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Understanding the Severe
Patient
What to do when CPAP fails!
Definition: Sleep Disordered Breathing
• A disorder of breathing during sleep only, or
significantly affected by sleep. In general, the
patient has little or no problem breathing
while awake.
• Not a true sleep disorder
Categories
• Mechanical : The inappropriate collapse of the
pharynx during sleep
– Snoring
– Inspiratory Flow Limitation
– Obstructive sleep apnea

• Chemical : Central Sleep Apnea
• Neuromuscular : paralysis of involuntary
muscle (diaphragm) or lack of adequate tidal
volume requiring ventilation at night
Continuum of Sleep Disordered
Breathing
Least
Mechanical

Severity
Chemical

Most
Neuromuscular
Continuum of Sleep Disordered
Breathing:
Treatment
Least

Severity

Most

Mechanical

Chemical

Neuromuscular

Oral Appliances
CPAP
Combination
Surgery
Tracheostomy

Cpap
Vpap
Oral Appliances
Combination
Oxygen

Ventilator
Tracheotomy
Combination
Continuum of Sleep Disordered
Breathing:
Treatment Success
Severity

Least

Mechanical

Chemical

CPAP <50%
?
OA’s >50%
TAP-PAP > 95%
Tracheotomy 100% ?

Most
Neuromuscular
Ventilator +
Tracheotomy = 100%?
TAP-PAP = 100%?
Why is the Passive Pharynx So
Important???
• Pharyngeal muscles are hypotonic during
sleep
• REM sleep causes atonia of pharyngeal
muscles.
• Allows the airway to collapse

© W. Keith Thornton D.D.S.
Sleep Eliminates Pharyngeal
Reflexes

© W. Keith Thornton DDS
Physics of Airway Collapse
• Poiseuille's Law
– Size of tube and effect on negative pressure to
breath and speed of airflow

• Bernoulli’s law
– Increase in speed of airflow decreases size of
flexible tube

• Pathology
– Large negative Inspiratory pressure
– And/or total collapse
© W. Keith Thornton D.D.S.
Neuromuscular Factors

P mus –P lum > atmosphere

Pharynx Open
© W. Keith Thornton DDS
Neuromuscular Factors

P mus - P lumin < atmospheric

Pharynx closed
© W. Keith Thornton DDS
Genioglossal EMG in OSA

© W. Keith Thornton DDS
No Mandibular Protrusion (Oshima et al.)

© W. Keith Thornton D.D.S.
Mandibular Protrusion (Oshima et al.)

© W. Keith Thornton D.D.S.
Inspiratory Flow Limitation

© W. Keith Thornton DDS
Inspiratory Flow Limitation : IFL

Airflow
Normal
Esophageal
pressure

IFL

Normal

© W. Keith Thornton DDS
Severe IFL, no OSA
90%

5 Minutes, RDI 0, T90 = approx. 80%, Severe Hypoventilation
Severe Inspiratory Flow Limitation, No heart rate variability
10 Minutes, Severe, RDI=96

16 events, RDI = 96
T90 = approx 20%
Little heart rate variability, 50-67
2 Minutes, Severe, RDI=96
90%

67 bpm

50bpm
16 events, RDI = 96
T90 = approx 20%
Little heart rate variablity 50to 67
Lowest desat 83%
2 Minutes, Severe, RDI=96
90%

67 bpm

50bpm
16 events, RDI = 96
T90 = approx 20%
Little heart rate variablity 50to 67
Lowest desat 83%
10 minutes, severe osa, RDI=66
90%

80bpm
40bpm

RDI = 66, T90= 75%, heart rate variability = 40-80
Lowest desat= 63
2 minutes, severe osa, RDI=66

90%

80bpm
40bpm

RDI = 66, T90= 75%, heart rate variability = 40-80
Lowest desat= 63
2 minutes, severe osa, RDI=66

90%

80bpm
40bpm

RDI = 66, T90= 70%, heart rate variability = 40-80
Lowest desat= 63
Patient controlled protrusion
Dose dependent improvement of pharyngeal
collapsibility in response to mandibular advancement
Velopharynx

Oropharynx
5

5

0

0

P’close
(cmH2O)

-5

-5

-10
-15

-10

Kato et© W. Keith Thornton D.D.S.
al., (2000, Chest)
Preliminary results
Patient #1
No IFL at 4mm advancement

Patient #2
No IFL at 10 mm advancement
0.20

0.15

10 mm
8 mm
6 mm
4 mm
2 mm
0 mm

0.15

Airflow
(L/s)

0.10
0.10

0.05

0.05

0.00

0.00

0

2

4

6

0

2

4

6

Oropharyngeal pressure (cmH2O)
(unpublished)
© W. Keith Thornton D.D.S.
Conclusions
• Protrusion increases the cross-sectional area
• Protrusion produces a hypotonic genioglossus
• Efficacy is dose dependant

© W. Keith Thornton D.D.S.
Maximum Protrusion

Voluntary

Induced
Stretched
© W. Keith Thornton D.D.S.
Treatment Position

Maximum protrusion: MP
Maximum passive protrusion: MPP
17 mm

Original Maximum protrusion 8mm
Present Maximum portrusion 17mm
170% of original maximum
23mm

23mm 185%
Macroglossia, Maxillary Hypoplasia
Severe IFL
Immediate TAP CS
Increase vertical
Patient History
• Loud snoring, excessive fatigue, several wrecks
• Uncontrolled hypertension, 5 different
medications per day
• Morning blood pressure on medication 175/120
• Stroke 5 years previous
• Four psg’s, no osa, no diagnosis, tried and failed
cpap
• HST: RDI 3, significant upper airway resistance
Before appliance therapy
After therapy
Macroglossia, Maxillary Hypoplasia

Lateral view,
Patient in occlusion

Centric Occlusion
5. Macroglossia, Maxillary Hypoplasia

Narrow arch,
High palate without
room for tongue

Normal
mandibular arch
size
Macroglossia, Maxillary Hypoplasia

Size of tongue

Normal posture of
tongue
Macroglossia, Maxillary Hypoplasia

Normal lip posture

Freeway space
Immediate TAP CS
• Moved screw forward to compensate for
maxillary hypoplasia
• Opened vertical 15 mm to accommodate
tongue
• Patient titrated himself 5mm beyond
maximum protrusion in first week
• Blood pressure on awakening 145/90
• No snoring, head aches, fatigue
Immediate TAP CS
15mm

5mm
TAP III from lab

Not enough vertical or protrusive
Encroachment on tongue
Final TAP III appliance

6mm

17mm

Initial vertical 8mm
Added 6mm to plate, 3mm to
bar
Total vertical, 17mm
Neuromuscular Patients
•
•
•
•
•
•

Post Polio
ALS
Muscular dystrophy
Brain tumors affecting motor function
Congenital
Spinal Cord Injuries
Neuromuscular Patients
• Generally need ventilatory assistance during
the day
• Paralysis of diaphragm
• Intercostal muscle deterioration
• Limited function of limbs
• Adequate dentition for retention
Neuromuscular Patients:
Treatment
• Tracheotomy (medical)
• Custom mask, oral appliance combination
(dental)
• No other choices except iron lung
Neuromuscular Patients:
History
45 yo, post polio
Paralyzed from neck down
Mask developed by DRI using
“bite block”
Pressure: 45 cmw
Volume ventilator
Could use intercostals during
day
Inserted by biting into trays
Neuromuscular Patients:
History
Problems:
Fabrication techniques
Retention
Leakage
Reparability
Bulk
Technique sensitivity
Caregiver issues
Treatment of the Severe Sleep
Apnic
An eight year history
2002- 2010
Patient: Ron Doe
HPI
2003
•
•
•
•
•

Hx of loud snoring starting in dental school
Recent weight gain of 100 lbs (300 lbs)
Hypersomnolence
Acid reflux
Htn
HPI
2003
•
•
•
•
•

Fibromyalgia
Night sweats
Joint aches
Numb feet
Nocturia
Family and Social Hx
• Divorced and remarried
• Father died at age 51 of HA
– Professional football player with very large neck

• Son and grandchild have osa by symptoms
• Orthodontist
– Focused on treating non-extraction and
developing airways
– Very knowledgeable in tmd and occlusion
Treatment Hx
• No initial sleep study or consultation with
physician
• Numerous oral appliances tried over 1 yr
– Herbst
– Silencer
– Snore guard
– Silent Knight

• Failure of all appliances
• Appliances still fit
Results
Before TAP

After TAP

© 2010 Airway Management, Inc.
TAP III 2010

Plate anterior to upper incisors
PSG
2/2/2009
Diagnostic

CPAP alone

TAP (4/4/09)

RDI

82.2

23.6

18.2

Minimum O2 Sat

74

77

75

Sleep Efficiency

88.1

65.9

NA

PLM

99

22

NA

Tried Bilevel CPAP at 11/7 cmw
Could not tolerate
TAP-PAP 2010
• TAP-PAP custom mask (TPCM)
PSG 12/28/2010
TAP

TAP-PAP
Custom

TAP-PAP
Universal

TAP-PAP
Nasal

RDI/ AHI

20.7/18.9

2.5/2.5

0/0

0/0

Mean O2 Sat

92.6 %

94%

93 to 94%

94 to 98%

Lowest O2 Sat 86.0%

94%

90%

94%

Time< 90%

0%

0%

0%

12-13 cmw

9 to 10 cmw

10 to 11 cmw

4.8%

CPAP pressure
Comments

Inadequately
treated alone

Mask leak,
Mask was not
attached
correctly

Sealed well,
Preferred by
patient
Understanding the Severe Sleep Apnic Patient: An Eight Year History

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