Snoring and Obstructive Sleep Apnoea

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What is snoring?

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Sleep related breathing disorders demonstrate, to varying degrees, the collapsibility of the pharyngeal airway, which characteristically occurs at the onset of sleep (Remmers et al., 1978). In patients with simple palatal snoring the problem is one of basic snoring, with no episodes of obstruction of the upper airway. The noise comes from vibration of the soft palate, velopharyngeal sphincter and upper oropharynx.

Prevalence of non-apnoeic snoring

Non-apnoeic snoring has been reported as being widely under-diagnosed in the United Kingdom (UK) adult population (Ohayon et al., 1997). It has been estimated to affect up to 45 per cent of the adult population (Rice and Perskey, 1986). However snoring also has profound effects on those in proximity to a snorer.

what are the symptoms

Snoring symptoms

In cases of simple palatal snoring the symptoms are most obvious to the partner of the sufferer. Whereas with OSA the snoring is itself a symptom of an apnoeic patient, for a non-apnoeic sufferer the symptoms are the audible snoring caused by vibration of the soft palate, velopharyngeal sphincter and upper oropharynx.

However non-apnoeic sufferers may also present with headaches during the night or in the morning, and may wake themselves and their partner causing problems associated to broken sleep. In addition sufferers may experience tenderness of the soft tissue of the upper airway.

A patient may present with what to them is a simple snoring problem that on further examination is a symptom of OSA.

consequences of snoring

Snoring has been estimated to affect up to 45 per cent of the adult population (Rice and Perskey, 1986). However snoring also has profound effects on those in proximity to a snorer.

Research by the British Snoring and Sleep Apnoea Association has shown that 80% of couples affected by snoring sleep in separate rooms. The psychological effects of snoring and resulting tension in relationships can put strain on partner relationships.

In addition the partner of a persistent snorer may not be able to experience a restful night's sleep resulting in them suffering some of the effects of sleep deprivation.

Daytime sleepiness

Excessive daytime sleepiness (EDS) in SBD can result from hypoxia and a poor quality of sleep due to multiple arousals, that terminate most of the respiratory events, leading to sleep fragmentation (Sink et al., 1986; Colt, 1991). The aetiology of EDS remains controversial, however Colt (1991) using a prospective randomised crossover study provided the strongest evidence relating EDS to sleep fragmentation rather than hypoxia. EDS can result in the sufferer falling asleep at unexpected and inappropriate moments. In extreme cases, this can be while talking or eating, with the subject managing to stay alert only if moving or being constantly stimulated. Adverse effects of EDS also include reduction in overall performance, inability to concentrate, poor memory and temporal disorientation (Kaplan, 1992; Jennum and Sjol, 1994). This can have a profound effect on the safety of both the individual and others if, for example they operate machinery or drive vehicles for an occupation. Research demonstrates that drivers suffering from pathological sleepiness were up to seven times more likely to be implicated in an accident than unaffected individuals (Haraldsson et al., 1990) and perform poorly under simulated driving conditions (Juniper et al., 2000). Sufferers may therefore find themselves unemployed, either because they feel unable to cope with their work or because they are required to give it up in case they become a danger to others.

Daytime sleepiness

The possibility exists that the snoring is a symptom of underlying OSA with the associated additional health risks.

snoring treatments

 

Mandibular Advancement Splints (generic name).

Mandibular Advancement Splints (MAS) are customised devices made for each patient to be worn at night time.

The Sleepwell â„¢ MAS is clinically proven to work and offers maximum comfort, retention and full patient adjustability.

Losing weight

Loss of weight can reduce or alleviate snoring and there are numerous other health benefits but it should be gradual.

Surgery

There are a number of surgical options but they are not always successful and are usually extremely painful.

 

Intra-oral appliances


Mandibular advancement splints (MAS)

The MAS is by far the most common form of intra-oral appliance used in the management of SBD (Schmidt-Nowara et al., 1995; Johal and Battagel, 2001). There is considerable variation in the design of MAS, but all posture the mandible forwards, to a varying extent, with a degree of vertical opening. Sleepwell â„¢ is the most clinically proven and effective.

Elimination of aggravating factors

Regardless of the severity of the SBD, it is prudent to eliminate co-existent conditions that either predispose to or worsen upper airway dysfunction during sleep. Subjects should therefore abstain from alcohol and caffeine during the evening, avoid the use of central nervous system depressants and ensure adequate control of any co-existing chronic obstructive airway disease, asthma or hypothyroidism. Furthermore, in subjects with a BMI above 25, research has demonstrated a weak correlation between the amount of weight loss and the clinical response (Smith et al., 1985; Kuna and Sant Ambrogio, 1991). A Cochrane review of lifestyle modifications for subjects with OSA could not identify any randomised controlled trials to support their use and concluded that there was no strong evidence to prevent instituting therapies of proven effectiveness, such as N-CPAP (Shneerson and Wright, 2002).

Changing sleeping posture

Research has demonstrated that, in a proportion of subjects, the frequency of SBD is substantially greater during sleep in the supine position compared with the lateral recumbent position (Cartwright, 1984). That author proposed that the effect of gravity on the tongue and enlarged soft palate collectively could lead to upper airway occlusion. Methods used to help subjects to sleep in the lateral recumbent position include the use of a tennis ball sewn into the back of their sleeping garment and positional alarms. In subjects whose symptoms are enhanced in the supine position, such treatment modalities have been demonstrated to reduce the AHI by 50 per cent (Cartwright et al., 1991).

Removal of nasal obstruction and nasal dilating devices

The presence of any nasal obstructions (see section 2.6.2) will lead to an increase in nasal airway resistance, which in turn will further promote collapse of the upper airway during inspiration. Despite the unpredictable direct effects of relieving nasal obstruction on SBD (Elsherif and Hussein, 1998), some authors suggest the removal of any obstructions as first line care in facilitating other treatment regimes (Kuna and Sant Ambrogio, 1991). The use of external nasal dilating devices to reduce nasal resistance has been shown to have beneficial effects in reducing the severity of snoring (Hoffstein et al., 1993; Ulfberg and Fenton, 1997).

In addition a range of surgical procedures address snoring however success varies. Short term results using surgical procedures have shown limited success, the long term results show that the snoring can return. Procedures include Tracheostomy, Nasal surgery, Pharyngeal surgery, Maxillo-facial surgery and Tongue base resection. In summary Uvulopalatopharyngoplasty (UPPP) is proven to be 50-90% successful for snoring but problems with the procedure include, pain, nasal regurgitation, swallowing problems and speech disturbances. Laser assisted uvulopalsty (LAUP) is 55-90% successful for snoring with similarly difficult side effect for the patient

What is Obstructive sleep apnea (OSA)

Sleep apnoea is defined as a cessation of airflow at the nose and mouth lasting at least 10 seconds, due to abnormal respiratory events. These abnormal respiratory events may take two forms: apnoeas and hypopnoeas. There are three distinct forms of sleep apnoea (Brown, 1994): central, defined by the absence of respiratory effort; obstructive, defined as continued respiratory effort against an occluded upper airway and mixed, which begins with a period of central apnoea and concludes with one or more obstructed breaths.

Hypopnoea has been defined as a reduction in tidal volume of greater than 50 per cent measured by a validated means, or a reduction in flow of 30-50 per cent associated with either an arousal or a desaturation of 3 per cent or greater, lasting more than 10 seconds.

The AHI, represents the number of apnoeas and hypopnoeas occurring per hour of sleep and thus gives an indication of the severity of OSA. The American Academy of Sleep Medicine Task Force (1999) defined mild OSA as an AHI of 5-15 events per hour, moderate OSA as an AHI of 16-30 events per hour and severe OSA as an AHI greater than 30 events per hour. It should be noted that any cut off in AHI score attempting to stratify the severity of OSA is arbitrary, as the severity can vary from night-to-night and symptoms from day-to-day in any individual. However, such stratification can be used when considering treatment strategies. The original definition of OSA by Guilleminault (1982), was the occurrence of five or more abnormal respiratory events per hour of sleep. However, there appears to be no universally accepted defining point for starting treatment for OSA subjects, with reported ranges from 5 to 20 (Guilleminault, 1982; Riley et al., 1983). Stradling (2001), proposed that rather than define a threshold for normality it would be better to accept that there is a spectrum of upper airway narrowing during sleep and the presence of snoring, hypopnoeas and apnoeas are arbitrary points along this spectrum. The adoption of this symptom-based approach to care avoids much of the ambiguity and encompasses less defined conditions, such as upper airways resistance syndrome.

Sleep related breathing disorders demonstrate, to varying degrees, the collapsibility of the pharyngeal airway, which characteristically occurs at the onset of sleep (Remmers et al., 1978). In OSA, despite the continued respiratory effort, the more severe degree of collapse and obstructed pharyngeal airway prevents effective ventilation, resulting in either apnoea or hypopnoea. In turn, hypoxia and hypercapnia quickly develop, necessitating arousal to re-establish airway patency and normal ventilation (White, 1995). The site of the obstruction is at the level of the velopharynx (behind the uvula and soft palate), oropharynx (behind the tongue), hypopharynx (behind the epiglottis and base of tongue) or some combination of the above (Pringle and Croft, 1993; Ryan.

 

Symptoms of Sleep Apnea

Snoring

Snoring occurs in virtually all OSA subjects and characteristically is loud (> 44 dB) and intermittent, graphically illustrating the fact that noise is created principally between apnoeas, when large tidal volumes are drawn through an airway that has just achieved patency (Brown, 1994).

Choking

Some patients awake with the feeling of choking or gagging. This is due to the increasing level of airway obstruction they are experiencing during the apnoeic cycle.

Abnormal motor activity

Subjects with OSA are experiencing asphyxiation during sleep due to upper airway obstruction and their sleeping behaviour reflects this. They may complain of restlessness, which may be manifest by increased tossing and involuntary movements during sleep.

Nocturia

The proposed mechanisms for this include: increased intra-abdominal pressure associated with the respiratory efforts against a closed upper airway; an alteration in the various humoral agents induced by hypoxaemia and more controversially, raised levels of atrial natriuretic factor (Roux et al., 2000).

Daytime sleepiness

Excessive daytime sleepiness (EDS) in SBD can result from hypoxia and a poor quality of sleep due to multiple arousals, that terminate most of the respiratory events, leading to sleep fragmentation (Sink et al., 1986; Colt, 1991). The aetiology of EDS remains controversial, however Colt (1991) using a prospective randomised crossover study provided the strongest evidence relating EDS to sleep fragmentation rather than hypoxia. EDS can result in the sufferer falling asleep at unexpected and inappropriate moments. In extreme cases, this can be while talking or eating, with the subject managing to stay alert only if moving or being constantly stimulated. Adverse effects of EDS also include reduction in overall performance, inability to concentrate, poor memory and temporal disorientation (Kaplan, 1992; Jennum and Sjol, 1994). This can have a profound effect on the safety of both the individual and others if, for example they operate machinery or drive vehicles for an occupation. Research demonstrates that drivers suffering from pathological sleepiness were up to seven times more likely to be implicated in an accident than unaffected individuals (Haraldsson et al., 1990) and perform poorly under simulated driving conditions (Juniper et al., 2000). Sufferers may therefore find themselves unemployed, either because they feel unable to cope with their work or because they are required to give it up in case they become a danger to others.

Depression and psychological dysfunction

There is increasing recognition of a link between OSA and depression. Sleep changes, most notably disturbances of REM sleep, are intrinsic to depressive disorders (Kaplan, 1992). Relief of mild to moderate sleep- and breathing-related disorders in children is associated with improved behaviour and psychological functioning (Ali et al., 1994).

Sexual problems

Abatement of sexual drive or impotence have been reported in patients with OSA (Karacan and Karatas, 1995). However, this may be a reflection of the age of the cohort rather than SBD (Schiavi et al., 1991).

Headaches

Morning headaches and headaches that are so severe they awaken the sufferer during the night are often reported in people with OSA. The former have been reported to be three times more common in subjects with SBD, than in the general population (Ulfberg et al., 1996). They are thought to be vascular in origin but their precise mechanism remains disputed.

Consequences of Obstructive Sleep Apnea

In contrast with the normal physiologic effect of sleep on the cardiovascular system, the acute haemodynamic consequences of OSA include: systemic and pulmonary hypertension; bradycardia at the onset of apnoea and tachycardia at the resumption of ventilation; decreased cardiac output and increased left ventricular after-load. These changes are primarily the result of sympathetic stimulation, alterations in intrathoracic pressure, hypoxia and hypercapnia (Roux et al., 2000). Thus, patients with SBD are thought to be 'at risk' of a range of severe medical complications. Although the review undertaken by Wright et al. (1997) on the health effects of OSA dismissed the relationship between SBD and cardiovascular disease, citing the lack of controlled prospective studies and the major difficulty in adjusting for confounding factors such as obesity, hypertension, diabetes mellitus, smoking and ageing. A prospective longitudinal randomised placebo-controlled study design could be regarded as being unethical for withholding quality of life improvement, resulting from reduced hypersomnolence, but in addition randomization of OSA subjects to a placebo treatment could potentially increase their risk of cardiovascular morbidity. Several recent epidemiologic studies (Lindberg et al., 1988; Grote et al., 1999; Lavie et al., 2000) and trials (Worsnop et al., 1998; Davies et al., 2000) have demonstrated an association between SBD and cardiovascular disease.

Hypertension

During an apnoeic event OSA patients show an increase in blood pressure, which then returns to normal levels as the obstruction clears. The resulting hypoxia and sympathetic discharge leads to peripheral vasoconstriction, bradycardia and decrease in cardiac output (Brown, 1994). Millman et al. (1991) concluded that the high prevalence of hypertension in OSA subjects was primarily related to age and obesity. Davies et al. (2000), however, in comparing OSA subjects with closely matched controls, found diastolic blood pressure to be increased during both the day and night together with an increase in nocturnal systolic pressure. The evidence supporting a possible cause and effect relationship between OSA and hypertension comes primarily from intervention studies, which have reported reductions in blood pressure following treatment (Faccenda et al., 2001; Pepperell et al., 2002). If OSA is a causative factor in hypertension, the proposed mechanism is the repeated hypoxia or arousals during sleep leading to increased sympathetic activity during both the awake and sleeping states (Brown, 1994). The findings of a prospective longitudinal population based study, suggested that snoring and upper airways resistance syndrome may be associated with an increased risk of cardiovascular disease (Lindberg et al., 1988).

Coronary heart disease

Andreas et al. (1996) reported a higher incidence of OSA amongst subjects suffering from coronary heart disease, with OSA being implicated as a risk factor in accelerating atherosclerosis of the coronary vessels. Confirmation of this theory has been provided by Peker et al. (1999), who found an independent association between OSA and coronary artery disease, once the results had been adjusted for the presence of other variables including age, obesity, hypertension, smoking and diabetes mellitus. This study may be criticized for its case-control design and a true population based prospective design may have been preferable.

Heart failure

Inspiration against a closed upper airway in OSA subjects generates a significant negative intra-thoracic pressure leading to a decrease in right atrial pressure and an increase in venous return to the right ventricle. This in turn can lead to isolated right ventricular hypertrophy and heart failure (Sanner et al., 1997).

Cerebrovascular disease

It is reported that approximately one-third of strokes take place during sleep, with snoring being identified as a potential risk factor (Palomaki et al., 1989). Marler et al. (1989), reported SBD as being associated with a three-fold increase in the risk of stroke. However, from these studies it is not clear whether SBD were an independent risk factor for stroke or if the increased stroke risk was due to the associated hypertension. SBD affect cerebral haemodynamics, with an estimated 50 per cent reduction in cerebral blood flow, related to the duration of apnoea, hypopnoea and consequent degree of oxygen desaturation (Roux et al., 2000).

Sudden death

This may be the result of a myocardial infarction or a cerebrovascular accident, as outlined above. Alternatively, sufferers of SBD are at risk of falling asleep whilst driving with lethal consequences (Haraldsson et al., 1990).

Thus, early diagnosis of SBD and, in particular, OSA with the instigation of suitable therapy not only offers symptomatic improvement but also improves long-term health prospects.

Obstructive Sleap Apnea treatments

The treatment options for OSA can be split depending on the severity. For severe OSA Continuous Positive Airway Pressure (CPAP) is the clear gold standard treatment, with the highest clinical success. MAS therapy tends to be the treatment of choice for mild to moderate Obstructive Sleep Apnoea as it very effective, less expensive and more patient friendly compared to CPAP.

Sleepwell ™ can be offered in conbination with CPAP as it holds the lower jaw forward thereby opening the airway hence reducing the air pressure required. Patients who have a low CPAP compliance threshold should be considered for Sleepwell ™.

There are two well established clinically proven treatment options :-

 

Mandibular Advancement Splints (generic name)

Mandibular Advancement Splints (MAS) are customised devices made for each patient to be worn at night time.

The Sleepwell â„¢ MAS is clinically proven to work and offers maximum comfort, retention and full patient adjustability.

Continuous Positive Airway Pressure – CPAP

CPAP is the gold standard for sufferers of severe Obstructive Sleep Apnoea, CPAP is not recommended for the treatment of simple snoring.

 

Intra-oral appliances

 

Mandibular advancement splints (MAS)

The MAS is by far the most common form of intra-oral appliance used in the management of SBD (Schmidt-Nowara et al., 1995; Johal and Battagel, 2001). There is considerable variation in the design of MAS, but all posture the mandible forwards, to a varying extent, with a degree of vertical opening. Sleepwell â„¢ is the most clinically proven and effective.

Nasal continuous positive airway pressure (N-CPAP)

N-CPAP is regarded as the major non-surgical, long-term treatment; the so-called 'gold standard'. Described by Sullivan et al. (1981), N-CPAP delivers a continuous stream of filtered air under low pressure (5 to 15cm H2O) through a nasal mask to the pharynx. N-CPAP acts as a pneumatic splint, by raising the intra-luminal pressure in the upper airways, preventing them from collapsing regardless of the subjectÍs position, but not enough to prevent expiration. All subjects undergo full polysomnographic studies in order for N-CPAP titration to be performed, to ensure that the pressure used is sufficient for maintaining airway patency and preventing apnoea in all sleep stages and postures. Most patients require lifelong treatment and to be reliably effective, N-CPAP should be used for 4 to 6 hours per night, 7 days a week (Engleman et al., 1998). The reported benefits of N-CPAP are: improved quality of life (Sanner et al., 2000); improved daytime cognitive function (Borak et al., 1996); elimination of snoring, and other night-time symptoms and reversal of daytime symptoms, in particular, sleepiness (Kiely et al., 1999) and reduced risk of road traffic accidents (Hack et al., 2000); long-term improvement in survival rates near to those of the general population (Chaouat et al., 1999). In addition, many of the beneficial effects have been shown to continue over the longer-term (Jenkinson et al., 2001). N-CPAP is the treatment for OSA with the firmest evidence base (Wright et al., 2002). However, randomised controlled trials of treatment for mild OSA do not support reduced objective sleepiness after N-CPAP and thus this should be reserved as a first line choice of therapy for those with moderate or severe OSA (Jenkinson et al., 1999; Barbe et al., 2001).

However, the use of N-CPAP is not without its problems: long-term compliance has been estimated at between 60 to 95 per cent, with intensive efforts (Engleman et al., 1998; McCardle et al., 1999); problems are often encountered with the nasal mask (Pepin et al., 1995); the face mask is considered anti-social and the machine noisy (Engleman et al., 1998). In an attempt to overcome some of the problems with N-CPAP, auto-titrating devices have been developed which raise pressure if they detect upper airway narrowing or obstruction and, conversely, lower pressure if the airway is not obstructed (Lloberes et al., 1996). However, they are more expensive than conventional N-CPAP machines and, as yet, there is no convincing evidence that they produce better outcomes in managing OSA over the long-term.

Elimination of aggravating factors

Regardless of the severity of the SBD, it is prudent to eliminate co-existent conditions that either predispose to or worsen upper airway dysfunction during sleep (see section 2.3.3). Subjects should therefore abstain from alcohol and caffeine during the evening, avoid the use of central nervous system depressants and ensure adequate control of any co-existing chronic obstructive airway disease, asthma or hypothyroidism. Furthermore, in subjects with a BMI above 25, research has demonstrated a weak correlation between the amount of weight loss and the clinical response (Smith et al., 1985; Kuna and SantÍAmbrogio, 1991). A Cochrane review of lifestyle modifications for subjects with OSA could not identify any randomised controlled trials to support their use and concluded that there was no strong evidence to prevent instituting therapies of proven effectiveness, such as N-CPAP (Shneerson and Wright, 2002).

Changing sleeping posture

Research has demonstrated that, in a proportion of subjects, the frequency of SBD is substantially greater during sleep in the supine position compared with the lateral recumbent position (Cartwright, 1984). That author proposed that the effect of gravity on the tongue and enlarged soft palate collectively could lead to upper airway occlusion. Methods used to help subjects to sleep in the lateral recumbent position include the use of a tennis ball sewn into the back of their sleeping garment and positional alarms. In subjects whose symptoms are enhanced in the supine position, such treatment modalities have been demonstrated to reduce the AHI by 50 per cent (Cartwright et al., 1991).

Removal of nasal obstruction and nasal dilating devices

The presence of any nasal obstructions (see section 2.6.2) will lead to an increase in nasal airway resistance, which in turn will further promote collapse of the upper airway during inspiration. Despite the unpredictable direct effects of relieving nasal obstruction on SBD (Elsherif and Hussein, 1998), some authors suggest the removal of any obstructions as first line care in facilitating other treatment regimes (Kuna and SantÍAmbrogio, 1991). The use of external nasal dilating devices to reduce nasal resistance has been shown to have beneficial effects in reducing the severity of snoring (Hoffstein et al., 1993; Ulfberg and Fenton, 1997).

Pharmacological therapy

The limited data available suggests that protriptyline (a non-sedating tricyclic anti-depressant) may be associated with a reduction in apnoeic episodes and daytime sleepiness (Clark et al., 1979; Bronwell et al., 1982). This may occur as a result of its REM-sleep suppressant effect or augmentation of upper airway muscle tone. However, the trials carried out have involved only a small number of subjects and the drug's anti-cholinergic effects are also limiting as they may exacerbate any cardiac problem. Smith et al. (2002), in their Cochrane review, concluded that no medication demonstrated a consistent response. Thus, the evidence base to date does not support the use of pharmacological therapy as effective first line therapy for OSA. More recently, however Modafinil, a wake provoking agent, has been shown to be an effective and well tolerated adjunctive therapy for the treatment of residual daytime sleepiness in OSA subjects whose apnoea is controlled by to N-CPAP (Kingshott et al., 2001; Schwartz et al., 2003).

In addition a range of surgical procedures address snoring however success varies. Short term results using surgical procedures have shown limited success, the long term results show that the snoring can return. Procedures include Tracheostomy, Nasal surgery, Pharyngeal surgery, Maxillo-facial surgery and Tongue base resection. In summary Uvulopalatopharyngoplasty (UPPP) is proven to be 50-90% successful for snoring but problems with the procedure include, pain, nasal regurgitation, swallowing problems and speech disturbances. Laser assisted uvulopalsty (LAUP) is 55-90% successful for snoring with similarly difficult side effect for the patient.

This topic is courtesy of www.s4sdental.com.