CASE

●
Hatice Özkardesler, 66 years, female. Comes to
your clinic due to husband cannot sleep !
– Brief statement of background and current problem

●
Height: 164cm, Weight: 69kg BMI:26
●
Symptoms: snoring, witnessed apnea, wake up
with respiratory distress, daytime sleepiness
●
HT, Hyperlipidemia,

●
Lung function obstructive otherwise normal

●
Smoker no

●
Alcohol. no

●
Drugs : Ator, osteocare,

●
Epworth Score: 12

●
Tentative Diagnosis
 Which of the following symptoms are the 2
must important in sleep apnea ?
1. Tiredness during the day
2. Snoring
3. Day sleepiness
4. Observed apneas
5. Dry mouth in the morning
6. Concentration problems
Clinical signs and symptoms in OSA !
 Clinical signs and symptoms in OSA

Risk factors for OSA:

– Obesity (upper body
adiposity)
– Male gender
– Craniofacial abnormalities
– Increased pharyngeal soft
or lymphoid tissue
– Nasal obstruction
– Endocrine abnormalities
(hypothyroidism,
acromegaly)
– Genetic factors
 Clinical signs and symptoms in OSA

Can be associated with the

disease
– Systemic hypertension
– Pulmonary hypertension
– Sleep fragmentation
– Sleep-related cardiac
dysrhythmias
– Nocturnal angina
– Gastroesophageal reflux
– Impaired quality of life
– insomnia
 Bixler
AJRCCM 1998 157 144-148
~60 yr
 Epworth sleepiness scale
A simple self-administered questionnaire
Sleep-related breathing disorders

Many subgroups
 Sleep-related
(breathing) disorders
Obstructive sleep apnea syndrome (OSAS)
• Obstructive sleep apnea syndrome (OSAS) is defined
as a chronic respiratory sleep disorder typified by
recurrent episodes of partial or complete upper
airway obstruction during sleep that cause cessation
of airflow in the presence of respiratory effort.
Critical Pressure during sleep

-10 cm H2O

-50 cm H2O

+
 Pathophysiology of Airway
Obstruction

Flow blockage (upper airway collapse)

under apnea and hypoapnea

Morrell et al. Eur Respir J. 2002; 20:451-7

 An imbalance between forces that
promote airway dilation
and forces that promote collapse
is associated with sleep apnea. 

The following factors promote collapse: The following factors promote patency:

• Small airway size • Pharyngeal dilator muscles

• Upper airway resistance • Larger airway and mandible
• Negative inspiratory • Higher lung volume
pressure
• Extraluminal tissue pressure
• Small mandible
• Supine position
• Upper airway inflammation
 The gold standard for diagnose!
• Polysomnography
• There are no absolute
contraindications
– Difficult / callibration
– Personal most be dedicated
– time consuming
• Split-night PSG
– first half of the total sleep episode is
dedicated to diagnosis and the latter
half is dedicated to a CPAP trial.
The generally accepted interpretations of the Epworth
sleepiness scale are as follows:

A score of 0-5 should be interpreted as supernormal.

A score of 5-10 should be interpreted as normal.
A score of 10-15 should be interpreted as sleepy.
A score of 15-20 should be interpreted as very sleepy.
A score of more than 20 should be interpreted as
dangerously sleepy. (Arrange transportation for
patient.)
 Epworth sleepiness scale
Excessive daytime sleepiness

– Discriminates between normals and

those with diseases that lead to
hypersomnolence
– Normal: 5.9 (2.2) – Range 2 – 10
– OSA: 11.7 (4.6) – Range 4 - 23
 Epworth sleepiness scale

Johns MW, Sleep 1991;14:540-545

 Prevalence ?
• ≈ 2% of women and 4% men age 30-60 years
• ≈ 4000 persons in North Cyprus will have
Sleep apnoa.
 BUT NO NEED FOR FURTHER PHARYNGEAL
TESTS BEFORE SURGICAL INTERVENTION IS
FIRST CHOISE OF TREATMENT
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2625324
 Polysomnography
• The term polysomnography was first introduced by
Holland et al in 1974
• Recording, analysis and interpretation of multiple,
simultaneous, physiologic parameters
• Essential in the diagnosis of many sleep disorders
• Essential to the understanding of normal and
abnormal sleep
 Polysomnography
• Sleep signals
EEG with at least 2 channels
EOG with two channels
EMG submentalis

• Respiration
Oronasal airflow
Respiratory effort / movement / snoring
Effect of respiration / oximetry / CO2

• Cardiovascular system
ECG

• Movement
EMG tibialis
Body position

- Indications and Standards for Cardiopulmonary Sleep Studies. ARRD 139: 559-568 (1989)
 Sleep Montage

•EEG C4-A1
•EEG C3-A2
•EOG left-A1
•EOG right-A1
•EMG mentalis

Rechtschaffen and Kales manual (1968)

 Whats happens
• Sleep apnea often worsens during REM sleep. muscle
tone of the hypopharyngeal and oropharyngeal
musculature decreases, resulting in upper airway collapse.

• Airway obstruction, oxygen desaturation, and (in severe

cases) retention of carbon dioxide cause the characteristic
arousals from sleep that are associated with sleep apnea.
 The Apnea hypoapnae index (AHI)
• An apnea is defined as a cessation of breathing for 10
seconds. In obstructive sleep apnea, the apnea is
accompanied by observed ventilatory effort (ie, a chest
rise/fall.)
• In central apnea, no ventilatory effort is seen. Central
apnea is rare.
• A mixed apnea is a disordered breathing event that begins
as a central apnea and ends as an obstructive one.
• A hypopnea is a partial reduction in ventilation with
continued effort for at least 10 seconds.
 Apnae is defined as a stop of ventilation lasting > 10s in air-flow.

Hypopnae is intermittent fall in ventilation >50% and lasting > 10s

The Apnae hypoapnae index (AHI) is defined as the number of episodes per hour of rest.

The Oxygen-desaturation index (ODI) as number of falls in saturation > 4% per hour of rest
 Back to your patient
• We did a sleep test !
 YAKIN DOĞU ÜNİVERSİTESİ TIP FAKÜLTESİ HASTANESİ
UYKU LABORATUVARI
POLISOMNOGRAFİ RAPORU

Patient: ÖZKARDEŞLER,HATİ Date:

CE

DOB: 5/18/1945 PSG Study #:

Age: 66 yrs 4 mos Referring Physician: ,

Sex: K Heightcm.): 164

PSG Tech: Weight(kg): 69
Scored by: Finn Rasmussen BMI: 26
 Time (min.) % of TST % of SPT % of

Total Recording Time (): 470.5 100 %

Total Sleep Time (TST): 391 100 % 84.0 % 83.1 %

Total Stage N1: 13.5 3.5 % 2.9 % 2.9 %

Total Stage N2: 272.5 69.7 % 58.5 % 57.9 %

Total Stage N3: 81 20.7 % 17.4 % 17.2 %

Total Stage R: 24 6.1 % 5.2 % 5.1 %

Total Movement Time: 0 0.0 % 0.0 %

Total Wake Time: 79.5 16.9 %

WASO: 76.0

Wake Time During SPT: 74.5 16.0 %

Latency to Sleep Onset: 3.5

Latency to Sleep: 0

Latency to Persistent Sleep: 75.5

Sleep Efficiency: 83.1 %

Sleep Maintenance: 84.0 %

 By Sleep Stage By Position

TOTAL
NREM Non-Supine Supine

Sleep Time (min.): 367 24 N/A N/A 391

Obstructive Apnea: 53 0 N/A N/A 53

Mixed Apnea: 0 0 N/A N/A 0

Central Apnea: 0 0 N/A N/A 0

All Apneas: 53 0 N/A N/A 53

Hypopneas: 37 0 N/A N/A 37

Apneas + Hypopneas: 90 0 N/A N/A 90

RERA: 0 0 N/A N/A 0

Apnea Index: 8.7 0 0 0 8.1

Hypopnea Index: 6.0 0 0 0 5.7

A/H INDEX: 14.7 0 0 0 13.8

RDI: 14.7 0 0 0 13.8
SaO2 Histogram
30

T 20
i
%
m
10
e

0
50 60 70 80 90 100
% O2
 Treatment?
• CPAP and oxygen ??
Stage Total Sleep,
Defining Traits

• EEG Wave
• I 2-5% Theta wave Light sleep, hypnic
jerks, conscious awareness
• II 45-55%Sleep spindles and K
complexes Consolidated sleep, loss of
conscious awareness, slowed heart
rate, decreased body temperature
III-(IV) 3-8% Delta/slow wave
Deep/restorative sleep, difficult to
arouse; no eye or muscle movements
REM 20-25% Alpha (wakefulness)
Dream sleep, paradoxical sleep,
paralysis, high cortical activity
 Cheyne-Stokes Breathing
-Central apnea

Periodic waxing and waning of ventilation without

pharyngeal obstruction

60 sec.
30 sec.
Included in the definition of OSAHS:
– AHI>5 and
– excessive daytime sleepiness
– Or 2 or more of the following:
• Choking or gasping during sleep
• awakenings
• unrefreshing sleep
• daytime fatigue
• impaired concentration

Sleep. 1999 Aug 1;22(5):667-89

 Relationship between AHI and clinical symptoms

Deegan et al. ERJ 1996;9:117-124

 Consequenses when not treated?
• Cardiopulmonary (myocardial infarction [MI],
arrhythmia, cor pulmonale)
• Memory (short-term memory loss)
• Dyslipidemia (elevated cholesterol,
triglycerides)
• Red blood cells (polycythemia)
• Blood pressure (independently associated with
snoring)
• Gastroesophageal reflux
• Ulcer
• Headache (Morning headaches may result
from carbon dioxide buildup that occurs during
apneic episodes.)
 OSAS Patients Exhibit High Prevalence Of
Cardiovascular Disease: Cross sectional studies

Source: Chest; University of Pennsylvania; PACE; William Bair & Co. estimates
 The spectrum of “obstructive sleep apnea”
still a matter of debate !

in increasing significance:

• primary snoring
• airway resistance syndrome (UARS) ?
• obstructive sleep apnea/hypopnea syndrome
(OSAH)

Snoring UARS OSAH

 Summary
Polysomnographic evaluation
• Although the severity of apnea is not measured by AHI
alone (clinical presentation [daytime somnolence],
hypoxemia, sleep fragmentation, and presence of
arrhythmias are also factors), the following is a simple
classification system of OSA severity:
• An AHI of less than 5 is classified as normal.
• An AHI of 5-14 is classified as mild apnea.
• An AHI of 15-29 is classified as moderate apnea.
• An AHI of more than 30 is classified as severe apnea
 Severity of OSAS according to AASM 1999
Poly(somno)grafie
AHI
• Mild : 5-15
Rating of severity of OSAS
• Moderate :15-30 should be based on the
• Severe : > 30 most severe component

Anamnesis
EDS unwanted napping during activities
• Mild : ..that require little attention (~indoor)
• Moderate : ..that require some attention (~outdoor)
• Severe : ..that require active attention (driving)
 Patients with More Pre-Tests:
Appointment with X ray
suspicious of
a Respiratory ECG
Sleep-related physician(OSA) or Blood
(breathing) Neurology (ex seizures) Ear-nose-throat exam.
Dental exam.
disorders
Physician:
GeneralNurse:
information
Contact information
Disease history
Body measurements
Physical examination
Fill in the sleep forms
PackageInformation
price must about test
include
Polysomnography date the all
Fill in the sleep forms
procedures
arrangement Polysomnography
Form a patient file
Good trustable
Give the and fixed
information prices
about
preparations
for polysomnography and CPAP
titration
Reminder by a phone call
Diagnose and
treatment is offered Sleep
Technicianreport is test
performs the
Responsible doctor must be
the patient made by dedicated
available during the test
Technician can call the doctor for
physician
every problem with the patients or
procedure

Sleep team meets and

discuss patient treatment
Otolaryngology,
odontology and
Pulmonology
(neurology)
Nonsurgical therapy
Weight loss
very effective in patients who are very obese

Improved sleep hygiene

Avoid alcohol or sedative-hypnotic medication prior to sleep.
Alcohol and sedative-hypnotic medications aid in more rapid sleep onset, but the sleep
in not as deep or "refreshing."

Positional therapy
avoidance of the supine position, to decrease snoring and potentially obstruction

Continuous positive airway pressure (CPAP)

CPAP behaves as a pneumatic splint that props open the pharyngeal
walls of the upper airway to prevent collapse.
CPAP is the criterion standard of therapy for obstructive sleep apnea
(OSA) and is the most commonly used initial treatment.
 Sleep Disorderd Breathing

Snoring Mild OSAS Moderate

Severe
osas

CPAP

MRA
Cons. Meas. CPAP
Conservative MRA
Measures

Surgery in selected patients?

ERS 2010
 Scientific evidence OSAS Therapy
Evidence level
• Conservative measures II

• CPAP (Cochrane 2006)

– Primary therapy moderate / severe OSAS: QOL, AHI, EDS I
– Reduction cardiovascular risk and short-term effects hypertension II

• MRA (Cochrane 2006, Syst. Rev Hoekema 2004 en RCT 2008)

– Primary therapy mild / moderate OSAS MRA = CPAP II
– CPAP-failure in severe OSAS II

• AHI MRA << CPAP I

• EDS MRA = CPAP II
• Qol MRA vs CPAP inconsistent

• ENT-Surgery (Cochrane 2006)

– No primary therapy (Cochrane) III
– Selected patients in mild /moderate OSAS (Dutch Nat. Guideline) III

• Bariatric Surgery II

Level I = Several Meta/Systemic analysis, Level II = good RCT’s, Level III = no RCT
 CPAP is the reference treatment
at least in moderate to severe OSA

 Compliance relatively high

 15% initial intolerance

 20% non compliant patients

Pépin Chest 1995; Lévy Sleep, 1996; Pépin AJRCCM, 1999; Petit
AJRCCM 2002; Lévy Sleep Med Rev, 2002
Sin DD et al, Circulation 2000;102:61–66
A patient being evaluated for OSA should be
assessed for surgically correctable causes of
OSA?

Who really wants to wear that mask!

 Effects of surgical weight loss on measures of obstructive sleep
apnea: a meta-analysis

Bariatric surgery significantly improved

obstructive sleep apnoea,
measured by the apnoea-hypopnoea index, but the
mean apnoea-hypopnoea index after surgery was
consistent with moderately severe residual disease,
suggesting that patients should not expect a cure
of sleep apnoea following surgical weight loss.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2625321/?report=abstract
 Main surgical techniques

Uvulo-palato-pharyngoplasty

Background
Ikematsu 1952
standardisation by Fujita 1980

Principle
to remove the redundant tissues (tonsils, uvula…)
to reduce the collapsibility of the velopharyngeal segment
 Main surgical techniques

Uvulo-palato-pharyngoplasty

Results (Sher Sleep 1996)

between 46% and 5% of rate of success
depending on the site of collapse: retrolingual collapse is
associated with a poor outcome

Indications
moderate OSA
velopharyngeal collapse
simple snorers
 Main surgical techniques

Uvulo-palato-pharyngoplasty

Complications
severe
acute respiratory failure
haemorrhage
short and long term
velopharyngeal insufficiency
pharyngeal stenosis as shown
here

Long term outcome ? The results seem to

consistently deteriorate over time
 Main surgical techniques
Phase I surgery

Objectives
enlarge UA
reduce collapsibility

targets

Hyoid bone
mandible
 Main surgical techniques
Phase I surgery

Limited invasivity
progressive steps

Very positive published results

Rate of success
67.0% (55 patients)
J Oral Maxillofac Surg 1989;47:159-64
61.1% (239 patients)
Otolaryngol Head Neck Surg 1993;108(2):117-25
75.0% (15 patients)
Otolaryngol Head Neck Surg 1994;11(6):717-21
 Main surgical techniques
Phase II: maxillo-mandibular ostetomy

Two strategies
Stanford : after phase I
Marburg : only osteotomy

Objectives
enlarge UA
reduce collapsibility
 Phase II: maxillo-mandibular osteotomy
120,0
90,0

Rate of success: 90 % (18/20)

60,0
AHI

59.3

Criteria
30,0

• IAH < 15
• and IAH reduced by more than
50%
11.1 • and normalisation of sleep
structure
0,0

Baseline Postop Am J Respir Crit Care Med 2000;162:641-9

 Effects and side-effects of surgery for snoring and obstructive
sleep apnea: a systematic review 2009

• There was no evidence of any effect from laser-assisted

uvulopalatoplasty (LAUP) or uvulopalatopharyngoplasty
and uvulopalatoplasty (TCRAFTA) on daytime
sleepiness, apnoea, quality of life or snoring
• Uvula removal carried a high risk of persistent side
effects

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2625321/?report=abstract
 Surgery & OSAS
• Nose surgery
• Palatal (for Fujita I obstruction)
• Uvulopalatopharyngoplasty (surgery, laser, RFT)

• Tonguebasis (for Fujita III obstruction)

– Hyoidthyroidpexia
– Genioglossus Advancement procedures
– Radiofrequency Therapy Tongue basis
• Multilevel (for Fujita II obstruction)
– Combined procedures
– Maxillomandibular osteotomy
• Tracheostomy
• Obesity Surgery
 Surgical intervention for treating
OSA is typically reserved for
patients in whom CPAP treatment
fails, whether due to
noncompliance, intolerance, or
ineffectiveness.
Thanks for your attention !!!