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Obstructive Sleep Apnoea

Even though obstructive sleep apnoea (OSA) is fairly common, it often remains undiagnosed in primary care. Because the disorder is associated with significant morbidity, family physicians, rural health physicians and general practioners need to be familiar with its clinical presentation and diagnosis.

Not until the 19th. Century, were theories on sleep based upon experimental findings in animals and humans. The introduction of the EEG in animals by Caton and in humans by Berger1, allowed the measurement of sleep depth without waking the sleeper for the first time. After discovery of the rapid eye movement (REM) sleep periods by Aserinsky and Kleitman1 in 1953 and the demonstration of sleep cycles by Dement and Kleitman1, polysomnography with simultaneous whole night recording of EEG, EMG, EOG and other physiological parameters was established as a major diagnostic tool.

The challenge to the clinician is to suspect the diagnosis when evaluating an awake patient. A carefully taken history can arouse appropriate suspicion. OSA is then diagnosed with the use of polysomnography by documenting repititive periods of upper airway closure during sleep.

Obstructive sleep apnoea is a condition characterized by repeated respiratory pauses due to the pharynx wall collapse, with subsequent obstruction to air flow2. Poper assessment of the upper airway for possible site(s) of obstruction is an important complemntary part of the management.

History: How important it is.

The spectrum of clinical presentations of obstructive sleep apnoea syndrome (OSAS) and their severity is variable ranging from neuro-cognitive complaints to serious cardio-respiratory consequences. OSAS has a significant impact on the quality of life (socially disturbing snoring, daytime somnolence with its sequelae (poor work performance, car accidents, disrupted social interactions). Clinical impression alone, however, has poor (50% to 60%) sensitivity and specificity (63% to 70%) 3, yet it might be able to suggest the presence or absence of OSA 4.

Snoring is said to be a disease of “listeners”, thus one of the social problems associated with snoring is the suffering of the bed partner and accompanied marital displeasure5. Moreover, snorers even with other symptoms may be passive in seeking help for their symptoms or may underestimate the severity of symptoms6. Therefore, it is advisable that the spouse or bed partner should attend the interview and participate in history taking.

Snoring is characterized by high frequency oscillations of the soft palate, pharyngeal walls, epiglottis and tongue. The pattern of snoring is different in OSA and non-apnoeic snorers 7. How well the subjective complaint of the listener is confirmed by objective measurement of snoring remains an area of controversy 8. In a recent study, Wilson et al9, analyzed snoring sound intensity of 1139 individuals undergoing polysomnography and examined the relationships between acoustic, polysomnographic and clinical variables. They concluded that there exists a very significant difference in sound intensity between apnoeic snorers and non-apnoeic snorers, however they were unable to show a significant independent relationship between the intensity of snoring sounds and a clinical history of arterial hypertension. Future research is needed that incorporates the measurement of snoring intensity and frequency variables, which link these acoustic variables to polysomnographic variables.

Since snoring and OSA are two parts of the same basic disorder (sleep related narrowing of the upper airway) 10, the second question is why don't all heavy snorers have obstructive sleep apnoea? It is suggested that airway collapse during sleep is favoured by a narrow velopharynx associated with large hypopharynx. Some heavy snorers may not have an oropharyngeal collapse because the peak inspiratory suction pressure could already be damped down at the level of the relatively narrow hypopharyngeal airway 11.

Daytime sleepiness is a significant complaint of the patient with OSA. Frequently, the patient falls asleep during sedentary activities. As daytime sleepiness becomes more excessive, the patient may report falling asleep in embarrassing situations. The patient often has to nap during the day but typically wakes up unrefreshed 12.

The development and use of the Epworth Sleepiness Scale (ESS), was described by Johns, 1991 13. It is a simple, self-administered questionnaire, which is shown to provide a measurement of the subject's general level of daytime sleepiness. Answers rate the chances that patients would doze off or fall asleep when in eight different situations commonly encountered in daily life. Total ESS scores significantly distinguish normal subjects from patients in various diagnostic groups including OSA, narcolepsy and idiopathic hypersomnia. ESS scores were significantly correlated with sleep latency measured during the multiple sleep latency tests (MSLT) and during overnight polysomnography. In patients with OSA, ESS scores are significantly correlated with the respiratory disturbance index and minimum SaO2 recorded overnight, while ESS scores of patients who simply snore don't differ significantly from controls 13, 14.

Investigating the reliability and internal consistency of the ESS on normal individuals and OSA patients, Johns, 1992 15, concluded that the questionnaire had a high level of internal consistency and that it was a simple and reliable method for measuring persistent daytime sleepiness as well as evaluating treatment effect 16.

Differential diagnosis of daytime sleepiness includes central nervous system pathologic abnormalities (such as narcolepsy and idiopathic CNS hypersomnia) and qualitative or quantitative sleep deficiencies (OSA, insufficient nocturnal sleep, misalignments of the body's circadian pacemaker with the environment as in jet lag or shift work). Therefore diagnosis of daytime sleepiness requires objective assessment such as MSLT and polysomnography 17, 18.

Analyzing the relations among ESS score, mean sleep latencies on MSLT and subjective assessments of severity of sleepiness in patients with suspected excessive daytime sleepiness, Chervin et al, 1997,19 concluded that ESS scores are correlated negatively, but not strongly with MSLT scores and ESS score of 14 and above predicted low mean sleep latency on the MSLT. The ESS score correlated with the degree to which patients complained of sleepiness and may be useful as an otherwise elusive link between patients' complaints and their objective findings on MSLT.

The relationship between headaches and sleep disturbances is complex and difficult to analyze. Both symptoms may have causal relations, or may be associated in the same patient with mutual reinforcements20. In one study 21, it is estimated that 5% of the general population reported experiencing headache often or very often upon awakening. However, in patients with heavy snoring and OSA, 18% reported experiencing headache often or very often upon awakening. Morning headache associated with sleep disorders relates closely to altered muscle activity, altered breathing and fluctuation in oxygen saturation levels 22. Morning headache is not more common in OSA than in other sleep disorders, yet analyzing its frequency in the light of polysomnographic results suggests that it is a nonspecific symptom in patients with sleep disorders and it is not a reliable symptom of sleep apnoea syndrome 23,24. However over 30% of patients with chronic headache and other symptoms of sleep apnoea have significant improvement in headache after appropriate treatment23.

The most common sleep disturbance is either an adjustment reaction to life events or a physical illness. Sleep disturbances caused by behaviours incompatible with sleep require counseling, while sleep disturbances due to psychiatric conditions require treatment of the underlying illness 25. Both nocturnal hypoxaemia and impairment of daytime vigilance have been suggested as the pathogenesis of neuropsychological deficits associated with OSA, yet it remains difficult to find good correlations between cognitive deficits and either of these parameters. Relative to non-snorers and non-apnoeic individuals, moderate and severe OSA patients show differences in many cognitive functions, and the severely affected show the greater differences. Further analyses reveal that reductions in general intellectual measures, as well as in executive and psychomotor tasks are all attributable to the severity of hypoxaemia, while other attention and memory deficits are related to vigilance impairment. Therefore, both vigilance impairment and nocturnal hypoxaemia may differently contribute to the cognitive dysfunctions found in OSA 26.

Cognitive executive functions include attention, short-term memory spans, learning abilities, planning and programming capacities, categorizing activities and verbal fluency. OSA patients were found to have a significantly decreased ability to initiate new mental processes and to inhibit automatic ones, in conjunction with tendency\for preservative errors. They were also affected with deficits of verbal and visual learning abilities and had reduced memory spans. Such defects were further evaluated via logistic regression against two criteria of the severity of the disease: the number of apnoea and hypopnoea per hour of sleep and the level of nocturnal hypoxaemia. Memory deficits were rather related to the former, whereas typical frontal lobe related abnormalities seemed rather consistent with the latter. The findings are discussed in the light of data from the literature concerning cognitive impairments described for patients with isolated daytime sleepiness versus hypoxaemia as illustrated in other pathological or physiological circumstances 27.

In their study on 1054 males and females (between 30-60 years of age), Jennum and Sjol, 1994 28, concluded that cognitive complaints show a high correlation to mood, insomnia, and hypersomnia. Habitual snoring and sleep apnoea show a correlation to concentration, but no memory complaints. This suggests that part of the association between snoring, sleep apnoea and cognitive dysfunction is related to the presence of sleep disturbances and daytime sleepiness. Borak et al, 1993 29, investigated the question of these changes being reversible after successful interference to treat OSA. Their results suggested that after 3 months of CPAP treatment the severity OSA improved significantly. However the observed tendency for cognitive functions to improve was not statistically significant.

The statement “hypnotics should not be used in patients with sleep apnoea as sedatives generally decrease pharyngeal muscle tone and can exacerbate obstructive sleep apnoea” is agreed upon by many authors 1,4, 10,12,30. The use of sedatives, particularly non-benzodiazepine hypnotics is questioned in central sleep apnoea on the assumption that they improve sleep as well as decrease the central apnoea frequency 31. Alcohol intake has been shown to worsen obstructive sleep apnoea and increase nocturnal hypoxaemia32,33,34. Animal studies suggested that a reduction in chemo- reflex sensitivity might be implicated 35. De-Borne et al, 199734concluded that the combination of increased inspiratory resistance and greater inspiratory effort produced by alcohol intake at bedtime would increase the tendency of an unstable upper airway to collapse and could account for the aggravation of OSA by alcohol.

Upper airway obstruction during sleep may be due to anatomical or functional factors. Functional factors in obstruction during sleep include: a) respiratory instability, b) increased extensibility of the lax tissues surrounding the oropharynx and C) deficient contraction of the pharyngeal dilator muscles during inspiration. These effects are worsened by sleep deprivation and fragmentation10. Rosenthal et al, 1997 36, studied the sleep/wake habits and suggested that sleep habits have an important modulatory effect on the level of sleepiness and this effect is lost as the severity of sleep disordered breathing increases. Normal sleep is not just a state of decreased consciousness, and it should be understood that both REM and non-REM stages of sleep are as different from each other as from the waking state. In REM sleep, the brain is active (near to or similar to wake state), with dreaming activity, rapid eye movements, very low muscle tone and respiratory instability. Therefore, taking sleep history should include 37,38:

Adolescence with excessive sleepiness added to ancillary symptoms of sleep paralysis, cataplexy, hypnogogic hallucination and possible familial tendency.

A helpful parameter to objectively evaluate sleep pattern is the Sleep Efficiency Index 39, which is {Total sleep time/total sleep period} X 100.

7. Symptoms of nasal obstruction:

Evidence of the role of nasal obstruction in OSA has appeared in the literature as early as the late 1800s. In 1892, Carpenter noted the association between disturbed sleep and impairment of daytime intellectual performance and memory. He attributed this impairment to nasal obstruction. Wells in 1898, described OSA patients in whom daytime hypersomnolence was improved when their nasal obstruction was corrected 40. In general terms, oropharyngeal collapse occurs when the subatmospheric pharyngeal pressure generated during inspiration exceeds, by some critical amount, the stabilizing force generated by the upper airway dilator muscles 41. Of importance in the generation of a critical airway collapsing pressure in the airflow resistance upstream, particularly that of the nose42. The role of nasal factor remains controversial in the literature 42. Series et al, 1992, 1993 43,44, stated that pre and post- operative evaluation of patients after corrective nasal surgery did not reveal any significant improvement in sleep disturbances especially in cases with abnormal findings in cephalometric analysis. Kerr et al, 199245, concluded that sleep architecture, incidence of apnoea periods and blood oxygenation did not improve after successfully reducing nasal airflow resistance. However it remains a constant observation that individuals with nasal obstruction do snore when asleep. Since breathing through the nose appears to be the preferred route during sleep, nasal obstruction frequently leads to nocturnal mouth breathing, snoring, and ultimately to OSA 46.

Hoffstein, 1996 47, reviewed 19 studies examining the association between snoring and hypertension. It was clearly shown that in the majority of them (14 studies) snoring was not found to be an independent risk factor. An association between snoring and cardiovascular and cerebrovascular disease is somewhat more difficult to assess. Analysis of 15 studies dealing with this issue shows that 9 of them concluded that snoring is a risk factor for vascular disease, whereas 6 studies reached the opposite conclusion. However, his detailed review of the studies showed positive association between snoring and vascular disease indicates that in some of them unsuspected sleep apnoea may have accounted for this increased risk. In addition, these studies exhibit a number of inconsistencies that raise doubts as to the true validity of association between snoring and vascular disease. Finally, it does not seem biologically plausible that snoring should be a risk factor for cardiovascular and cerebrovascular disease without also being a risk factor for hypertension. Consequently, one cannot conclude that snoring is an independent risk factor for such adverse vascular complications as hypertension, cardiovascular and cerebrovascular disease.

OSA, on the other hand, is a multisystem disorder with pathologic sequelae that become apparent after a number of years. Patients with OSA, in addition to loud snoring, experience nocturnal oxygen desaturation and repetitive disruptions from sleep that extremely lead to daytime hypersomnolence. Numerous complex interactive pathophysiologic events occur during each obstructive episode, and it is important for the clinician to be aware of the cardiopulmonary and neurological manifestations associated with this condition. Alveolar ventilation during an apnoeic episode is immediately reduced to zero, and the metabolic demands for oxygen must be met by oxygen stores within the body. With repetitive episodes of obstruction, the oxygen stores within the lungs are diminished and the rate of arterial oxyhaemoglobin desaturation increases. During apnoeic episodes, the systemic blood pressure increases while heart rate and cardiac output decrease. Bradydysrhythmias have been noted with the obstructive apnoeic episodes, and ventricular dysrhythmias are associated with episodes of severe oxyhaemoglobin desaturation. Coexisting cardiopulmonary or neuromuscular disease in patients with OSA, contribute to the development of hypoventilation, serious gas exchange derangements, and general cardiovascular instability 48.

Comparing the general health status in 103 OSA patients, Formas et al, 199549, found no significant differences in the general health status and the degree of daytime sleepiness, but there were significant differences between OSA patients and control subjects. It was concluded that in spite of the fact that OSA patients showed a deterioration of general health status parameters in comparison with healthy subjects, these parameters do not correlate with the physiological disturbances of OSA expressed as the number of respiratory events per hour.

Kimoff et al, 199150reviewed all articles on OSA published in English and French languages between 1970 and 1990 and indexed in Index Medicus and concluded that OSA leads to various neuropsychological and cardiovascular complications.

Proper history taking should raise the suspicion index of OSA and perhaps more important, to guide general practitioners and rural health doctors to report and refer cases with high risk. It takes further steps of examining the upper airway to localize the possible site(s) of obstruction in addition to polysomnography, which is believed by many authors to be the corner stone to diagnose OSA.

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