Swallowing Exam 2

Disordered Swallowing can be due to:

speed/timing or strength/weaknees

etiologies of dysphagia

1. Neurogenic= CN

Penetration

material in laryngeal vestibule

aspiration

material past VF's

On MBS or FEES do we see the etiology or consequence?

We see the consequence (residue

sarcopenia

the loss of muscle mass/fatigue that comes with aging *Affects tongue

Aging and Acute Care

*Over 70% of dysphagia referrals were for older patients of 60 years and above *42% over 80 yrs

With age:

1. Bolus transit times increase

2. UES pressure drop is delayed

3. UES pressure minimum increases to a significant positive value

4. Functional swallow but risk factor

Oral phase dysphagia symptoms

Longer chewing times

Oral Phase dysphagia Signs

1. Drooling

2. Pocketing of food in buccal and labial sulci (oral residue post swallow)

3. Difficulty manipulating and organizing the bolus

4. Difficulty chewing

5. Prolonged oral prep time

6. Loss of control of bolus (anterior or posterior)

7. Prolonged/delayed transit

Oral Phase dysphagia neuro reasons

-Motor planning

Pharyngeal phase dysphagia signs/symptoms bedside

1. Gurgly/wet voice quality at baseline

2. Gurgly/wet voice after bolus

3. Coughing after swallow- Immediate or after meal

4. Choking- airway obstruction

5. Multiple swallows per bolus

6. "Something is stuck"

What does a gurgly voice mean?

extra liquid on vocal folds -sensation impaired if pt doesn't cough

Pharyngeal Phase dysphagia on FEES/MBS

1. Delayed onset of swallow: Bolus has been pumped into pharynx

Pharyngeal phase dysphagia etiologies

1. Hemispheric stroke: Weakness opposite side

2. LMN injuries: disease

Neurogenic causes of dysphagia

1. CVA

2. TBI

3. Neoplasm

4. Progressive neurodegenerative disease

CVA statistics with dysphagia

**30-65% of patients with CVA have initial dysphagia (Often resolves over 6 months) **7-29% develop PNA (pneumonia) secondary to dysphagia

Dysphagia is highly correlated with

dysarthria

CVA characteristics

1. Hemorrhagic versus ischemic

2. Unilateral vs bilateral

3. Cortical and subcortical

4. symptoms worse at acute and then plateaus in recovery

5. undamaged hemi takes over in recovery

6. self feeding issues if damage on dominate side

7. Cognition and perception issues

CVA common issues

• Reduced lingual control • Slow oral transit • Decreased sensation: Delayed trigger of swallow response • Reduced pharyngeal wall contractions • Increased pharyngeal transit time • Reduced laryngeal sensation • Reduced laryngeal elevation • Vallecular and pyriform stasis • Penetration and aspiration

RCVA vs LCVA

RCVA- cognitive and perception issues

The severity of dysphagia correlates with

• dysarthria • aphasia • low FIM score (functional independent measure) • level of cognitive functioning

Bedside presentation correlates with

MBS

Functional Independence Measure (FIM)

18-item

Brainstem lesions: Pons

-more oral stage stuff -V and VII

Brainstem lesions: Medulla

-More pharyngeal phase • VII sensory

Wallenberg's syndrome (lateral medullary syndrome)

-result of CVA of posterior inferior cerebellar artery (PICA) • Medial PICA supplies part of medulla • Dysphagia and dysphonia

TBI issues

•Cognitive issues: Following directions

TBI dysphagia strategies

• Recommend safe consistency •control environment: distraction free

A stroke in brainstem has

more bilateral deficits because it's so small

TBI injury types

-Diffuse axonal injury: Bilateral UMN= spasticity

Progressive degenerative diseases issues

• contraindicated?? Pt's swallow will only get worse

Parkinson's disease and dysphagia oral stage

-impaired mastication and lingual movements -increased number of swallows per bolus

• tongue pumping

• premature or uncontrolled loss of bolus from the oral cavity -increased oral transit duration

• decreased suction pressure

• residue on the tongue and anterior and lateral sulci after the swallow

Parkinson's disease and dysphagia pharyngeal stage

1. delayed trigger of the pharyngeal swallow reflex

2. prolonged laryngeal movement

3. decreased pharyngeal contraction pressure

4. vallecular and pyriform sinus residue

5. inability to adapt hyoid bone movement to changes in bolus characteristics

6. aspiration

Esophageal dysfunction neuro symptoms

-Sensation that food is stuck (not precise!) -Sensation that food comes back up -Odynophagia

Esophageal dysfunction neuro signs

• Regurgitation to pharynx • Ineffective peristalsis • Poor clearance

Neuro etiology esophageal dysfunction

• Esophageal motility depends on intact sensory motor function:

• Relaxation of UES and LES

• Esophagus must sense presence of bolus for secondary peristalsis

• Muscle contraction for peristalsis: strength and coordination

Cricopharyngeal dysfunction

-Hypertonicity of UES -striated muscle

• Tx: myotomy (incision)

Achalasia

• In esophagus: failure of LES to relax -Smooth muscle

• absent peristalsis -bolus gets through to stomach very slowly

Cricopharyngeal Bar

structure that protrudes and is in the way of bolus -neural based as it's not a growth

Esophageal spasms: Diffuse esophageal spasm (corkscrew on barium)

• High amp distal (smooth) muscle contractions

• Long duration multiple contractions

Esophageal spasms: Nutcracker esophagus

-Hypertensive peristalsis that's normal in sequence

• Pain! -Unknown etiology

• Tx with med

Parkinson's disease characteristics

in resting tremor

Parkinson's disease dysphagia signs

•Reduced taste and tongue sensation • drooling •Impaired strength

PD- Oral Phase

•Reduced jaw opening; impaired mastication •Impaired lingual movements • tongue pumping (festinated tongue movement • increased number of swallows per bolus

PD- pharyngeal stage

•delayed onset of the pharyngeal swallow response •prolonged laryngeal movement •decreased pharyngeal contraction pressure •vallecular and pyriform sinus pooling before and residue after swallow •inability to adapt hyoid bone movement to changes in bolus characteristics and •Silent aspiration

PD Treatments

•LSVT- makes pt way louder

Huntington's Disease characteristics

•Hereditary d/z of basal ganglia •Deterioration of cognition

Huntington's dysphagia

•Signs: oral bolus retention •Impaired bolus formation and voluntary swallow initiation •Delayed

HD therapy

•Posture; lemon ice prior to food(makes them more aware

ALS characteristics

•Amyotrophic lateral sclerosis •Degeneration of both upper and lower motor neurons with the CNS •Dysphagia is often an early symptom •As the disease progresses aspiration and aspiration pneumonia become common

ALS therapy

•Diet modification •Timely (early) feeding tube placement •CONTROVERSY: STRENGTHENING!!!- complete strength training

Guillain-Barre'

• G-B is toes to nose progression

• demyelinating condition effecting primarily motor nerves

• Three stages of Disease: Progressive (12 days)

cerebral palsy

90% had: Oral phase delays

Myasthenia Gravis

•Receptor cites for ACh do not function •Reduced efficiency in muscle contraction

Myasthenia Gravis Treatment

•In early stages

Multiple Sclerosis

•Demyelinating disease •Cognition •Dysphagia in at least 1/3 of patients •Signs/symptoms depends on site: Corticobulbar

Structural disorder types

-Neural innervation -Muscles -Cartilage -Connective tissue -Bone

What are some of the reasons for lesions to RLN/SLN?

•Can be stretched or cut •RLN: Paresis or paralysis of movement of vocal folds

• U VFP on strobe •SLN: Pitch glide is affected

• Laryngeal EMG to confirm that it's truly paralyzed or something else is affecting it

Patients with unilateral VF impairment

•Decreased pharyngeal stripping wave: pharyngeal residue •Decreased laryngeal elevation and epi inversion •Abnormal Cricopharyngeal function

carotid endarterectomy

removal of plaque from an occluded carotid artery

thyroidectomy

complete or partial removal of thyroid gland

Anterior cervical spine discectomy and fusion

•Protruding inter-vertebral disc is reduced •Plate is placed fusing vertebrae together -larynx is moved over -RLN and SLN can be stretched -Edema -Pharyngeal wall bulging -UES hypertonicity -Esophageal perforation

osteophytes

• Bony outgrowths

• Middle aged-elderly -in c spine -protrude into pharynx and near UES -bad posture can lead to this

intubation

-Transient reduced sensation: silent aspiration -Greater risk with #days intubated- take longer to recover -Won't be able to cough if aspirate -Recover 2-10 days -unilateral vocal fold paresis -arytenoid dislocation -scarring between arytenoids

Post intubation dysphagia

-Aspiration was seen in 45% of subjects with in 24 post extubation -1/2 were silent -check on patients 48 hours after extubation for bedside test

nasogastric tube

-Inflammation and ulceration at the posterior larynx -Abductor paralysis! Midline fold! -dysphagia and airway compromise: If dysphagic with NG tube

Zenker's diverticulum

•Outpouching or "herniation" of the posterior hypopharyngeal mucosa •Killian's triangle- weak as it has no muscles behind it -above UES -Worse with particulate food (rice)! -Not just solved with double swallow! -Rare prior to age 40 (mean age 67)

Killian-Jamieson diverticulum

-Just below UES -Less common than Zenker's

GERD

gastroesophageal reflux disease -stomach acid coming up through LES and esophagus -Mucosal changes

GERD symptoms

-substernal pain

hiatal hernia

-Protrusion of stomach tissue through the hiatus of the diaphragm -can be associated with GERD

GERD therapy

-Elevate HOB 30 degrees -Sit up 3-4 hours after meal (do not recline!) -Avoid certain foods •ETOH

Strictures

•Esophageal narrowing caused by inflammation or trauma/compression •Can be caused by GERD

Strictures therapy

dilate the narrowing every so many months

Schatzki's ring

-stricture -DISTAL esophagus -Can result in poor: Esophageal clearance

CP bar and Zenkers

The increased resting tone of the cricopharyngeus muscle has been implicated in the formation of a Zenker's diverticulum

CP treatment

•Botox: -Reduced effects compared to CP myotomy -Still need total anesthesia •CP myotomy more effective

Head and Neck Cancer Surgery

-Excision of oral cavity structures: Tongue

Effects on swallow during/after radiation

•Mucosa: -erythema

SLP's job during radiation

•Pre-Tx counseling •Find tolerated consistency •Moist

Delayed effects of radiation

•Xerostomia •Permanent injury to salivary glands: Thick ropy secretions; ph is off

Late effects of radiation

•Radiation necrosis/fibrosis syndrome -Sclerosis (pathologic change) of soft tissue (muscle

MBS Pros

•Good because you can visualize: before

MBS cons

•Concerns: •Positioning •Medical complexity (transport) •Follow commands •Needs to be brief recording (radiation) •Can't assess well: •VP movement •Vocal fold mobility •Tissue health- can't see color of tissue •Secretion management! - can't see saliva

FEES pros

•Visualize: •VP closure as you pass the scope •Laryngeal A&P •Glottal attack

Reasons for fees

•Resonance / VP function •Voice/laryngeal function •Respiratory status/secretions? •Pharyngeal/laryngeal surgical Hx -MBS not feasible

FEES cons

•Oral phase •Zenker's •Esophageal phase problems

Assess during fees

•Anatomy •Abnormal appearance of structures: Normal? Color? Inflammation? Secretions? •Reconstruction

•Physiology: •VP function (dun-uh-dun-uh-dun-uh) •Pharynx (high pitch /i/) •Laryngeal function •Hold breath

Valsalva (pressure you have when you lift something up)

FEEs visual

•Premature spillage of bolus to pharynx •Pharyngeal onset •Penetration and aspiration before or after swallow •Pharyngeal residue after swallow •Signs of penetration and aspiration during the swallow •Can try therapeutic strategies •Entire meal! •Lots of time due to no radiation

when does aspiration occur

90% of all aspiration occurs before or after the swallow

MBS vs FEES

•Phases you can see •Time benefit •Fees sees larynx •Fees secretion •Fees see velum

High pitch /i/ tests??

Pharyngeal wall closure

dun-uh-dun-uh-dun-uh tests?

VP function

Valsalva tests?

VF closure

ihi ihi ihi test?

VF function

purpose of bedside

• Safe to eat: What consistency liquids

Speech

language