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All you need to know about … obstructive sleep apnoea

Obstructive sleep apnoea is a condition that tends to "creep up on you", as long-term snorers are often unaware that their snoring has deteriorated over the years. Marianne J Davey, Director of the British Snoring & Sleep Apnoea Association, explains …

Marianne J Davey
MSc
Director
British Snoring & Sleep Apnoea Association
Member of the Royal Society of Medicine, British Sleep Society and British Thoracic Society

Obstructive sleep apnoea (OSA) is a condition that belongs to a spectrum of breathing abnormalities known as "sleep disordered breathing" and is related to increased airway resistance (see Figure 1). It is characterised by loud heavy snoring and intermittent episodes of "not breathing" that disrupt normal sleep architecture, and is associated with excessive daytime sleepiness.

[[nip41_fig1_74]]

Clinical presentation
The simple definition for OSA is the cessation of airflow at the nose and mouth during sleep due to an obstruction of the upper airway. The clinical recognition of OSA is a cessation of breathing > 5/h and each apnoea event lasting > 10 seconds, with an accompanying dip in arterial blood oxygen saturation levels of > 4%. The clinical features of OSA can be divided into nocturnal and daytime symptoms (see Table 1).

[[nip41_table1_74]]

Who is at risk?
Most studies estimate the prevalence of OSA to be approximately 4% in middle-aged men and 1-2% in middle-aged women.(1-3) It is generally a consequence of being obese or overweight and is particularly associated with a large collar size. There are also anatomical features that can predispose an individual to OSA (see Figure 2), and from recent research we know that OSA can be hereditary.(2,4,5) Other factors such as cigarette, alcohol and sedative use tend to exacerbate the condition as they are thought to increase muscle relaxation and depress arousal response.

[[nip41_fig2_74]]
 
Getting a diagnosis
In addition to the signs and symptoms listed in Table 1, a number of other parameters should be considered:

  • Epworth Sleepiness Scale (see Figure 3).
  • Perspective of the bed partner.
  • BMI, waist and neck circumference (an abnormal waist circumference of around 102 cm (38 inches) or a hip/waist ratio of 0.95 for men of 0.8 for women would be likely to produce a positive result on a polysomnography).
  • History of other illnesses such as hypertension, heart disease, stroke and type 2 diabetes. The reasons snorers and individuals with OSA are more at risk of developing type 2 diabetes is due to obstruction of the upper airway. This leads to oxygen desaturation, which in turn leads to increases in catecholamines and cortisol levels that trigger the metabolic processes involved in insulin action and glucose regulation.
  • Current medications.
  • Examination of the upper airway to determine crowded airway or enlarged tonsils.
  • Examination of facial profile for conditions such as retrognathia (posterior positioning of the jaw) or micrognathia (small jaw).

[[nip41_fig3_76]]

Although a clinical assessment can often determine whether OSA is present, an overnight sleep study, known as polysomnography (PSG), can be undertaken. PSG measures a range of sleep parameters including: apnoea hypopnoea index (AHI)*; snoring sounds; oxygen saturation; body movements/position; eye movements (EOG); brain activity (EEG); heart rhythm (ECG); skeletal muscle activation (EMG); and breathing or respiratory flow during sleep.
It is not always possible to provide such a detailed investigation and in many cases it is not necessary. A more limited study may be offered whereby the patient will be provided with the equipment to use at home. Research has consistently confirmed that data from a "home" sleep study is equally efficient as a full PSG in diagnosing OSA.
*Hypopnoea is the reduction of airflow passing through the airways. The AHI is used to determine the severity of OSA.

The consequences of OSA
Patients with OSA generally have a reduced quality of life, but there is also a large body of evidence linking OSA with chronic diseases such as hypertension, cardiovascular disease, stroke and diabetes.(1-3,6-8)

Blood pressure
Although there is no definitive data to determine whether OSA causes cardiovascular disease, current literature suggests a strong association between OSA and hypertension, which may have cardiovascular consequences.(8) More than 50% of patients with OSA have systemic hypertension whereas only 25% of patients with hypertension have OSA. Controlling hypertension by conventional means has been found to be more difficult in patients with OSA than in hypertensive individuals without OSA.(8)

Heart disease
The incidence of heart disease is three times higher among patients with OSA than in the general population. The exact mechanisms of this relationship are still not fully understood, but we can offer some conceivable explanations:

  • The physiological responses to repetitive surges in blood pressure.
  • Oxidative stress.
  • Oxygen desaturations associated with acidosis.
  • Sympathetic nervous system overactivity.
  • High levels of catecholamines.

Stroke
There is a high incidence of OSA (90%) found in stroke patients, but does OSA cause stroke? Some studies have found both snoring and OSA to be risk factors.  Considering the cardiovascular effects of OSA there is every likelihood of this being the case.(8)

Diabetes
It is thought that the decrease in oxygen saturation caused by the apnoea increases catecholomine and cortisol levels, thereby increasing insulin resistance.6 However, there may be other confounding factors. We know that around two-thirds of OSA patients are overweight or obese, and studies have found that even adjusting for BMI, patients with OSA are five times more likely to develop diabetes than nonapnoeics.

Prevention is better than cure
Individuals should be aware that OSA is a preventable disease. In almost all cases many years of loud heavy snoring precedes OSA. This should be the warning signal for patients to address their snoring and lifestyle in order to avoid the debilitating effects of OSA. It should be known that treating simple snoring is much easier than treating OSA and the health implications surrounding the disease.
 
Treatment options
The "gold standard" treatment for OSA is continuous positive airway pressure (CPAP), which reduces both nocturnal and daytime symptoms and allows the patient to lead a "normal life". However, it is still not clear whether CPAP has a beneficial effect on the chronic diseases associated with OSA. For some, its intrusive nature and possible side-effects can impair compliance. The side-effects include rhinitis, conjunctivitis, sinusitis, skin abrasions and abdominal distention, and therefore CPAP is not ideal for all patients. Mandibular advancement device therapy (MAD) has been shown to be a successful treatment for OSA and is recommended as an alternative for those who refuse or are unable to tolerate CPAP as a primary treatment.(9,10) MAD therapy comprises an oral device that brings the lower jaw and tongue forward to increase the upper airway, provide upper airway muscle tone and reduce pharyngeal collapse. Over the last decade, there has been increasing evidence to support the use of these devices, with robust studies demonstrating their efficacy. MAD therapy is often a more attractive choice of treatment for individuals who suffer mild or moderate OSA as it easy to use, less bulky than CPAP and not dependent on electricity. Additionally, for some, using a MAD is perceived to be more socially acceptable than wearing a CPAP mask.

Conclusion
OSA is a common disorder that affects men more than women. It is typically a condition of obese and overweight individuals, with snoring and excessive daytime sleepiness being the most prevalent symptoms. CPAP is an effective therapy, but MAD therapy is also recommended for mild or moderate OSA.

References

  1. Dart RA, Gregoire JR, Gutterman DD, et al. The association of hypertension and secondary cardiovascular disease with sleep disordered breathing. Chest 2003;123:244-60.
  2. Leineweber C, Kecklund G, Janszky. Snoring and progression of coronary artery disease. Sleep 2004;27:1344-9.
  3. Stradling JR, Davies RJ. Sleep. 1: Obstructive sleep apnoea/hypopnoea syndrome: definitions, epidemiology, and natural history. Thorax 2004;59:73-8.
  4. British Snoring & Sleep Apnoea Association. Snoring is bad news ... for your health. Presentation at the British Sleep Society Annual Conference, 2007.
  5. Dahlqvist J, Dahlqvist A, Marklund M, et al. Physical findings in the upper airways related to obstructive sleep apnea in men and women. Acta Otolaryngol 2007;127:623-30.
  6. Al-Delaimy WK, MansonJE, Willett WC, et al. Snoring is a risk factor for type II diabetes mellitus: a prospective study. Am J Epidemiol 2002;155:387-93.
  7. Bananian S, Lehrman SG, Maguire GP. Cardiovascular consequences of sleep-related breathing disorders. Heart Dis 2002;4:296-305.
  8. Dincer HE, O'Neill W. Deleterious effects of sleep-disordered breathing on the heart and vascular system. Respiration 2006;73:124-30.
  9. National Institute for Health Clinical Excellence. CPAP for the treatment of OSA/hypopnoea syndrome. London: NICE; 2007. p. 1-25.
  10. Scottish Intercollegiate Guidelines Network. Management of OSA/hypopnoea syndrome in adults. Edinburgh: SIGN; 2003.