Treatment Of Sleep Apnoea And Snoring

The approach to treatment will vary according to severity of symptoms, severity of hypoxaemia during sleep and cost. In the absence of significant data showing a deleterious effect of asymptomatic sleep apnoea, treatment for prognosis alone is probably inappropriate. However, patient denial may produce an 'asymptomatic' patient, so if there is a highly positive diagnostic study in an 'asymptomatic' patient, it is advisable to check with relatives about any symptoms.

Weight Loss

A number of studies have demonstrated a reduction in sleep apnoea severity after weight loss, either through caloric restriction or bariatric surgery. However, it is important to reassess patients after weight loss and ensure there is little residual disordered breathing. Most published reports indicate that, although there is a reduction in apnoea index, a significant degree of apnoea persists, which in most cases warrants further treatment (86-88). Weight loss associated with apparently successful bariatric surgery may have limited efficacy in reducing sleep apnoea as many patients also have maxi-llo-facial abnormalities predisposing them to OSA (80). Recent data from the SOS Study show a marked reduction in sleep apnoea symptomatology in obese subjects 2 years after surgically induced weight loss compared with controls.

Lifestyle Factors

Some studies have suggested that reduction of smoking and alcohol consumption will lead to reduced self-reported snoring and reverse mild sleep apnoea (89). Sleep deprivation may reduce upper airway tone and chemosensitivity and should be avoided. Drugs such as benzodiazepines or opiates should be avoided at bedtime, particularly in patients with severe OSA or OHS.

Devices

Positive Airway Pressure

Until the early 1980s, tracheostomy was the only form of treatment available for sleep apnoea and was usually performed on patients with severe symptomatic disease. The advent of nasal CPAP revolutionized the management of OSA and allowed a wider range of patients to be treated (90,91). A CPAP machine delivers varying pressure to the upper airway through a nose or face mask, providing a 'pneumatic' splint which prevents upper airway closure. CPAP treatment leads to normalization of sleep architecture, decreased upper airway oedema and a reduction in daytime sleepiness (91,92). CPAP improves cognitive function and quality of life, as well as the associated symptoms listed in Table 27.1 for patients with all degrees of severity of OSA (93). CPAP is not a cure for sleep apnoea. Cessation of treatment will lead to a recurrence of sleep-disordered breathing and accompanying symptoms.

Nasal CPAP is an effective treatment, but compliance is variable (94,95), ranging between 40 and 80%. Problems affecting compliance with nasal CPAP include a sense of claustrophobia, mask air leaks, nasal congestion and dryness of the mouth and throat (usually associated with mask or mouth air leaks), and the inconvenience of using a machine. Patients with mild disease or those requiring high pressures are most likely to be non-compliant. Obese patients generally require higher CPAP pressures (96).

Devices that allow variation between the set inspiratory and expiratory pressures, known as bilevel positive airway pressure were originally introduced to improve compliance in CPAP users (97). Although not proven to improve compliance, this form of positive airway pressure therapy has been used increasingly in the management of severe respiratory failure and hypoventilation during sleep, such as OHS.

Mandibular Advancement Splints

The use of an orthodontic device designed to advance the mandible and thus increase the upper airway aperture has produced a major reduction in sleep apnoea severity in several studies (98) and is the subject of a large randomized clinical trial at present in Canada (A. Lowe, personal communication). The efficacy of these devices is likely to be reduced in the obese patient, as skeletal factors are less important in the genesis of upper airway obstruction. In general, these devices are less effective in patients with severe OSA (99). Data on compliance and the prevalence of side effects related to the temporomandibular joint are needed.

Surgery

Tracheostomy

Prior to the introduction of nasal CPAP as a treatment for OSA, tracheostomy was the major therapeutic modality. Tracheostomy is only currently indicated in patients with severe OSA who have been unable to comply with CPAP or related therapies. Tracheostomy can produce significant morbidity, particularly in the obese fat-necked individual and will be only partly effective in treating OHS. However with skilful minimalist surgery and close follow-up, tracheostomy may be a 'last-resort' therapeutic option in some patients.

Uvulopalatopharyngoplasty (UPPP) and Other Upper Airway Surgery

This operation was developed for the treatment of heavy snoring in the early 1950s and involves careful removal of the uvula and part of the soft palate. The introduction of UPPP for the treatment of OSA into North America occurred in 1981 (100) but despite early enthusiasm the operation has never lived up to its promise as a 'cure' for sleep apnoea (101). There are no preoperative tests that satisfactorily predict the response to surgery. There is a significant morbidity and even mortality (101). Excessive removal of palatal tissue will lead to velopharyngeal incompetence and nasal regurgitation and speech changes. Many studies report particularly poor results in obese patients. More recently UPPP has been performed with a surgical laser or high-frequency radio-waves ('somnop-lasty'), aiming at stiffening palatal tissue rather than complete removal. Meaningful outcome data are lacking and, as in conventional UPPP, subjective reports of snoring improvement are not supported by objective benefit. There is clearly a 'placebo' effect in snoring surgery that has been demonstrated in other forms of surgical intervention, such as simple sternotomy for severe angina.

More complex maxillo-facial surgery, usually involving UPPP in combination with genioglossus advancement via a mandibular osteotomy and hy-oid myotomy, has been used with some success in the treatment of OSA. However, this surgery is less effective in patients with severe disease ( > 60 events per hour and desaturation to 70%) and in the morbidly obese (102).

Figure 27.3 Efficacy of nasal ventilation in a patient with OHS. (a) Recordings of oxygen saturation show marked falls in oxygen level during sleep. (b) Addition of CPAP and low-flow oxygen results in normal oxygen saturation in NREM sleep but persisting hypoxaemia in REM sleep. (c) Use of nasal ventilation, either pressure support or volume cycled, will prevent oxygen desaturation and rises in CO2 levels (Tc CO2, transcutaneous CO2) in REM sleep.

Figure 27.3 Efficacy of nasal ventilation in a patient with OHS. (a) Recordings of oxygen saturation show marked falls in oxygen level during sleep. (b) Addition of CPAP and low-flow oxygen results in normal oxygen saturation in NREM sleep but persisting hypoxaemia in REM sleep. (c) Use of nasal ventilation, either pressure support or volume cycled, will prevent oxygen desaturation and rises in CO2 levels (Tc CO2, transcutaneous CO2) in REM sleep.

Management of Sleep Apnoea with Awake Respiratory Failure Including OHS

Many centres prefer to manage these patients in hospital, even for brief periods. While most patients starting CPAP require only one night of sleep monitoring to adequately determine required pressure, patients with sleep apnoea and awake respiratory failure require more detailed assessment. In these patients, oxygen alone should be used with caution and with close monitoring of hypercapnia. This is one group in whom sedation or use of hypnotics is contraindicated. Until recently, high CPAP pressures or CPAP plus added oxygen were needed in the first weeks of treatment until blood gases improved (91,103) or, for the obtunded hyper-capnic patient, a short period of intubation and ventilation may have been required. Currently, the bi-level positive airway pressure systems can deliver effective non-invasive pressure support ventilation to these patients and successfully treat hypercapnic respiratory failure (Figure 27.3). Home use of these devices is then prescribed with or without oxygen, depending on the degree of intrinsic lung disease.

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