BTS sleep Course. Sleep studies Management nasal CPAP Future challenges

Transcription

1 BTS sleep Course Module 3a Sleep Apnoea and snoring (prepared by J Stradling) What is sleep apnoea? What causes it? What are the symptoms? Sleep apnoea and driving Sleep apnoea and the cardiovascular system Epidemiology Definitions and diagnosis Sleep studies Management nasal CPAP Future challenges

2 BTS sleep Course Modules 1, 2 and 3 Acknowledgements With many thanks to Richard Horner, Toronto University for permission to use some material from his sleep course Some images have come from Some images came from internet searches via Google Others have come from published articles/books Most of the images are therefore copyright and cannot be used other than for personal study Others come from Prof J Stradling who wrote these modules

3 What is sleep apnoea? The sleep apnoeas are a group of related conditions that are characterised by abnormal breathing during sleep. Divided into:- Obstructive (airway is partially or completely blocked) Failure of the upper airway to maintain adequate patency when the upper airway dilator muscles relax with sleep Cessation of airflow but continuing effort (+paradox) Central (patient fails to make any effort to breathe) Cessation of airflow with no effort

4 What is obstructive sleep apnoea? The term obstructive sleep apnoea is used to describe the actual obstructive events during a sleep study. The term obstructive sleep apnoea syndrome is used to describe the occurrence of obstructive abnormalities on a sleep study combined with symptoms, usually excessive daytime sleepiness Although we use the term apnoea, in reality the obstruction to breathing may not be complete (apnoea), but partial. Partial obstruction may lead to hypopnoea (under breathing) or just increased inspiratory effort (upper airway resistance syndrome) Hence sometimes called the sleep apnoea/hypopnoea

5 What is obstructive sleep apnoea? Thus obstructive sleep apnoea syndrome is:- Pharyngeal incompetence brought on by sleep Recurrent brief arousal from sleep to clear the airway Markedly fragmented sleep throughout sleep Daytime consequences of sleep fragmentation, mainly excessive daytime sleepiness

6 Obstructive sleep apnoea midline coronal section through the upper airway of a cadaver main area of airway collapse in OSA Pharyngeal muscles required to maintain patency Reason for recovery position and jaw thrust in unconscious subjects

7 Flash MRI images of an apnoea Awake - Asleep - Asleep - Awake - Air column (black) fully open Air column collapsed behind tongue Air column collapsed from uvular to larynx Air column fully open again

8 Beginning of night Overnight (8 hours) oxygen saturation levels (oximetry) in OSA: >400 dips/apnoeas in total 1 st hr 2 nd hr 3 rd hr End of night 8 th hr 60 minutes

9 Obstructive Sleep Apnoea

10 What is the arousal stimulus to waking up in OSA? Is it the hypoxia, the hypercapnia or the inspiratory effort? Kevin Gleeson s experiment in normals exposed to hypoxia, hypercapnia, or inspiratory loading. This shows that the subjects woke at a particular inspiratory effort, regardless of the cause of that increase in effort. Thus in most it is the increaed inspiratory effort that awakes the patient with an obstructed upper airway.

11 Sleep increases upper airway resistance (nose to larynx) in normals

12 Balance of forces across the upper airway Obesity Small jaw Tonsils

13 Effect of neck circumference on OSA Not obesity In 20s Approx 17 inches

14 Normal OSA MRI images Sagittal views Note more upper body fat in OSA and angled jaw Axial views Axial views before (A) & after (B) weight loss

15 Retrognathia causing OSA 17 year old boy very small retroglossal airway extensive teeth removal by orthodontist due to overcrowding ( forme fruste of Pierre Robin syndrome) Many patients with OSA have smaller lower jaws

16 Average cephalograms OSA (red) versus normal (black) Mandible down, back, and less angled Compensatory hyoid descent

17 Why do so many people have small lower jaws (that cannot accommodate all their teeth) and may predispose them to OSA? Chimpanzee Human Suggested that chimps (and other non-human primates) have a strong jaw, and big jaw muscles (temporalis muscle) with extensive attachments to extra thick bone on the top of its skull that limit cranial expansion expansion.

18 Human jaw evolution All humans have a frameshift mutation of a myosin (MYH16) gene that in nonhuman primates produces the long jaw (occurred 2.4 m years ago) via more powerful masticatory muscles. Small temporalis attachment compared to other primates Small muscle fibres compared to other primates Did the evolution of human brain expansion depend on losing a big powerful jaw and thus make us prone to upper airway compromise during sleep? Stedman et al, Nature 2004;428(6981):373-4

19 Tonsillar hypertrophy in OSA Usual cause in children and responds to tonsillectomy. Much less common in adults and may not respond to tonsillectomy.

20 Upper airway grading in OSA Abnormalities of the upper airway can be categorised using the Mallampati score originally devised for anaesthetic practice. The Mallampati class correlates with both OSA severity and required CPAP pressure Mallampati et al. Can J Anaesth 1985;32:429-34

21 Alternative pharyngeal grading system Sampsoon-Young classification system Correlates with the presence of OSA Samsoon et al. Anaesthesia 1987;42: Tsai et al. AJRCCM 2003;167:

22 Endoscopy during OSA By courtesy of Mary Morrell

23 Causes of snoring/obstructive sleep apnoea Obesity ü Lower facial shape ü Tonsils ü Nasal problems Hypothyroid Alcohol Smoking Menopause Acromegaly Mucopolysaccharidoses Neuromuscular diseases/stroke? Reduced airway reflexes/increased arousal response

24 Symptoms of Obstructive sleep apnoea Common (>60%) Loud snoring Excessive daytime sleepiness Choking or shortness of breath sensations during sleep Restless sleep Unrefreshing sleep Changes in personality Nocturia Less common (10-60%) Morning headaches Enuresis Reduced libido Nocturnal sweating Spouse worried by apnoeic episodes Rare (<10%) Recurrent arousals/insomnia Nocturnal cough Symptomatic oesophageal reflux

25 Sleepiness at work These photographs were taken by this man s work colleagues prior to his retirement party. Retired unnecessarily on health grounds unable to work due to excessive sleepiness. Sleepiness resolved on nasal CPAP for his OSA

26 Epworth Sleepiness scale for measuring sleepiness. Least sleepy=0 Most sleepy=24

27 Patients with OSA

28 Sleep Apnoea and Driving George et al Thorax 2001;56: (similar French data, Chest 1997;112:1561) Driving accidents for 3 years before and 3 years after nasal CPAP (n=210), versus control population. Ontario public record data. Crashes/driver/year Before (A) After (B) Controls 1 Controls (p<0.001) Rate remained high in 27 untreated pts Before (113 accidents) After (38 accidents)

29 Bad Driving simulator performance Good Normal subjects, influence of alcohol, and effects of OSA Normal subjects given enough alcohol to put them just over the legal limit George et al AJRCCM 1996

30 OSA and driving simulation Start of drive End of drive (30 minutes) OSA Increasing tendency to wander off road Repeated on treatment, 1 month later. No deterioration

31 Cost of road accidents (UK department of transport official figures) Douglas and George Thorax 2002;57:93-4 Fatal accident 1.25 million +Injury 49.8 thousand Property damage 1,300 Treating 500 pts for 5 years prevents 1 fatal accident, 75 injury accidents, and 224 property damage accidents. 5.3 million saved, against estimated treatment cost of 0.4 million (12.3 times return on investment!)

32 Sleep Apnoea and health costs Canadian data Bahammam et al Sleep 1999;22: patients with OSA, versus controls: health expenditure during 5 years prior to treatment and 2 years after. Hospital stays, similar difference. Similar US data Kapur et al Sleep 1999;22:749 (1 year prior to diagnosis versus matched controls). $2720/yr versus $1384/yr, correlated with OSA severity even after allowance for BMI.

33 Costs of delivering CPAP, Qalys, UK calculations Sleep study, 3 outpatient visits, CPAP set up, machine, mask, 1,000 in the UK. Chilcott et al, Trent Institute for Health Services Research, October 2000 (Guidance for purchasers). Annual maintenance thereafter approximately 250 (generous) Minimum Qaly gain estimated (from SF36 data) = 0.1/year Making assumptions about patients investigated and not put on treatment, and those put on treatment who stop using it, BUT NOT ALLOWING FOR ANY COST SAVINGS, the Cost per Qaly/yr depends on the time period on treatment considered:- =10 x yearly maintenance cost ( 250) = 2500 (NSCLC 15,000)

34 Arterial blood pressure during OSA Recurrent dips with every obstructed breath Rise with every arousal

35 Survival in OSA, effect of tracheostomy, uncontrolled study pre CPAP era Partinen et al 1990

36 Blood pressure in OSA, and matched control subjects Davies C et al Thorax 2000

37 Toronto dog model of OSA Sleeping BP Awake BP OSA Noise OSA Noise

38 Control 24hr blood pressure before, and after 1 month of ncpap, therapeutic versus sub-therapeutic control ncpap Pepperell et al, Lancet 2002

39 Severe untreated OSA Up to 12 year follow up of patients with varying severity of OSA. Fatal, and nonfatal, cardiovascular events. Marin et al Lancet 2005;365:

40 Effect of compliance on survival in chronic heart failure. Results from the CHARM programme. Granger et al Lancet 2005;366: High compliers Low compliers 80% v 65% of tablets taken People who decline medical therapy probably do not take other medications (statins, antihypertensives etc.) Poor compliance is a powerful and complex adverse risk factor

41 OSA and cardiovascular disease conclusions Should we treat OSA and expect to reduce blood pressure? Yes in typical clinic obstructive sleep apnoea, but we do not know if this confers long term morbidity/mortality benefit Currently, the evidence favours the benefit being in the sleepy patients with more severe OSA on sleep study criteria (not adequately proven) Non-symptomatic patients should have any hypertension treated conventionally as this is evidence based

42 Epidemiology of OSA How common is sleep apnoea? Critically depends on how sleep apnoea is defined What thresholds do you use (rather like the problem with defining hypertension)? Do you use sleep studies, symptoms or both?

43 Snoring and OSA are part of a continuum Increasing symptoms Never snores Snores supine all the time Apnoeas only when supine and drunk Snores only when supine and drunk! Snores any posture Apnoeas on back only Severe OSA all the time These occurrences are arbitrary points along the scale of severity

44 Evolution of snoring and sleep apnoea (after Lugaresi)

45 Changes in adult obesity (BMI > 30) in US and UK over the last 25 years National Health and Nutrition Examination Survey (NHANES) USA % subjects with BMI > 30 (aged 20-74) UK men UK women US men US women

46 European obesity league tables

47 Average wt in lbs of domestic cats Not just humans!

48 Prevalence of Obstructive sleep apnoea Depends on definition thresholds and exact components Depends on levels of obesity In the UK approximately 1% of men have severe OSA worthy of CPAP treatment In the UK approximately 5% of men have significant OSA likely to be increasing their degree of sleepiness (In the US (and Western Samoa!) the prevalence is higher - 3% & 15%) In certain populations, e.g. type II diabetics, the prevalence is much higher In a population of snorers the prevalence of severe OSA is much higher

49 Definitions of OSA/syndrome 1970 s >5/hr of >10s apnoeas (or >35/night) based on sleep study findings only, in small numbers of subjects s >5/hr of >10s apnoeas or hypopnoeas or >10 or >15/hr. Hypopnoeas, <50% preceding baseline ±>4% dip in SaO 2. Variable definitions. Large night to night variation in indices. Now:- Sleep-induced upper airway obstruction leading to symptomatic sleep disturbance.

50 Correlation between AHI or microarousals and objective tests of sleepiness, MSLT or MWT. Kingshott et al ERJ 1998;12:1264 MSLT MWT AHI Arousals

51 Clinical approach to OSA and its variants History:- Compatible symptoms? Are symptoms bad enough to consider therapy? Sleep Is there evidence of upper airway narrowing that study:- leads to sleep fragmentation? QUALITATIVE DECISION Decision:- Has the sleep study revealed anything that accounts for the patient s daytime symptoms, and is a trial of nasal CPAP justified?

52 BTS sleep Course Module 3a (appendix) Sleep history taking, and clinic activities Importance of a full history Use of screening questionnaires Points in the History Use of proforma clerking sheets Points in the examination Clinic investigations

53 Sleep History Taking Needs to cover all aspects of abnormal sleep and its symptoms. Although there may be an apparently obvious cause, there is often another cause of sleepiness at least as important at the more obvious one. When the treatment for the original diagnosis doesn t work, the tendency is to plug on rather than review the diagnosis the possibility of other diagnoses is best highlighted early on.

54 There are many aspects of a sleep history unfamiliar at first. Therefore a clerking proforma can be useful, but is not a substitute for the usual way of taking a history general review with more specific questions based on early ideas as to the diagnosis. Some centres use postal questionnaires for patients and partners to fill in before coming to outpatients. This may save time and allow an accurate sleep diary to be kept. However they have poor sensitivity and specificity and are no substitute for a proper assessment.

55 Example of simple screening questionnaire for Obstructive sleep apnoea

56 It is best to interview the patient along with their partner. Important information is available from the partner that the patient may not know, or admit to. The following list is designed to cover the main areas that need to be covered. It is not exhaustive and much more detail may be required around the areas of interest. Based on a table in Clinicians Guide to Sleep Medicine, Douglas NJ, Arnold 2002.

57 Presenting Complaint Specific reason for presenting Patient or partner complaining? Duration of symptoms Age at onset Progression of symptoms Severity of symptoms Sleep Duration and Quality Normal bed or lights out time working days and weekends Usual time to fall asleep Time of final awakening working days and weekends Number and duration of awakenings throughout the night Cause of nocturnal awakenings if known Daytime Naps Refreshing or not Shift working Precise timing and pattern of shifts Symptoms better when on holiday? Associated symptoms Snoring, including frequency, severity, and position dependence Witnessed apnoeas/nocturnal choking Nocturia Unrefreshing sleep Nocturnal acid reflux Decreased libido Cataplexy Hypnagogic hallucinations Sleep paralysis Witnessed recurrent limb movements during sleep Restless legs during waking hours

58 Predisposing Factors Weight gain, especially recently Quantity of alcohol consumed Family History of:- sleep apnoea narcolepsy sleep paralysis Psychological/psychiatric history Drug history, potentially sedative or alerting agents Caffeine (coffee, tea, colas, Red Bull, Jolt, Dr Pepper, Irn-Bru etc OTC drugs, e.g. Pro Plus, herbal weight loss remedies Severity of Sleepiness Epworth Sleepiness Scale Frequency of sleep episodes Impact on daily life, work, home Impact on driving, any sleep-related accidents or near misses Overall effect on quality of life Past Medical History Previous ENT surgery, tonsillectomy etc. Cardiovascular disease Hypertension Hypothyroidism Diabetes Head injury Brain irradiation

59 Two examples of some clerking sheets to cover these points.

60 Courtesy of Simone DeLacey, St Thomas s Hospital, London

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63 Specific points in the examination, if indicated Possible OSA Awake snoring Obesity and its distribution (neck circumference) Backset jaw Tongue size Tonsils and other masses Nasal patentcy relevant to possible CPAP use Blood pressure (best measured away from clinic) Evidence of cor pulmonale, resting SaO 2 Evidence of neuromuscular disease

64 Specific investigations that may be indicated Possible OSA Thyroid function Cardiovascular screen, glucose, cholesterol, ECG IGF1 (acromegaly) Oximetry, if <95% then arterial/capillary blood gases Spirometry (COPD, overlap syndrome) Sleep studies (covered elsewhere) Possible narcolepsy HLA typing CSF hypocretin/orexin (not widely available) MSLT sleep onset REM (covered elsewhere)

65 End of part 1 on OSA, module 3a Next section (module 3b) will cover:- Sleep studies Management nasal CPAP Future challenges

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