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Laryngology > Dysphagia and Aspiration > Flashcards

Dysphagia and Aspiration Flashcards

1
Q

√What are the classifications of dysphagia?

A

Difficulty initiating vs. food “sticks” after swallowing:
- Initiating = Oropharyngeal dysphagia
- Sticks = Esophageal Dysphagia

Esophageal dysphagia - Solids only or solids and liquids:
- Solids only = Mechanical obstruction
- Solids and liquids = Motility disorder

Mechanical obstruction: Intermittent or progressive?
- Intermittent = Esophageal ring
- Progressive = Stricture/Malignancy

Motility disorder: Intermittent vs. Progressive?
- Intermittent = Esophageal spasm
- Progressive = Achalasia / scleroderma

Flow Chart Vancouver 206

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2
Q

What are the 4 stages of swallowing / phases of deglutition? What nucleus innervates the pharyngeal phase?

A
  1. Oral Preparatory
  2. Oral
  3. Pharyngeal (nucleus tractus solitarius/ambiguous - nucleus ambiguus provides fibers that innervate the somatic muscles of the pharynx, larynx, and soft palate)
  4. Esophageal
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3
Q

Name the 6 different sphincters that regulate normal swallowing

A
  1. Lips/oral commissure
  2. Tongue with hard palate
  3. Tongue base with soft palate (palatoglossus)
  4. Velopharynx
  5. Larynx (true folds first, false folds next, then epiglottis and aryepiglottis folds)
  6. Cricopharyngeus (upper esophageal sphincter)
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4
Q

What are 7 events that have to occur during normal pharyngeal phase of swallowing?

A
  1. Breathing cessation
  2. Palate elevation and closure of nasopharyngeal isthmus
  3. Glottic closure (three levels) - True VF, False VF, epiglottic collapse + anterior arytenoid tilt
  4. Laryngeal elevation
  5. Pharyngeal peristalsis
  6. Cricopharyngeal relaxation
  7. Dilation of pharyngoesophageal segment
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5
Q

List the layers of the esophagus. What are the types of muscles within the esophagus?

A

From inside to out:

  1. Mucosa (ELM)
    a/ M1 = Epithelium
    b/ M2 = Lamina propria
    c/ M3 = Muscularis mucosa
  2. Submucosa
  3. Muscularis Propria
    a/ Inner circular layer
    b/ Outer longitudinal layer
  4. Adventitia

*Basement membrane divides epithelium from rest of the esophagus

UES and Proximal 1/3 esophagus = skeletal muscle
LES and Distal 2/3 esophagus = smooth muscle

Kevan Page 49

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6
Q

What is the arterial supply and innervation of the esophagus?

A
  1. Upper third = inferior thyroid artery
  2. Middle third = Thoracic aorta branches
  3. Lower third = Left gastric artery

Innervation: Vagus/sympathetic chain

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7
Q

Describe the Grading system of Erosive / Reflux Esophagitis

A

Los Angeles Classification System:

Grade A:
- ≥1 mucosal break < 5mm
- Does not extend between the tops of two mucosal folds

Grade B:
- ≥ 1 mucosal break ≥5mm
- Does not extend between the tops of two mucosal folds

Grade C:
- ≥ 1 mucosal break that is continuous between the tops of 2 or more mucosal folds
- < 75% of the esophageal circumference

Grade D:
- >75% of the esophageal ciircumference involves

Kevan Page 50

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8
Q

What are the different types of swallowing investigations? 6

A
  1. MBS (tests all phases)
  2. Manometry
  3. Barium swallow
  4. FEES/FEEST
  5. Scintigraphy
  6. CXR
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9
Q

Differentiate a barium swallow, modified barium swallow, and FEES. What features do each evaluate? List 4 differences

A

Barium Swallow:
- Swallowing test with a single swallowed medium (large volume), essentially a “contrast esophagram”
- Done by a radiologist only and shows static images (SLP not involved)
- Good at evaluation of esophageal anatomy, but not of esophageal function (e.g. Good at obstruction, not at aspiration)
- Image is performed in SUPINE position (lie on x-ray table)
- No therapeutic component to the exam, just diagnostic

Modified Barium Swallow:
- aka. VFSS Video Fluoroscopic Swallowing Study
- Performed by a Radiologist + SLP
- Provides many textured mediums (thin fluids to solids), each with small amounts of barium contrast material
- Evaluates all 4 phases of swallowing (oral prepatory, oral transit, pharyngeal, esophageal)
- Functional evaluation (e.g. aspiration)
- Image is performed in UPRIGHT position
- Can be therapeutic and diagnostic functions

FEES = Functional Endoscopic Evaluation of swallowing:
- Video endoscopy with direct evaluation of pharynx/larynx before/after/during swallowing with different consistencies
- Better for evaluation of aspiration
- Can also be used to assess therapeutic response
- Can be combined with sensory testing (FEESST)

Features Evaluated (food/liquid/ice chips mixed with green food colouring):
- Premature spillage: loss of bolus into pharynx before the initiation of swallowing
- Laryngeal penetration: into laryngeal inlet but not into VF
- Tracheal aspiration: below vocal folds
- Pharyngeal residue
- Coughing/throat clearing
- Secondary re-swallow
- Rising Tide Sign: Post-swallow regurgitation out of the esophagus into the pharynx (esophagopharyngeal reflux). May indicate the presence of a Zenker’s diverticulum or profound esophageal dysmotility

Other points of assessment:
1. Nasopharygneal closure
2. Symmetry of palate at rest
3. Quantity of pooled secretions
4. Larynx inspection for lesion and vocal fold mobility
5. Ability to close the supraglottis with breath holding
6. Pharyngeal squeeze maneuver to evaluate pharyngeal muscle contraction

Things that can be modulated during FEES:
1. Texture
2. Volume
3. Compensatory maneuvers
4. Patient position

Kevan Page 35

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10
Q

What is a FEESST? What nerve does it test, and how do you interpret the results?

A

FEESST = FEES + SENSORY TESTING
- Sensory testing: Ability of tactile stimulus to elicit the laryngeal adductor reflex (Nerve = Internal branch of SLN)
- Sensory testing is performed with the tip of the scope touching the AE fold, or with air-pulse stimulator blowing puffs of air on the AE fold

Air pulse stimulator results: Quantified the air pressure (mmHg) required to stimulate the laryngeal adductor reflex
- Normal < 4 mmHg
- Moderate deficit: 4-6 mmHg
- Severe deficit: >6 mmHg

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11
Q

Comparing MBS and FEES, what are the advantages and disadvantages among them? name 3 of each

A

MODIFIED BARIUM SWALLOW

Advantages:
1. Non-invasive
2. Evaluates oral, pharyngeal, and esophageal phases of swallow
3. Visualization of cervical hardware after spinal surgery or cervical osteophytes
4. Evaluation of hyolaryngeal elevation
5. Allows for evaluation of the pharyngoesophageal segment (during “white-out”)
6. Allows for screening of the esophagus

Disadvantages:
1. Radiation exposure (exam time may be limited)
2. Fluoroscopy unit is turned off between bolus presentations, so possible to miss salient event if not imaging between swallows
3. Exam usually requires transport to radiology department or mobile unit

FUNCTIONAL ENDOSCOPIC EVALUATION OF SWALLOWING

Advantages:
1. More sensitive than MBS for aspiration or penetration
2. Lower cost, no radiation exposure
3. Provides direct view of anatomy structures to evaluate laryngeal and pharyngeal structures
4. May be performed at bedside
5. Uses real food and liquid
6. Exam can last throughout a meal to evaluate for fatigue if needed

Disadvantages:
- Whiteout period during height of swallowing limits evaluation
- Examiner must make inferences regarding laryngeal penetration vs. aspiration during the swallow
- Time and expense involved with decontamination of endoscope

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12
Q

Name four different uses of a modified barium swallow

A
  1. Define an oral or pharyngeal motility disorder
  2. Identify aspiration
  3. Assess the speed of swallow
  4. Assess effects of therapeutic strategies
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13
Q

What are the differences in advantages and disadvantages between barium and gastrograffin?

A

GASTROGRAFFIN:

Advantages:
1. Less risk of inflammation in case of mediastinal extravasation (water soluble, easier to wash out)

Disadvantages:
1. If aspirated, can cause significant pneumonitis (important consideration with concomitant laryngeal injury)

BARIUM:

Advantages:
1. More sensitive than gastrograffin

Disadvantages:
1. High risk of inflammation in case of mediastinal extravasation (More difficult to wash out)
2. Airway inflammation with aspiration/pneumonitis (but less than gastrograffin)

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14
Q

How can you confirm chronic aspiration in a child? List 4 different diagnostic tests

A
  1. CXR
  2. MBS
  3. FEES
  4. Barium swallow
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15
Q

√What are 8 possible causes / differential diagnosis of esophagitis?

A

INFECTIOUS:
1. Fungal (Candida)
2. Viral (CMV, HIV, HSV)

INFLAMMATORY:
1. Allergic (eosinophilic)
2. GERD (30% of patients with LPR have esophagitis)
3. Bullous dermatitis (TEN, SJS, EM)

TRAUMATIC:
1. Chemical/Caustic (e.g. Lyme)
2. Traumatic (nasogastric tube)
3. Post-XRT

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16
Q

√Regarding Eosinophilic Esophagitis, discuss:
1. What is the typical epidemiology/phenotype? 4
2. Clinical presentation? 5
3. What are the diagnostic methods? 3. Scope findings 5
4. Treatment options? 8

A

EOSINOPHILIC ESOPHAGITIS:
- Autoimmune/allergic esophagitis

EPIDEMIOLOGY:
1. Young teens/adults
2. 70% males
3. History of atopy
4. Often have refractory GERD

CLINICAL PRESENTATION:
1. Refractory GERD
2. Dysphagia with sensation of food getting stuck (globus)
3. Food impaction
4. Esophageal strictures
5. Abdominal pain in pediatrics

DIAGNOSIS:
1. Esophagoscopy
- Linear Furrows
- Rings/trachealization of esophagus
- White exudates
- Esophageal narrowing
- “Crepe paper mucosa”

  1. Biopsy proven local eosinophilic infiltrate (>15eosinophils/hpf)
  2. Allergy testing

TREATMENT:
1. Conservative:
- Food allergy evaluation
- Hypoallergenic diet - e.g. six-food elimination diet

  1. Medical:
    - Swallowed topical steroids (e.g. Fluticasone, Budesonide)
    - Swallowed montelukast (LTRA)
    - Allergy medications (e.g. antihistamines, leukotriene inhibitors, etc.)
    - PPI (though generally poor response)
    - Biologics (Dupilumab anti IL4Ra)
  2. Surgical:
    - Dilation of Strictures

Vancouver 207 image
Kevan Gen #136

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17
Q

On manometry, what is normal LES pressure? What 4 environmental things can affect LES pressure?

A

10-40mmHg

Affected by:
- Diet (fat, chocolate, EtOH, mint)
- Caffeine
- Smoking (relaxes)
- GERD

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18
Q

√Discuss Achalasia:
1. What is it and what is the pathophysiology?
2. What is Auerbach’s Plexus and Meissner’s plexus?
3. Clinical presentation? 4
4. What imaging would be used in its workup? What other workup can be considered? 3 total
5. What is the manometry findings?
6. What is the differential diagnosis for achalasia? 3
7. What is the treatment? 4

A

Achalasia = neuromuscular disorder caused by degeneration of Auerbach’s Plexus, resulting in failure of peristalsis but preservation of LES tone, thus causing progressive esophageal dilatation
- Auerbach’s Plexuses = Part of the enteric nervous system, located in the muscularis propria, responsible for peristalsis (between the circular and longitudinal layers of the GI tract)
- Meissner’s Plexuses = Located in the submucosa, responsible for sensory function

Clinical Presentation:
- Aperistalsis
- Esophageal dilation
- Failed LES relaxation
- Progressive disease = leads to fibrosis and atrophy of muscle

Imaging:
- Barium Swallow finds “Bird’s Beak Esophagus’ caused by esophageal dilatation proximal to the tight LES (see Kevan page 50)
- Esophagram: Esophageal distention, air-fluid level, aperistalsis, absence of LES relaxation, retension of barium
- Can use smooth muscle relaxants (methacholine, nitroglycerin) to differentiate from stricture

Other workup:
1. Can consider esophagoscopy
2. Esophageal manometry

Manometry findings:
1. Increased LES pressure (40-60mmHg)
2. Aperistalsis
3. Absent LES relaxation

Differential Diagnosis:
1. Distal esophageal or upper gastric carcinoma
2. Chagas Disease - caused by parasitic infection by Trypanosoma Cruzi, results in damage to ganglion cells of the esophagus/Auerbach’s plexus
3. Central or peripheral neuropathies (stroke, DM)
4. Amyloidosis
5. Strictures secondary to reflux esophagitis
6. Scleroderma
7. Zenker’s Diveriticulum

Treatment: GI consult
1. Early symptomatic = Calcium channel blockers, or nitrates to stimulate LES relaxation
2. Botox injections
3. Esophagoscopy with Dilatations
4. Heller Myotomy (LES myotomy) if failed dilation or higher risk of dilation (e.g. previous perforation, epiphrenic diverticula, adjacent aortic aneurysm)

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19
Q

√Discuss CREST syndrome. What are the classic findings? 6

A

CREST Syndrome = limitied cutaneous form of systemic sclerosis.

C: Calcinosis
R: Raynaud’s Phenomenon
E: Esophageal Dysmotility
S: Sclerodactyly
T: Telangiectasia

Findiings: Anti-centromere antibodies (blood test)

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20
Q

√How do esophageal motility disorders typically present? How are they classified and list a differential. What are the common investigations?

A

Features:
- Dysphagia
- Globus pharyngeus
- Non-cardiac chest pain

Classified into Hyperkinetic and Hypokinetic disorders

Hyperkinetic:
1. Nutcracker esophagus
2. Diffuse esophageal spasm (aka. distal esophageal spasm)
3. LES hypertonia

Hypokinetic:
1. Achalasia
2. Ineffective esophageal motility
3. Systemic Sclerosis (e.g. Scleroderma, or CREST which is limited cutaneous systemic sclerosis)

Investigations:
1. Esophageal Manometry
2. Impedence monitoring (e.g. MII-pH monitoring, can assess bolus transit)

Kevan Page 51 for flowchart of esophageal disorders

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21
Q

√Discuss Nutcracker Esophagus:
1. What are the classic findings? 3
2. What is it often associated with? 1
3. What is the treatment? 3

A

Findings:
1. Manometry: Normal peristalsis, high amplitude esophageal contractions
2. Bolus transit usually normal
3. Fluoroscopy usually normal

Associations:
1. Reflux

Treatment:
1. Reassurance
2. Anti-reflux treatment and/or pH testing
3. Nitrates and Calcium channel blockers may reduce intensity of contractions

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22
Q

√Discuss Diffuse Esophageal Spasm
1. What is it and what is the pathophysiology?
2. What are the classic findings on imaging/investigations? 2
3. What is the treatment? 5

A

Pathophysiology:
- Non-peristaltic motility disorder
- Uncoordinated contractions of the esophagus, which affect bolus transit

Findings:
1. Barium Swallow: Corkscrew esophagus
2. Manometry: >20% but < 100% of wet swallows produce simultaneous contractions. Onset velocity of perstaltic wave >8cm/s

Treatment:
1. pH testing and anti-reflux therapy
2. Possible efficacy in case series: PDE inhibitors, CCBs, peppermint oil, visceral analgesics, botox injections
3. Esophageal dilatation may be helpful
4. Myotomy can be considered in extreme cases

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23
Q

√Discuss LES Hypertonia:
1. Definition
2. What are the classic findings and features? 2
3. What is the treatment? 2

A

Definition:
1. LES resting pressure > 45mmHg on manometry

Features:
- Typically does not cause dysphagia as long as esophageal peristalsis is normal (decreased peristalsis + preserved LES tone = achalasia)
- Can also be symptomatic if the LES fails to relax completely (remains >8mmHg)

Treatment:
1. Botox injections
2. Surgical myotomy

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24
Q

√Discuss Ineffective Esophageal Motility:
1. What is it and what is the pathophysiology?
2. What are its features on investigations?
3. What is the treatment?

A

What is it? Common hypokinetic esophageal disorder that may cause globus or dysphagia

Findings:
1. Manometry: 50% or more swallows with amplitudes < 30mmHg in distal esophagus
2. 50% will also have impaired bolus transit on impedence testing

Treatment:
1. Address reflux
2. Bethanechol (muscarinic receptor agonist) may improve distal esophageal contractility

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25
Q

√Discuss Systemic Sclerosis/Scleroderma
1. What is it and what is the pathophysiology?
2. What are the common investigational findings?
3. What is the treatment?

A

What is it?
- Multisystem collagen vascular disease (causes chronic inflammation in connective tissues)
- Results in fibrosis and atrophy of SMOOTH MUSCLE (ie. LES and lower 2/3 esophagus)
- GI symptoms present in 90% of SS, with the distal esophagus being the most common site involved (as it is made up of smooth muscle)

Findings:
1. Manometry: Poor peristalsis, weak contractions/absent LES contraction (< 10mmHg), or aperistalsis of lower 2/3 esophagus, esophageal dilation
2. May have CREST syndrome: Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, and telangiectasias
3. Incompetent LES increases risk for reflux and its sequelae

Treatment:
1. Antireflux therapy
2. Immunosuppressive agents

26
Q

√Discuss Dermatomyositis:
1. What is it and what is the pathophysiology?
2. What are the associated risks?
3. How does it typically manifest in the head and neck?
4. What are the esophageal manometry findings if it is affected?

A

DERMATOMYOSITIS:
- Idiopathic inflammatory myopathy of striated muscle (ie. Esophagus = Proximal 1/3 and UES)

Associations:
1. Rashes
2. Higher risk of esophageal malignancy

H/N Manifestations:
1. 50% weakness in neck muscles
2. Dysphagia 30%

Manometry:
1. Aperistalsis of upper 1/3 of esophagus
2. Frequent nasal regurgitation

27
Q

√Regarding Plummer Vison Syndrome, discuss:
1. What is Plummer Vinson Syndrome?
2. What are the risks of the syndrome?
3. What is the epidemiology of it?
4. What is the cliniical presentation? 8
5. What tests should be ordered?
6. What is the treatment? 4

A

Triad of:
1. Hypopharyngeal or esophageal webs
2. Iron deficiency anemia
3. Dysphagia

RISKS:
Increased risk of hypopharyngeal and esophageal cancer

EPIDEMIOLOGY:
- Unclear epidemiology and etiology, but thought to be due to nutritional deficiency (iron)
- Increased prevalence in Caucasian middle aged women (especially US, Wales, Sweden)
- Increased prevalence of Scandinavian descent

CLINICAL PRESENTATION:
1. Dysphagia (degeneration of esophageal muscle)
2. Esophageal stricture, pharyngoesophageal webs
3. Glossitis
4. Iron deficiency anemia (microcytic hypochromatic anemia)
5. Cheilitis (fissures at corners of lips)
6. Koilonychia (nails are flattened and have concavities)
7. Splenomegaly
8. SCC of the post-cricoid region and cervical esophagus
9. Hypothyroidism
10. Hiatal hernia
11. Achlorhydria (stomach does not produce hydrochloric acid)

TESTS:
1. CBC, iron levels
2. Contrast esophagram
3. Esophagoscopy

TREATMENT:
1. Endoscopic web rupture
2. Iron replacement (improves most symptoms)
3. Esophageal dilation
4. Monitor for esophageal and hypopharyngeal carcinoma

28
Q

√Regarding Cricopharyngeal dysfunction, discuss:
1. What are the types?
2. What are the possible causes?
3. What is the common anatomic abnormality seen?
4. What is the treatment? 4

A

Types: Primary or Secondary

Causes:
1. Idiopathic
2. Associated with intrinsic disorders of the muscle, such as e.g:
- Polymyositis
- Muscular dystrophy
- Parkinson’s
- Hypothyroidism
- Reflux

Anatomic abnormality: Cricopharyngeal bar

Treatment:
1. Diet modification
2. Dilation
3. Botox injection
4. Cricopharyngeus myotomy

29
Q

√Regarding Cricopharyngeal spasm, discuss:
1. What are the common causes?
2. What are the common investigations and findings? 2
3. How do you differentiate this from achalasia?
4. Treatment? 2

A

COMMON CAUSES: May be secondary to neurologic disorders:
- Poliomyelitis
- Oculopharyngeal dysphagia
- Stroke
- Amyotrophic lateral sclerosis (ALS)
- Diabetic neuropathy
- Myasthenia gravis
- Peripheral neuropathies

Investigations:
1. EMG
2. X-ray
3. Note: Normal LES opening differentiates this from achalasia

X-RAY FINDINGS:
1. Corkscrew pattern

EMG FINDINGS:
1. Lack of synchrony between cricopharyngeus relaxation and inferior constrictor contraction

TREATMENT:
1. Calcium channel blockers
2. Transthoracic myotomy

30
Q

√What is Boyce’s Sign

A

Gurgling with manual manipulation of the neck, associated with Zenker’s diverticulum or laryngocele.

31
Q

√Describe 3 natural regions of weakness of the esophagus.

A
  1. Killian’s Triangle: Between the cricopharyngeus and inferior constrictor muscle
  2. Killian-Jamieson Triangle: Between the oblique and transverse fibers of the cricopharyngeus
  3. Laimer’s Triangle: Between the Cricopharyngeus and the most superior esophageal circular muscle

Nadia Zenker’s notes pictures, Vancouver 209

32
Q

√What are the different classifications on how to describe a diverticulum/diverticulae, in the context of the GI system?

What are the 3 common locations of diverticulae in the upper GI tract, and what type of forces cause these?

A

True or False Diverticulae:
1. True Diverticulum: Herniation of all layers of the gastrointestinal wall (e.g. Meckel’s Diverticulum)
2. False Diverticulum: Herniation of only some of the wall of the GI wall, such as just mucosa and submucosa (e.g. Zenker’s Diverticulum)

Traction vs. Pulsion Diverticulae:
1. Traction: External pulling force causes formation of the diverticulum due to adjacent inflammation (e.g. inflammation, neoplasm, TB lymphadenitis in mediastinum)
2. Pulsion: Internal pushing force (ie. increased intraluminal pressure) causes formation of the diverticulum; hernation through an area of weakness (e.g. Zenker’s)

LOCATIONS:
1. Pharyngoesophageal (Zenker’s): Usually due to pseudo-pulsion diverticulum
2. Mid-esophageal (mid-thoracic): Usually due to traction, and usually true diverticula
3. Epiphrenic: Usually due to pulsion

33
Q

√Discuss Zenker’s Diverticulum:
1. What is it and what is the pathophysiology?
2. What is its epidemiology? What are the risk factors?
3. What are the classic features on exam?
4. How is it diagnosed?
5. How is it classified?
6. What is the treatment? What are the indications for surgical 4 vs. non-surgical treatment?

A

What is it?
- False pulsion diverticulum located at Killian’s triangle

Pathophysiology:
- Weakness of Killians area with spasm or persistent elevated resting tone of the cricopharyngeus muscle
- Multiple theories, with the common theme being a CP muscle issue that causes the formation of ZD

Epidemiology:
- Incidence 2/100000
- Men 2-3x greater
- More common 7-8th decade of life
- More commonly left sided herniation (carotid artery is more lateral and less adherent to prevertebral fasia on the left; esophagus also slightly convex to the left) – case series 2/3 midline, 25% left, 10% right
- Most common symptomatic esophageal diverticula

Features/Clinical Presentation:
- Progressive dysphagia (90%)
- Regurgitation of food, even hours after a meal
- Noisy deglutition (borborygmi)
- Unprovoked aspiration
- Belching
- Belching, Halitosis, choking, coughing, hoarseness, globus, weight loss
- Recurrent respiratory infections
- Boyce’s Sign - Swelling in the neck that gurgles on palpation
- Hypopharyngeal mucous collection that initially clears with swallowing, then recurs (rising tide sign)

Risk factors:
- Reflux
- Hiatal Hernia

Diagnosis:
1. Barium Swallow Radiography (Define size and position of sac)
2. Fiberoptic endoscopy (rule out other causes)

Classification Schemes
1. Lahey 1930
- Stage 1: Small mucosal protrusion, spherical in shape
- Stage 2: Pear shape
- Stage 3: Glove-fingered shape

  1. Brombart and Monges 1964
    - Stage 1: Thorn-like diverticulum (longitudinal axis of 2-3mm visible only during contraction phase of upper esophageal sphincter)
    - Stage 2: Club-like diverticulum (longitudinal axis of 7-8mm visible only during contraction phase of upper esophageal sphincter
    - Stage 3: Bag-shaped diverticulum (caudally oriented axis >1cm in length) without compression of the esophagus
    - Stage 4: Compression of the esophagus, which is displaced ventrally
  2. Morton and Bartley 1993:
    - Stage 1: < 2cm
    - Stage 2: 2-4cm
    - Stage 3: >4cm
  3. Van Overbeek and Groote 1994
    - Stage 1: Over one vertebral body
    - Stage 2: 1-3 vertebral bodies
    - Stage 3: More than 3 vertebral bodies

Treatment Options:
Nonsurgical: Close monitoring for aspiration, alternate enteral feeding via PEG/NG
Indications:
- Asymptomatic
- Minimal problems/complications

SURGERY (Primary definitive management)
Surgical: Transvercervical
- Diverticulectomy + CP myotomy
- Diverticular inversion + CP myotomy (flipping ZD inside out but not removing it)
- Diverticulopexy + CP myotomy

Surgical: Endoscopic:
- Endoscopic staple diverticulotomy (doing the staple diverticulotomy also simultaneously does an internal CP myotomy)
- Endoscopic CP myotomy
- Endoscopic laser diverticulotomy

*CP myotomy always needed to be done to reduce recurrence rate

Indications for Surgical Management:
1. Severe symptoms of dysphagia
2. Aspiration or complications of aspiration/recurrent pulmonary infections
3. Cachectic/dehydration due to poor PO intake
4. Concern for malignancy within the diverticulum

See Chapter 70 (my notes) and Cummings, Kevan Page 53

34
Q

What is the normal resting pressure of the UES and LES?

A

UES: 100mmHg
LES: 10-45mmHg

35
Q

√Discuss Barrett’s Esophagus:
1. What is it and what is the pathophysiology?
2. What does it increase risk of?
3. What are the common endoscopic findings?
4. What are the pathology findings?

A

What is it?
- Metaplasia of the esophageal squamous epithelium to the columnar gastric mucosa
- Normally the squamous epithelium of the esophagus interfaces with the columnar epithelium of the stomach at the Gastroesophageal junction (where the stomach meets the esophagus)
- The transition zone between the squamous epithelium and columnar gastric epithelium is called the squamocolumnar junction (SCJ)
- When the SCJ is not at the GEJ (ie. it’s more proximal), this suggests Barrett’s

Increases risk of: esophageal adenocarcinoma (around 30x)

Endoscopic findings:
1. Hiatal Hernia: When GE junction extends >2cm above diaphragmatic compression
2. Barrett’s Esophagus: When SCJ is proximal to the GE Junction - suggests metaplasia

Pathology Findings:
1. Intestinal metasplasia (columnar cells)
2. Goblet cells
3. High grade dysplasia suggests high risk of malignancy and is treated equivalently to an esophageal carcinoma

36
Q

√Discuss Esophageal rings. What are the differences between three types?

A

Esophageal rings are classified as A or B or C (very rare) rings

A Rings:
- Esophageal ring due to muscular hypertrophy, usually a few centimeters proximal to the LES /proximal LES
- Rarely symptomatic
- If symptomatic, chemical or surgical myotomy is most effective

B Rings:
- Most common cause of intermittent solid food dysphagia and food impaction
- Ring due to reflux
- Aka. Schatzki ring
- Occurs at the squamocolumnar junction, usually with squamous mucosa superiorly and gastric mucosa inferiorly (distal margin of LES)
- Causes: Commonly associated with hiatal hernia, GERD, or Congenital
- Considered to be reflux related
- Diagnosis: Barium swallow
- Management involves addressing (1) reflux and (2) dilatation

C Rings:
- Rare
- Occur due to indentation by the diaphragm crura

Kevan Page 54

37
Q

√What is the difference between an esophageal ring vs. esophageal web? 3

A

Rings:
- Circumferential
- Can consist of mucosa or muscle
- Most commonly occur in the distal esophagus

Webs:
- Only part of the esophageal lumen
- Always mucosal
- Usually located in the proximal esophagus
- May be associated with iron deficiency (e.g. Plummer-Vinson syndrome)

38
Q

√What are the causes of aspiration? List 8 main categories and 2-3 examples of each.

A
  1. Acute Neurologic Causes
    - CVA, embolism
    - Intracranial hemorrhage or infection
    - Anoxic brain injury / head injury
  2. Chronic Neurological causes
    - ALS
    - Parkinson’s Disease
    - Parkinson Plus Diseases (MSA, PSP)
    - Multiple sclerosis
  3. Neuromuscular disorders
    - Poliomyelitis
    - Myasthenia Gravis
    - Lambert-Eaton Syndrome
  4. Muscular Disorders
    - Muscular dystrophies
    - Myopathies
  5. Peripheral Nerve Disorders
    - Guillain Barre Syndrome
    - Vagal injury
    - Trauma
  6. Pharyngeal Disorders
    - Malignancy
    - Post-surgical dysfunction
    - Post-radiation dysfunction
    - Zenker’s diverticulum
    - Cricopharyngeal dysfunction
    - Stricture
    - Presbylaryngeus / glottic gap
  7. Esophageal disorders
    - Reflux / GERD
    - Achalasia
    - Other motility disorders
    - Caustic injury
  8. Miscellaneous
    - Severe illness/deconditioning
    - Multisystem disease
    - Drug intoxication
    - Trauma
39
Q

√What are the signs and symptoms of chronic aspiration? (9)

A
  1. Bronchorrhea (>100cc watery sputum, secondary to chronic bronchitis)
  2. Pneumonia/pneumonitis
  3. Chronic cough/throat clearing
  4. Dysphagia
  5. Weight loss
  6. Hoarseness
  7. Pulmonary fibrosis
  8. Bronchiectasis
  9. Lung abscess/empyema
40
Q

√What are 3 types of sources of aspirated material?

A
  1. Orally ingested material
  2. Oropharyngeal secretions
  3. Gastric contents
41
Q

√When can aspiration occur with regards to the pharyngeal phase of swallowing, and why?

A
  1. BEFORE: Reduced tongue control or delayed pharyngeal swallow
  2. DURING: Incompetence of airway sphincters
  3. AFTER: Reduced laryngeal elevation, tongue base control, delayed pharyngeal constriction, Cricopharyngeus dysfunction
42
Q

√Describe the workup and possible investigations for chronic aspiration

A
  • Multidisciplinary evaluation

Physical Exam:
- Complete head and neck examiination
- Cranial nerve examination
- FNL

Possible investigations:
- CXR
- MDL or esophagoscopy (can send for lipid liden macrophages)
- Pulmonary function testing
- Barium swallow (Anatomy, Zenkers)
- FEES (± sensory testing FEESST)
- MBS/VFSS
- Reflux testing

43
Q

√List all the types of management options for chronic aspiration, including conservative and irreversible and reversible surgical options.

A

CONSERVATIVE
1. Change consistency of food (e.g. thickening)
2. Modifying bolus size and speed
3. Sensory enhancement (e.g. carbonation of liquids)
4. Swallowing maneuvers (see other swallowing maneuver flash card)
5. Compensatory postures

PROCEDURAL/ADJUNCTIVE:
1. Reduces production of aspirate (can aspirate food, reflux, or salivary secretions. These strategies aim to decrease one or more of these components):
- NG tube insertion
- Gastrostomy tube
- Jejunostomy tube
- Vocal fold medialization (Type 1 thyroplasty, injection thyroplasty, arytenoid adduction)
- Salivary duct ligation
- SMG resection
- Botox injection or Cricopharyngeal myotomy
- Elevation of the interarytenoid area
- Laryngeal suspension

SURGICAL:
1. Pulmonary toilet (tracheostomy)
2. Separate airway from esophagus, divided into reversible and irreversible procedures :

Reversible (>90% successful)
- Laryngotracheal separation (LTS)
- Lindeman Procedure - Tracheo-esophageal diversion (TED)
- Epiglottic flap laryngeal closure
- Endolaryngeal stent (e.g. Eliachar stent)
- Double barrel tracheostomy
- Partial cricoidectomy (posterior cricoid resection)
- Vertical laryngoplasty
- Supraglottic laryngoplasty

Irreversible:
- Subperichondrial cricoidectomy
- Laryngectomy (narrow field - described as narrow field because it preserves the hyoid, straps, and as much hypopharyngeal mucosa as possible)
- Total Laryngectomy
- Glottic closure

*Irreversible procedures generally affect the glottis itself, reversible preserves the glottis/true VF structures

Vancouver 212

SURGICAL THERAPY FOR CHRONIC ASPIRATION - Wisdom et al. 1997
1043-1810/97/0804-0012505.00/0

44
Q

√What are all the medical management options for chronic aspiration?

A
  1. NPO with tube feeds
  2. Oral hygiene
  3. Speech therapy: Swallowing retraining, diet modifications, postural compensation maneuvers, head position maneuvers, oral motor exercises
  4. Optimization of pulmonary status
  5. LPR prophylaxis
  6. Anti-sialagogues
45
Q

√Describe briefly what a narrow field laryngectomy is and what are the advantages and disadvantages in its use for managing chronic aspiration?

A

Irreversible Procedure:
- Effective separation of the digestive tract and respiratory tract
- Like a laryngectomy but preserves hyoid, straps, and as much hypopharyngeal mucosa as possible compared to laryngectomy (that is used for oncologic reasons)

Advantages:
- Excellent control of aspiration

Disadvantages:
- Loss of voice, psychosocial aspects, not reversible

Vancouver 213

46
Q

√Describe briefly what a subperichondrial cricoidectomy is, how it works, and what are the advantages and disadvantages in its use for managing chronic aspiration?

A

Irreversible surgical option for chronic aspiration.
- Definitive surgical separation of upper respiratory and digestive tracts
- Requires tracheostomy
- Anterior aspect of the cricoid is exposed, perichondrium is divided vertically in the midline to expose the cricoid
- Anterior cricoid is then removed, preserving the perichondrium
- Inner perichondrium and subglottic mucosa then trasected horizontally, inverted, and then closed to create a subglottic blind sac to close the airway

Advantages:
1. High success rate
2. Simplicity
3. Lower morbidity than laryngectomy

Disadvantages:
1. Needs tracheostomy
2. Fistula into upper trachea
3. Not reversible

Kevan Page 46

47
Q

√Describe briefly what a partial cricoidectomy is, how it works, and what are the advantages and disadvantages in its use for managing chronic aspiration?

A

Reversible surgical option for chronic aspiration
- Posterior cricoid perichondrium is elevated (unlike the anterior perichondrium with a subperichondrial cricoidectomy)
- Posterior half of the cricoid is then removed without entering mucosa
- Cricopharyngeal myotomy and tracheostomy necessary
- Functions to enlarge the pharyngeal inlet and narrow the laryngeal inlet to reduce aspiration

Advantages:
- Preserves voice

Disadvantages:
- Does not complete separate the respiratory tract and digestive tract
- Still requires tracheostomy

48
Q

√Describe briefly the procedure of endolaryngeal stents, how it works, and what are the advantages and 4 disadvantages in its use for managing chronic aspiration?

A

Reversibly occludes the laryngeal opening to reduce aspiration; currently only recommended for short term use and has not gained wide acceptable for chronic aspiration management.
- Requires tracheostomy

Advantages:
- Reversible
- Can separate airway from digestive tract

Disadvantages:
- Leakage around stent possible
- Discomfort
- Can displace tracheostomy tube
- Tracheostomy required
- Stent dislodgement can be life threatening

49
Q

√Describe briefly the epiglottic flap closure procedure, how it works, and what are the advantages and disadvantages in its use for managing chronic aspiration?

A

Reversible surgical treatment for chronic aspiration
- Infrahyoid pharyngotomy performed to access the supraglottic larynx
- Edges of epiglottis, AE folds, and arytenoids are denuded and sutured togetether
- Modification leaves the posterior laryngeal inlet open to allow for phonation

Advantages:
- Reversible
- Allows deglutition and speech preservation if leaving posterior laryngeal inlet open
- Leaves true vocal folds in tact

Disadvantages:
- Tracheostomy required
- High rate of dehiscence
- Only about 50% effective in literature

Kevan Page 47, Vancouver 212

50
Q

√Describe briefly what a vertical laryngoplasty is, how it works, and what are the advantages and disadvantages in its use for managing chronic aspiration?

A

Reversible surgical management option for chronic aspiration
- Initially described the prevent aspiiration in patients who had a total glossectomy for advanced oral cavity SCC
- Incision made along the outside of the epiglottis and AE folds
- Supraglottic larynx then closed together in 2 layers to form a tubular supraglottis. Small opening left superiorly

Advantages:
- Voice maintained
- Allows swallowing

Disadvantages:
- Dehiscence
- Tracheostomy required (although can be temporarily occluded for phonation)

Kevan Page 47

51
Q

√Describe briefly what a glottic closure is, how it works, and what are the advantages and disadvantages in its use for managing chronic aspiration?

A

Irreversible surgical option for chronic aspiration management.
- Larynx is complete closed at the level of the true and false vocal cords
- Both true and false VFs are denuded and sutured to one another

Advantages:
- Effectively ablates aspiration

Disadvantages
- Irreversible
- Tracheostomy required

52
Q

√Describe briefly what a tracheoesophageal Diversion (TED) and Laryngotracheal Separation (LTS) is, how it works, and what are the advantages and disadvantages in its use for managing chronic aspiration?

A
  • TED and LTS are essentially the same, except for what is done with the proximal end of the trachea
  • Both are reversible as the larynx are RLNs are preserved

Tracheoesophageal Diversion (TED)
- aka. Lindeman Procedure
- Trachea is divded and the proximal stump is anastomosed to the esophagus to divert secretions
- The distal stump is connected to the neck as a tracheostomy stoma

Laryngtracheal Separation (LTS)
- Used in situations where the proximial stump iis too short to anastomose to the esophagus (e.g. with a high tracheostomy tube)
- TED is preferred in patients who have not had a high tracheostomy (no blind pouch)
- The proximal stump is instead closed into a blind pouch, while the distal stump is formed into a tracheostoma like before

Advantages:
- Reversible
- Completely separates repiratory and digestive tracts
- Dependable and consistent results

Disadvantages:
- Fistula formation (worse with LTS than TED)
- Risk of tracheal stenosis post reversal
- Riisk of Tracheoinnominate fistula
- Loss of air powered speech

Kevan Page 48
Vancouver 212

53
Q

√Review the different postural techniques and different swallowing maneuvers for patients with chronic aspiration

A

Postural Techniques:
1. Head Back - uses gravity to clear oral secretions (decreases oral transit time)
2. Chin down - Widens vallecula to prevent bolus entering airway, and pushes epiglottis back to protect airway
3. Head rotation - Rotation towards the dysfunctional site (e.g in VFP) increases vocal fold closure by applying extrinsic pressure, puts epiglottis in a more protective position, and directs bolus away from damaged side
4. Head tilt - Tilt towards stronger side directs bolus down stronger side (food goes in direction of tilt in the oral cavity/pharynx)
5. Lying down on one side - Eliminates gravitational effect on pharyngeal residue (gets the residue to stick on pharyngeal walls rather than fall down airway)
6. Shaker exercise: strengthens the suprahyoid muscles

Swallowing Maneuvers (Mnemonic: MESS)
1. Mendelsohn Maneuver
- A form of supraglottic swallow where the patient mimics upward motion of the larynx by voluntarily keeping larynx elevated
- Increases duration that the cricopharyngeal opening is present
- Steps: (1) Swallow and then hold swallow for 2-5 seconds, (2) patients are advised to hold their larynx at the peak position (they can palpate to landmark where this is), and (3) complete swallow

  1. Effortful swallow
    - This increases posterior tongue base movement (useful in posterior tongue base not moving well or is deficient)
    - Steps: (1) Swallow HARD, (2) Keep lips closed tightly together, (3) Push tongue against roof of mouth while swallowing
  2. Supraglottic Swallow
    - Aka. Voluntary breath hold
    - Simultaneous swallow and breath holding
    - Patient can then cough afterwards to expel any residue in the vestibule
    - Steps: (1) Take a deep breath and hold breath, (2) Keep holding breath while swallow (cover tracheostomy tube if applicable), (3) Cough immediately after swalow
  3. Super-Supraglottiic swallow
    - Supraglottic swallow + valsalva effect
    - Involves performing a supraglottic swallow while simultaneously performing a valsalva
    - Valsalva has the added benefit of tilting arytenoid over and narrowing glottic inlet (useful if glottic incompetence)
54
Q

√What are the most common benign esophageal lesions?

A
  1. Leiomyoma (most common)
  2. Polyps
  3. Hemangioma
  4. Adenoma
  5. Neurofibroma
  6. Granular cell tumor
55
Q

√List the possible etiologies of an esophageal perforation (7)

A
  1. Iatrogenic (most common, usually in cervical esophagus, posterior wall)
  2. Trauma (blunt, penetrating)
  3. Toxic - caustic ingestion
  4. Inflammatory
  5. Neoplastic
  6. Spontaneous - Mallory-Weiss, Boerhaave
  7. Diffuse idiopathic skeletal hyperostosis - dysphagia secondary to spinal osteophytes –> high risk of esophageal perforation during endoscopic
56
Q

√List a differential diagnosis of esophageal hemorrhage 5

A
  1. Perforation
  2. Ulcer
  3. Malignancy
  4. Mallory Weiss Tear
  5. Varices
57
Q

√Regarding Mallory-Weiss tears, discuss:
1. Causes?
2. Pathophysiology of how bleeding occurs?
3. Clinical presentation
4. Treatment
5. Complications

A

Mallory-Weiss tears: UGI bleed, usually secondary to vomitting/retching

CAUSES:
- Most common: secondary to vomitting / retching

PATHOPHYSIOLOGY:
1. Non-penetrating mucosal tear at lower esophagus/cardia, tearing the submucosal arteries

CLINICAL PRESENTATION:
1. Significant bleed
2. Hypovolemic shock in 50%

TREATMENT:
1. Bleeding usually stops spontaneously
2. May require endoscopic cautery or vasoconstrictor application

COMPLICATIONS:
1. Mediastinitis
2. Pneumothorax
3. Pneumomediastinum
4. Pleural effusion

58
Q

√Regarding Boerhaave syndrome, discuss:
1. What is it?
2. Where is the most common location to occur?
3. Clinical presentation?
4. Treatment?

A

BOERHAAVE SYNDROME:
- Spontaneous esophageal rupture due to vomitting, coughing, heavy lifting or straining

LOCATION:
- Typically left sided & transmural

CLINICAL PRESENTATION:
1. Mediastinitis-like symptoms: picket fence fevers (spikiing fevers), retrosternal pain, tachycardia, arrhythmias
2. Indolent course –> decompensates quickly

TREATMENT:
1. Surgical drainage of mediastinum/pleura
2. Repair of perforation
3. Nutritional support

59
Q

√What are 6 contraindications to esophagoscopy?

A
  1. Severe erosive burns to esophagus
  2. Aortic aneurysm
  3. Chronic steroid use
  4. Laryngeal inflammation/edema
  5. Combative patient
  6. Spine abnormalities - severe cervical/thoracic

“BASICS:
Burns
Aortic aneurysms
Spine abnormalities
Inflammation of larynx
Combative patient
Steroid use chronic

60
Q

√What is the 6 food elimination diet?

A

Take the top 6 most common food allergens out of your diet for 6-8 weeks
1. Milk products
2. Eggs
3. Wheat
4. Soy
5. Peanut/tree nuts
6. Fish/shellfish

61
Q

√What are the treatment options for impacted food bolus?

A
  1. Esophagoscopy with extraction or pushing into stomach
  2. Glucagon (relaxes smooth muscle and LES to promote passage)
62
Q

√Regarding oculopharyngeal muscular dystrophy, discuss:
1. What is the genetics?
2. Epidemiology?
3. Clinical presentation? 4
4. Scope findings?
5. Treatment? 2
6. Prognosis?

A

OCULOPHARYNGEAL MUSCLAR DYSTROPHY
- Commonly seen in french people
- Onset of symptoms around 40 years old, slowly progressive thereafter

GENETICS:
- Autosomal dominant PABPN1 gene

CLINICAL PRESENTATION:
1. Significant bilateral ptosis
2. Progressively worsening dysphagia (cricopharyngeal spasm)
3. Eventually can have voice weakness, cough, aspiration
4. Eventually can develop systemic muscle weakness

SCOPE:
- Normal vocal fold function
- Lots of pooling secretions

TREATMENT:
1. Dysphagia: Cricopharyngeus myotomy, consider G-tube eventually
2. Ptosis: Blepharoplasty, brow lift, supportive (no cure, progressive)

PROGNOSIS:
1. Progressive
2. Usually normal life expectancy
3. Eventually die of anorexia, aspiration

Laryngology (8 decks)

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