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Understanding the Severe Patient What to do when CPAP fails!

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Page 1: Spreecast

Understanding the Severe Patient

What to do when CPAP fails!

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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

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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

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Continuum of Sleep Disordered Breathing

Mechanical

SeverityLeast MostChemical Neuromuscular

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Continuum of Sleep Disordered Breathing:Treatment

SeverityLeast Most

ChemicalCpapVpapOral AppliancesCombinationOxygen

NeuromuscularVentilatorTracheotomyCombination

MechanicalOral AppliancesCPAPCombinationSurgeryTracheostomy

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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% ?

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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

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Sleep Eliminates Pharyngeal Reflexes

© W. Keith Thornton DDS

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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.

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Neuromuscular Factors

© W. Keith Thornton DDS

P mus –P lum > atmosphere

Pharynx Open

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Neuromuscular Factors

Pharynx closed

P mus - P lumin < atmospheric

© W. Keith Thornton DDS

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Genioglossal EMG in OSA

© W. Keith Thornton DDS

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No Mandibular Protrusion (Oshima et al.)

© W. Keith Thornton D.D.S.

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Mandibular Protrusion (Oshima et al.)

© W. Keith Thornton D.D.S.

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Inspiratory Flow Limitation

© W. Keith Thornton DDS

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Esophagealpressure

Inspiratory Flow Limitation : IFL

© W. Keith Thornton DDS

NormalAirflow

Normal

IFL

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

Severe IFL, no OSA90%

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10 Minutes, Severe, RDI=96

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

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90%

67 bpm

50bpm

2 Minutes, Severe, RDI=96

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

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90%

67 bpm

50bpm

2 Minutes, Severe, RDI=96

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

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10 minutes, severe osa, RDI=66

80bpm

40bpm

90%

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

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2 minutes, severe osa, RDI=66

80bpm

40bpm

90%

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

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

2 minutes, severe osa, RDI=66

80bpm

40bpm

90%

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Patient controlled protrusion

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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.

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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.

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Conclusions

© W. Keith Thornton D.D.S.

• Protrusion increases the cross-sectional area

• Protrusion produces a hypotonic genioglossus

• Efficacy is dose dependant

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Maximum Protrusion

© W. Keith Thornton D.D.S.

Voluntary

Induced

Stretched

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Treatment Position

Maximum protrusion: MP

Maximum passive protrusion: MPP

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Original Maximum protrusion 8mm

Present Maximum portrusion 17mm

170% of original maximum

17 mm

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23mm 185%

23mm

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Macroglossia, Maxillary HypoplasiaSevere IFL

Immediate TAP CS

Increase vertical

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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

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Before appliance therapy

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After therapy

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Macroglossia, Maxillary Hypoplasia

Lateral view,Patient in occlusion

Centric Occlusion

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5. Macroglossia, Maxillary Hypoplasia

Narrow arch,High palate without room for tongue

Normal mandibular arch size

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Macroglossia, Maxillary Hypoplasia

Size of tongueNormal posture of tongue

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Macroglossia, Maxillary Hypoplasia

Normal lip posture Freeway space

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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

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Immediate TAP CS

15mm

5mm

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TAP III from lab

Not enough vertical or protrusive Encroachment on tongue

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Final TAP III appliance

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

6mm 17mm

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Neuromuscular Patients

• Post Polio

• ALS

• Muscular dystrophy

• Brain tumors affecting motor function

• Congenital

• Spinal Cord Injuries

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Neuromuscular Patients

• Generally need ventilatory assistance during the day

• Paralysis of diaphragm

• Intercostal muscle deterioration

• Limited function of limbs

• Adequate dentition for retention

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Neuromuscular Patients:Treatment

• Tracheotomy (medical)

• Custom mask, oral appliance combination (dental)

• No other choices except iron lung

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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

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Neuromuscular Patients:History

Problems:Fabrication techniquesRetentionLeakageReparabilityBulkTechnique sensitivityCaregiver issues

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Treatment of the Severe Sleep Apnic

An eight year history

2002- 2010

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Patient: Ron Doe

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HPI2003

• Hx of loud snoring starting in dental school

• Recent weight gain of 100 lbs (300 lbs)

• Hypersomnolence

• Acid reflux

• Htn

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HPI2003

• Fibromyalgia

• Night sweats

• Joint aches

• Numb feet

• Nocturia

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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

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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

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Results

Before TAP

After TAP

© 2010 Airway Management, Inc.

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TAP III 2010

Plate anterior to upper incisors

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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

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TAP-PAP 2010

• TAP-PAP custom mask (TPCM)

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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

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