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

Mechanical

SeverityLeast MostChemical Neuromuscular

Continuum of Sleep Disordered Breathing:Treatment

SeverityLeast Most

ChemicalCpapVpapOral AppliancesCombinationOxygen

NeuromuscularVentilatorTracheotomyCombination

MechanicalOral AppliancesCPAPCombinationSurgeryTracheostomy

Continuum of Sleep Disordered Breathing:

Treatment Success

SeverityLeast Most

Chemical?

NeuromuscularVentilator +Tracheotomy = 100%?TAP-PAP = 100%?

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

Why is the Passive Pharynx So Important???

© W. Keith Thornton D.D.S.

• Pharyngeal muscles are hypotonic during sleep

• REM sleep causes atonia of pharyngeal muscles.

• Allows the airway to collapse

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

© W. Keith Thornton DDS

P mus –P lum > atmosphere

Pharynx Open

Neuromuscular Factors

Pharynx closed

P mus - P lumin < atmospheric

© 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

Esophagealpressure

Inspiratory Flow Limitation : IFL

© W. Keith Thornton DDS

NormalAirflow

Normal

IFL

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

Severe IFL, no OSA90%

10 Minutes, Severe, RDI=96

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

90%

67 bpm

50bpm

2 Minutes, Severe, RDI=96

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

90%

67 bpm

50bpm

2 Minutes, Severe, RDI=96

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

10 minutes, severe osa, RDI=66

80bpm

40bpm

90%

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

2 minutes, severe osa, RDI=66

80bpm

40bpm

90%

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

RDI = 66, T90= 70%, heart rate variability = 40-80Lowest desat= 63

2 minutes, severe osa, RDI=66

80bpm

40bpm

90%

Patient controlled protrusion

Dose dependent improvement of pharyngeal

collapsibility in response to mandibular advancement

-10

-5

0

5

P’close

(cmH2O)

Velopharynx

-15

-10

-5

0

5

Oropharynx

Kato et al., (2000, Chest)© W. Keith Thornton D.D.S.

0 2 4 6

0.00

0.05

0.10

0.15

0.2010 mm

8 mm

6 mm

4 mm

2 mm

0 mm

0 2 4 6

0.00

0.05

0.10

0.15

Airflow

(L/s)

Preliminary results

Oropharyngeal pressure (cmH2O)

Patient #1

No IFL at 4mm advancementPatient #2

No IFL at 10 mm advancement

（unpublished）

© W. Keith Thornton D.D.S.

Conclusions

© W. Keith Thornton D.D.S.

• Protrusion increases the cross-sectional area

• Protrusion produces a hypotonic genioglossus

• Efficacy is dose dependant

Maximum Protrusion

© W. Keith Thornton D.D.S.

Voluntary

Induced

Stretched

Treatment Position

Maximum protrusion: MP

Maximum passive protrusion: MPP

Original Maximum protrusion 8mm

Present Maximum portrusion 17mm

170% of original maximum

17 mm

23mm 185%

23mm

Macroglossia, Maxillary HypoplasiaSevere 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 tongueNormal 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

Initial vertical 8mmAdded 6mm to plate, 3mm to barTotal vertical, 17mm

6mm 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 polioParalyzed from neck downMask developed by DRI using “bite block”Pressure: 45 cmwVolume ventilatorCould use intercostals during dayInserted by biting into trays

Neuromuscular Patients:History

Problems:Fabrication techniquesRetentionLeakageReparabilityBulkTechnique sensitivityCaregiver issues

Treatment of the Severe Sleep Apnic

An eight year history

2002- 2010

Patient: Ron Doe

HPI2003

• Hx of loud snoring starting in dental school

• Recent weight gain of 100 lbs (300 lbs)

• Hypersomnolence

• Acid reflux

• Htn

HPI2003

• 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 cmwCould not tolerate

TAP-PAP 2010

• TAP-PAP custom mask (TPCM)

PSG 12/28/2010TAP TAP-PAP

CustomTAP-PAPUniversal

TAP-PAPNasal

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% 4.8% 0% 0% 0%

CPAP pressure 12-13 cmw 9 to 10 cmw 10 to 11 cmw

Comments Inadequately treated alone

Mask leak,Mask was not attached correctly

Sealed well,Preferred by patient