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Ariane Hawkins

Aspiration Pneumonia And The Role Of The Speech-Language Pathologist: Using Evidence To Determine Risks Associated With Oral Feeding

Ariane Hawkins

Ariane Hawkins

Ariane Hawkins

SPEAKER:James L. Coyle, PhD, CCC-SLP, BRS-S

2/6/2010

1

Dysphagia Practice: Aspiration Pneumonia and the Role of the Speech‐Language PathologistMarch 6th, 2010Pittsburgh, PA

James L. Coyle, Ph.D., CCC‐SLP, BRS‐S ([email protected])Department of Communication Science and DisordersUniversity of Pittsburgh

Outline

• 8:00–8:30 Anatomy and Physiology of the Respiratory System R/T Dysphagia

• 8:30–9:30 Pneumonia Types; Differential Diagnosis of Aspiration Pneumonia

• 9:30–9:45 Break• 9:45–11:15 Differential Diagnosis of AP (continued)• 11:15–12:15 Lunch (on your own)

2

5 5 ( y )• 12:15–1:00 Non‐Dysphagia Pneumonia Risk Factors:

Attributing Risk With Logic• 1:00‐1:45 Pulmonary Function Tests and Treatments for

Respiratory Diseases• 1:45–2:00 Break• 2:00–2:45 Dysphagia Interventions and Aspiration: Thick

Liquids, Water Protocols, (Tubes), and Common Sense• 2:45–3:45 Case Studies

Dysphagia is Not a Disease

D h i

Disease, Condition:

Disease, Condition:

3

DysphagiaNeurologicTraumaticNeoplasticStructuralIatrogenic

“Deconditioning”Pulmonary

Others

PulmonaryNutritional

Community -AcquiredSocial

PsychologicalOthersAging

Aspiration Pneumonia and the SLP James L. Coyle, Ph.D., CCC-SLP, BRS-S

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Medical SLP

Role of Modern Medical SLP

What is the nature of the patient’s dysphagia?

How likely is current disease related to dysphagia?

What is risk of future disease due to dysphagia?

Can that risk be lowered?

How?

These questions are far less commonly asked by referring physicians, of other professionals

4

Medical SLP

Adverse outcomes in our patients

Pulmonary diseases

Malnutrition, dehydration

Blood glucose managementg g

Airway obstruction

Social isolation, depression

All are costly (economic cost)

Most can cause premature death (human cost)

5

Essential Knowledge

Anatomy, physiology respiratory system

Pathophysiology of common conditions

Natural history of common conditions

Eff t d id ff t f di ti Effects and side effects of common medications

What do test results mean

Imaging, laboratory, bacteriology, PFT, etc.

What is considered “normal” swallowing function?

6


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Pre‐test

Where does diaphragm’s innervation originate?

What cranial nerve supplies facial sensation?

What about tongue sensation?

All i t h i ll i ti All pneumonias are technically aspiration pneumonias. True or false?

Feeding tubes prevent aspiration. True or false?

Eliminating dysphagia is the best way to reduce aspiration pneumonia risk. True or False?

7

Aerodigestive tract anatomy

8

Digestive:

9


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Digestive System

FOOD

10

Inside the body, cells, absorbed nutrients

waste

Digestive System

Esophagus ‐Transports food to digestive system

Stomach ‐ Breaks down proteins

Duodenum ‐ Breaks down fats, carbohydrates

Jejunum ‐Absorbs carbohydrates and proteins

Ileum –Absorbs fats

Colon: transport waste, absorb water Cecum, ascending, transverse, sigmoid, rectum…

11

Digestive System

Esophagus

Muscular tube

Sphincters

Pierces diaphragm

Bolus transit

12


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Digestive System

Stomach

GE junction

Fundus, body, pylorus

Pyloric sphincter

13

Pyloric sphincter

Mucosa secretes:

HCl

Proteolytics

Hormones

Mucus

Digestive System

Duodenum

14

Digestive System

Jejunum

Villi absorb dissolved nutrients

Nutrients transported in blood to target organs

15


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Digestive System

Large intestine

Removes water from remaining waste

Eliminates waste FO

16

OD

waste

Aero:

17

Respiratory System Functions

Ventilation

Transfer of oxygen rich air into lungs

Transfer of oxygen depleted/waste air out of lungsg

Respiration

Transfer of oxygen to circulatory system, then to working organs

Removal of some metabolic waste from working organs, via circulatory system

18


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Ventilation

19

20Airways CONDUCT air to alveoli…NO GAS EXCHANGE

Respiratory Gross Anatomy

Parietal pleura

Visceralpleura

21

riblungP<atm


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Ventilation Principles

Lungs (alveoli) have a tendency to collapse

Elastance (or surface tension)

Chest wall has a tendency to expand

Elastance Elastance

Chest wall is connected to lungs, which

Maintains lungs partially inflated at rest

Maintains chest wall partially collapsed at rest

22

Major Events in Ventilation

PhrenicNerve

activates diaphragm

Diaphragm contracts,

pulling on lung and pushing on

viscera

Alveolar inertia

overcome, lung volume increases

Atmospheric air fills

Intra‐alveolar pressuredecreases

(Boyle’s Law)

Al l i i

Inspiration

Expirationair fills

pressure void in lungs

Phrenic nerve impulses cease,

diaphragm relaxesElasticity of

viscera, alveoli are now

unopposed

Compressed viscera, stretched

alveoli, recoil

Alveolar volume

decreases, pressure increases

Alveolar air is “pushed” out

to atmosphere

23

Ventilation‐Rest= Pleural linkage

24

ribrib

Diaphragm

lunglung

P=Patm P=Patm


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Ventilation‐Inspiration

25

ribriblunglung lunglung

P<Patm P<Patm

Ventilation‐Expiration

26

ribrib

Diaphragm

lunglung

P>Patm P>Patm

27

Inspiration Expiration


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Respiration

28

Terminal Respiratory Structures

Respiratory Gross AnatomyRespiratory Gross Anatomy

29

Terminal Respiratory Structures

Respiratory Gross AnatomyRespiratory Gross Anatomy

30


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Respiration

Physiologic requirements

Eliminate accumulated waste

Acquire nutrients

Oxygen and Carbon Dioxide concentrations Oxygen and Carbon Dioxide concentrations are balanced by the respiratory system

31

Medullary, peripheral centers sensitive to pH changes

Rate, depth of ventilation quickly altered by response to pH

32

Photo: John A Beal, PhDDep't. of Cellular Biology & Anatomy, Louisiana State University Health Sciences Center Shreveport

Lungs

Circulation&

Respiration

ExternalRespiration

(Blood Atmosphere)

capillaries

Right Heart Left

Heart

33

Give Off CO2Pick Up O2

InternalRespiration

Blood Organs

Working Tissues & Organs


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External External RespirationRespiration

Alveoli exchangewith blood

34

with blood

Breathing and Swallowing

35

Respiration and Deglutition

Upper aerodigestive tract is shared

Ventilation stops Ventilation stops with swallowing (apnea)

Larynx closes “bottom to top”

36

Charbonneau et al., 2005; Hiss et al., Charbonneau et al., 2005; Hiss et al., 2003; 2003; Perlman et al., 2005 Perlman et al., 2005


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Normal Spirometry

IRVInspiration (expansion)

Max. lung volume

37

TV

ERV

REL

RV

Expiration (“collapse”)

Seconds>. . . . . .

20 s.

RR=20

breaths


In Normals...

Exhale Swallow Exhale; Young and Old1

Respiratory rate (young) is about 16/min.2

“ “ (elderly) “ “ 20/min.y

Total Swallow Duration, Swallow Apnea Duration3

Increase with age

Decrease with lower lung volumes

38

1.1. Perlman et al., 2005; Hiss et al., 2002; Leslie et al., 2002; Perlman et al., 2005; Hiss et al., 2002; Leslie et al., 2002; 2.2. Leslie et al., 2002;Leslie et al., 2002;3.3. Gross et al., 2003; Hiss et al., Gross et al., 2003; Hiss et al., 2003; 2003; Leslie et al., 2005.Leslie et al., 2005.

inspiration Swallow apnea1.5 – 2.5 seconds

Total Swallow Duration=1.5 – 2.5 seconds

Normal Respiratory Rate‐swallow on expiration

expiration

Seconds

Respiratory Rate = 16/min

39


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Exhalation begins Swallow begins Swallow ends, exhalation resumes

40

One swallow


Subglottic pressure

volume

swallow

41

pressurepA

+

_

tongue

mandible

Thyrohyoid

mandiblemandible

epiglottis

mandible C4

bolus

velumvelum

valleculae

Rest breathingInhalation: pressure above atmosphericExhalation: pressure below atmospheric

42

larynxlarynx

C7

C6

C5Post. Phar.

wall

UES


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mandible

tongue

mandiblemandiblemandible C4

bolus

velumvelum

Thyrohyoid

Swallow breathing‐swallow onsetTakes place at onset of exhalation

4343

larynxlarynx

C7

C6

C5Post. Phar.

wall

Airflow from lungsPressure > atmospheric

mandiblemandible

Tongue

mandiblemandible C4

bolus

velum During SwallowExhaled airflowobstructed by

mechanical closure

444444

larynx

C7

C6

C5Post. Phar.

wall

UES

Airflow from lungsPressure > atmospheric

Breathing and swallowing

Abnormalities

Stroke: volumes, duration, airflow direction

Shorter cycle duration at rest*

Direction of airflow after swallow**

Normals: 96% expiration after swallow

Stroke: 60% expiration after swallow (p<.01)

Laryngectomy ***

Evidence of maintained pattern in laryngectomy

45

*,**Leslie et al., 2002 a,b***Charbonneau et al., 2005


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Breathing and swallowing Abnormalities

Cheyne Stokes respiratory pattern

Periodic apnea 1 minute

46

inspiration

Swallow apnea1.5 – 2.5 seconds

Breathing and swallowingAbnormalities: Tachypnea

Abnormalities

expiration

Seconds

Respiratory Rate = 36/min

Abnormalities

47

Pneumonia and Respiratory Diseases

480830


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Aging and Disease

2005: 20 million chronic‐disease deaths

Cardiovascular 30%

Cancer 13%

Chronic respiratory 7%p y 7

Diabetes mellitus 2%

Devastating events and comorbidity

Stroke, neurodegenerative disease PLUS above

49

Pneumonia

Most frequent infectious cause of death*

2nd most common nosocomial infection (UTI) in hospitals*** 13%‐48% of all Nursing Home Infections

6 d h i ** 63,000 deaths in 2003**

40% higher incidence in elderly

Case fatality rate 55% (elderly)

50

Marston, et al., 1997*; National Center for Health Statistics, 2003**; ***Niederman, et al., 2002;

What is Pneumonia?

Causes

Microbiological etiology

Pneumococcal, Legionnaire’s, RSV, bacterial

Location (site)

h l l l b l l b Bronchoalveolar, lobular, lobar

Type

Primary (inhale or aspirate pathogen)

Secondary (opportunistic pathogen infects damaged epithelium)

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What is Pneumonia?

Setting of onset

Community acquired pneumonia

Health care associated (nosocomial) pneumonia

Predisposing factors

Ventilator associated pneumonia

Aspiration pneumonia

52

What is Pneumonia?

An inflammation of pulmonary parenchyma (alveoli, airways, both)…

C d b i f ti …Caused by infectious pathogens

Treatment:

Infection must be treated

Respiratory distress, failure must be treated

53Illustration: Patrick J. Lynch

What is Pneumonia?

Phase 1: Edema

Pathogen infiltrates, infects alveoli

Draws nourishment from alveolar epithelium

O2

p

Damaging alveolar epithelium

Producing metabolic byproducts (toxins)

Irritants to alveoli

Inflammation

54

Mandell & Wunderink, 2007Capillary – RBC, WBC

O2

O2

O2

O2O2

O2

CO2

CO2

CO2

CO2


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What is Pneumonia?

Phase 2: Red hepatization phase.

Alveoli become excessively permeable

O2

permeable Red blood cells “leak” from capillaries

Immunological response Inflammation of the lung = Pneumonitis

55Capillary – RBC, WBC

O2

O2

O2

O2

O2

O2

CO2

CO2

CO2

CO2

What is Pneumonia?

Alveoli fill with RBC, WBC, serum, infectious debris

Respiratory surface area is reduced by infiltrate

Dyspnea, hypoxemiaO2

O2O2

O2

O2

CO2

Dyspnea, hypoxemia

Epithelium thickens

Surfactant production is diminished

Reduces compliance of lung

…further source of dyspnea

Can spread with cough

56capillary

O2

O2 CO2

CO2

CO2

Infiltrates Clear alveoli

57

Thickened epithelium


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What is Pneumonia?

Phase 3: Gray hepatization phase

RBC’s destroyed

Infection contained

Bacteria absent

O2

Bacteria absent

Infiltrates diminish

Phase 4: Resolution

Immunological “clean‐up”

Epithelium “heals”, surfactant restored

58capillary

O2

O2

O2

O2

O2

O2

CO2

CO2

CO2

CO2

Types of Pneumonia

CAPNosocomialPneumonia

All PneumoniaBacterial, viral, Legionella, RSV, etc.

59

DAPNon‐DAP

TypicalVAP

Atypical

AspirationPneumonia

DAP = Dysphagia‐related Aspiration Pneumonia

Non‐VAP

Types of Pneumonia

Community Acquired Pneumonia (CAP)

Pneumonia not acquired in a health care facility

4‐5 million cases per year* **

600 000 hospitalizations 45 000 deaths** 600,000 hospitalizations, 45,000 deaths**

Incidence**

12 per 1000 persons

20 per 1000 elderly persons (60% greater)

60

*Niederman, 2002; **Mandell & Wunderink, 2007


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C.A.P.

Pathogens responsible

Typical: Streptococcus, Klebsciella pneumoniae

Atypical *: H. influenzae, RSV, Legionella, E. coli, Staph. aureus, others

61

*El Solh, et al., 2001; CDC guidelines

Cost of CAP

Human Costs of Community Acquired Pneumonia

Pneumonia after stroke*

26.9% mortality, vs. 4.4% in stroke w/o pneumonia

Economic Costs of Community Acquired Pneumonia

Cost of pneumonia: $8‐10 billion (1998)** ***

62

*Katzan, et al., 2003; ** Niederman, et al., 1998; Mandell & Wunderink, 2007

Types of Pneumonia

Nosocomial Pneumonias: Ventilator Associated, Nursing Home Acquired Pneumonia

Pathogens:

Pseudomonas aeruginosa, Proteus species, staph. Aureus

63MRSA P.mirabilis


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Types of Pneumonia

Ventilator Associated Pneumonia

Exposure to mechanical ventilation

Contaminated respiratory circuits

Contaminated suction, bronchoscopic equipment

Gastroesophageal reflux common in Ventilation

Early, late onset

Early: typically CAP pathogens

Late: MRSA, other drug‐resistant pathogens

64

Aspiration Pneumonia (AP)

Aspiration

Foreign matter enters the respiratory system

Pneumonia

Infectious acute inflammation

Reaction to pathogen

Aspiration Pneumonia

Pulmonary infectioncaused by aspiration of colonizedmatter

65


CAP

Nosocomial


AP can originate in the community or in a hospital/HCF

Has reached epidemic proportions in the US*

66*Baine, Yu, & Summe, 2001


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Human Costs of Aspiration Pneumonia

AP admissions highest case‐fatality rate

23.1% during hospitalization*

Is fatal in 20%‐50% of confirmed cases Is fatal in 20%‐50% of confirmed cases

Annual mortality (1998 numbers) >25,000 annual deaths due to AP

Economic Costs of Aspiration Pneumonia

$1.5 billion

67

*Baine et al, 2001;

Importance:

If we reduce the incidence of AP by a modest 20%

5,000 saved lives each year

If we reduce the admissions or length of stay for AP by a modest 20%

$300 million saved

68

Data extrapolated from Mandell & Wunderink, 2007; Baine et al, 2001

Patient with dysphagia

…and other risk factors favoring pneumonia

aspirates colonized oral secretions

What is Dysphagia‐Related Aspiration Pneumonia (DAP)?

…aspirates colonized oral secretions

…causing infection of airways and/or alveoli

Where do these pathogens come from?

69


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Oral biofilm development

70http://bioinfo.bact.wisc.edu/themicrobialworld/streptococci_biofilm.jpg; Public health image library #3074, Centers for Disease Control

Oral biofilm

Variety of microorganisms in dental plaqueOral anaerobes

How Does DAP Develop?

Host Risk Factors

Mental status, immunological health, oral condition, upper GI obstruction, etc.

What was aspirated?

And what is its pathogen load?

Iatrogenic Risk Factors (institutionalized)

Feeding tube, postoperative impairments, medications, etc.

71* CDC/MMWR 46, RR‐1, (1997); **Langmore et al, (1998)

Where Does DAP Develop?

Site of occurrence:

Can occur in a health care facility (HCF)

Nosocomial Aspiration Pneumonia

Can occur outside of the HCF

Community Acquired Aspiration Pneumonia

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Aspiration Pneumonitis

Non‐Infectious

Acute Lung Injury caused by aspiration of caustic or particulate matter

Inflammation of alveoli by effects of irritants

No infection (sterile/non‐pathogenic material)

Inflammatory edema reduces surface area

Gastric contents

Sterile, acidic, caustic

Damage to airways, alveoli

73

O2O

O2

CO2

74capillary

2O2

O2

O2

O2O2

CO2CO2

CO2

O2

O2O2

O2

O2

O2

O2O2

CO2

CO2

CO2

CO2

CO2 CO2

A new source of AP?

Gastric contents are normally sterile

pH : 2‐3* (nothing can survive)

However….

When stomach is de‐acidified and patient When stomach is de acidified, and patient exhibits GE reflux or emesis, , aspirated, colonized gastric contents can produce pneumonia

Increased use of acid suppressing drugs**

Raise gastric pH to 4.0 to 6.0*

75

*Feldman & Barnett, 1991; **Laheij, et al., 2004.


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A new source of AP?

Laheij et al., 2004*

365,000 patients

Users and non‐users of acid suppression drugs

Some were prior usersp

5,551 patients developed pneumonia

PPI users were twice as likely to develop pneumonia

OR = 1.94‐2.28

H2 receptor agonist users

OR = 1.36‐1.64

AND…Eurich, et al., 2010; Herzig, et al., 2009

76*Marik, 2001; Marik and Zaloga, 2002; Laheij, et al., 2004;

Distinguishing AP, Aspiration Pneumonitis, Other Pneumonias

77

The Medical Record contains important clues

HISTORY OF ONSET

The course and progression of the disease

Presence/absence of underlying source/cause of Presence/absence of underlying source/cause of aspiration

Results of lab, radiographic tests

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Differential Diagnosis

Dysphagia‐related Aspiration Pneumonia (DAP)

Non‐dysphagia‐related Aspiration Pneumonia (NDAP)Pneumonia (NDAP)

Other pneumonias

79

DAP

Associated with dysphagia

Non‐dysphagia related AspirationPneumoniaPneumonia

Aspiration does not occur because of dysphagia

Safely swallowed material

Gastroesophageal reflux or emesis (colonized)

Deacidified gastric contents

80

DAP vs. other Pneumonias

1. Location of chest infiltrates

DAP: typically gravity dependent segments

Lower lobes an segments

DAP

segments

Position while aspirating

81

NDAP

Giorgio Conrad (P.D.)


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Radiographic evidence

Infiltrates

Chest x‐ray shows “shadows” at sites of infection‐ induced inflammation

Advanced pneumonia may involve entire lobes Advanced pneumonia may involve entire lobes

Infection can spread

Aspiration Pneumonitis ‐Does not spread…

82

Aspiration Related Infiltrates

83

Aspiration produces pneumonitis or pneumonia in gravity dependentgravity dependent portions of lung(s).“Dependence” depends on posture when aspiration occurs“Dependence” depends on posture when aspiration occurs, density & volume aspirated.

(R) Basilar infiltrates(R) Upper & middle lobe infiltrates


1. Location of chest infiltrates

CAP, VAP, NosocomialPneumonia:

Diffuse

VAP: often well distributed

84


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85

RRUL and RML infiltrates in patient with pneumonia

86


87



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88

Multilobar community acquired pneumonia

2. Signs and symptoms

DAP, CAP, Nosocomial Pneumonia: similar.

Dyspnea

Hypoxemia

Malaise


Malaise

Fever

Productive cough

Purulent sputum

Leukocytosis

89

3. Bacteriology

DAP: oral pathogens/oral flora

CAP: Strep. pneumoniae, Klebsciella pneumoniae, H. influenzae, RSV, Legionella, E. coli, Staph. aureus

VAP: pseudomonas, proteus species, Staph. Aureus


p , p p , p

Typically multiple organisms

Nosocomial pneumonia: pseudomonas, proteusspecies, Staph. aureus

Leukocytosis (elevated WBC)

Normal: 4.5 – 10.5 k cells/microliter

90


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4. History

DAP: Dysphagia! Dysphagia‐producing disease, Symptom onset following oral intake; position during oral intake; esophageal dysmotility

Dependent for feeding/oral care, oral biofilm


91

4. History

CAP: pt. not institutionalized; insidious onset

Nosocomial Pneumonia: institutionalized patient, insidious onset

VAP: mechanically ventilated patient; typically


VAP: mechanically ventilated patient; typically NPO at onset

92

Examination data collection

5. Course of Pneumonia

What you see on assessment is not baseline

Elevated respiratory rate

Mental status

Cough is present in background

Count coughing before, during, and after oral trials

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Examination data collection

Sign Interview Oral Facial Exam

Swallow Trials A

Swallow Trials B

Post‐swallow trials

Cough 112

0.4 sx/min all phases

11 3

0.4 before oral trials, 1.1 during oral trials, 0.2 after oral trials

Throat clear

Vocal quality

other

94

TimeTime Time TimeTime Time

duration duration duration duration duration

5 min 5 min 5 min 5 min 5 min

2

1

1

11 1

1 3

32

1

Summary‐pneumonia

Knowledge of normal and abnormal function is essential

Not just swallowing function…

Elderly possess many risk factors for pneumonia that are unique to the elderly

There are many clues pointing to, or away from, a diagnosis of DAP

95

Things to remember

Aspiration can occur without dysphagia

Aspiration is one potential source of pneumonia pathogens

Summary‐pneumonia

All respiratory illnesses are NOT dysphagia related

ALL PNEUMONIAS ARE NOTASPIRATION RELATED

Patient appearance with pneumonia is NOT baseline

History, course, physical signs are data for the SLP

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Respiratory System & Diseases

The structures involved

The respiratory conditions seen in the elderly

Are they suspicious for a dysphagia etiology?

970945

Aging and Disease

Obstructive Diseases

Inspired air is obstructed from the respiratory membrane

Obstructed gas exchange

Respiratory pump works

Restrictive Diseases

Airflow or volume is mechanically restricted

Gas exchange is intact

Patient cannot inhale sufficient volume

98

Aging and Disease

Chronic respiratory conditions

COPD

Progressive airway/alveolar destruction (emphysema)

Chronic bronchitis

Congestive Heart Failure

Hypertension

Right heart, left heart

Pulmonary Edema, Pleural Effusions

Pulmonary Fibrosis

Asthma

99


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Aging and Disease

Acute respiratory conditions

Pneumonia

Pneumothorax

Atelectasis

ARDS

Other acute pneumonitis

100

Respiratory Disease‐obstructive

Obstructive diseases air is “obstructed” from

contact with respiratory membrane

R d d l

obstruction

Reduced oxygen supply

Reduced waste elimination Acidosis

Increased respiratory rate Overlap with swallow

101

Alveolarmembranedestroyed

Airway Obstruction

Caused by dysphagia?

Very possible

Causes dysphagia?


y p g

No

102


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COPD

Chronic bronchitis

chronic mucus…obstruction

Emphysema

Alveoli and capillary destruction,


p y ,

Resistance to blood flow into lungs

Can cause heart failure

Increased rate

Decreased cough effort

Reduced mucociliary clearance

103

Obstructive Pulmonary Disease

Respiratory membrane Respiratory membrane surface area is destroyedsurface area is destroyed

emphysemaemphysema

Respiratory membrane surface area is obstructed Chronic bronchitis

104

COPD: Caused by dysphagia?

Rarely but possible…

Chronic aspiration can produce

Alveolar destruction


Airway disease

Asthmatic bronchitis

Chronic irritation due to chronic aspiration

105


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CHF

106

Lungs

capillaries

CHF

Lungs

1. “Bottlenecked” Pulmonary Circulation (R) Ventricle Fails

2. “Bottlenecked” Systemic Circulation (L) Ventricle Fails

Right Heart

Left Heart

107

Give Off CO2Pick Up O2

Working Tissues & Organs

IntakeOutput

InterstitialFluid

Plasma

Lymphatics

Na+

Na+

Capillary membraneBlood Vessel

108

IntracellularFluid

Cell membrane

Fluid

Na+ Na+

Na

osmosis

Hypertension and Edema:Normal Fluid “Balancing” Working Organs


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Intake HIGH PRESSUREOutput

Hydrostatic pressurepushes water into interstitial space around organs Interstitial

Fluid

PlasmaHIGH PRESSURE

Na+

Na+

Capillary membrane

Hypertension

Hypertension and Edema:

Abnormal Fluid “Balancing”

109

Cells/Organs

Cell membrane

Fluid

Na+ Na+

Na

osmosis

Cells/Organs

Common in CHF hypertension

Caustic ingestion Increased capillary permeability

Obstructive Pulmonary Disease

Pulmonary Edema

Pneumonitis

Increased rate / reduced inspiratory capacity

110

Respiratory Disease‐Restrictive

Restrictive Diseases

Limit amount of air that can be inhaled

Mechanical

restriction

Pain, paralysis, fibrosis

Poor compliance

111


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Restrictive Pulmonary Disease

Asthma

A. Allergic/reactive

bronchial smooth muscle spasm

narrow airway, yincreased resistance, reduced flow

B. Asthmatic bronchitis

Mucus production

Obstructive component

112

Asthma Dysphagia related? Maybe. Chronic aspiration can cause

asthmatic bronchitis

Cause of dysphagia? Short‐term/acute, maybe

Respiratory Disease‐Restrictive

113


Mechanically restrictive disease

Disable complete expansion of thoracic cavity

Kyphosis

Abnormally flexed thoracic spine, compressed thorax

Pulmonary fibrosis

Tough, leathery segments tether adjacent segments

Paralysis

114


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Dysphagia related?

Kyphosis, no

Pulmonary fibrosis? Maybe

Chronic aspirationp

Effects on respiration/swallow

Increased rate / reduced inspiratory capacity

115

Restrictive Pulmonary Disease Pneumothorax

Perforation caused by empyema/abscess

Chronic aspiration

116

Atelectasis

Areas of collapsed alveoli


117


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Pleural Effusion

118

CHF (transudative), Inflammatory (exudative)

Aspiration and Lung Damage

Idiopathic Pulmonary Fibrosis (IPF)

Fibrosis: toughening

Idiopathic: from an unknown cause/etiology

Tobin et al., 1998

119

IPF


Acute Lung Injury caused by aspiration of caustic or particulate matter

Restrictive Plus Obstructive

Restrictive

Inflammation of alveoli by effects of irritants

No infection Pulmonary edema

Obstructive

Fluid filled alveoli

120


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Gastric Contents: Massive Acute Inflammation

Sterile acidic Sterile, acidic

Airways, respiratory membrane damage

Opportunistic secondary infection

ARDS

121

ARDS

122Ware & Matthay, 2000

Normal acute resolution

Iatrogenic causes of respiratory conditions

Iatrogenic condition: a disease cause by treatment of another disease

Sedation (restrictive)

CNS depression

Disruption of pleural linkage (restrictive)

Cardiothoracic surgery

Phrenic nerve injury (restrictive)

Cardiothoracic surgery

123


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Respiratory Swallow Tactics

Effects on interventions

Mainly on behavioral interventions

Timing of airway closure

Consider added fatigue of “eating and drinking”g g g

Increase respiratory rate even more?

Mitigating rate increases with supplemental O2

…because we can’t pull off more CO2.

124

Summary

Pulmonary disease affects swallow/breathing coordination

Pulmonary disease can cause, or be caused by, dysphagiaby, dysphagia

Mainly characterized by disruption of swallow‐respiratory coordination

1251115

Next – Risk Factors Favoring Pathogenesis of Pneumonia (Besides Dysphagia!)

126


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Risk Factors for Pneumonia

Host Risk Factors

Something about the host (patient) predisposing them to an adverse outcome

Oral colonization, aging, dependence, underlying pulmonary, neurological or digestive disease

Iatrogenic Risk Factors

Increased risk for an adverse event caused by treatment of another condition

Medications, intraoperative injury, artificial airway

127

1215

Dysphagia‐a host risk factor

Little disagreement regarding dysphagia

Aspiration obstructs airways

Enables secondary infection

Stroke, neurological diseases, cause dysphagia, g , y p g

But pneumonia is always multifactorial…

We often CANNOT eliminate dysphagia

What else can we do to mitigate pneumonia risk?

128

Non‐Dysphagia Risk Factors

Langmore, et al., 1998

189 institutionalized males (non‐ICU)

CSE, VFS, 3 scintigraphic exams (GE reflux, esophageal motility)

Half also had FEES test

VFS repeated if dysphagia suspected

Dental exam, salivary flow measurement, saliva and throat cultures, interview (repeated annually)

Outcome: pneumonia

SBC >12,000 + fever >100.5F + new infiltrate on CXR

129


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Non‐Dysphagia Risk Factors

Patients who developed pneumonia had significantly more:

Feeding tubes in place

COPD, CHF, GI diagnoses, , g

Decayed teeth, periodontitis, did not brush teeth

Multiple medical diagnoses, multiple medications

Dependent for oral care and feeding

Reduced activity

What is the evidence in these areas?

130

Feeding Tubes‐iatrogenic

Feeding tubes as pneumonia risk factor

Bacterial contamination of stomach and mouth*

44% PEG, 54% NG

E. coli, Proteus, multi‐organism: NG > PEG (p<.001)

Feeding tube reservoirs contaminated**

44% stroke patients with NG develop pneumonia***

…without worsening dysphagia****

131

Segal, et al., 2006; **Wagner, et al., 1994; ***Dzeiwas et al., 2004; Dzeiwas et al., 2008

Feeding Tubes

Pneumonia incidence is high *, **, ***, ****

Short‐term, long‐term

Other complications

Agitation and self extubation*g

Do not improve risk of death or poor outcome #

132

*Ciocon, et al., 1988; Dzeiwas et al., 2004; Finucane, et al., 1996; Gomes et al., 2004# Lindeboom, 2005


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Pulmonary Disease‐host risk

COPD

Alters swallow physiology

Inspiration following swallow more frequent*

Damaged mucociliary clearanceg y

Reduced ability to clear contaminants

Impaired cough

133*Gross et al., 2009;

Pulmonary Disease

CHF

Increased respiratory rate due to

Pleural effusion, pulmonary edema

COPD and CHF: present significantly more in patients diagnosed with pneumonia *, **

134

Langmore et al., 1998; Langmore et al., 2002

Pulmonary Disease

Active smoking

4.1 times higher pneumonia risk *

Pharyngeal and glottic protective reflexes are attenuated by active smoking**

135

Langmore et al., 1998; Dua et al., 2002


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Medications‐iatrogenic

Antipsychotics*

60% increase pneumonia risk in a case‐control study of elderly patients

Risk in first week of treatment: 450% increase

Subsides (does not disappear) over time

Most events with atypical antipsychotics

Clozapine, Abilify, Risperdal

Extrapyramidal effects, sedation

Typical drugs: sedation (haloperidol, chlorpromazine

136

*Knol, et al., 2008;

Medications

Multiple medications

Increase risk of pneumonia 15% *

Medications that reduce LES tone

Cholecystokinin secretin progesterone Cholecystokinin, secretin, progesterone, glucagon, neurotensin, dopamine, atropine, butylscopolamine, theophylline, nitrates, alcohol, fat, chocolate

Barbiturate, cigarettes, benzo., Ca channel blockers (cardizem), caffeine, anticholinergics

137

*Langmore et al., 1998;

Medications

Acid suppression medications

Administered for stress ulcer prophylaxis in ICU

3 studies show increased incidence of pneumonia in patients taking acid suppressing drugs

Proton pump inhibitors (omeprazole, etc.)

H2 receptor antagonists (ranitidine, etc.)

Increased pneumonia risk (discussed earlier)

Enables survival of pathogens in stomach

138


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Medications

LaHeij et al., 2004 (>300,000 OP subjects)

Treated patients who developed pneumonia were matched to up to 10 age/gender/lifestyle

Currently using PPI: 89% higher pneumonia risk over those who stopped using PPI

H2 antagonists: 63% higher pneumonia risk

Herzig et al., 2009 (>60,000 IP subjects)

52% inpatients treated

5% treated patients, 2% untreated, pneumonia

30% higher risk of pneumonia (adjusted)

139

Medications

Eurich et al., 2010

248 patients post‐pneumonia admission, compared to 2500 patients with no pneumonia hx.

5.4 years average follow up

Some continued, some stopped PPI use

Acid suppression (current/past): 12% incidence

Current users: all of the incidence was with current

Non‐acid suppression: 8% incidence

140

Medications

Interesting contrast

SDD (selective decontamination of the digestive tract (sterilizes gastric contents without acid suppression)

Reduced pneumonia incidence in CVA patients*

141

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Medications

There is evidence that acid suppression therapy may increase pneumonia risk

…and that the stomach is a reservoir for pathogens

Mechanism: alteration of gastric pH (normally 2‐3) allows bacterial survival and colonization

142

Colonization‐host risk or iatrogenic Gastric colonization

Discussed previously

Oral colonization

Systematic review Systematic review

Good evidence that aggressive oral care/hygiene reduces pneumonia in high risk adults

Relative risk reduction=34‐83%

Causes: oral, dental disease, xerostomia, medications

143

Azarpazhooh, et al., 2002

Colonization

Oral Colonization (cont’d)

Worsened with*:

Antibiotic use

Oral disease

Xerostomia

Malnutrition

Presence of teeth! **

144

*Gomes et al., 2003; **Wan et al., 2003


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Colonization

Oral colonization (cont’d)

Up to 1/3 of stroke patients cultured, found to have:

aerobic* (pseudomonas, e.g.)

and anaerobic** (E. coli, e.g.)

…pathogens in mouth

Combine oral colonization with the fact that all normals aspirate at times ***

145

Gosney, et al., 2006*; Millns, et al., 2003**; Huxley, et al., 1978, & Gleeson, et al., 1997***

G.E. Reflux

Regurgitation of gastric contents aspiration

If colonized pneumonia

If not colonized ? Pulmonary fibrosis*

24 hour pH probe4 p p

Compared IPF to ILD patients

Significant incidence of pH <4 in top, bottom of esophagus in IPF, not in ILD

146

*Tobin et al., 1998

Aging

Senescent sensorimotor changes

Reduced physiologic reserve

StrokeBaseline

147

Young Middle Aged

Old Very Old

Non Well‐Being

Physiologic Reserve

Healthy

Not Healthy


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Aging

Diminished esophageal motility

Reduced cricopharyngeal compliance

Reduced intrabolus pressure generation (swallowing)(swallowing)

Immune system degradation

148

Other iatrogenic risk factors

Postoperative sensorimotor impairments

Predispose to dysphagia

Anterior cervical fusion*

Esophagectomy**

Thyroidectomy, carotid endarterectomy

Aortic repairs

Phrenic, vagus n.

149*Kriskovich, et al., 2000; **Atkins, et al., 2007)

Airway manipulation

Mechanical ventilation

Endotracheal intubation

Tracheostomy

Other iatrogenic risk factors

y

All raise the patient’s pneumonia risk (VAP)

150


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Mechanical Ventilation

Complications of PPV Barotrauma (alveolar damage, excessive pressure) Pneumothorax

Diffuse alveolar damage

At l t i ( l l ll i ffi i t P ) Atelectasis (alveolar collapse, insufficient P a)

Infection ETT, tracheostomy: direct pathogen route Nosocomial pathogens VAP

Respiratory deconditioning

Alveolar hypo‐ hyperventilation

Hypotension

151

Endotracheal Intubation

Complications

malfunction, mucus plug, leak, position

Self extubation

Mucosal necrosis

Pneumonia

Laryngeal edema

Tracheal erosion

152

Prolonged Intubation

Definition

Generally, >24‐48 hours

Dependent on other host risk factors

Age, method of intubation, underlying disease

>24 hours (frail elderly)

153


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Prolonged Intubation

Evidence

Ajemian et al., 2001

48 patients > 48 hours intubation, < 48 hours extubated

27/48 (56%) aspirated 12/27 (44%) silent aspiration 27/48 (56%) aspirated, 12/27 (44%) silent aspiration

19/27 thin liquid aspirators, 9/27 puree

154

ElSohl et al., 2003

42 elderly, 42 nonelderly; all > 48 hours intubation

FEES at 2 days post‐extubation, and 5,9,14 days (aspirators)

/ ld l / ld l i i 22/42 elderly, 15/42 non‐elderly, aspiration

13% elderly persistent dysphagia after 2 weeks

0% non‐elderly)

155

Tracheostomy

Open pathway for pathogens to colonize lung

156


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Respiratory System Testing and Treatments

1300‐1345

Testing the Respiratory System

158

Pulmonary Function Parameters

FVC = forced vital capacity

VC = vital capacity

FEV1 = forced expiratory volume in 1 second

TLC = total lung capacity TLC = total lung capacity

Reduced in restrictive disease

RV = residual volume

159


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Normal Resting Spirometry

inspired

160

expired

Spirometry Subtests

Post‐bronchodilator FEV1

FEV1/FVC

Rate of decline

B d l th h Body plethysmography

Exhaled CO (carbon monoxide)

Confirms current smoking status

161

Imaging of the Chest

Chest x‐ray

Chest CT

162


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Chest x‐ray

Shadows

X‐rays penetrate air filled areas and strike film

X b b d b d ti X‐rays are absorbed by denser tissue

Differences in grayscale color indicate areas of “more solid” matter

Cases a shadow on the film

163

Posterior AnteriorRight Left

Right lung

164

RUL, RML, RLL, LLL

Anterior PosteriorRight Left

Left lung

165

LUL, LLL


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Chest x‐ray

Film

BodyPart

X‐ray source

166

Shadow

Chest x‐ray

Film

BodyPart

Same

X‐ray source

167167

SameShadow

Chest x‐ray: AP Film

Ant. Post

Film

BodyPart

X‐ray source

Ant. Post

Film

BodyPart

X‐ray source

168

Shadow

ShadowShadow is near the bottom = Shadow is near the bottom???


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Chest x‐ray: AP & lateral

Film

BodyPart

X‐ray source

Right Left

Lateral filmAP film

Ant. Post

Film

BodyPart

X‐ray source

169

Shadow

Shadow

Shadow is near the bottom of body part + Shadow is on the left= Shadow is on bottom left

Chest x‐ray reports

Terms

Consolidation, density, opacity:

“I see a shadow.”

Does not indicate nature of “more solid” matter

Infiltrates:

More solid matter has infiltrated a space

Alveolar, airway

Edema: Fluid saturating area

Alveolar, interstitial

Effusion: fluid fills a body cavity (pleural)

170


Terms

Atelectasis: collapsed alveoli

Obstructive

Blocked airways; gas within alveoli absorbed into blood

Non‐obstructive

Compressive

Alveoli pressed closed – extrinsic

Dependent

Pt. position prevents inflation of alveoli; poor inspiration

Adhesive: lack of surfactant cause collapse

Passive: widened pleural space enables collapse

171


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Terms

Pulmonary vascular congestion

NOT airway congestion

Blood back‐up in pulmonary vessels

Poor perfusion, (R) heart failure

pulmonary artery congestion

Arterial hypertension, (L) heart failure

pulmonary vein congestion

Alveolar infiltrates are inside alveoli!

The rest of these are NOT alveolar infiltrates.

172

173

Pneumothorax

174

ARDS (bilaterally) with (R) Pneumothorax


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175

Pulmonary edema (before, after)

176

Left lung mass; patchy (R) infiltrates

National Cancer Institute

177

ARDS – Massive pneumonitis


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178

Pleural Effusions (R>L)

Chest CT

Slices of body part are looked at

179

right

Rostralslice

Caudal slice

Middle slice

top

Plane film wouldlook like this

180


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Chest CT

Reduced parenchyma

COPD

181

Emphysematous “holes”

Loss of alveolar surface area

Other tests

Exercise tolerance

Treadmill test, 6 minute

Resting SpO2

After 10 minutes rest After 10 minutes rest

Biomarkers

Sputum, exhaled gas condensate, metabolites

DNA; Markers for surfactant, etc.

Questionnaires

Depression, QOL, fatigue, dyspnea

182

Other tests

Body Plethysmography: TLC and RV

Inhalation Challenge Tests: allergen

Exercise stress test

G diff i Gas diffusion

ABG

183


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Blood Gases Reading Blood Gas Data (ABG)

p = partial pressure (mm/Hg)

a = arterial

v= venous (blood gases from venous l )sample)

O2= oxygen, CO2= carbon dioxide

S = saturation

H = hydrogen ion

Index of acidity

184

Blood Gases

Arterial blood gases & normal ranges

paCO2 = partial pressure of CO2

38‐45 mmHg

paO2 = partial pressure of O2 paO2 = partial pressure of O2

85‐100 mmHg

pH: acidity

~7.4

SaO2 = % hemoglobin O2 saturation

90‐100%

185

Pulmonary Disease Treatment

…and adapting the SLP evaluation to accommodate them…

186


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Treatment of Respiratory Conditions

Bronchodilators

Nebulizer

Metered Dose Inhaler (MDI)

187


Oxygen monitoring

ABG

Pulse oximetry

Continuous

Intermittent

188


Hyperinflation therapy Patient generated Incentive spirometry (IS)

Positive pressure “Mechanical bronchodilator”

CPAP One level

Bipap‐2 level IPAP, EPAP

IPPB

189


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Bronchopulmonary Hygiene

Percussion and postural drainage

Suctioning

190


Supplemental oxygen

Nasal cannula

Facemask

Non‐rebreather

Prevents inspiration of

Room air

Exhaled air

Delivery parameter = LPM flow

Adaptations?

Facemask: can pt. use cannula/oximizer?

191


Venturi mask

Mixes room air with O2 to a fixid FiO2

Delivery parameter = FiO2, not flow (LPM)

192

Adaptations: Can patient use cannula during PO?


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Observe all important vital signs

Respiratory rate in context of…

Oxygen saturation

Pulse oximetry does not help with dysphagia assessment; identifies hypoxemia over longer periods

Endurance/fatigue

Speaking, feeding, etc.

Overall mental status

Can the rate be brought down, temporarily?

i.e. the duration of a “meal”

193

Examination considerations

Medication timing and the evaluation

Assess patient functions r/t recent medications

Bronchodilators, sedating medications, anxiolytics

Timing of “breathing treatments”g g

Duration of endurance

Can influence meal duration/frequency

Patient who is “safe” for short periods

Mix and match

The above parameters can be flexibly manipulated

194

Tracheostomy Management

Establishment of OralEstablishment of Oral‐‐Nasal Nasal AirflowAirflow

Screening for Aspiration of Screening for Aspiration of Oropharyngeal SecretionsOropharyngeal Secretions

Tolerance of Cuff DeflationTolerance of Cuff Deflation

Patient Fails to Wean from Patient Fails to Wean from Mechanical VentilationMechanical Ventilation

Patient Survives Acute Patient Survives Acute Illness/DiseaseIllness/Disease

Acute Illness Requiring Acute Illness Requiring Mechanical VentilationMechanical Ventilation

195

Tolerance of Tolerance of InspiratoryInspiratory and and Expiratory OcclusionExpiratory Occlusion

Clinical / Clinical / Instrumental Instrumental Evaluation of SwallowingEvaluation of Swallowing

Tolerance of Expiratory Tolerance of Expiratory Occlusion; SpeechOcclusion; Speech

Patient is Patient is DecannulatedDecannulated

Patient Successfully Weans Patient Successfully Weans from Mechanical Ventilationfrom Mechanical Ventilation

Tracheostomy is Placed*Tracheostomy is Placed*

*Heffner & Zamora, 1990; Holevar et al., 2008


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High End Life Support ECMO

Extracorporeal membrane oxygenation

196

After Mechanical Ventilation

Weaning

Prolonged endotracheal intubation

Ventilator associated pneumonia

Cli i l l ti f t h t ti t Clinical evaluation of tracheostomy patients

Instrumental Testing

197

Dysphagia Interventions

198

1400‐1445


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Interventions

Designed to

Prevent adverse events

Biomechanical

Aspiration, bolus misdirection, etc.

Global health outcomes

Pneumonia, malnutrition, dehydration

Psychosocial impairments

Isolation etc.

199

Interventions

Topics

Thickening of liquids for dysphagia management

“Free water” protocols

Enteral feeding tubes in dysphagic patientsg y p g p

Common theme:

hydration/nutrition vs. aspiration…

Choosing the better of 2 or more bad choices

200

Water

Main fluid medium of all cells (except fat)

75‐80% cell volume = water

Necessary for normal cellular functions

Other chemicals dissolved suspended Other chemicals dissolved, suspended

Concentrations at cell membrane

2011540‐1625


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Water

Intake of water: ~2300 mL per day

2100mL through intake

200 mL synthesized by body (CHO metabolism)metabolism)

Variations in water intake

Climate, habits, physical activity

202

Water

Loss of water: ~2300 mL per day

Evaporation: 700 mL per day

Respiratory system (300mL), through skin (400mL)(400mL)

Not sweating

Urine: 1400 mL

Sweat: 100 mL

Feces: 100 mL

203

IntakeOutput

InterstitialFluid

Plasma

Lymphatics

Na+

Na+

Capillary membrane

204

IntracellularFluid

Cell membrane

Fluid

Na+ Na+

Na

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Dehydration

Kidneys constantly excrete fluid

Elimination of excess solutes

Ingested or metabolic byproducts

+ Evaporation Evaporation

= dehydration

Sodium concentration rises

Hypernatremia with loss of extracellular fluid

205

Dehydration

Hypernatremia ADH increases fluid conservation by kidneys

Threshold for drinking

AKA Thirst!

Heart, kidney, neuron, other organs do not function

Cellular activity depends on concentration of sodium and other ions in plasma, cells.

206

Thick liquids

207


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Pneumonia and aspiration

Thin liquids aspirated most frequently

Compared to other viscosities

Spawned experimentation with thick liquids

208

Thickened liquids

Theory for dysphagia use:

Slowing the flow

Compensates for mistimed airway closure

What do we know about them?

209

Thickened liquids

Use in SNF’s

11 companies that own 20% of all SNF’s in US

Randomly selected facilities to avoid bias

252facilities in 41 states (~29000 beds)

Analyzed by CMS region

210Castellanos et al., 2004)


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Results by facilities

Use in SNF: 0% to 100%

Facilities that use thickened water: 91.6%

Results by patients

8.3% patients receive thick liquids

Nectar (60%), Honey (33%), Pudding (6%)

Assessedwith instrumentation:45% (0‐100%)

211Castellanos et al., 2004)

Thickened liquids

Reduces aspiration of thin liquids

Kuhlemeier et al., 2001; Logemann et al., 2008

Does not increase pharyngeal residue

B dt t l Bogaardt, et al., 2007.

Swallow apnea later/longer with thick liquids

Hiss et al., 2004; Butler et al., 2004

More effort needed to clear thick

Nicosia et al., 2001

212

Thickened liquids

Patients do not like thick liquids

Garcia, 2005: prepackaged vs. mixed

Prepackaged better : Whelan, 2001

Great variability in thick liquids Great variability in thick liquids

Prepackaged & mixed: UW/VA Swallowing Research Lab, 1999

Prepackaged: Garcia, et al., 2005; Steele, 2005

Mixed by clinician: Glassburn & Deem, 1998

213


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Thickened liquids

And…

Mixed vs. packaged thick liquids

Not same viscosity

And…And…

Barium mixtures vs. packaged thick drinks:

Not same viscosity

Other properties make up “thickness”

…not just viscosity

214

Thickened liquidsAdd liquid to

cylinder Remove cylinderSpread distance over time (50 mm)

Line Spread Testvs.

Brookfield Viscometer

215

LST: Similar Viscosity Fluids

Material Viscosity Line Spread - 50Pre-thickened honey 1 675 9Pre-thickened honey 2 832 8.75Pre-thickened honey 3 909 10.42P thi k d h 4 1117 9 33

Dysphagia Treatment Methods

216

Pre-thickened honey 4 1117 9.33Honey thick barium 710 18.75Karo syrup (93%) 1038 13.6

Pre-thickened nectar 1 260 12.8Pre-thickened nectar 2 300 13Pre-thickened nectar 3 264 11.7

Nectar thick barium 200 17.2

UW/VA Swallowing Research Lab, 1999


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Thickened liquids

Among 25 experienced SLP’s

Nectar: r= +0.02, Honey: r= ‐0.03

Within subject (1st vs. second mixing of h i t )each consistency)

Nectar: r= +0.26‐0 to +0.33

Honey: r= +0.67

Glassburn and Deem, 1998

217

Thickened liquids

0.6

0.8

1

ability

Moderate relationshipModerate relationship

Strong relationshipStrong relationship

218

‐0.2

0

0.2

0.4

Nectar Honey Nectar Honey

Repeata

No relationshipNo relationship

Weak relationshipWeak relationship

Moderate relationshipModerate relationship

N=25 experienced SLP’s

Glassburn and Deem, 1998.

interjudge intrajudge

Thickened liquids

Hydration and thick liquids

Sharpe et al., 2007

Assessed water absorption

>95% water absorbed from thick mixtures95

No difference between water, thick water

219


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Thickened liquids


Reduced fluid intake when thick prescribed

Whelan, 2001

24 stroke patients24 stroke patients

Mean fluid intake = 455 mL/day

220

Thickened liquids


Reduced fluid intake when thick prescribed

Finestone, et al., 2001

2 groups: 2 groups:

1‐enteral diets with thick liquids (21 days)

2‐diets with thick liquids (21 days)

Both groups inadequate fluid intake with thick liquids

Reduced fluid intake as weaned from tube

221

Thickened liquids

Large study data

Logemann et al., 2008; Robbins et al., 2008

711 Patients with Parkinson disease, dementiadementia

Aspiration on qualifying VFSS

Randomized order of presentation

Chin‐down/thin, Nectar, Honey

Results…

222


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Thickened liquids

Part 1: eliminating liquid aspiration

Honey nectar chin down posture (all groups)

Overall aspiration: 53%, 63%, 68%Overall aspiration: 53%, 63%, 68%

Half of patients aspirated on all 3

More aspiration on later trials

Patient preference:

Chin down posture, nectar, honey

Part 2

223

Thickened liquids

Protocol 201 Part 2 (515 patients)

Patients with aspiration on none or all:

½ chin down posture with thin liquids (259)

½ thick liquids (256) ½ thick liquids (256)

½ nectar, ½ honey (133, 123)

3 month follow up

Pneumonia, hydration, other outcomes

Results:

224

Thickened liquids

Results – Protocol 201 Part 2

52/515 patients developed pneumonia (11%)

Much less than expected

Other adverse outcomes Other adverse outcomes

More dehydration in thick liquids patients

6% vs. 2%

More UTI in thick liquid patients

6% vs. 3%

225


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Thickened liquids

Median hospital LOS with pneumonia

Honey (18 d.), nectar (4 d.), CDP (6 d.)

226

Thickened liquids

Summary on thickened liquids

Reduces aspiration but is not preferred

Thick liquids do not dehydrate

Reduced intake of fluidsReduced intake of fluids

Probable source of dehydration

Test results do not match diet thickness

Anticipated results cannot be expected

227

Thickened liquids

Summary on thickened liquids

Compliance

Patient preferences

Patient satisfaction

Aspiration of thick liquids may produce a worse pulmonary consequences than thin liquids

If treatment plan will not be implemented…

2281625


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Evidence Summary for using Free Water Protocols

“Free Water” Protocols

2291625‐1700

Frazier Rehab Institute Water Protocol Kathy Panther, M.S., CCC, Louisville, Kentucky

“... Concern over patient and family non‐compliance with thin liquid restrictions compliance with thin liquid restrictions both within the facility and after discharge led us to alter our protocol in 1984. …oral intake of water became a major feature in both treatment and day to day hydration. Features of Frazier’s program …”

230

Retrieved 01/20/09 from http://www.speech‐languagepathologist.org/archives/chat/SLP/April212003.html

Free Water Protocols

Literature search

1. “Free Water”, + Deglutition Disorders

2. Panther, K.

One citation on semantic relations in JSHD 1983

Perspectives article in 03/05 describing protocolPerspectives article in 03/05 describing protocol

“Currently there is no published evidence that will give dysphagia clinicians a definitive scientific basis for the safe delivery of water to patients with dysphagia”

ASHA journal (pre “Leader”) piece in 1998

231

Leonard, L. B., Steckol, K. F., & Panther, K. M. (1983). Returning meaning to semantic relations: some clinical applications. Journal of Speech and Hearing Disorders, 48, 25‐36.


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Developers discuss

Safety of Water

Hydration

Compliance

“Free Water” Protocol Principles

p

232

1. “Safety of Water”

“Small amounts of water … are quickly absorbedinto the body pool.”


Large amounts are not.

“Water has a neutral pH…is free of bacteria…”

“Aspiration of other liquids can lead to respiratory infections and pneumonia.”

Cited evidence: animal studies, drowning case studies

233



Drowning

Water fills air spaces

Plasma is hypertonic

Meaning: it contains lower concentration of water

At membrane, water flows into capillary

234capillary

Na+Na+ Na+

Na+

water

Effros, et al., 2000


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Example: seawater contains

High NaCL concentration

Is hypertonic Is hypertonic

Compared to plasma

Seawater drowning

Plasma enters lung

Similar with aspiration of any hypertonic solution

235capillary

Na+Na+ Na+

Sea waterNa+

Na+Na+

Na+

Na+

Na+

Na+

Na+

Na+

1. “Safety of Water”

“Water provides a safe means of assessing patients”

Opinion


Opinion

“All patients (of any diagnosis) referred to Speech Pathology are screened for dysphagia with water.

OK

“Water is safely utilized in daily treatment

“Swallow compensations can be practiced with thin liquid.

236

2. “Hydration”

“Free water consumption is encouraged for all patients and makes a significant contribution in hydration for many.”


hydration for many.

Evidence?

“The risk and cost of IV fluids should be decreased.

“Post‐discharge surveys… indicate water often is the primary means of hydration.”

237



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3. “Compliance”

“Patients reported thickened liquids did not quench thirst.

“ ti t l i t h l ”


“…patient complaints are now much less”

“…patients object to thickened liquids.

“…patients appear more likely to comply with the thin liquids restriction.”

238



3. “Compliance”

“…preparation of thickened liquids (is) burdensome.

“family may tire of patient complaints and abandon thi k d li idthickened liquids.

“Availability and cost of thickening may preclude compliance.

“Thick liquid preparation, … can overwhelm many families.”

239

Free Water Protocols Evidence

Bronchoalveolar lavage

Whelan et al. (2001) reduced fluid intake in patients prescribed thick liquids

Numerous citations on dehydration in Numerous citations on dehydration in dysphagia

Animal studies of water aspiration

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Garon et al., 1997

20 aspiration‐documented CVA patients

Aspirated liquid only on VFSS

Randomized to

(C): Thick liquids only at all times (10)

(E): All liquids thickened, AND free water (10)

Duration: treatment + 30 day follow up

Small and underpowered study

Yet the main evidence for protocol

241

Garon et al., 1997

Exclusion

“Severe cough” when aspirating

Cannot rinse and expectorate

Cannot self‐feed

Pre‐existing hydration concern

148 patients screened: 13% enrolled

34 patients declined participation

94 patients ineligible

242

Garon et al., 1997

Water placed out of reach

No water with meal or within 1hour

No compensatory swallow therapyp y py

Outcome variables

Pneumonia, hydration, time to no aspiration

Fluid intake

243


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Garon et al., 1997

Results

No patient in either group developed pneumonia, dehydration, complications

Intake of fluids comparable between groups

1210 mL (C) ‐ all thick

1318 mL (E): 855mL thick, 463mL thin

244


Garon et al., 1997

Time to recovery of aspiration

Experimental: 19.1 days (range 7‐35 days)

Control: 27.2 days (range: 8‐64 days)

Control: 42% longer to recover

More severe aspirators in control so OK

Small sample

Time to pneumonia outcome: adequate?

245


Garon et al., 1997

“Much less water than expected” by investigators (“we were surprised…”)

Satisfaction: only one control patient was satisfiedwith thick liquid

“all study patients satisfied with water”

246


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Robbins et al. 2008. Protocol 201

Pneumonia‐no difference

Thin liquids/chin‐down posture: 10%

Thick liquids: 11%

Nectar: 8%, Honey: 15%

Dehydration: Thin: 2%, Thick: 6%

UTI: Thin: 3%, Thick: 6%

3 times longer hospital stay in honey‐thick who developed pneumonia

247

Two recent studies

Two presented at ASHA 2008

Bronson‐Lowe, et al., 2008. Effects of a free water protocol for patients with dysphagia.

Free Water Protocols

Becker et al., 2008. An oral water protocol in rehabilitation patients with dysphagia for liquids.

248

Bronson‐Lowe, et al., 2008

1. Retrospective study comparing patients with historical controls (via chart review)

Pneumonia, dehydration: no difference

Free Water Protocols (#1)

Fluid intake greater in treatment group (p=.03)

2. Sample of convenience concurrent comparison

Fewer pneumonia and more fluid intake

249


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Authors’ discussion

Authors could not determine whether results were influenced by

Increased oral hygiene in the treatment group

Increased oral hydration in the treatment group

More compliance with aspiration precautions in treated More compliance with aspiration precautions in treated patients

Hydration not affected by treatment/control assignment

This needs to be replicated prospectively

250

Bronson‐Lowe, et al., 2008


Randomization to water protocol or prescribed dietary fluid (26 patients)

17 patients requiring feeding assistance

8 assigned to control 9 to treatment8 assigned to control, 9 to treatment

9 independent feeding patients

3 assigned to control, 6 to treatment

All received oral care four times per day

Becker, et al., 2008

251

Dependent Variables

Adverse events (pneumonia, UTI, death)

Objective measures not assigned by clinician/judges

FIM, FCM scores


,

not blinded, assigned by treating clinician/judges

Length of stay

252



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Results

Pneumonia: 1 patient in each group

UTI: 2 patients in each group

Death: 2 treatment deaths, no control deaths


,

FIM: no significant difference

FCM: no significant difference

Length of stay: 29.1 days (control) vs. 15.8 (tx)

Diet influence length of stay?

253


Other findings:

Independent patients consumed significantly lessfluid than dependent patients (p<.01), regardless of group

254


255Becker, et al., 2008


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Discussion

The presence of two deaths in the treatment group cannot be ignored

…and may underscore the importance of clinical


judgment in applying this and other treatments

Both patients that died had chronic pulmonary conditions

256


Other issue – implied endorsement

257

“Free water protocols”

Summary

25 years experience by developers

No published, peer reviewed data

anecdote only

Minimal objective evidence

No pneumonia difference

Other differences seem to exist

258


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“Free water protocols”

Summary

Physiologic justification exists

But not for all patients

Severe pulmonary disease

One size does not fit all

Developers obligation to publish data

Opinion here: there is no one protocol that is appropriate for every patient

259

Feeding tubes

260

Feeding tubes

Indications

Artificial nutrition

Gastric decompression

Digestive system incompetenceg y p

Paralysis, obstruction, absorption disease

“Transfer dysphagia”

Oropharyngeal transfer disorder

Delivery:

Directly to gut blood (enteral)

Directly to blood (parenteral)

261


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Non‐Oral Nutrition Enteral nutrition Delivered to the gut

Utilizes digestive system

Tube name entry, deliverydelivery Naso‐gastric (NG); gasatrojejunostomy (GJ)

Depth: sphincters, absorption

262

Non‐Oral Nutrition

Parenteral nutrition Bypasses the digestive system‐intravenous

Central, peripheral Percutaneous Intravenous Central Catheter

i f b h d proteins, fats, carbohydrates, etc.

Peripheral vein – few nutrients can be delivered

TPN, PPN

263


Nasopharyngeal entry

Fluoroscopic

Blind

264


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Surgical entry

Fluoroscopically guided

Endoscopically guided

PEG

Open surgical

All involve opening abdominal wall so all are surgical

265


PEG

266

267


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Enteral Tube Indications

Intractable aspiration

Failed interventions

Recurrent illness attributed to prandialaspirationp

Permanenttemporary

Replacement/substitute for oral intake

Supplement to oral intake

Replacement for types of materials aspirated

268

Contraindications

Ileus/Gastroparesis, SBO

Paralysis, obstruction

Absorption Deficits

Default to parenteral nutrition Default to parenteral nutrition

Prior abdominal resections/anatomy diff.

Surgically inserted abdominal enteral tubes

GER, severe.

269

Feeding Tubes

Aspiration

Is not mitigated (25‐40% in PEG)

Saliva production

may increase – new site (Metheny et al., 2006)y ( y , )

270


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Complications

271

Feeding Tubes Evidence

272

Enteral Tube Feeding

N= 70 tube fed patients, age 65‐95, over 11 mo. Indications refusal to swallow 50%

dysphagia without obstruction 47%

h l b i % esophageal obstruction 3%

Nutrition: weight, hgb, hct, serum albuminCiocon et.al, (1988)

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NGT complications in first two weeks self‐extubation (67%) , AP (43%)

GT complications in first two weeks pneumonia (56%), dysfunction 50% self‐extubation 44% self extubation 44%

Late NGT complications pneumonia (44%), self‐extubation (39%)

Late GT complications pneumonia (56%),dysfunction 38% self‐extubation 0%

40% died

274

Ciocon et.al, (1988)

Mortality in tube fed patients is high

Because they have multiple conditions

Dementia: 25‐50% mortality

¼ d ti ti t di i h it l f ll i PEG


¼ dementia patients die in hospital following PEG placement (McClave & Chang, 2003)

Callahan et al., 2000 (150 PEG cases)

7‐14 days 16%

30 day 22%, 1 year 50%

275

The SLP and the Feeding Tube

1. Patient education most important

Empower patient to ask questions

Neutral pro’s and con’s

2 Clinician personal opinion irrelevant2. Clinician personal opinion irrelevant

3. Clinician understanding of all the “ins and outs”

Our patients are sick

Balance of risks = medical care

276


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Thank you.

[email protected]

And now for some cases…

277


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