall asleep in the situations described above, in contrast to just feeling tired?
Situation	Score
Sitting and reading
Watching television
Sitting in a public place (e.g. theatre or 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 lunch without alcohol
In a car, while stopped for a few minutes in the traffic

How do you diagnose the condition?

When the condition is suspected and other causes of EDS have been excluded, referral to appropriate specialty is advised for further investigation. The specialties involved in the management of OSAHS differ between countries. In Malaysia, suspected cases are generally referred to respiratory physicians or ear, nose and throat (ENT) surgeon.

Pulse oximetry is useful as a screening tool for OSAHS. It is universally available and cheap. However, limited data is available to define abnormal frequency of desaturation or oxygen desaturation index (ODI). The sensitivity and specificity of pulse oximetry increase in more severe disease, indicating that it may be an effective tool for screening in certain groups of patients.¹⁷

The gold standard for diagnosis is polysomnography (PSG). When adequately supervised, it provides comprehensive information on sleep and breathing pattern. PSG is a multichannel recording of sleep and breathing variables. Apart from identifying patients with OSAHS and quantifying severity, it also analyzes abnormal sleep behaviours, thus facilitating other diagnosis such as periodic limb movement disorder and central sleep apnoea. Other indications for PSG are to evaluate effectiveness of treatment and titration of CPAP pressures. It is traditionally performed overnight but can also be done during daytime nap. In the latter, care must be taken in interpretation of results as it may underestimate severity.

PSG is routinely done in a dedicated sleep lab. Various electrodes and wires are attached to the patient non-invasively, at specific body position, to detect and measure different variables simultaneously during sleep. The variables or data is translated into digital signals to allow interpretation of results.

Electroencephalogram (EEG), electrooculogram (EOG) and electromyogram (EMG) records brain, eye and muscle activities, respectively during sleep. The recordings help to define wakefulness and stages of sleep. Defining the sleep stage can assist in determining significant respiratory events, as apnoea and hypopnoea commonly occurs in REM sleep.

Changes in respiratory effort and airflow are detected using a thoracic and abdominal belts, and nasal pressure cannulae, respectively. Interpretation is done in conjunction with pulse oximetry, measured at earlobes or fingers. This portion of PSG is central to making a diagnosis of OSAHS.

Other variables measured include body position, electrocardiograph, limb movements and snoring.