|SNORING AND OBSTRUCTIVE SLEEP APNOEA
(CHILDREN AND ADULTS)
AIMS AND OBJECTIVES
Know the specific questions in the history that distinguishes simple snoring from Obstructive Sleep Apnoea
Be able to identify the risk factors for and complications of obstructive sleep apnoea
Understand the principles of investigation and treatment of patients who snore and who suffer with obstructive sleep apnoea
Snoring, noisy breathing during sleep, is caused by vibration of one or more areas of the upper airway. Such noisy breathing occurs in 45 per cent of the population from time to time and an estimated 25 per cent are habitual snorers1,2. Although, snoring is the cardinal symptom of obstructive sleep apnoea, the prevalence of obstructive sleep apnoea is notably lower at 0.5- 4%1,2.
SPECTRUM OF THE CONDITION
Snoring and Obstructive Sleep Apnoea form the opposite ends of a spectrum of disorders under the umbrella of Obstructive Sleep related breathing disorders (SRBD). Depending on the degree of obstruction and associated symptoms, individuals are categorised into one of the following categories.
Simple snoring is disruptive snoring without any impact on the patients sleep pattern or increased daytime sleepiness. As the severity of the obstruction increases, greater respiratory effort is required which leads to increased sleep disruption and resultant daytime sleepiness. Upper airways resistance syndrome (UARS) is categorised by the presence of these symptoms without evidence of obstructive apnoeas or de-saturations. It is characterised by increased respiratory effort identified by oesophageal pressure analysis. Further progression of airway obstruction leads to near total or total obstruction of airflow. Obstructive sleep apnoea hypopnoea syndrome (OSAHS) is categorised by the co-existence of excess daytime sleepiness with interrupted and repeated collapse of the upper airway during sleep, usually with associated de-saturations. This collapse can be complete with total cessation of airflow (apnoea) or partial with significant hypo-ventilation (hypopnoea).
Frequency of the apnoeas and hypopnoeas are used to assess the severity of OSAHS and is called the apnoea/hypopnoea index (AHI) or the respiratory disturbance index (RDI). OSAHS is categorised as mild (5-14 events per hour), moderate (15-30 events per hours) or severe if they are greater than 30 events per hour3. Although AHI is often used to assess the severity of OSAHS, clinically significant OSAHS is only likely to be present when the AHI is greater than 15 events per hour, in association with unexplained day time sleepiness or a minimum of 2 of the other features of the condition as identified in Table 13.
Table 1:- Symptoms associated with OSAHS
Excessive daytime sleepiness
Choking episodes during sleep
Snoring and obstructive apnoea only occur during sleep and not during wakefulness. In humans, the airway between the posterior end of the nose and the larynx is unprotected by cartilaginous or bony structures and reliant on muscle tone for its patency. With the onset of sleep, pharyngeal muscle tone falls progressively as sleep condenses to deeper levels. This phenomenon is present in all humans and yet not all humans snore or have OSAHS. Factors that have been found to increase the risk of SRBD are:
a) Age. There is a progressive increase in the prevalence of snoring and obstructive sleep apnoea up to the 6th and 7th decade of life independent of the Body mass index (BMI)1. The mechanism is unclear.
b) Sex. Population based studies have found that men have between a two and five fold increased risk of OSAHS compared with age and weight matched women2. The reasons for the sex difference are not clear. However, the prevalence of snoring and obstructive sleep apnoea in women increases post-menopause. Oestrogen plus progesterone replacement therapy in post menopausal women has shown to decrease OSAHS.
c) Obesity. The most important risk factor. The prevalence of respiratory events (RDI) has been shown to directly correlate with BMI. Seventy percent of individuals with BMI of 40 or greater suffer with OSAHS. Conversely, up to 50% of patients with OSAHS may have a BMI below 30. Central obesity indicators such as neck circumference index and waist hip ratio are better predictors of OSAHS than obesity or BMI in general.
d) Obstructive Upper airway anatomy. Craniofacial abnormalities are associated with a higher prevalence of SRBD. These include abnormalities such as retro or micrognathia, midfacial or mandibular hypoplasia and macroglossia. Adenotonsillar hypertrophy, though common in children as a cause of snoring and OSAHS, its role in adults is significantly less. Decreased nasal airway due to turbinate hypertrophy, septal deviations or nasal polyposis significantly increases upper airway resistance. These can contribute to snoring and UARS, but are unlikely to be the sole cause for OSAHS.
e) Social Habits. Social habits such as smoking and alcohol increase the risk of SRBD.
f) Other risk factors. The relative risk of OSAHS may be two- to fourfold greater in first degree relatives even after adjustment for BMI and craniofacial variations. Certain medical conditions such as Hypothyroidism and acromegaly are associated with OSAHS. Neuromuscular diseases also predispose to OSAHS though central apnoeas are more likely. Drugs associated with central depression such as hypnotics and opioids increase the risk of SRBD. Chronic lung disease does not pose a direct risk for SRBD. However, in both obstructive and restricted lung disease, OSAHS tends to be more severe with deeper events of oxygen de-saturation resultant from the hypo-ventilation and the lower lung reserve.
CONSEQUENCES OF SLEEP RELATED BREATHING DISORDERS
Although simple snoring has a significant social impact it has no detrimental impact on the individual’s health. Conversely, OSAHS is known to have significant cardiovascular consequences.
a) Neurocognitive effects. Excessive day time sleepiness (EDS) is the commonest complaint of patients with obstructive sleep apnoea. Cognitive performance is notably impaired with deterioration in memory, intellectual capacity and motor co-ordination4. There is evidence to suggest a 1.3 – 12 fold increase in accident rates amongst patients with OSAHS2,5. Sleepiness at the wheel is estimated to cause 20% of road traffic accidents on major highways, although it is unclear how many of these are due to OSAHS.
b) Cardiovascular consequences. There is compelling evidence that OSAHS is associated and contributes to systemic hypertension 6,7. This association is independent of confounding factors such as obesity, age, gender and alcohol consumption. Furthermore, treatment with continuous positive airway pressure (CPAP) reduces blood pressure by up to 5mmHg over 24 hours8. Over a 5-10 year period, reduction in blood pressure of this magnitude can decrease cardiac events by 20% and stroke risk by 40%. There is some data suggestive of an association between OSAHS and coronary artery disease and cerebrovascular events. The evidence is in-direct and yet equivocal.
c) Others. Patients with OSAHS have been known to have potential problems with impotence and increased likelihood of gastroeosophagal reflux.
The aims of the history, clinical examination and investigations are
1) Identify if the patient has OSAHS
2) Identify the potential causes and predisposing factors
3) Localise the level(s) of obstruction in the upper airway
a) Epworth sleepiness scale (ESS) is a validated method of identifying excessive daytime sleepiness. However, the correlation between ESS and OSAHS is relatively weak and it cannot be used as a screening tool for OSAHS 9. Physical examination of the upper airway is essential and usually performed by an ENT surgeon. However, there is poor correlation between clinical findings and predictability of OSAHS. A formal assessment of nasal airway and pharyngeal anatomy needs to be undertaken preferably with an endoscope (flexible or rigid). An assessment should be made of the oropharyngeal inlet including tonsil, tongue and mandibular size. The possibility of hyperthyroidism, acromegaly and Marfan’s syndrome should always be considered in patients presenting with snoring or OSAHS.
b) Sleep Studies are indicated in all patients presenting with snoring or suspected sleep apnoea. OSAHS should always be excluded in patients before considering surgery for snoring. OSAHS can be present in over 30% of snorers presenting without symptoms of overt sleepiness 10 and Uvulopalatopharyngoplasty may compromise future nasal CPAP therapy 11. Patients with COPD and snoring should have an urgent sleep study as the combination is potentially dangerous. All patients who drive long distances, heavy goods vehicles or handle hazardous machinery as part of their profession must have a sleep study as part of their assessment. There are many levels of sleep studies depending on the local circumstances.
i) Polysomnography (PSG) is considered the gold standard for diagnosis of OSAHS. The assessment entails an in-patient study involving overnight assessment of variable number of parameters including- EEG, electromyogram, electro-oculogram, respiratory airflow, thoraco-abdominal movement, ECG, oximetry, body position, snoring sound and video. Clearly, it is a relatively intrusive and costly study whose interpretation can be complex.
ii) Ambulatory Pulse Oximetry is a useful screening tool for OSAHS. However, there is a high incidence of false negative results (30%) and in patients with COPD, a high false positive result. When compared to PSG, oximetry has shown to have a mean sensitivity of 87% and a mean specificity of 65% 12. Due to the high false negative rate, it is a useful screening tool to diagnose OSAHS, but cannot be relied to exclude OSAHS.
iii) Limited Sleep Studies usually incorporate some measurement of respiratory signals-airflow, thoraco-abdominal movement, oximetry and pulse measurement. As these studies can often be performed in an ambulatory basis and are less invasive than a PSG, it is a common practice in the UK. Disadvantages include inability to identify sleep stages, conditions such as Restless Leg Syndrome, equipment failure and night to night repeatability. Whilst these concerns are appreciated, limited studies can be useful, cost effective and an accepted method of assessment.
c) Upper airway pressure assessment. Advancements in technology have allowed simultaneous assessment of respiratory indices aimed at identifying OSA, to be combined with airway pressure sensors to provide localisation of the level of obstruction 13,14. Such investigations may improve the outcome of upper airway surgery by better patient selection 15.
The choice of treatment is dictated by
1) Diagnosis - In moderate to severe OSAHS, the aim is to eliminate the episodes of apnoeas/hypopnoea, de-saturations, and associated daytime sleepiness. Here, the gold standard of treatment is Continuous positive airway pressure (CPAP).In the simple snorer the aim is a reduction of the duration and intensity of snoring to socially acceptable levels. Here life style changes, oral devices and limited surgery is appropriate. In UARS and mild OSAHS the goal is reduction in snoring but also the upper airway resistance and associated sleep fragmentation. Here most modalities of treatment are appropriate depending on patient choice and the predominant symptom – snoring noise reduction or sleep disturbance.
2) Accurate localisation of the level of airway obstruction - Other than life style changes and CPAP, other modalities of treatment are site specific. Therefore, the efficacy of the treatment is dependent on accurate localisation of the obstruction. Clinical and radiological examinations are known to be poor at localising the level of obstruction25. Fibreoptic upper airway endoscopy, with our without sedation, are limited as they are not performed during natural sleep and are uni-positional. Upper airway pressure recordings and acoustic reflectometry are promising techniques 15, 16 though they are not widely available or practiced in UK.
a) Behavioural Changes. For simple snoring, simple measures such as allowing the partner to fall asleep first, using ear plugs, or sleeping on your side rather than the back can often suffice.
c) Weight Loss. Obesity is the single most important factor in increasing upper airway resistance. Weight reduction has been shown to reduce snoring, the number of apnoeas and hypopnoeas, sleep efficiency and oxygenation. The most dramatic results have been reported with surgical weight loss. It should be recognised, that substantial weight loss by non surgical means is both difficult to achieve and hard to maintain.
d) Lifestyle changes. Patients who smoke should be encouraged to stop smoking for general health reasons. While there is evidence linking smoking with OSAHS, there is no evidence that stopping smoking improves apnoeic events. Alcohol, especially close to bed time, exaggerates loss of pharyngeal muscle tone during sleep and episodes of airway collapse. For similar reasons, sleeping tablets, sedative antihistamines and tranquillizers should be avoided at bedtime.
e) Continuous Positive Airway Pressure. CPAP applied via a nasal mask has been shown to be the most effective treatment for OSAHS. It has been shown to eliminate apnoeas/hypopnoeas, improve daytime alertness, neurocognitive functions, mood and cardiovascular sequelae. Despite its effectiveness, it suffers from notable compliance limitations. Approximately, one third of patients offered CPAP are unwilling to use it and from various studies, average nocturnal use averages between 4-5 hours per night. Compliance can be improved by initial habituation to the mask for several days before CPAP usage, eliminating oral leakage with chin straps, heated humidification to reduce nasal dryness, Bi-level positive airway pressure (BIPAP) or Auto-CPAP to reduce exhalation pressure. Often the most important factor is supportive and accessible medical staff.
f) Intra-Oral Appliance. Several intraoral devices have been designed to enlarge pharyngeal airway by moving and fixing the mandible in an anterior position. The devices have been shown to be effective in improving snoring and mild OSAHS. Side effects relating to excessive salivation, jaw discomfort, teeth/gum discomfort and temromandibular joint dysfunction have been reported in a significant proportion (60-65%) of patients.
g) Pharmacological Treatments. Drugs used in treatment of OSAHS are either respiratory stimulants for increasing upper airway muscle tone, or drugs for treating excessive day time hypersomnolence. Protrytyline, acetozolaminde and progesterone, are respiratory stimulants and also known to suppress rapid eye movement sleep (sleep stage most prone to airway collapse). These drugs have not been shown to be curative in the treatment of OSAHS. There is some evidence to show that addition of alerting drugs such as modafanil, may have some beneficial effect on reducing daytime sleepiness in patients who remain sleepy despite CPAP usage. However, its use cannot be considered as an alternative to CPAP as it fails to address the underlying pathology.
h) Upper Airway Surgery
The success of upper airway surgery is dependent on accurately identifying the level/s of obstruction and effective surgical treatment for that level of obstruction. Identification of the level of obstruction has traditionally been based on clinical assessment and/or investigations under sedation. With technical advancements, techniques combining assessment for OSAHS and level of obstruction during natural sleep are likely to improve the outcome from surgical intervention13-16.
i) Tracheostomy. This was the first surgical procedure used in the treatment of OSAHS. It is rarely performed today. Current surgical approaches are designed to widen the upper airway- nasal, oropharyngeal or retrolingual. These procedures are usually single site and non-invasive for simple snoring and multiple level and invasive for moderate to severe OSAHS.
ii) Nasal Surgery. Nasal pathology increases the upper airway resistant and results in an increased negative pressure in the pharynx during inspiration. Surgical approaches to correct deviated septum and address nasal polyposis and turbinate hypertrophy can significantly reduce upper airway resistance. However, the reported impact on snoring is variable (39-87%) and there is a known relapse after several years 17. In patients with OSAHS, nasal procedures can improve compliance with nasal CPAP but does not improve OSAHS per say18.
iii) Uvulopalatopharyngoplasty (UPPP). This probably has the longest track record than any other procedure for widening the oropharyngeal airway. The procedure involves tonsillectomy, uvulectomy and excision of a variable segment of the soft palate. In the appropriately selected group i.e. suspected obstruction solely at the level of soft palate/oropharynx, success rates for simple snoring vary between 75-85%19,20 and 52.3% for OSAHS21. However, it is notable that the success rate decreases with increasing follow-up periods.
iv) Laser-Assisted Uvulopalatoplasty (LAUP). Though originally developed as a modification of the traditional UPPP, has evolved notably in the last decade. There are some 24 different techniques in the literature though the principles of the different procedure are quite similar. Using visual analogue scores, the success of LAUP has been reported between 51-89% dependent on the time of follow up22. Studies show that though LAUP is more effective than doing nothing in OSAHS, it is less effective than conventional UPPP 22,23.
v) Radiofrequency (RF) procedures of the tonsil, palate and tongue base are based on the principle of submucosal application of low frequency radiowaves to create thermic lesions and subsequent volume reduction and scarring. The advantages of the technique include mucosal sparing and emphasis on volume reduction rather than resection. A few long term studies show an approximate 80% reduction in subjective snoring at one year. There is very limited published data with respect to OSAHS. A study with multilevel radiofrequency (tonsil, palate and tongue base) in a small cohort showed a decrease in AHI of 32.6 to 22.0 after surgery24. The author’s experience (unpublished data) with a modification involving palatal incisions with submucosal channelling, coined Coblation Assisted Upper Airway Procedures (CAUP), has shown a reduction in AHI from 21 to 9.3 at one year. The technique shows promise but results with long-term follow up are required.
vi) Maxillofacial and Multilevel Surgery is usually performed for patients with moderate to severe OSAHS. It includes a range of procedures to improve the retrolingual airway and the retropalatal airway. These procedures are extremely invasive and there use is limited to patients who fail to use CPAP.
SNORING AND OBSTRUCTIVE SLEEP APNOEA IN CHILDREN
Although OSAHS in children has many similarities with the adult form, there are some notable differences (Table 2)25. It is unclear whether the condition in children is the same as that in adults. Unlike adults, the incidence is equal in both sexes and does not increase with age. The peak occurrence is between the ages of 2 and 5 years, when the adenoids and tonsils are largest in relation to the oropharyngeal size. Children with OSAHS frequently show signs of failure to thrive rather than obesity. Symptoms in children are similar to adults with the exception of sleepiness. Paradoxically, children often demonstrate restlessness and hyperactivity. Other potential consequence in children includes secondary enuresis.
Table 2 Differences in characteristics of obstructive sleep apnoea between Children and adults
Peak- 2-5 years
Increases with age
Male = Female
Hyperactive, Developmental Delay
Although OSAHS in children is associated with Adenotonsillar hypertrophy, it is unlikely to be the only cause. Firstly, these children with OSAHS do not obstruct during wakefulness. Secondly, studies have failed to show a correlation between adenotonsilar size and OSAHS. Thirdly, a small percentage of children with adenotonsillar hypertrophy and no other risk factors do not improve with adenotonsillectomy. Finally, long term studies show that there is a cohort of children who initially improve with adenotonsillectomy but have a recurrence in there adolescence25. Other anatomical factors which predisposing to OSAHS include choanal stenosis/atresia, macroglossia, micrognathia, mid face hypoplasia (e.g. Down’s, Crouzon’s and Apert’s syndromes, achondroplasia) and Mandibular Hypoplasia (e.g. Pierre-Robin and Cornelle De Lange syndrome).
Medical sequaele such as pulmonary, systemic hypertension, cor pulomonale and congestive heart failure are described but is rare and is usually associated with severe cases. Neurobehavioural and developmental consequences are more common including poor school performance, poor learning skills, Attention deficit hyperactivity disorder and behavioural problems. A study on children performing poorly in school (lowest 10th percentile) showed a high prevalence (18%) of OSA. In this cohort, children treated with adenotonsillectmy improved in their grades in the following year, whereas untreated children showed no improvement26.
Full polysomnography is rarely used in children in regular clinical practice in UK. Furthermore, the diagnostic criteria are different as an AHI of greater than 1 is considered abnormal. The natural course and long term prognosis of childhood OSAHS are unknown. It is not known whether childhood OSAHS is a precursor of adult OSAHS or two diverse diseases affecting discrete populations.
Sleep related breathing disorders is a spectrum of condition spanning from simple snoring to severe obstructive sleep apnoea.
Obstructive sleep apnoea/hypopnoea syndrome is associated with systemic hypertension and notable neurocognitive sequeale.
Patients who must be considered for sleep studies
- Patients with COPD as the combination is potentially dangerous
- Any patient describing daytime sleepiness and working with dangerous machinery or drive for their profession
- Patients being considered for surgery for snoring
Surgical procedures for SRBD should be guided by the diagnosis and level/s of obstruction
There are notable differences between the adult and childhood form of OSAHS
OSAHS Obstructive Sleep apnoea/Hypopnoea Syndrome
SRBD Sleep Related Breathing Disorders
UARS Upper Airway Resistance Syndrome
AHI Apnoea/Hypopnoea index
RDI Respiratory Disturbance Index
CPAP Continuous Positive Airway Pressure
BMI Body Mass Index
EDS Excessive Day Time Sleepiness
1 Stradling JR, Crosby JH. Predictors and prevalence of obstructive sleep apnoea and snoring in 1001 middle aged men. Thorax 1991;46:85-90.
2 Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N
3 Management of Obstructive Sleep Apnoea/Hypopnoea Syndrome in Adults. A national Clinical Guideline. Scottish Intercollegiate Guideline network. June 2003. available from www.sign.ac.uk
4 Engleman HM, Martin SE, Deary IJ, Douglas NJ. Effect of continuous positive airway pressure treatment on daytime function in sleep apnoea/hypopnoea syndrome. Lancet 1994;343:572-5.
5 Teran-Santos J, Jimenez-Gomez A, Cordero-Guevara J. The association between sleep apnea and the risk of traffic accidents. Cooperative Group Burgos-Santander. N Engl J Med 1999;340:847-51.
6 Worsnop CJ, Naughton MT, Barter CE, Morgan TO, Anderson AI, Pierce RJ. The prevalence of obstructive sleep apnoea in hypertensives. Am J Respir Crit Care Med 1998;157:111-5.
7 Davies CW, Crosby JH, Mullins RL, Barbour C, Davies RJ, Stradling JR. Case-control study of 24 hour ambulatory blood pressure in patients with obstructive sleep apnoea and normal matched control subjects. Thorax 2000;55:726-8.
8 Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, Mullins R, Jenkinson C, Stradling JR, et al. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 2002;359:204-10.
9 Engleman HM, Hirst WS, Douglas NJ. Under reporting of sleepiness and driving impairment in patients with sleep apnoea/hypopnoea syndrome. J Sleep Res 1997;6:272-5.
10 Miljeteig H, Mateika S, Haight JS, Cole P, Hoffstein V. Subjective and objective assessment of uvulopalatopharyngoplasty for treatment of snoring and obstructive sleep apnea. Am J Respir Crit Care Med 1994;150:1286-90.
11 Mortimore IL, Bradley PA, Murray JA, Douglas NJ. Uvulopalatopharyngoplasty may compromise nasal CPAP therapy in sleep apnea syndrome. Am J Respir Crit Care Med 1996;154:1759-62.
12 Ross SD, Allen IE, Harrison KJ, Kvasz M, Connelly J, Sheinhait IA. Systematic review of the literature regarding the diagnosis of sleep apnea. Rockville (MD): Agency for Health Care Policy and Research; 1999. AHCPR publication No. 99-E002. [cited 28 Apr 2003]. Available from url: http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat1.chapter.2 [section 3.5.3] [section 3.5.4] [section 3.6]
13 Tvinnereim M, Cole P, Haight J S J, Hoffstein V. Diagnostic Airway Pressure recordings in Sleep Anpoea syndrome. Acto Otolaryngol (Stockh) 1995, 115:449-454.
14 Rollheim J, Tvinnerium M, Sltek J, Osnes T. Repeatability of sites of sleep-induced upper airway obstruction. A 2-night study based on recordings of airway pressure and flow. Eur Arch Otorhinolaryngol 2001, 258 : 259-264
15 Skatvedt O. Continuos pressure measurements during sleep to localise obstructions in upper airways in heavy snorers and patients with obstructive sleep apnoea syndrome. Eur Arch Otorhinolaryngol 1995; 252(1): 11-14
16 Faber C E, Grymer L. Available techniques for objective assessment of upper airway narrowing in snoring and sleep apnoea. Sllep and Breathing 2003;7:77-87
17 Hormann K, Verse T. Surgery for Sleep disordered breathing. Springer-Verlag Berlin Heidelberg 2005
18 Friedman M, Tanyeri H, Lim JW, Landsberg R, Vaidyanathan K, Caldarelli D. Effect of improved nasal breathing on obstructive sleep apnea. Otolaryngol Head Neck Surg 2000;122:71-4.
19 Hicklin LA, Tostevin P, Dasan S. Retrospective survey of long-term results and patient satisfaction with uvulopaslatopharyngoplasty for snoring J Laryngol Otol 2000;114:675-681
20 Levin BC, Becker GD. Uvulopalatopharyngoplasty for snoring:Long-term results. Laryngoscope 1994;104 1150-1152
21 Sher AE, Schechtam KB, Piccirillo LF. The efficacy of surgical modifications of upper airway in adults with obstructive sleep apnoea syndrome. Sleep1996;19:156-177
22 Berger G, Stein G, Ophir D, Finkelstein Y. Is there a better way to do laser-assisted uvuloplatoplasty? Arch Otolaryngol Head Neck Surg 2003;129:447-453
23 Ferguson KA, Heighway H, Ruby RRF. A randomised trial of laser assisted uvulopalatoplasty in the treatment of mild obstructive sleep apnoea syndrome. Am J Respir Crit Care Med 2003;167:15-19
24 FisherY, Khan M, Mann WJ. Multilevel temperature controlled radiofrequency therapy of soft palate, base of tongue and tonsils in adults with obstructive sleep apnoea. Laryngoscope 2003;113:1786-1791
25 Marcus CL. Sleep disordered breathing in Children. Am J Respir Crit Care Med 2001;164:16-30
26 Gozal D. Sleep Disordered breathing and school performance in children. Pediatrics 1998;102:616-620