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Is Snoring Bad For You? Dr. Shanthi Paramothayan BSc MBBS PhD LLM MScMedEd FHEA FCCP FRCP Consultant Respiratory Physician Honorary Senior Lecturer St.

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Presentation on theme: "Is Snoring Bad For You? Dr. Shanthi Paramothayan BSc MBBS PhD LLM MScMedEd FHEA FCCP FRCP Consultant Respiratory Physician Honorary Senior Lecturer St."— Presentation transcript:

1 Is Snoring Bad For You? Dr. Shanthi Paramothayan BSc MBBS PhD LLM MScMedEd FHEA FCCP FRCP Consultant Respiratory Physician Honorary Senior Lecturer St. Helier University Hospital 8 th September 2012


3 History Mr. AN  35 yearsNon smoker  Cab driverMinimal alcohol  DivorcedPoor sleep  DepressedFatigue  Snores loudlyUn-refreshed  Daytime somnolence

4 History New girlfriend reports:  Loud snoring  Apnoeas  Snorts and grunts

5 Examination  Obese : Wt = 182 kg, Ht = 190 cm, BMI = 50  Collar size = 23 inches  BP = 150/95  Narrow oropharynx  Chest clear  Epworth Sleepiness Score: 16

6 Epworth Sleepiness Score How likely are you to doze off or fall asleep during the following situations, in contrast to just feeling tired? Score of 0 to 3 where 0= would never dose; 1= slight chance; 2= moderate chance; 3 = high chance. SituationScore 1. Sitting and Reading 2. Watching TV 3. Sitting inactive in a public place 4. As a passenger in a car for an hour Without a break 5. Lying down to rest in the afternoon 6. Sitting and talking to someone 7. Sitting quietly after lunch (no alcohol) 8. In a car while stopped in traffic

7 Epworth Sleepiness Score  Score of < 6: Normal  Score of > 8: Possible sleep disordered breathing  Score of > 12: Probability of OSA  Score of > 16: High probability of OSA  Score of > 20: Consider narcolepsy  Maximum score = 24

8 So what is the diagnosis? Differential diagnosis of snoring: 1. Simple snoring – consider ENT causes (e.g deviated septum). May be positional and exacerbated by alcohol, sedatives 2. Upper airways resistance syndrome (UARS) 3. Obstructive sleep apnoea (OSA)

9 Hypersomnolence 1. UARS 2. OSA 3. Narcolepsy 4. Obesity-hypoventilation (Pickwickian) syndrome 5. Insomnia/other sleep related disorders 6. Restless Leg Syndrome (periodic limb movement) 7. REM behaviour disorder 8. Chronic insufficient sleep

10 Obstructive Sleep Apnoea  Apnoea means “without breath” in Greek  People with OSA stop breathing repeatedly during their sleep, often for a minute or longer, even up to 100 x every night  Apnoea: complete obstruction of airways for > 10 secs  Hypopnoea: Partial obstruction of airways (30 –50 %) for > 10 secs  AHI: apnoea/hypopnoea index (no / hour, same as RDI)  Mild OSA: AHI of > 10 / hr  Moderate OSA: AHI of > 20 / hr  Severe OSA: AHI of > 30 / hr

11 Obstructive sleep apnoea and upper airways resistance syndrome UARS:  Snoring with brief, repetitive arousals due to increases in resistance to airflow and increased respiratory effort  Negative intrathoracic pressure  autonomic and CV changes hypertension. No oxygen desaturations  Sleep fragmentation results in daytime somnolence OSA:  Snoring with apnoeas and hypopnoeas and oxygen desaturations ( 4% from baseline)  The AHI is a continuous variable like BP, so separating normal from abnormal is difficult.

12 Epidemiology of OSA  Common: 5 % of women and 10 % of men aged over 35 (USA: Wisconsin cohort study, 9-24% in M and 4 – 9% in F)  M:F = 2-3 : 1 ( in F after menopause)  Prevalence increases with age  Race: Prevalence > in African-Americans  Mortality and Morbidity: retrospective data suggest the greater mortality in patients with AHI > 20 / hour

13 Risk Factors for OSA  Obesity: BMI > 25, collar size > 17 inches  Age: loss of muscle mass in airways and neck and excess fat  Nasal problems that impede airflow  Enlarged tonsils and adenoids (children)  Hypothyroidism  Acromegaly  Other structural abnormalities: retrognathia, micrognathia  Amyloidosis, neuromuscular disorders, Marfan’s, Down’s  Can be exacerbated by: supine position, alcohol and sedatives

14 Low threshold for referral in   Overweight patients   Snoring or disturbed sleep   Unexplained tiredness   Unexplained sleepiness   Lack of concentration, memory, libido   Resistant hypertension (requiring many antihypertensives   Metabolic syndrome: Diabetes, HT, hypercholesterolaemia   Cardiovascular disease (heart failure, arrhythmias,

15 So what happens in OSA?  Site of obstruction is soft palate, extending to the region at the base of the tongue (no rigid structures to hold airway open)  When awake, muscles in the region keep passages open  When asleep, muscles relax, and there is reduced neuromuscular activity, causing airway collapse and obstruction of airway  This results in an oxygen desaturation  When breathing stops, the sleeper awakens (arousal) for a few seconds and there is a rise in BP  Repeated arousals cause sleep fragmentation (no REM sleep) and un-refreshed sleep

16 Normal

17 Sleep apnoea-hypopnoea syndrome

18 Upper airway resistance increases during sleep in normal subjects

19 Typical presentation of OSA  Symptoms are insidious and often present for years  Snoring, loud and habitual and bothersome to others  Witnessed apnoeas that end with a loud snort  Gasping and choking sensations  Restless sleep, frequent arousals, nocturia  Feeling un-refreshed, morning headaches  Excessive sleepiness during day  Poor: concentration, memory, libido  Problems with family and work  Road traffic accidents (RTA)

20 Approach to a patient with possible OSA  Get clear history and talk to witnesses (partner)  Driving history and occupation (truck drivers, train drivers)  Assess daytime sleepiness (ESS) and other symptoms  Weight, height and calculate BMI  Collar size  Oropharynx (tonsils)  Nasal airflow  Blood pressure  Cardiovascular and respiratory examination

21 Investigating patients with possible OSA  Bloods: FBC, U+E’s, glucose, thyroid function  Epworth sleepiness score  (Multiple sleep latency test)  If necessary: ECG, CXR  ENT referral

22 Investigating patients with possible OSA  Overnight pulse oximetry  Overnight limited sleep study: oximetry, thoracic and abdominal wall movement, oronasal airflow, snore volume, BP  Full polysomnography: as above plus Leg movements (anterior tibialis EMG) and video, Sleep stages (EEG, EMG, EOG) ECG and blood pressure



25 Consequences of OSA  Untreated OSA is related to a significant mortality risk, 3X (Sleep, American Heart Association, American College of cardiology,  OSA is a risk factor for developing nocturnal hypertension (independent of other factors (Davies, Thorax 1998)  Recent evidence that OSA causes hypertension and treatment with CPAP improves BP (Becker et al, Circulation 2003, 107:68-73, Nieto et al, JAMA 2000, 283:1829-1836, Peppard P, N Engl J Med 2000, 342: 1378-1384)  OSA increases risk of stroke, heart block and MI  Risk of OSA is increased in patients with pulmonary hypertension  Link between OSA and heart failure (also with central sleep apnoea)  Increased risk of RTA

26 Evidence of link between OSA and CV disease   Animal models   Epidemiology   Association long suspected ? Confounding factors?   Wisconsin Sleep Cohort study – –18 year follow up of 1522 (30-60 yrs) with mild, moderate, or severe OSA or no OSA – –Mortality was 19% with severe OSA v 4% with no OSA   Sleep study (Australia) – –14 year study of 380 – –Moderate-to-severe sleep OSA was an independent risk factor for dying (33% in severe OSA v 7.7% in no OSA)

27 Mechanism of increased cardiovascular morbidity in OSA  OSA associated with increased CV morbidity  Intermittent hypoxia increases formation of reactive oxygen species and oxidative stress  Reactive oxygen species cause rupture of unstable atherosclerotic plaques  Inflammatory pathways activated  Inflammatory cytokines and adhesion molecules: cell/leukocyte/platelet interaction  Endothelial dysfunction

28 Syndrome Z  Hypertension  Central ObesitySyndrome X  Insulin resistance  Hyperlipidaemia  OSASyndrome Z  So suspect OSA in patients with above risk factors


30 Management of patients with OSA Depends on severity of OSA and symptoms General:  Weight reduction (dietician, medication)  Advice on sleep position (tennis ball !)  Avoidance of alcohol and sedatives  Treat nasal congestion  Try devices to stop snoring (e.g snorban)  Information, telephone numbers and websites  Information about Driving : Patient must inform DVLA if they are being investigated for OSA

31 Management of patients with OSA  Oral appliances  CPAP  Medication: Modafinil (Provigil)=stimulant. For patients still symptomatic despite CPAP  Surgery: uvulopalatopharyngoplasty (UPPP), craniofacial reconstruction, tracheostomy

32 Oral Appliances  Oral appliances move tongue or mandible forward  Suitable as 1 st line therapy for mild OSA if patient doesn’t tolerate CPAP  Not as effective as CPAP (Engleman, 2002)  Mandibular advance devices move lower jaw forward  Tongue-retaining devices pull tongue forward  Should be fitted by specialist dentist/maxillofacial surgeon  Side effects: TMJ pain, excessive salivation

33 CPAP (Continuous Positive Airways Pressure)  Treatment of choice in moderate and severe OSA  CPAP improves snoring, sleep quality, daytime sleepiness, mood, cognitive function, QOL (Becker, 2003)  CPAP decreases BP and has other cardiovascular benefits in patients with OSA (RCT evidence)  Compliance is a major problem: 50 – 70 % use it regularly and significantly  Common side effects: rhinorrhoea, dry mouth, dry eyes, nose bleeds, claustrophobia, aerophagia  Need regular assessment, advice, help with mask fitting, humidifier etc – so need competent technical staff  Patients with OSA can drive once established effectively on CPAP


35 So what happened to my cab driver?  Overnight limited sleep study showed significant OSA  Patient given information about weight reduction, referred to dietician  Patient referred urgently for CPAP  Patient advised NOT to drive and to inform DVLA until established on CPAP


37 Now what about you?  Do you snore?  What is you ESS?  If you snore and your ESS is > 12…………

38 Central Sleep Apnoea  Absent/reduced ventilatory drive Congenital  Ondine’s curse Acquired  Destructive brain lesions  Neuromuscular disease  Severe obesity  Chest wall abnormalities

39 Conclusions  OSA is common. Need increased awareness (especially GP’s) and referral for sleep study  Pulse oximetry suitable for majority with OSA but will miss UARS and mild OSA, or patients with hypoxia for other reasons  Limited sleep study can be done at home and will be sufficient for the majority with OSA but may miss other problems  Increasing evidence that OSA is a significant risk factor for systemic hypertension, cardiovascular disease, pulmonary hypertension and all cause mortality  Evidence that treatment of OSA reduces risk  OSA responsible for a significant number of road traffic accidents  CPAP is the treatment of choice for OSA


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