OSA is an entity that is increasingly being managed by otolaryngologists...Hope this presentation helps to clear any doubts regarding its diagnosis and management!

1. Dr Dhaiirya Joshi
Resident ,IGGMC

2.  Physiology of sleep
 Definitions
 Pathophysiology of OSA
 Clinical features
 Investigations
 Medical Management
 Surgical Management

3.  Obstructive sleep apnoea syndrome
described as Pickwikian syndrome in Charles
Dicken‟s work-‟The Pickwick papers”
 Guilleminult,Eldridge and Dement described
first sleep apnoea in 1973,and established
first sleep clinic.

4.  Behavioral and neurobiological state which is
characterized by a change in the state of
consciousness and bodily as well as
neurological behavior.
 Involuntary cyclic process which is
dependent on environmental and internal
circumstances of an individual

5. Divided into
REM (Rapid Eye Movement) sleep
NREM (Non-Rapid Eye Movement) based on
 Environmental Responsiveness
 General Physiology
 EEG waveforms (of muscle and eye
movement)
 Muscle tones
 Mental activity

6. Principal characteristics of REM and NREM sleep
REM SLEEP SLOW-WAVE/NREM SLEEP
EEG De-synchrony EEG Synchrony (slow
(irregular, low voltage waves)
high freq)
Lack of Muscle Tones Moderate Muscle Tones
Rapid Eye Movement Slow or Absent Eye
Movement
Genital Activity Lack of Genital Activity
Dreams
Dreams -
Increased autonomic
activity

8. NREM sleep divided into 4 stages
 Stages 1 and 2- EEG voltage low and freq
mixed.
 Stages 3 and 4- EEG voltage high and freq
slow. So also referred as Slow wave
sleep(SWS)
 Stage 2 – Predominant sleep stage
50% of sleep time

9. REM sleep
 Occurs 1st time 90 min after onset of sleep
 Recurs 4-6 times throughout night
 Accounts for 25% of total sleep
 Increasing age, alcohol and sedatives
decrease REM sleep.
 Helps in brain development, promote learning
and strengthening memories.

10.  Reticular activating system-promotes
wakefulness when active.
 Controls the intrinsic sleep drive, which
increases with time spent awake.
 Adaptive sleep drive-influenced by behavioral
responses to environment and reflex
responses to sensory stimulation.

11.  Suprachiasmatic nucleus-
- Controls the circadian rhythm.
- Keeps the sleep/wake cycle in sequence with
the environment,but does not initiate sleep.
 Melatonin
- Released by pineal gland in response to
darkness.
- Promotes sleep.
- Acts on suprachiasmatic nucleus to
change circadian rhythm and reduce
body temp.

12.  Reduced chemical and mechanical drives to
breathe.
 Respiratory output via phrenic nerve and
other motor nuclei to spinal cord.
 NREM sleep- Diaphragmatic activity - N
Intercostal ms activity –
-Expansion of ribcage and diaphragmatic
activity.
 REM sleep – Diaphragmatic activity –
- Intercostal ms activity -

13.  REM sleep
- Reduction of lung compliance.
- Decrease in lung volume.
- Increases V/P mismatch.
- Increase in abdominal contribution to
breathing.
 So overall-reduction in ventilation

14.  Hypoventilation with mild hypoxemia and
hypercapnia.
 Metabolic rate reduced by 10-25 %.
 Arterial PCO2 increases- 0.5 kPa
 Arterial PO2 decreases – 0.5-2 kPa
 Hypocapnic apnoeic threshold more sensitive.
 Upper airway dilating capacity decreases
partially due to hypercapnoea due to
hypoventilation.

16.  OBSTRUCTIVE SLEEP APNOEA(OSA)
Condition characterized by repetitive upper airway
obstruction leading to apnoea and hypopnoea
causing sleep fragmentation, cardiovascular
stimulation and oxygen desaturation during
sleep.More than 5 apnoeas per hour of sleep.
 UPPER AIR WAY RESISTANCE SYNDROME(UARS)
Increased respiratory efforts(as identified by
esophageal pressure measurements) with frequent
arousals as measured from EEG during diagnostic
overnight polysomnography,but without apnoeas and
hypopnoea

17.  OBESITY HYPOVENTILATION SYNDROME(OHS)
Daytime respiratory failure in presence of
obesity(BMI > 30kg/m2 ) in absence of airway
obstruction from respiratory spirometry.
Respiratory failure is defined as PaCo2 >
45mmHg and PaO2 < 70mmHg
 CENTRAL SLEEP APNOEA
◦ Cessation of ventilation during sleep due to
loss of ventilatory drive
◦ ≥ 10 second pauses with no associated
respiratory effort

18.  Upper airway more prone to collapse if
-Upper airway narrowing
-Decreased intraluminal pressure
-Extraluminal pressure increased
 When –ve pressure by inspiratory muscles
exceeds the force generated by dilator
muscles Collapse
 Critical pressure(Pcrit) – pressure reqd to
collapse upper airway.

19.  OSAH
+ve Pcrit with airway collapsing at
atmospheric pressure.
So +ve pressure to relieve obstruction.
 Normally –ve pressure required to collapse
airway.

20.  Upper airway dilating muscles influencing
-Hyoid position- eg Geniohyoid
-Tongue position- eg Genioglossus
-Palate position- eg Tensor palitini
 Geniohyoid and genioglossus – Phasic
inspiratory activity maintained during NREM
sleep.
 Tensor palatini – Tonic actvity which
decreases during sleep.

22.  Upper airway dilating muscles activated by
–ve airway pressure stimulating nasal and
laryngeal receptor.
 Activity by hypoxia.
 Progesterone dilating activity.
 Serotonin dilating activity and reduced in
patients with OSA.

23.  Supine position-
-Posterior displacement of tongue and
mandible.
-Loss of tone and gravity.
-More marked in REM sleep.
 Obesity- fat deposition around upper airway.
 Shape of airway - More oval upper airway.
 Chronic vascular over perfusion-upper airway
edema.

24.  Upper airway edema secondary to mechanical
trauma during snoring and recurrent airway
obstruction.
 Further reduction in airway – perpetuates
obstruction
 Overuse myopathy of dilating muscles due to
increase workload.
 Chronic sleep deprivation impairs dilating
activity.

27.  Obesity
Strongest risk factor for OSA
◦ Present in > 60% of patients referred for
a diagnostic sleep evaluation
 Alters upper airway mechanics during sleep
1. Increased parapharyngeal fat deposition:
neck circumference: > 17” males
> 16” females
With subsequent smaller upper airway
 increase the collapsibility of the pharyngeal
airway

28. 2. Changes in neural compensatory mechanisms that
maintain airway patency:
 diminished protective reflexes which otherwise
would increase upper airway dilator muscle
activity to maintain airway patency
3. Waist circumference
Fat deposition around the abdomen produces
 reduced lung volumes (functional residual
capacity) which can lead to loss of caudal
traction on the upper airway
 low lung volumes are associated with
diminished oxygen stores

29. MALE GENDER
 Increased neck and waist circumference
 Pharyngeal airway length
 ? Women not reporting the classic symptoms
 ? Differential response of bed partner to
symptoms
of obstructive breathing during sleep
 ? Healthcare providers have lower index of
suspicion
for considering OSA in men than women

30.  CRANIOFACIAL ABNORMALITIES
• Mandibular body length
• Retrognathia
• Tonsilar hypertrophy
• Enlarged tongue or soft palate
• Inferiorly positioned hyoid bone
• Maxillary and mandibular retro position
• Decreased posterior airway space

31.  OTHER
• Smoking
• Alcohol consumption
• Sedatives (benzodiazepines)
 reduce nerve output to compensatory
dilator
muscles
 increase OSA severity in patients with
preexisting syndrome.

32. NOCTURNAL SYMPTOMS
 Snoring
– reflects the critical narrowing
- population survey: habitual snorers
25% of men, 15% of women
- prevalence increases with age
- the most frequent symptom of OSA
- absence makes OSA unlikely
(only 6% of patients with OSA did not report)

33.  Witnessed apneas
 Nocturnal choking or gasping
- report of waking at night with a choking
sensation; passes within a few seconds
 Insomnia
- sleep maintenance insomnia
- few have difficulty initiating sleep

34. DAYTIME SYMPTOMS
 Excessive daytime sleepiness(EDS)
- severity can be assessed
 subjectively = questionnaires
(Epworth Sleepiness Scale)
 objectively
MSLT = Multiple Sleep Latency Test
MWT = Maintenance of wakefulness
Test
Osler Test

35.  Fatigue
 Memory impairment
 Personality changes
 Morning headaches or nausea
 Depression

36. American Academy of Sleep Medicine Criterias
A. Excessive daytime sleepiness that is not better
explained by other factors
B. Two or more of the following that are not
better explained by other factors:
-choking during sleep
-recurrent awakenings
-unrefreshing sleep;
-daytime fatigue
-impaired concentration
C. AHI (five or more obstructed breathing
events per hour during sleep)

38. QUESTIONNAIRE
 Does pt snore?
 Is the pt or the partner troubled by snoring?
 How severe is the snoring?Audible if
 in the same room
 in an adjacent room?
 downstairs/anywhere in the house?
 next-door noeghbour?
 Is the snoring positional or does it occur in all
sleep positions?

39.  For how long pt has been snoring?
 Are there clinical features suggestive of OSA?
 regular multiple apnoeic episodes most
nights?
 cerebrovascular complications like stroke,
HTN,MI.
 endocrine co-morbidity like DM or
hypothyroidism.

40. Are the any aggravating factors?
 alcohol,how many per week?
 smoking how many per day? passive
smoking?
 current wt and whetehr this is increasing?
 previous tonsil or adenoid surg?
 other upper aerodigetive tract abnormalities?

41.  Have any conservative treatment tried such as
wt loss,mandibular advancement splints or
nasal valve dilators?
 Does this pt represent an anesthetic risk?
 is airway anatomically difficult?
 does the pt have cardiovascular,repiratory or
cerebral disease that would significantly
increase risk of anaesthesia?

42. Examination of oropharynx,hypopharynx and
larynx to establish whether
 Nasal airway is patent
 Postnasal space is small
 There is long redundant soft palate with swollen uvula
 Palatine and/or lingual tonsils enlarged
 Tongue base is prominent
 There is large floppy epiglottis
 Vocal cord palsy
 Retrodisplaced Mandible
 Retro-displaced hyoid complex
 Dental malocclusion or large tongue

46. FRIEDMAN PALATE POSITION

47. TONSIL SIZE

49. PALATE VARIATIONS

50. ESS > 15 significant

51. OVERNIGHT OXIMETRY
 Measures O2 saturation and provides pulse
data.
 Assumes that when individual has apnoea or
hyponoea O2 saturation falls.
 Once apnoea or hyponoea relived- O2
saturation rises.
 Falls and rises – Oxygen dips
 Dip of 4 or more % regarded as meaningful.

52.  Oxygen desaturation index(ODI)- No of times
O2 saturation falls by 4% per hr.
 ODI > 15 /Hr siggestive of OSA.
 Good specificty and +ve predictive value but
poor sensitivity and _ve predictive value.
 In UK some sleep centres use it as a sceening
test

54. HOME MULTI CHANNEL TESTING
 Kit consists of
-Nasal/oral flow by pressure cannulae
-Chest and abdominal movts by Velcro belts
-Pulse oximetry
 Disdvantage- Sensor failure and loss of signal
 Chest and abdominal belts allow to determine if
apnoeas are related to respiratory effort
-Central apnoea – no chest or abdominal
movts
-OSA – movts +

55. HOME MULTI CHANNEL KIT

56.  Apnoea- compete cessation of airflow for
atleast 10secs irrespective of oxygen
desaturation or arousals.
 Hypopnoeas
– Reduction in airflow(amplitude of signal)
between 50 -90%(with or without a 3% O2
desaturation and/or EEG arousal) OR
- Reduction in airflow of <50% + 3% or more
O2 desaturation and/or EEG arousal

58. POLYSOMNOGRAPHY
 Measurements
◦ EEG, EOG, submental EMG – used to identify
stages of sleep
◦ Airflow – measured by nasal prongs with pressure
transducer, give a quantitative measure of
inspiratory airflow
◦ Respiratory Effort
◦ O2 saturation
◦ ECG
◦ Body position
◦ Anterior tibialis EMG – to detect limb movements

59.  Derived Information
◦ Total Sleep Time
◦ Sleep Efficiency
◦ Sleep stage latency
◦ Sleep stage distribution
◦ Arousals
◦ Apneas
◦ Hypopneas
◦ Indices
◦ Snoring
◦ Body position
◦ Oxygen desaturations
◦ Limb Movements

61. Apnea-Hypopnea Index (AHI) – total number of
apneas and hypopneas per hour of sleep.
 Mild- 5 to 20 per hour.
 Moderate- 21 to 30 per hour.
 Severe- >30 apnoea per hour.

62.  Respiratory effort-related arousal(RERA) –
events like hypopneas, with less than 4% drop
in saturation
 Respiratory disturbance index(RDI)
Apneas + hypopneas+ RERA‟s/hour
-RDI > 5 is considered OSA
-RDI 5 –20, mild
-RDI 20 –40, moderate
-RDI > 40, severe

63. DYNAMIC NASOPHARYNGOLARYNGOSCOPY
 Flexible fiberoptic scope to examine the
upper airway.
 Determine whether there are any fixed
blockages in the upper airway such as a
deviated septum or nasal polyps.
 Demonstrate the dynamic behaviour of the
airway under conditions that promote
collapse or which help to prevent collapse.

64. Flexible Fiberoptic Scope
View of the nasopharynx
Structures to note are the
adenoids and the depth
and height of the
nasopharynx.

65.  View of the velopharynx
The velopharynx is bounded
by the soft palate (top), the
back of the throat, and a
muscle complex on each side.
 View of the oropharynx
and hypopharynx
This is the part of the upper
airway that contains the
tonsils and the tongue.

66.  View of the glottis

67. MULLER‟S MANOEUVRE
 The patient is asked to breathe in while the
mouth is closed and the nose is pinched shut.
 This generates a –ve pressure in the upper
airway.
 Just snorers, slight inward movement of the
soft palate and the back of the throat but the
glottis remains visible.
 OSA show varying degrees of collapse in the
side walls of the velopharynx, at the base of
the tongue, and at the back of the throat which
narrows the airway by more than 25%.

68. MULLER‟S MANOEUVRE
Resting airway Severe airway collapse
during Muller's
manoeuvre

69. JAW THRUST OR MANADIBULAR ADVANCEMENT
 Enlarges the airway by several mechanisms
mostly the base of the tongue is pulled forward.
 Also lifts the pharyngeal muscles off the spine
and places them under tension.
 Enlarges and stabilizes the airway at several
levels.
 Patients who show a good response to this
manoeuvre can use a dental appliance for
treatment of their snoring or OSA (provided that
their teeth are in good shape).

70. JAW THRUST
Resting airway Airway with jaw thrust

71. SLEEP NASOENDOSCOPY
[Drug induced sleep endoscopy (DISE)]
 1st described by Croft and Pringle in 1991
 Pt sedated with propofol to a level sufficient to
induce snoring.
 Operator examines upper aerodigestive tract in
supine position to determine levels of
obstruction.
 Anaesthetist must be present with full cardiac
monitoring and resuscitation facilities.
 Respiratory stimulants can be used to encourage
snoring.

72. Sleep nasoendoscopy gradings
Grade Obstruction
1 Simple palatal level snoring/palatal
flutter
2 Single level palatal obstruction
3 Palatal level obstruction with
intermittent oropharyngeal
involvement
4 Sustained multi segmental obstruction
5 Tongue base level obstruction
6 Isolated epiglottic involvement

73. ESOPHAGEAL MANOMETRY
 Used in conjunction with screening sleep
studies to diagnose apnoeas and
hypoapnoeas.
 Evaluate relationship between reflux and OSA.

74. DYNAMIC ULTRAFAST MRI
 Can be used in awake and asleep pts to
assess the site of obstruction.
 Midline saggital and cross sections at various
levels most useful.
 In awake pts with OSA-very close correlation
with videoendoscopy found.
 Not widely used due to high cost and time
taken.
 Sleep in an MRI machine may not be
representative of normal sleep patterns.

76. 3-DIMENSIONAL CT
 Retropalatal space is most relevant area.
 Gives an idea about modifications in palatal
surgeries required to increase lateral
dimensions of this space

78. CEPHALOMERTRY
For size of airway,bulkiness of surrounding
tissues & anatomical abnormalities
 S sella
 N nasion
 ANS anterior nasal spine
 A subnasale
 B supramentale
 PAS posterior airway space
 Go gonion
 Gngnathion

79. NASAL SPRAY TEST
Using topical nasal decongestant on alternate
nights and comparing severity of snoring and
apnoea.

80. STANFORD METHOD
Craniofacial
Measurements
 Palatal Height
(distance D - F): mm
=P
 Maxillary Intermolar
Distance: mm = Mx
 Mandibular Intermolar
Distance: mm = Mn
 Overjet: mm = OJ
 Angle AC is 20 degrees

81. The Stanford Score =
{P + (Mx - Mn) + 3 x OJ} + {[Max(BMI - 25, 0)] x
(NC/BMI)}
= {Craniofacial Score} + {Obesity Score}
 If > 70 patient has OSA; and if < 70, there is a
10% chance of OSA
 If the jaw is too small, there will not be enough
room for the tongue. This is reflected in the
Craniofacial Score.
 If the person is obese and/or has a very thick
neck it can lead to collapse of the throat during
sleep. This is reflected in the Obesity Score.

82.  Weight Loss/Exercise
 Nasal Obstruction/Allergy Treatment
 Sedative Avoidance
 Smoking cessation
 Sleep hygiene
◦ Consistent sleep/wake times
◦ Avoid alcohol, heavy meals before bedtime
◦ Position on side
◦ Avoid caffeine, TV, reading in bed

83. SLEEP POSITION
TRAINING
Use of a tennis
ball sewn into
the back of a
night shirt as a
means of
training the
patient to avoid
the supine
position and
sleep in the
lateral
position.

84. CONTINUOUS POSITIVE AIRWAY PRESSURE(CPAP)

85. CPAP
 Mainstay of treatment
 Acts as a „pneumatic splint‟.
 Blowing air via a mask and tube supports
pharyngeal and palatal walls to prevent
collapse.
 Two types
-Fixed pressure type
-AutoCPAP

86. CPAP

87. MASKS
 Can be nasal or full face.
 Chin straps can be used keep mouth closed.
 Kept in place with Velcro straps.
 Have expiratory port to prevent reinhalation
of expired air.

88. SETTING UP ON CPAP
 Patient education
 Group video workshops
 Pressure(cm H2O)=(0.16 x BMI) + (0.13 x NC)
+ (0.04 x AHI) – 5.12
NC=Neck circumference
 Split night- Diagnostic PSG and halfway
through night CPAP started.
 Set fixed pressure is 95th percentile-pressure
reqd to elilimnate 95% of apnoeas and
hypopnoeas.

89.  Has been shown to objectively
◦ Decrease blood pressure
◦ Decrease day time sleepiness
 Problems
By 3 years of treatment 12-25% have discontinued
treatment due to
◦ Mask discomfort
◦ Claustrophobia
◦ Aerophagia
◦ Nasal stuffiness
◦ Skin abrasions
◦ Ulcerations over nasal bridge
◦ Leaks
◦ Rarely pulmonary barotrauma

90.  BiPAP
◦ Useful when > 6 cm H2O difference in
inspiratory and expiratory pressures
◦ No objective evidence demonstrates
improved compliance over CPAP

91. ORAL APPLIANCES
 Mandibular advancement device
 Tongue retaining device
◦ Protrude the mandible forward and hold
tongue more anteriorly, away from the
posterior pharyngeal wall
◦ More effective in patients with mild –
moderate OSA, AHI 5-15

93. INDICATIONS FOR SURGERY
 Apnea-Hypoapnea index>15
 O2 desaturation<90%
 AHI>5 or<14 with day time sleepiness.
 Upper airways resistance syndrome.
 Cardiac arrhythmias with obstruction.

94.  Nasal Surgery
◦ Limited efficacy when used alone
◦ Verse et al 2002 showed 15.8% success rate
when used alone in patients with OSA and
day-time nasal congestion with snoring
(RDI<20 and 50% reduction)
 Adenoidectomy (children)

95. Uvulopalatopharyngoplasty(UPPP)
 1st described by Ikematsu in 1950‟s.
 Popularized by Fugita in 1985.
 Resection of strip of soft palate and uvula +
tonsillectomy.
 Tonsillar pillars then sutured.
 Used in pts of severe snoring with OSA.

96. COMPLICATIONS OF UPPP
 Severe post op pain.
 Haemorrage.
 Respiratory obstruction due to laryngospasm.
 Post –op pulmonary edema.
 Velopharyngeal insuffiency.
 Nasopharyngeal stenosis.
 Dry throat due to loss of lubricating function of
uvula.
 Voice changes.
 Taste disturbances.

98. Cahali, 2003 proposed
the new Lateral
Pharyngoplasty technique
for patients with
significant lateral
narrowing

100.  Laser Assisted Uvulopalatoplasty(LUAP)

101.  Introduced by Kamami in France,1993.
 Can be done as OPD procedure.
 Lignocaine+adrenaline injected at the base of
uvula and 1cm lateral to midline on soft
palate.
 Partial vapourization of the uvula with a CO2
laser.
 Stiffens soft palate and minimizes palateal
flutter.
 May require repeated sessions.

102. LAUP

103. RADIOFREQUENCY ABLATION

104.  Similar to diathermy but
-lower power (2-10 W)
-lower tissue temperatures(60-90o C )
-freq of 460 Hz
 Applied to specific submucosal sites causing
-fibrosis of muscular layer
-volumetric tissue reduction
 3 types of radiofrequency devices
-Somnus unit
-Celon device
-Coblator unit

105. Pillar Palatal Implant System
 Three Implants Per Patient
 Implants are
• made of Dacron®
• 18 mm in length and 1.8 mm in diameter
• meant to be permanent
• can be removed
 FDA Approved for SNORING
 FDA Approved for mild to moderate SLEEP
APNEA - AHI UNDER 30

106.  Antibiotic 1 hour pre-op
 Mouth Rinse (chlorhexidine gluconate or
equivalent)
 Hurricane or Equivalent Topical Spray
 Ponticane or Equivalent
 Topical Jelly Anesthetic, optional.
 Local Anesthetic Infiltration: 2 to 3 cc.
Beginning at the junction of the Hard and Soft
Palate inject entire “Target Zone”. (lidocaine
with epinephrine or equivalent)
 Have available: Flexible Scope, Angled Tonsil
Forceps

107. 2 m.m. apart
Minimum
Palate Length
25 mm

108.  Needle through the
mucosa layer into the
muscle.
 The insertion site
should be as close to
the junction of the
hard and soft palate
as possible.
 Needle advancement
continued in an arcing
motion until the “Full
insertion depth
marker” is no longer
visible.

109. INSPECTION
 Inspect the needle
insertion site.
 If a portion of the
implant is exposed, it
must be removed with a
hemostat.
 Inspect the nasal side of
the soft palate using a
Flexible Naso Scope.
 If the implant is
exposed, it must be
removed.
 An angled tonsil forceps
is recommended.

110. PREFERRED PATIENT
 BMI less than 32
 AHI Less than 30
 No Obvious Nasal Obstruction
 Small to Medium Sized Tonsils
 Mallampati Class І or Class ΙΙ
 Friedman Tongue Position I and II
 Minimum 25mm Palate to treat

111. TONGUE BASED PROCEDURES
 These are rarely done alone
 Part of multilevel surgery
 Knowledge of anatomy and important
structures is critical
 Address the tongue base by three
mechanisms
-Tissue reduction
-Improved tension
-Increased airway space

112. TONGUE BASE ANATOMY
 Hypoglossal nerve, lingual artery
neurovascular bundle
 Foramen cecum and sulcus terminalis
 Retromolar trigone
 Lingual tonsil
 Epiglottis
 Hyoid

113. Radiofrequency base of tongue ablation
 Advantages
-Relatively safe (3.5% overall complication
rate)
-Can be performed on outpatient basis
-Can be performed in as little as one sitting
 Disadvantages
Can only ablate a small amount of tissue

114. Submucosal minimally invasive lingual
excision(SMILE)
 Lingual arteries found and marked using
doppler
 Midline of tongue one centimeter anterior to
the circumvallatepapillae an incision is made
using 15 blade
 Coblator wand to ablate tissue to vallecula
 Stay within 1 cm of midline, and medial to the
markings for artery
 Leave open for drainage

115. SMILE

116. LASER MIDLINE GLOSSECTOMY AND
LINGUALPLASTY

117. GENIOGLOSSUS ADVANCEMENT

118. REPOSE(SUTURE SUSPENSION OF TONGUE)
 Intraoral incision is made in the frenulum and
a titanium screw is placed in the lingual
cortex of the geniotubercle
 Permanent suture is passed through the
paramediantongue musculature to the tongue
base and then back through.
 1 cm lateral to midline, and 1 cm below
foramen cecum
 Pulls the tongue base anteriorly
 Increase tension, and posterior airway space

119. LINGUAL SUSPENSION

121. HYOID MYOTOMY
AND SUSPENSION
◦ Advances hyoid bone
anteriorly and
inferiorly
◦ Advances epiglottis
and base of tongue
◦ Performed in
conjunction with
other procedures
◦ Dysphagia may result

122. Maxillary-Mandibular Advancement
◦ Severe disease
◦ Failure with more conservative measures
◦ Midface, palate, and mandible advanced
anteriorly
◦ Limited by ability to stabilize the segments
and aesthetic facial changes
◦ Performed in conjunction with oral surgeons
◦ Temporary or permanent paresthesia

124. TRACHEOSTOMY
 Ultimate treatment modality
 Temporary treatment while other surgery is
done
 Morbid obesity
 Severe OSA when more conservative
treatment failed,refused or not tolerated
 Life threatening cardiopulmonary
complications
 Significant anesthetic/surgical risks
 Once placed, uncommon to decannulate

125. ALGORITHMS
 Stanford Protocol
• Riley et al 1992 Studied 2 phase approach for
multilevel site of obstruction
• Phase 1: Genioglossal advancement, hyoid
myotomy and advancement, UP3
• Phase 2: Maxillary-Mandibular advancement in 6
months if phase 1 failed
• Reported >90% success rate in patients who
completed both phases
• Testing is done at 6 months

126. FRIEDMAN ALGORITHM
 Chance of success with surgical management
decreases with increasing Friedman stage
 Stage I and II patients have good success with
UPPP and tongue base procedures
 Stage III and IV patients have much lower
rates of success following UPPP/tongue base