Swallowing Exam 2

Disordered Swallowing can be due to:

Disordered Swallowing can be due to:

speed/timing or strength/weaknees

etiologies of dysphagia

1. Neurogenic= CN, Neuro lesions, neuro diseases

2. Structural= something physical, injury, surgery

3. Medical= infection, swelling, pain

4. Deconditioning= too weak all over, older people just degenerate

5. Psychogenic= believes they can't swallow, only can control it in oral phase

Penetration

material in laryngeal vestibule, above VF

aspiration

material past VF's, in trachea

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

We see the consequence (residue, etc) and need to work backwards to figure out the physiology (reduced HL excursion, etc) and etiology (CN V lesion)

sarcopenia

the loss of muscle mass/fatigue that comes with aging

*Affects tongue, UES, and sensory changes

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, cutting up food, avoiding certain consistencies

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, discoordination, weakness, paralysis, muscle rigidity, muscle spasticity

-Etiology: CN lesions: V VII XII; Cortical and subcortical lesions

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, hyoid hasn't moved, Vallecular and pyriform "pooling" before swallow trigger, Penetration, Aspiration(Before, during or after swallow)

2. Reduced HL excursion: leads to Penetration; aspiration, limited UES opening

3. Reduced laryngeal airway closure: leads to Penetration/aspiration

4. Poor BOT to PPW contraction: leads to Vallecular residue, No help inverting the epiglottis

5. Reduced pharyngeal stripping wave: leads to Vallecular stasis, Pyriform sinus stasis, Coating of pharyngeal wall

6. Poor UES opening: leading to Pyriform residue, Aspiration off pyriform residue

Pharyngeal phase dysphagia etiologies

1. Hemispheric stroke: Weakness opposite side

2. LMN injuries: disease, trauma, surgery

3. Brainstem injuries

4. Degenerative disease affecting muscles

5. Common in large, multiple diffuse injuries to brain

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, RCVA= impulsive, visual field, awareness deficits)

8. Contralateral weakness: lower half of face (VII), tongue (XII)

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, probably will not be able to complete compensatory strategies, deficit in awareness,

LCVA- cognitively able to complete compensatory strategies

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, 7-level scale that assesses severity of disability in performing basic life activities, 1=total assist

-lower score=more at risk for dysphagia

Brainstem lesions: Pons

-more oral stage stuff

-V and VII

Brainstem lesions: Medulla

-More pharyngeal phase

• VII sensory, CPG

• Pharyngeal muscle function asymmetry

• Unilateral laryngeal paralysis (ipsi)

• Reduced Cricopharyngeal/ UES opening\

• Vallecular and pyriform residue

• Penetration and aspiration

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, Food recognition, Attention

• Behavioral issues: Compliance with strategies (memory, impulsiveness), Self-feeding

• Polytrauma: trach, jaw and face fracture etc.

• Emergent Care: Intubation effect on larynx

• Medications

TBI dysphagia strategies

• Recommend safe consistency

•control environment: distraction free, not a ton of people

• feed assist: help with memory and compensatory strategies

A stroke in brainstem has

more bilateral deficits because it's so small