Presentation is loading. Please wait.

Presentation is loading. Please wait.

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

Similar presentations


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

2

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

23

24

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: , Peppard P, N Engl J Med 2000, 342: )  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

29

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

34

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

36

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

40


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

Similar presentations


Ads by Google