Swallowing Exam 2

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Disordered Swallowing can be due to:

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Disordered Swallowing can be due to:

speed/timing or strength/weaknees

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etiologies of dysphagia

  1. Neurogenic= CN, Neuro lesions, neuro diseases

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  1. Structural= something physical, injury, surgery

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  1. Medical= infection, swelling, pain

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

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

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Penetration

material in laryngeal vestibule, above VF

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aspiration

material past VF's, in trachea

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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)

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sarcopenia

the loss of muscle mass/fatigue that comes with aging

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*Affects tongue, UES, and sensory changes

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Aging and Acute Care

*Over 70% of dysphagia referrals were for older patients of 60 years and above

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*42% over 80 yrs

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With age:

  1. Bolus transit times increase

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  1. UES pressure drop is delayed

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  1. UES pressure minimum increases to a significant positive value

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  1. Functional swallow but risk factor

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Oral phase dysphagia symptoms

Longer chewing times, cutting up food, avoiding certain consistencies

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Oral Phase dysphagia Signs

  1. Drooling

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

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  1. Difficulty manipulating and organizing the bolus

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  1. Difficulty chewing

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  1. Prolonged oral prep time

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

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  1. Prolonged/delayed transit

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Oral Phase dysphagia neuro reasons

-Motor planning, discoordination, weakness, paralysis, muscle rigidity, muscle spasticity

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

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Pharyngeal phase dysphagia signs/symptoms bedside

  1. Gurgly/wet voice quality at baseline

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  1. Gurgly/wet voice after bolus

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  1. Coughing after swallow- Immediate or after meal

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  1. Choking- airway obstruction

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  1. Multiple swallows per bolus

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  1. "Something is stuck"

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What does a gurgly voice mean?

extra liquid on vocal folds

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-sensation impaired if pt doesn't cough

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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)

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

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

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

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

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

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Pharyngeal phase dysphagia etiologies

  1. Hemispheric stroke: Weakness opposite side

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  1. LMN injuries: disease, trauma, surgery

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  1. Brainstem injuries

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  1. Degenerative disease affecting muscles

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  1. Common in large, multiple diffuse injuries to brain

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Neurogenic causes of dysphagia

  1. CVA

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  1. TBI

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  1. Neoplasm

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  1. Progressive neurodegenerative disease

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CVA statistics with dysphagia

**30-65% of patients with CVA have initial dysphagia (Often resolves over 6 months)

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**7-29% develop PNA (pneumonia) secondary to dysphagia

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Dysphagia is highly correlated with

dysarthria

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CVA characteristics

  1. Hemorrhagic versus ischemic

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  1. Unilateral vs bilateral

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  1. Cortical and subcortical

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  1. symptoms worse at acute and then plateaus in recovery

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  1. undamaged hemi takes over in recovery

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  1. self feeding issues if damage on dominate side

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  1. Cognition and perception issues, RCVA= impulsive, visual field, awareness deficits)

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

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CVA common issues

• Reduced lingual control

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• Slow oral transit

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• Decreased sensation: Delayed trigger of swallow response

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• Reduced pharyngeal wall contractions

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• Increased pharyngeal transit time

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• Reduced laryngeal sensation

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• Reduced laryngeal elevation

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• Vallecular and pyriform stasis

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• Penetration and aspiration

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RCVA vs LCVA

RCVA- cognitive and perception issues, probably will not be able to complete compensatory strategies, deficit in awareness,

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LCVA- cognitively able to complete compensatory strategies

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The severity of dysphagia correlates with

• dysarthria

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• aphasia

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• low FIM score (functional independent measure)

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• level of cognitive functioning

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Bedside presentation correlates with

MBS

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Functional Independence Measure (FIM)

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

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-lower score=more at risk for dysphagia

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Brainstem lesions: Pons

-more oral stage stuff

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-V and VII

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Brainstem lesions: Medulla

-More pharyngeal phase

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• VII sensory, CPG

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• Pharyngeal muscle function asymmetry

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• Unilateral laryngeal paralysis (ipsi)

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• Reduced Cricopharyngeal/ UES opening\

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• Vallecular and pyriform residue

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• Penetration and aspiration

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Wallenberg's syndrome (lateral medullary syndrome)

-result of CVA of posterior inferior cerebellar artery (PICA)

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• Medial PICA supplies part of medulla

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• Dysphagia and dysphonia

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TBI issues

•Cognitive issues: Following directions, Food recognition, Attention

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

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• Polytrauma: trach, jaw and face fracture etc.

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• Emergent Care: Intubation effect on larynx

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• Medications

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TBI dysphagia strategies

• Recommend safe consistency

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

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• feed assist: help with memory and compensatory strategies

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A stroke in brainstem has

more bilateral deficits because it's so small

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