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Laryngology > Benign Pathology, Functional Disorders, Stenosis > Flashcards

Benign Pathology, Functional Disorders, Stenosis Flashcards

1
Q

l

√What is the differential diagnosis of benign vocal fold lesions? Name 12

A
  1. Vocal fold polyp (most common) - mucoid or angiomatous
  2. Vocal fold Nodules (bilateral)
  3. VF Cyst (mucous retention or epithelial inclusion)
  4. Pseudocyst (no capsule)/fibrous mass
  5. Polypoid degeneration/Reinke’s edema
  6. Granuloma
  7. Sulcus vocalis
  8. Papilloma
  9. Lymphatic/vascular malformations
  10. Granular cell tumor (posterior VC)
  11. Schwannoma
  12. Chondroma - posterior cricoid
  13. Sarcoid
  14. Amyloid
  15. Hemangioma/lymphatic malformation
  16. Paraganglioma
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2
Q

What is the most common cause of viral laryngitis?

A

Rhinovirus
- 30-60% of acute, infectious, laryngopharyngitis in adults is due to self-limiting viral infections as part of the common cold.
- Rhinovirus is the most common cause of a cold.

Other possible causes:
1. Influenzae
2. Parainfluenza

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3
Q

Most common cause of bacterial laryngitis in an adult?

A
  1. Hemophilus influenza
  2. Strep pyogenes (GAS)
  3. Staph Aureus
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4
Q

Regarding Laryngeal Diphtheria, discuss:
1. What is it?
2. Causes?
3. Findings/symptoms? 5
4. Treatment? 5

A

LARYNGEAL DIPHTHERIA:
- Inflammatory reaction with vascular dilation

CAUSES:
1. Corynebacterium diphtheriae (gram positive pleomorphic aerobic bacillus)

FINDINGS:
1. Exudative membranous tonsillitis
2. Fever
3. Dysphonia
4. Myocarditis (diphtheria exotoxin)
5. Neurologic sequelae (caused by diphtheria exotoxin)

TREATMENT:
1. Tracheostomy (not intubation - could dislodge exudate)
2. Anti-toxin
3. High dose penicillin
4. Erythromycin
5. Tetracycline

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5
Q

What is a turban shaped epiglottis associated with? 2

A
  1. Sarcoidosis
  2. Tuberculosis

Kevan Page 16

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6
Q

Describe the 5 histopathologic features of sarcoidosis

A

PLANS mnemonic:

  1. P = PAS+ (Periodic Acid Schiff) inclusions
  2. L = Langhans giant cells
  3. A = Asteroid bodies (small, intracytoplasmic eosinophilic star shaped structures)
  4. N = Non-caseating granulomas
  5. S = Schaumann bodies (calcium and protein inclusions include of Langhans giant cells as part of granuloma)

https://www.pathologyoutlines.com/topic/skinnontumorsarcoidosis.html

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7
Q

What are 10 granulomatous diseases of the larynx that may simulate cancer?

A
  1. Tuberculosis (most common)
  2. Pachydermia laryngitis
  3. Coccidiomycosis
  4. Histoplasmosis
  5. Blastomycosis
  6. Rhinoscleroma
  7. Leprosy (supraglottic coalescent nodules)
  8. Syphillis (secondary - raised grey plaque)
  9. Sarcoidosis (turban epiglottis)
  10. GPA
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8
Q

A patient presents with laryngitis. What features may suggest a neurologic cause? List 13 different clinical features, and 5 different examination findings.

A

Speech problems:
1. Asthenia
2. Breathiness
3. Pitch instability
4. Lack of vocal inflection
5. Abnormal resonance
6. Dysarthria

(Think about all the SLN problems)

Swallowing problems:
1. Oral incompetence
2. VPI
3. Instability to initiate swallow
4. Aspiration

Breathing abnormalities:
1. Fluctuanting inspiratory stridor
2. Weak, breathy cough
3. Gurgly breathing noises

Examination findings:
1. Tremor (facial, blepharospasm, resting tremor)
2. Muscle wasting
3. Fasciculations (e.g. tongue fasciculations)
4. Focal neurologic deficits (e.g. in MS)
5. Ptosis (e.g. MG)

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9
Q

List 4 common focal dystonias affecting the head and neck

A
  1. Spasmodic dysphonia = larynx
  2. Blepharospasm = forced involuntary eye closure
  3. Torticollis = neck
  4. Oromandibular = face/jaw/tongue
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10
Q

NOT IN VANCOUVER

Define Dystonia. How are they classified and what are the subdivisions of the classification?

A

Dystonia = Disorder resulting in sustained involuntary skeletal muscle contractions, which can cause twisting, repetitive movement, or abnormal posture. Thought to be due to a lesion in the basal ganglia.

PRIMARY DYSTONIA = Normal at Rest, action induced
SECONDARY DYSTONIA = Fixed Dystonia

Classified across 2 axes:
1. Axis 1 = clinical features
2. Axis 2 = etiology

Axis 1 Clinical Features Dimensions of Classification:
1. Age at onset
a/ Infancy (birth to 2 years)
b/ Childhood (3-12 years)
c/ Adolescence (13-20 years)
d/ Early adulthood (21-39 years)
e/ Later adulthood (40 years and older)

  1. Body distribution
    a/ Focal (one body part)
    b/ Segmental (2 or more contiguous body parts)
    c/ Multifocal (2 or more non-contiguous body parts)
    d/ Generalized (involving trunk and at least 2 other sites, divided into 2 subtypes “with leg involvement - ambulatory” or “without leg involvement - non-ambulatory”)
    e/ Hemidystonia (half of the body)
  2. Temporal pattern
    a/ Disease course (static vs. progressive)
    b/ Short term variation (e.g. persistent, action specific, diurnal, or paroxysmal)
  3. Associated features
    a/ Isolated (with or without tremor)
    b/ Combined (with other neurologic or systemic features)

Axis 2 Etiology Dimension for Classification:
1. Nervous system pathology
a/ Degenerative
b/ Structural (e.g. focal static lesions)
c/ No degenerative or structural pathology)

  1. Heritability
    a/ Inherited (e.g. sex linked, autosomal dominant or recessive, or mitochondrial)
    b/ Acquired (e.g. brain injury, drugs/toxins, vascular, or neoplastic)
  2. Idiopathic
    a/ Sporadic
    b/ Familial (usually autosomal dominant)
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11
Q

What is Meige’s Syndrome?

A

Syndrome that is a combination of 2 types of dystonia:
1. Blepharospasm
2. Oromandibular dystonia

Also known as craniocervical dystonia
May also present with torticollis and spasmodic dysphonia

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12
Q

Name 9 hyperfunctional laryngeal disorders

A
  1. Laryngeal Dystonia
    a/ Abductor spasmodic dysphonia
    b/ Adductor spasmodic dysphonia
    c/ Mixed laryngeal dystonia
    d/ Adductor breathing dystonia
    e/ Singer’s laryngeal dystonia
  2. Muscle Tension Dysphonia
  3. Essential Tremor
  4. Myoclonus (oculopalatolaryngopharyngeal myoclonus)
  5. Pseudobulbar Palsy
  6. Stuttering
  7. Tic (Tourette’s)
  8. Functional Dysphonia/aphonia
  9. Paradoxical movement of the vocal folds
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13
Q

What causes pseudobulbar palsy?
What are the common features - 5
How does it differentiate with other types of dystonia? 4

A

PBP is caused by bilateral lesions of the corticobulbar tract

Features: Muscle spasticity, hyperreflexia of the pharynx, palate, lips, tongue, larynx

Differentiating features: Hypernasality, slow/labored articulation, emotional lability, cognitive impairment

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14
Q

List 5 hypofunctional laryngeal disorders and a classification system for them

A

Think based on Localization:
1. Central (brain)
2. Brainstem
3. Spinal cord
4. Anterior horn cells
5. Roots
6. Peripheral nerve
7. Neuromuscular junction
8. Muscle
9. Other

Central:
1. Arnold Chiari Malformation
2. Stroke
3. Multiple Sclerosis
4. Parkinson’s Disease
5. Parkinson-Plus Syndromes

Brainstem:
1. Arnold Chiara Malformation
2. ALS (degeneration of both UMN and LMNs)
3. Medullary strokes (e.g. Wallenberg aka. Lateral Medullary Syndrome)

Peripheral Nerve:
1. Vocal fold paralysis

Neuromuscular Junction:
1. Myasthenia Gravis
2. Lambert-Eaton Syndrome

Muscle:
1. Myopathies
2. Muscular dystrohpies

Other:
1. Psychogenic / Malingering
2. Post-polio syndrome

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15
Q

What is the difference between the pathophysiology of Myasthenia Gravis and Lambert-Eaton Syndrome? How can you differentiate them on assessment of dysphonia?

A

Myasthenia Gravis: Antibodies against Acetylcholine receptors at the neuromuscular junction lead to LMN weakness which worsens with prolonged use. Can be tested with the tensilon (acetylcholinesterase inhibitor challenge) which results in immediate symptom reversal

Lambert-Eaton Syndrome: Antibodies target voltage gated calcium channels at presynaptic nerve terminals leading to a decrease in the release of Ach. These will not have a good response to the Tensilon challenge (because overall have less ACh released in the first place)

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16
Q

What is the cause of Parkinson’s disease? 2
What are the general requirements for diagnosis? 3
What are the clinical symptoms? 4
How can the voice be managed? 1

A

Extrapyramidal syndrome caused by cell death in the substantia nigra and degradation of dopaminergic neurons of the basal ganglia

Criteria diagnosis require that a patient be first diagnosed with Parkinsonisms, which is defined as bradykinesia + resting tremor OR rigidity

Following those criteria, the diagnosis needs to meet further strict criteria.

Clinical Symptoms:
1. Tremor
2. Rigidity
3. Akinesia
4. Reductino or loss of movement and postural changes

Plus low concentration of dopamine in the basal ganglia

TREATMENT:
1. Lee-Silverman voice training

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17
Q

What are the 3 main problems in Parkinson’s voice?
What are the perceptual voice abnormalities in Parkinson’s disease? 6

A

THREE PROBLEMS IN PARKINSON’S ARE:
1. Decreased vocal drive
2. Poor self-perception
3. Inability to regulate output

Others:
1. Rough
2. Breathy
3. Unstable (Tremulous)
4. Reduced vocal intensity
5. Lower variation of fundamental frequency
6. Decreased speech speed

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18
Q

What are two different types of Parkinson-Plus Syndromes? Describe them. What are some airway considerations for management of these patients?

A

Parkinson Plus Syndrome = PD + other features

Types:
1. Progressive Supranuclear Palsy
2. Multiple System Atrophy

Multiple System Atrophy: aka. Shy-Drager Syndrome
Parkinsonism with autonomic dysfunction:
- Orthostatic hypotension
- Urinary and/or fecal incontinence
Vocal fold paralysis in a patient with parkinsonism is highly suggestive of MSA. Trach may be necessary if within goals of care

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19
Q

What are bamboo nodes?

A

Inflammatory laryngeal nodules associated with rheumatoid arthritis.

Kevan page 19

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20
Q

List 5 different laryngeal manifestations of rheumatoid arthritis

A
  1. Mucosal edema/hyperemia
  2. Arytenoid swelling
  3. Cricoarytenoid joint ankylosis
  4. Vocal fold immobility
  5. Bamboo nodules
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21
Q

What are the two types of muscle tension dysphonia according to ASHA classification manual for voice disorders?

A
  1. Primary Muscle Tension Dysphonia
    - Dysphonia in the absence of current organic vocal fold pathology
    - Possible triggers include illness, allergies, reflux, irritants, anxiety, emotional trigger, or increased vocal demand
  2. Secondary Muscle Tension Dysphonia
    - Dysphonia in the presence of current organic vocal fold pathology, psychogenic, or neurologic etiology, originating as a compensatory response to the primary etiology
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22
Q

What is the typical clinical presentation of Muscle Tension Dysphonia? What are the risk factors, list 4?

A
  1. F>M 2:1
  2. Associated with professional voice use
  3. Associated with stress/anxiety
  4. Will often have a preceding trigger (e.g. URTI, laryngitis)

Symptoms:
- Dysphonia with neck and shoulder tension, increasing over time

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23
Q

Describe in detail the two types of classification systems of types of muscle tension dysphonia.

A

Morrison-Rammage Classification (1993)
1. Type 1: Laryngeal isometric = posterior glottal gap
2. Type 2: Laryngeal hyperadduction states
2a/ Glottic hyperadduction
2b/ Supraglottic hyperadduction
3. Type 3: Supraglottic AP contraction
4. Type 4: Conversion Aphonia = the vocal folds have full movement and can adduct normally for cough, but they stop short of sufficient adduction for voicing with an attempt to speak. Will also have generalized laryngeal hypertonicity
5. Type 5: Psychogenic Bowing = bowed vocal folds outside the context of vocal fold atrophy
6. Type 6: Adolescent Transitional Dysphonia = aka. Puberphonia (seen in adolescents trying to maintain vocal pitch during puberty)

Koufman-Blalock Classification
1. Type 1: Persistent posterior glottic gap during phonation;; increase muscular tension (e.g. elevated larynx, palpable neck tension/tender, breathy or strident voice, ± VF nodules)
2. Type 2: Medial compression of the false vocal folds during phonation;; (most severe = plica ventricularis where false folds are used for phonation)
3. Type 3: Anteroposterior supraglottic contraction;; (epiglottis and arytenoids may obscure at least 50% of laryngeal aditus)
4. Type 4: Complete supraglottic sphincteric closure (epiglottis/arytenoids contact, with lateral constriction)

Note: If the glottis is difficult to see, ask the patient to inhale and this will decrease the anterior-posterior compression

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24
Q

List 6 options for the treatment of muscle tension dysphonia?

A
  1. Voice hygiene (avoid yelling, speaking in noisy environments, throat clearing, limiting use of alcohol and caffeine and smoking)
  2. Voice therapy with SLP
  3. Circumlaryngeal massage
  4. Treat GERD if concomitant
  5. In refractory cases, topical lidocaine or botox
  6. Biofeedback
  7. Secondary MTD: Treat the underlying cause
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25
Q

How do you clinically differentiate muscle tension dysphonia from spasmodic dysphonia? List 4 differences.

A

Spasmodic dysphonia is NOT a functional disorder like MTD. However adductor spasmodic dysphonia can appear very similar to Type 2 MTD (lateral hyperadduction).

In particular, spasmodic dysphonia is:
1. Task specific (ad: voiced vowels, Ab: voiceless consonants)
2. Will often improve with singing or with alcohol
3. Often associated with another dystonia or tremor (12-20% have family history of dystonia; often will also have essential tremor)
4. Doesn’t improve with voice therapy

Muscle tension dysphonia however is:
1. Less task specific
2. Improves with voice therapy

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26
Q

Name the laryngeal disorder associated with the following vocal fold closure patterns:
1. Posterior gap
2. Spindle
3. Hourglass
4. Asymmetric

A
  1. Posterior gap = MTD Type 1, or can be physiologic in women
  2. Spindle = vocal fold atrophy, presbylarynx
  3. Hourglass = vocal fold nodules
  4. Asymmetric = Vocal fold lesion (e.g. polyp, cyst, tumor, etc.)
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27
Q

What are the treatment options for a posterior glottic gap in the context of vocal fold paralysis?

A
  1. Arytenoid adduction
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28
Q

Describe arytenoid abduction and arytenoid adduction procedures. What action do they mimic? How are they performed, what are their indications?

A

Arytenoid ADDuction:

  1. Mimics the action of the lateral cricoarytenoid to internally rotate the arytenoid to close the glottis
  2. Performed by placing a suture in the muscular process of the arytenoid through the paraglottic space to the inferior cornu of the thyroid ala - applies anterior traction
  3. Indications: If thyroplasty is insufficient for medialization (e.g. significant flaccid paralysis and glottic incompetence), or height mismatch

Arytenoid ABDuction:
1. Mimics the action of the posterior cricoarytenoid to displace the vocal process laterally
2. Performed by placing a suture in the muscular process of the arytenoid and applying traction posteriorly and inferiorly - Applies posterior traction
3. Indications: Widens the glottic airway in patients with bilateral vocal fold paralysis

Kevan Page 20

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29
Q

How can you distinguish a psychogenic cause (e.g. conversion, malingering) of voice loss from true voice loss? What else can you distinguish with this test?

A

Psychogenic cause/conversion dysphonia
- Somatoform = Not produced by the patient intentially
- Can present as aphonia or hypophonia

  1. Have the patient cough
    - Vocal folds abduct during the inspiratory phase, then close tightly for compressive phase, then open widely
    - Also useful for differentiating psychogenic stridor from true bilateral VFP (patients will abduct vocal fold prior to cough)
    - Useful for differentiating aphonic malingering patients (patients may not adduct vocal folds fully when asked to phonate, but will when coughing).
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30
Q

What are the types of spasmodic dysphonia, and the relative incidence of each?

What is the overall epidemiology of SD (F:M)?

A
  1. Adductor SD (80%)
  2. Abductor SD (15%)
  3. Mixed laryngeal dystonia (< 5%)
  4. Adductor breathing dystonia (< 5%)
  5. Singer’s laryngeal dystonia

Female:Male 8:1

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31
Q

List the voiced consonants compared to voiceless consonants, nasal consonants, and plosives

A

Voiced consonants: B, D, G, J, L, M, N, Ng, R, Sz, Th(as in the word “then”), V, W, Y, and Z.

Voiceless consonants: Ch, H, F, K, P, S, Sh, T, and Th(as in “thing”)
- Do not use the vocal folds to produce their hard, percussive sounds (tongue, teeth, and lips used)

Nasal consonants: M, N, Ng

Plosives: P, B, T

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32
Q

What are three indicators of a hyperfunctional laryngeal dysphonia on indirect laryngoscopy?

A
  1. Anteroposterior compression of the larynx
  2. Aryepiglottic fold contraction
  3. False vocal fold compression (medial compression)
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33
Q

√Discuss the clinical presentation and physical exam of adductor vs. abductor spasmodic dysphonia.
How do they differ on clinical presentation and voice characteristics? Name 2-3 characteristics each
How do you elicit findings on physical exam?

A

SPASMODIC DYSPHONIA:
- Action induced laryngeal motion disorder
- Focal dystonia, which may have an associated family history of other dystonias in 12%
- All are task specific, better with EtOH, worse with anxiety, better with singing/laughing

ADDUCTOR SD

Clinical Presentation:
1. Harsh, strained strangled quality with voice breaks in connected speech
2. Some compensate with low, breathy voice (sounds like ABdSD)
3. Worse with words that BEGIN with vowels and after voiced consonants

Physical Exam:
1. Elicit phrases that begin with vowels (e.g. count from 80-89, we eat eggs every day)

Laryngeal exam:
1. Inappropriate adduction of vocal folds with hyperfunction of supraglottis
2. Insertion of scope may diminish voluntary contractions and normalize speech (Geste Antagonist)

ABDUCTOR SD

Clinical Presentation:
1. Sustained breathiness with breathy voice breaks in connected speech
2. Worse for vowels following a VOICELESS consonant (vocal cords are relaxed, allowing air to flow freely from the lungs to the mouth, where the tongue, teeth, and lips engage to modulate the sound)

Physical Exam:
1. Elicit phrases of voiceless consonants - listen for a delayed onset of phonation after voiceless consonants (count from 60-69, the puppy bit the tape, Harry had a hard head)

Laryngeal Exam:
1. Inappropriate vocal fold abduction during connected speech
2. Insertion of scope may diminish voluntary contractions and normalize speech

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34
Q

√What is the Geste Antagonist?

A

A sensory trick, which is a manoeuvre used by patients with dystonia to ameliorate their dystonic movements or posturing.

With spasmodic dysphonia, this can sometimes occur with the insertion of a scope - and this may diminish their voluntary contractions and normalize speech

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35
Q

What are the sentences used to determine the type of spasmodic dysphonia?

A

ADductor:
1. Counting 80-89
2. We mow our lawn all year
3. We eat eggs every easter
4. Where were you one year ago
5. A dog dug a new bone
6. Eee eee eee

ABductor:
- Counting 60-69 (lower case b looks like 6)
- Harry hit the hammer hard
- The puppy bit the tape
- Peter will keep at the peak
- See See See

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36
Q

√What are the options of treatment for spasmodic dysphonia? 5

A
  1. Voice therapy: minimal role, but can help differentiate between AdSD and MTD
  2. Geste antagonist (sensory trick): Certain actions that temporarily interrupt dystonias (e.g. pulling on an ear) - not really a treatment modality though
  3. Medical: Anticholinergics, muscle relaxants (limiited benefit)
  4. Botox injections
  5. Surgery
    - Adductor SD: denervation of RLN ± reinnervation to ansa - crush, neurolysis
    - Adductor SD: Type 2 lateralization thyroplasty, bilateral TA±LCA myectomy
    - Abductor SD: Type 1 Thyroplasty, PCA myoplasty (limited evidence
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37
Q

√What are the surgical options for spasmodic dysphonia?
3 AdSD, 2 for AbSD

A

Adductor SD:
1. SLAD-R: Selective laryngeal adductor denervation-reinnervation
2. Type 2 thyroplasty (not typically done in North America)
3. Bilateral TA ± LCA myectomy

ABductor SD:
1. Bilateral Type 1 thyroplasty, with or without botox
2. PCA myoplasty

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38
Q

√Discuss SLAD-R: Selective laryngeal adductor denervation-reinnervation. How does it work and how long does it take for tone to return?

A
  1. Anterior branch of the RLN is severed to denervate the spasming laryngeal adductors (TA and LCA).
  2. Ansa is then anastomosed to the severed nerve
  3. As with laryngeal reinnervation, it takes 3 months for tone to return
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39
Q

√How many types of botox are there? Which one is the most clinically useful and why?

A

7 types A to G

Type A is the longest lasting and therefore the most clinically useful

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40
Q

√What is the mechanism of action of botulinum toxin? How long does it take to reach effect?

A

Irreversibly blocks release of acetylcholine at neuromuscular junction (cleaves SNAP-25 proteins), causing muscles relaxation instead of contraction. Function returns only as new axons/receptors grow.

  1. 2 days (48 hours) to onset
  2. 2 weeks for maximal effect
  3. 2-6 months maximal duration of effect
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41
Q

√What is the dosage of botulinum toxin for treatment of AdSD and AbSD?
Which muscle do you inject for each, and through what approach?
What is the frequency of injection?
What are the side effects? 7 AdSD, 4 AbSD

A

Adductor SD:
1. Muscle: Thyroarytenoid muscle, or lateral cricoarytenoid (can do bilateral at once, or alternate unilateral)
2. Dosage: 1-5u (start 0.5u per side; range 0.05-10u); some say 1-1.25U
3. Approach: Commonly inject via cricothyroid membrane, thyrohyoid membrane, or transthyroid membrane; 15-30deg lateral and 30deg superior
4. Frequency of injection: q3-4 months bilaterally. Some individuals find benefit from unilateral injections at shorter intervals
5. Side effects: breathiness, difficulty swallowing liquids (1-3 days post injection, can last up to 2 weeks), aspiration, weak voice, hyperventilation, sore throat, bloody sputum
6. 90% success lasting ~15 weeks

Abductor SD:
1. Muscle: Posterior cricoarytenoid - unilateral ONLY per visit
2. Dosage: 2-5u (usually start 1u); Some say 1-3.75U
3. Side effects: Stridor with airway compromise (must scope to assess glottal adequacy prior to PCA injection, and only unilateral injections), Dysphagia (due to leakage to cricopharyngeus), sore throat, bloody sputum
4. More difficult to treat, 30-60% success, ~10 weeks

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42
Q

√What are the different approaches to the posterior cricoarytenoid muscle for botox injection of abductor SD? 5
How do you confirm location

A
  1. Anterior/transcricoid approach - via cricothyroid membrane, then through posterior cricoid ring.
  2. Lateral/retrocricoid/retrolaryngeal approach - through inferior constrictor
  3. Lateral/retrocricoid/retrolaryngeal approach with laryngeal rotation
  4. Transoral
  5. Transnasal

Confirmation of PCA location by EMG with SNIFFING

Nadia Botox Grand Rounds

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43
Q

√What are the different approaches for botox injection of adductor SD? 4

A
  1. Trans-cricothyroid membrane (most common)
  2. Trans-thyroid cartilage
  3. Trans-oral/trans-nasal

Nadia Botox Grand Rounds

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44
Q

√How is botulinumtoxin quantified? What is the lethal dose in humans?

A

Quantified in units, where 1 unit is the amount lethal to 50% of mice

1 bottle typically has 100 units

Lethal dose in humans is unknown, but based on primate studies likely around 2700-3000 units

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45
Q

√List 5 contraindications to botulinum toxin injection

A
  1. Pregnancy
  2. Neuromuscular disorders (E.g. myasthenia gravis, lambert-eaton)
  3. Infection at site of injection
  4. Aminoglycosides (interfere is neuromuscular transmission)
  5. Allergy to component

A PINA colada

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46
Q

√What are 3 signs of systemic toxicity from botulinum toxin?

A
  1. Descending flaccid paralysis
  2. Normal mentation
  3. No fever
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47
Q

vRegarding Adductor Breathing Disorder, discuss:
1. What are the other names? 1
2. What is it/characteristic findings? 3
3. How can it be reversed?
3. Causes? 2
4. Epidemiology/phenotype? 5
5. PFT findings?
6. Treatment? 3

A

Aka. Paradoxical vocal fold movement (PVFM)

CHARACTERISTICS:
- Adduction of vocal folds while inspiring = stridor and dyspnea
- Do NOT become hypoxic, do NOT need a trach
- Characteristic posterior glottic gap while adducting
- VF abducts when SNIFFING

CAUSES:
1. Organic causes: Brainstem compression, upper motor neuron or LMN injury, irritant exposure, LPR
2. Non-organic (malingering, conversion)

PHENOTYPE:
1. Young females
2. Type A personality
3. Astham in 60%
4. Anxiety
5. Athlete

PFT (similar to bilateral VFP):
- Blunting/flattening of inspiratory loop (variable extrahoracic) if symptomatic compared to asthma, which impairs the expiratory loop

TREATMENT:
1. Acute: heliox, positive pressure ventilation, reassurance, anxiolytics
2. Long term: speech/SLP therapy, Psychiatry
3. Bilateral Thyroarytenoid botox in severe cases

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48
Q

√How do you differentiate asthma and paradoxical vocal fold motion based on:
1. Quality of respiratory noise
2. Scope
3. CXR
4. Flow volume loops

A
  1. Quality of respiratory noise: PVFM = inspiratory/biphasic stridor; Asthma = wheeze
  2. Scope: PVFM = Vocal fold adduction on inspiration; asthma = no abnormalities
  3. CXR: PVFM = Normal; Asthma = 75% normal, but some will have pulmonary hyperinflation, pulmonary edema, and bronchial wall thickening
  4. Flow volume loops:

ASTHMA:
1. Flow loop = elliptical
2. FVC = Usually Decreased
3. FEV1 = Decreased > 20%
4. FEF = Decreased
5. FEV1/FVC = FEV1 decrease > FVC decrease
6. FEF/FIF = Ratio < 1

PVFM:
1. Flow loop = Truncated or flattened
2. FVC = Normal or Decreased
3. FEV1 = Normal or Decreased
4. FEF = Normal
5. FEV1/FVC = No change
6. FEF/FIF = Ratio > 1

Vancouver 201

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49
Q

What is a posterior glottic chink? List 3 conditions where this may be seen.

A

PGC = Posterior triangular gap extending from the posterior wall of the glottis to the tip of the vocal processes present on maximal closure of the glottis.

Conditions:
1. Muscle tension dysphonia (Type 1)
2. Paradoxical vocal fold motion
3. Physiologic in women

https://www.researchgate.net/profile/Ahmed-Fayed-3/publication/327109160/figure/fig1/AS:661770603606017@1534789815521/Vocal-cord-during-normal-inspiration-left-and-in-patient-with-vocal-cord-dysfunction.png

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50
Q

What is Plica Ventricularis?

A

Phonation via vibration of the false vocal folds, also known as ventricular phonation.

Can also be considred a type of Koufman-Blalock Type 2 muscle tension dysphonia (lateral hyperadduction)

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51
Q

√What are the neurological disorders that demonstrate vocal tremor?

A

“T-SPASM”

  1. T: Tic (Tourette’s)
  2. S: Spasmodic dysphonia
  3. P: Paradoxical/Parkinson’s disease or Parkinson-plus syndromes (including multisystem degeneratiion, shy-drager syndrome, basal ganglia degeneration, stroke, progressive supranuclear palsy)
  4. A: Ataxia disorders (Friedrich ataxia FNX gene); Aphonia/functional dysphonia
  5. S: eSSential tremor
  6. M: Myastenia gravis, Myoclonus, MTD, MS
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52
Q

√Differentiate between essential tremor and spasmodic dysphonia

A

SD = Dystonic contraction of specific intrinsic laryngeal muscles

EXAM:
- Key phrases elicit dystonia, but have no effect on essential tremor

Treatmetn:
- ET: Propranolol, primidone ± botox
- SD: Botox

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53
Q

√Regarding vocal tremor, discuss:
1. What is it?
2. Epidemiology?
3. Clinical presentation 5
4. Voice sounds like what 3
5. Exam findings 3
4. What is the treatment? 3
5. Describe 6 characteristic patterns of ESSENTIAL tremor.
6. How do essential tremor characteristics differ from laryngeal or vocal tremor?

A

VOCAL TREMOR:
- Involuntary, voca tremor (purposeless rhythmic movement) in the absence of other neurologic disorders (6-8Hz)

EPIDEMIOLOGY:
1. Bimodal age of onset (second and sixth decades of life)

CLINICAL PRESENTATION:
1. Most patients have tremor in the upper extremities ± head
2. Symptoms worsen over months to years
3. Can be absent or seen at rest, but attenuated at end of movement, maximal during posturing and exaggerated during phonation
4. Tremor worsens with anxiety, improves with EtOH
5. Tremor affects ALL laryngopharyngeal muscles compared to SD which affects intralaryngeal muscles only

Voice during vocal tremor:
1. Altered pitch and loudness
2. Phonation stoppages
3. Decreased intelligibility

Exam Findings:
- Variiable groups of muscles affected, from strap muscles, palate and intrinsic laryngeal muscles to being isolated to intrinsic laryngeal muscles
- Periodic/rhythmic modulation of vocal pitch and loudness
- Most noticeable during prolongation of vowels

Treatment:
1. Propranolol and Primidone first line (variable effect in improving voice)
2. Botox into most severely affected muscles (commonly sternohyoid and sternothyroid) if propranolol and primidone are ineffective

CHARACTERISTIC PATTERNS OF ESSENTIAL TREMOR:
1. Absent at rest
2. Maximal during maintence of a posture (end of movement, posturing, phonation)
3. Reduced with movement
4. Accentuated at the termination of movement
5. Bilateral
6. Symmetric

Compared to Vocal tremor:
1. Parallel the onset of other symptoms, or presents in isolation
2. Sudden onset that can cause rapid deterioration in speech intelligibility
3. Greater with emotional stress or fatigue
4. Seen at rest with quiet inspiration on examination of the larynx.

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54
Q

√What are 6 treatment options for laryngeal tremor?

A

Medications:
1. Benzodiazepines
2. Propranolol
3. Primidone (Barbituate)

Procedural:
1. Botox injection (doesn’t eliminate tremor, but makes it less severe) - injected into the muscles that seem most affected by tremor

Surgical:
1. Deep brain stimulation
2. Thalamotomy

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55
Q

√What is the approach to botox injection for laryngeal tremor?

A

Predominately horizontal glottic tremor = bilateral thyroarytenoid muscles are injected with an initial dose of 1 unit per side.

Predominately vertical laryngopharyngeal tremor = bilateral strap muscles are injected with an initial dose of 2.5 to 5 units per side. This diminishes the up-and-down motion of the larynx, thereby decreasing the amplitude of the tremor and making speech more fluent.

If there is both vertical and horizontal tremor, injections can be alternated 3 to 8 weeks apart to avoid dysphagia and aspiration.

Cummings Page 835

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56
Q

What is the pathophysiology of Myasthenia Gravis? What are 3 diagnostic tests that can be used in an ENT setting?

A

Pathophysiology:
- Auto-antibodies formed against Acetylcholine receptors at the post-synaptic neuromuscular junction
- Results in a fatiguable neuromuscular response

Diagnostic tests:
1. Endoscopy: Repeated vocal use results in laryngeal fatigue
2. Serum antibodies to ACh receptor
3. Edrophonium (Tensilon) Test

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57
Q

List 8 treatment options for myasthenia Gravis, and their classifications.
What are 3 indications for thymectomy?
What are 3 indications to NOT do a thymectomy

A

Acetylcholinesterase inhibition (symptomatic relief)
1. Pyridostigmine
2. Neostigmine

Chronic immunosuppressive therapy:
1. Steroids
2. Azathioprine
3. Mycophenylate

Rapid immunomodulation
1. IVIg
2. Plasma exchange

Surgery
1. Thymectomy

Indications for Thymectomy:
1. Thymoma
2. Generalized MG with Age < 60 AND either AChR-antibody associated with MG OR Seronegative MG
3. Disabling ocular MG

No thymectomy for any of the following:
1. ≥ 60 years old
2. MuSK antibody-associated MG
3. Nondisabling ocular MG

Kevan Page 22

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58
Q

NOT IN VANCOUVERS

What is the diagnostic criteria for Parkinson’s disease?

A

Parkinson’s Disease requires all of the following:
1. Parkinsonism (bradykinesia + tremor/rigidity)
2. No “red flags”
3. No absolute exclusion criteria
4. At least ≥ 2 supportive criteria

Red Flags:
1. Rapid deterioration of gait
2. Absence of motor symptom progression over 5 years
3. Early bulbar dysfunction
4. Respiraotry dysfunctin
5. Early severe autonomic failure
6. Early recurrent falls due to misbalance
7. Disproportionate anterocollis
8. Absence of common non-motor features of disease during >5 years
9. Pyramidal tract signs
10. Bilateral symmetric presentation

Absolute exclusion criteria:
1. Cerebellar signs
2. Supranuclear gaze palsy
3. Established diagnosis of BVFTD
4. Parkinsonism is restricted to the lower limbs only for >3 years
5. Treatment with an antidopaminergic, or with dopamine-depletion agents
6. Absence of response to levodopa
7. Sensory-cortical loss
8. No evidence for dopaminergic deficiency on functional imaging
9. Other parkinsonism-inducing condition

Supportive Criteria:
1. A clear and dramatic positive response to dopaminergic therapy
2. Levodopa-induced dyskinesia
3. Documentation of resting tremor of a limb
4. A positive diagnostic test of either olfactory loss or cardiac sympathetic denervation on scintigraphy

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59
Q

List 4 vocal presentation of Parkinson’s disease

A
  1. Hypokinetic dysarthria (45%)
  2. Decreased loudness (poor breath support)
  3. Monotone
  4. Prosodic insufficiency
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60
Q

List 6 Endoscopic / Stroboscopy findings of Parkinson’s disease

A
  1. Vocal folds may be adynamic and/or bowed
  2. Increased jitter and shimmer
  3. Decreased harmonic/noise ratio
  4. Tremor
  5. May have laryngeal rigidity –> strained voice similar to in SD
  6. Pooling of secretions/aspiration
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61
Q

What is the Lee Silverman Method of Speech Therapy?

A

Speech therapy for Parkinson’s Disease.

Based on 5 components:
1. Increase AMPLITUDE of phonatory effort (think loud, be loud)
2. Improving sensory PERCEPTION of effort (think loud)
3. Administering treatment in high EFFORT style (recalibration)
4. Intensive FREQUENCY sessions (4 sessions per week x 4 weeks = 16 sessions)
5. QUANTIFY all speech and voice output (sound meter)

62
Q

What are 3 goals of voice therapy?

A
  1. Vocal hygiene
  2. Decrease phonotrauma
  3. Increase coordinated voice production via decrease tension and increase breath support
63
Q

List 12 different voice therapy techniques

A
  1. Confidential Voice (reduce laryngeal tension and hyperfunction by beginning with an easy and breathy voice quality and building up)
  2. Resonant Voice (based on oral cibratory sensations, with goal to achieve the strongest, “cleanest” possible voice with the least effort)
  3. Voice function exercises
  4. Lee-Silverman Voice Therapy
  5. Manual Circumlaryngeal Therapy (Reduce MSK tension and hyperfunction and reposturing the larynx during phonation)
  6. Straw Phonation (phonating through straw or tube)
  7. Accent Method (Based on accentuated, rhythmic, speech production in association with abdominal diaphragmatic breathing)
  8. Yawn-Sigh
  9. Inhalation phonation
  10. Respiratory re-training exercises
  11. Alexander technique
  12. Vegetative and reflexive techniques
64
Q

What are 5 absolute contraindications to performing for a professional voice user?

A
  1. Submucosal hemorrhage
  2. Enlarging vocal fold varix (blood vessel)
  3. Break in vocal fold mucosa
  4. Significant systemic illness
  5. Severe laryngitis

BLESS
break in mucosa
laryngitis
enlarging varix
submucosal hemorrhage
significant systemic illness

65
Q

List 6 risk factors for developinig benign vocal fold lesions

A
  1. GERD
  2. Smoking
  3. Allergies
  4. Voice abuse
  5. Occupational voice use
  6. Infection
66
Q

Describe the management of dysphonia in the professional voice. List 7 behavioural techniques, 6 avoidance behaviours, 4 medical options, and an additional option beyond those.

A

Behavioural:
1. Voice hygiene (minimizing throat clearing, coughing)
2. Avoiding excessive voice use; voice rest
3. Adequate hydration
4. Humidification
5. Discontinue smoking
6. Conservative measures for reflux
7. Psychological counselling/support

Avoidance of:
1. Inhaled steroids (irritates mucosa, risk of fungal infection)
2. Antihistamines (dessicating)
3. Decongestants (dessicating)
4. Aspirin (risk of hemorrhage)
5. Topical analgesics (increases risk of overwork injury)
6. Mentholated preparations (drying, habit forming)

Medical:
1. PPI
2. Systemic steroids (if little chance of vocal damage)
3. Mucolytics (e.g. Guanefisin)
4. Antibiotics as needed

Surgery if medical or behavioural therapy is unsuccessful

67
Q

√What are the phases of postoperative recovery after laryngeal microflap surgery for a professional voice user? What types of activities should be done in each phase?

A
  1. Phase 1: 7-14 days; Voice rest
  2. Phase 2: 7-28 days; Graduated voice use with SLP
  3. Phase 3: 4-12 weeks; Vocal reeducation (singing with pedagogue)
  4. Phase 4: 3-18 months; Professional activity
68
Q

What are the effects of masses, nodules, polyps, and cysts on the mucosal wave?

A
  1. Masses generally change the vibratory properties, decreasing fundamental frequency and prevent closure
  2. Nodules: minimally reduce mucosal wave
  3. Polyps: normal to minimally reduced mucosal wave
  4. Cysts:
    - Within mucosa: normal to minimal disruption dependin gon size
    - Within ligament: significant reduction in mucosal wave
69
Q

What are two vocal fold masses that will increase mucosal wave amplitude?

A
  1. Laryngeal myxedema
  2. Polypoid degeneration (Reinke’s edema)

Vocal fold polyp does NOT increase mucosal wave?? Controversial

70
Q

What lesions would cause a reduced mucosal wave? 4

A
  1. Sulcus
  2. Scarring
  3. Aging
  4. Lesions adding mass
71
Q

Discuss vocal fold nodules:
1. What are the causes and epidemiology? 2
2. What layer of the vocal fold is affected (1)?
3. What are the endoscopy and stroboscopy findings? 5
4. What are the treatment options? 3

A

Causes:
1. Voice overuse / misuse
2. GERD / LPR

Epidemiology:
1. Male > Female
2. Almost always vocal overdoers

Layer of vocal fold affected: Epithelium basal layer (basement membrane)

  • Most commonly occurs at strike zone of the vocal folds (~border between the anterior and middle third of the vocal cord)
  • At the junction between the phonatory and respiratory portion of the vocal folds:
  • Phonatory airway = anterior 2/3
  • Respiratory airway = posterior 1/3

Endoscopy/Stroboscopy findings:
1. Hourglass closure pattern
2. Normal mucosal wave
3. May have mucous string sign
4. Always bilateral, but not always symmetric
5. Involves strike zone (at 1/3 mark on anterior VF), mid-membranous

Treatment:
1. Voice therapy with SLP
2. Voice hygiene
3. PPI
4. NON operative (avoid especially on singers; correct underlying problem)

Any lesion that does not improve with behavioural modification is not a vocal fold nodule (per Rosen in Baileys); Cumming’s disagrees and says surgery can be offered if failure of a 3 month trial of voice therapy

Kevan Page 24
Vancouver Page 189

72
Q

Discuss vocal fold polyps:
1. What are the causes? 4
2. What layer of the vocal fold is affected?
3. What are the endoscopy and stroboscopy findings? 6
4. What are the types of polyp materials? 2
5. What are the treatment options? 3

A

What is it? Gelatinous substance without a capsule, stemming from inflammation in Superficial lamina propria

Causes:
1. Voice overuse/misuse
2. GERD
3. Smoking
4. Hypothyroid

Layer of vocal fold affected: Superficial lamina propria (Reinke’s space)

Endoscopy/Stroboscopy findings:
1. Can be Sessile or Pedunculated
2. Can be hemorrhagic or non-hemorrhagic
3. Usually unilateral, mid-membranous, but can have contralateral reactive lesion or sulcus
4. Exophytic with thin overlying mucosa
5. Typically translucent in appearance
6. Normal or minimally reduced mucosal wave (more with larger polyps)
7. May interfere with glottic closure

TYPES:
1. Mucoid
2. Angiomatous

Treatment:
1. Voice therapy and voice hygiene (less successful)
2. Management of reflux if present (PPI)
3. Surgery often required - microsurgical excision (micro-flap or truncation)

Kevan Page 25
Vancouver 190

73
Q

Discuss Vocal Fold cysts
1. What is the classification?
2. What are the common causes?
3. What layer of the vocal fold is affected?
4. What are the endoscopy and stroboscopy findings?
5. What are the different types of cysts and how are they formed?
6. What are the treatment options?

A

What is it? Encapsulated lesion of the vocal fold (less common than polyps)

Causes:
1. Vocal abuse/misuse

Classification: Subepithelial or Ligamentous
1. If capsule is adherent to microflap on elevation in surgery = subepithelial
2. If capsule is deep to microflap = ligamentous
3. If a large cyst spontaneously unroofs, this may become a sulcus vocalis

Layer of vocal fold affected:
1. Subepithelial = SLP
2. Ligamentous = ILP/DLP (vocal ligament)

Endoscopy/Stroboscopy findings:
1. Pale, raised, unilateral vocal fold mass
2. May have a reaction lesion on contralateral fold, but can also be bilateral
3. Mucosal wave minimally decreased if subepithelial (depending on size)
4. Mucosal wave MARKEDLY decreased if ligamentous

Types of cysts:
1. Mucous retention cyst (ductal cyst) - formed by occlusion of glandular duct
2. Epidermoid cyst (inclusion cyst) - formed by invagination of epithelium (keratin filled, more often associated with abuse)

Treatment:
1. Does not respond to voice therapy (may be more useful for epidermoid cysts)
2. PPI
3. Surgery (microflap and resection)
- DISTINCT capsule. ofa cyst. isseen, differentiates it from polyp

Vancouver notes 190 for diagram classification of cysts

74
Q

Discuss vocal fold fibrous mass
1. What is the classification? How does it differ from a vocal fold cyst?
2. What layer of the vocal fold is affected?
3. What are the endoscopy and stroboscopy findings? 4
4. What are the treatment options? 3

A

Classified into subepithelial or ligamentous.

Key difference between mass and cyst is the findings intraoperatively:
1. If encapsulated = cyst
2. If poorly defines borders/amorphous material = fibrous mass

Layer of vocal fold affected:
1. Subepithelial = SLP
2. Ligamentous = ILP/DLP (vocal ligament)

Endoscopy/Stroboscopy findings:
1. Mucosal wave significantly decreased
2. Can be unilateral or bilateral
3. Grayish pale (unlike a polyp which is more translucent)
4. Amorphous appearance with extensions anterior and posteriorly in the vocal fold

Treatment:
1. Does not respond to voice therapy
2. PPI
3. Surgery (microflap and resection)
- Will have indistinct borders without a defined capsule
- Can often be difficult to distinguish between the vocal ligament intraoperatively

75
Q

Discuss vocal fold pseudocysts.
1. What are the causes and epidemiology? 1
2. What layer of the vocal fold is affected?
3. What are the endoscopy and stroboscopy findings? 3
4. What are the treatment options? 3

A

Causes: ALWAYS associated with chronic glottal incompetence

Layer of vocal fold affected: Subepithelial (SLP)

Endoscopy/Stroboscopy findings:
1. Appears like a clear water blister
2. Can be unilateral or bilateral
3. Mucosal wave normal

Treatment:
1. May respond to voice therapy (~60%)
2. Phonomicrosurgery
3. Underlying glottal incompetence must be addressed as well to avoid recurrence

76
Q

Discuss reactive vocal fold lesions.

  1. What are the causes? 1
  2. What are the endoscopy and stroboscopy findings? 3
  3. What are the treatment options? 2
A

Causes: paired with a contralateral vocal fold lesion (therefore by definition is unilateral lesion)

Endoscopy/Stroboscopy findings:
1. Contralateral to a vocal fold lesion
2. Normal mucosal wave (asymmetric)
3. May have a cup and saucer appearance (indented)

Treatment:
1. Address the primary lesion; the reactive lesion itself often does not require separate treatment
2. Steroid injection is occasionally beneficial

Kevan Page 26

77
Q

Discuss NSVFL (Non-specific vocal fold lesions). What are they? How are they treated?

A

NSVFL is a term to account for patients that had symptomatic improvement with conservative therapy without resolution or diminuition of lesion size.
- Compared to vocal fold nodules for example, which don’t require surgery but will resolve or get smaller with non-surgical treatment

Patients in these groups have persistent lesions that could not be defined further without going to the OR.

Kevan Page 26

78
Q

Discuss Polypoid Corditis.

  1. What is it?
  2. Name 4 causes/risks
  3. What layer of the vocal fold is affected?
  4. What are the endoscopy and stroboscopy findings? 4
  5. What are the treatment options? 5
A

Aka:
- Reinke’s edema
- Polypoid degeneration of the vocal folds

What is it?
- Accumulation of gelatinous mucoid material (inflammatory exudate) in the superficial lamina propria

Causes/risk factors:
1. Women > Men
2. Smoking
2. GERD
3. Voice overuse

Layer of vocal fold affected: SLP (Reinke’s space)

Endoscopy/Stroboscopy:
1. Edematous, gelatinous vocal folds (SLP layer)
2. VF may prolapse inward during inspiratory phonation
3. Increased mucosal wave amplitude
4. Decreased fundamental frequency due to increase in mass of vocal fold and amplitude (slower vibration)

Treatment:
1. Management of reflux
2. Smoking cessation (does not reverse)
3. Voice hygiene
4. Voice therapy (case by case basis)
5. TSH if hypothyroidism suspected (poor evidence)
6. Surgery (usually does not go away without this): Microflap and aspiriation, or CO2 laser resurfancing)

Kevan Page 27

79
Q

Discuss vocal fold vascular lesions.

  1. What are they?
  2. What is the pathophysiology? - 2
  3. What are the causes and epidemiology? 2
  4. What layer of the vocal fold is affected?
  5. What are the endoscopy and stroboscopy findings? 4
  6. What are the treatment options? 5
  7. What are 6 indications for surgery?
  8. What are 2 surgical approaches?
A

What are they?
- Subepithelial blood vessels on the vocal folds
- No standard nomenclature; has been described as “vascular ectasias, capillary/venous lakes, varices, spider telangiectasias, etc.”

Pathophysiology:
- Repeated vibratory microtrauma causes capillary angiogenesis
- Dilated capillaries (from anterior to posterior) then increase mucosal vulnerability to further trauma

Layer affected: Subepithelial

Causes:
1. Vocal overuse (repeated microtrauma)
2. F>M preponderance (some speculation of an estrogen effect)

Endoscopy/Stroboscopy findings:
1. Abnormal dilatation of long arcades that proceed mostly from anterior to posterior
2. If they become confluent, often termed a capillary/venous lake
3. May have some vocal fold swelling
4. May form hemorrhagic polyp

Treatment:
1. Medical: hydration; avoid NSAIDs, ASA, blood thinners if appropriate
2. Management of reflux (e.g. PPI)
3. Voice hygiene - reduce voice training duration period, avoid sudden explosive vocals
4. Patient counselling on risk of hemorrhage (~2.68%)
5. Surgery (if meet indications; don’t need to treat all of them)

Indications for surgery:
1. Recurrent hemorrhage
2. Enlarging varices
3. Continuing dysphonia despite maximal medical and behavioural management
4. Decreased vocal endurance (decreasing good voice time before onset of huskiness)
5. Intermittent bruising
6. Hemorrhagic polyp

Options for surgery: Cold steel excision vs. laser ablation with spot coagulation to interrupt blood supply (KTP, PDL, CO2)
- Visible spots should involute spontaneously

80
Q

Discuss vocal fold hemorrhage.
1. What are the causes and 7 risk factors?
2. What are the symptoms? 4
3. What are the endoscopy and stroboscopy findings? 4
4. What are the treatment options? 8
5. What is the prognosis?

A

Causes:
1. Voice misuse, typically on a background of chronic voice overuse

Risk factors:
1. Voice abuse / extreme vocal effort (e.g. sporting event, forceful singing, sneezing)
2. Anticoagulants
3. Laryngitis
4. Preceding vascular ectasia / varicosities / capillary ectasias ± rupture
5. Perimenstrual women (just before or during menstruation)
6. Women in hormone supplement withdrawal
7. Pregnant women

Symptoms:
1. Sudden significant voice change with increased voice use or vocal abuse (e.g. singing, yelling, prolonged public /intense speaking)
2. Reduction in vocal range
3. Increased vocal fatigue
4. ± Association with URTI

Endoscopy/Stroboscopy:
1. Usually unilateral
2. May arise from varicosity on the medial vibrating edge of the vocal fold
3. Reduced amplitude and mucosal wave
4. May have a diffuse bruise or a deep blood blister (may stiffen the fold, lead to hemorrhagic polyp)

Treatment:
1. Absolute voice rest (usually x1 week minimum, up to 14 days) - no coughing, throat clearing, speaking, singing, or whispering
2. Performance cancellation if professional/applicable
3. Voice hygiene
4. Hydration
5. Stop anticoagulation (if possible)
6. Resumption of hormone therapy (for women in hormone withdrawal)
7. Serial clinical examination - reassess every 7 days
8. Surgery: microlaryngoscopy and evacuation of hematoma via small superiorly based cordotomy
- Acute indications: Evacuation can be considered if large hematoma does not resolve over a few days
- Subacute indications: Recurrent hemorrhage + vascular ectasia, enlarging varix, continued dysphonia

Prognosis:
- Majority: swelling from hemorrhage resolves spontaneously with voice rest
- If organized hematoma during follow up: OR for laryngoscopy, evacuation as above
- Hematoma/hemorrhage used to be thought as a “career-ending” event for a singer. Recent evidence suggests this is not true, and vast majority of professionals recover without any consequences

81
Q

Discuss Sulcus Vocalis.

  1. What is it?
  2. What is the classic cause? Can you name 5 others?
  3. How is it typically classified?
  4. Symptoms 3
  5. What are the endoscopy and stroboscopy findings? 6
  6. What are the treatment options? 6
A

Sulcus Vocalis = Epithelial lined groove at the free edge of the vocal fold, which can result in dysphonia by affecting mucosal wave and due to glottic leakage.

Cause:
1. Rupture of a VF cyst (classic thought)
2. History of voice overuse
3. Iatrogenic
4. LPR
5. Infection
6. Congenital

Ford Classification of Sulcus Vocalis
1. Type 1
- Epithelial invagination into the superficial lamina propria only.
- Normal voice
- Considered physiological
2. Type 2 (sometimes called 2a)
- Loss of a functional SLP
- Epithelial invagination into the vocal ligament, atrophic mucosa
- Moderate dysphonia
- Also known as a sulcus vergeture
3. Type 3 (sometimes called 2b)
- Epithelial invagination extends to the bottom of the vocal ligament and may involve the vocalis muscle
- Severe dysphonia
- Also known as a true sulcus vocalis

SYMPTOMS:
1. Chronic hoarseness
2. Diplophonia
3. Aphonia at certain frequencies - voice is worse than NP exam appears

Endoscopy/Stroboscopy:
- Bowed or curved free vocal fold edges
- Increased vocal fold stiffness (decreased mucosal wave)
- Glottic incompetence
- May have compensatory ventricular hypertonia
- Decreased vocal fold volume
- Adynamic segments seen on strobe

Treatment Options:
1. Medical: Voice therapy, PPI (not great)
2. Injection laryngoplasty
3. Surgery

Surgical options (also not great):
1. Excision with secondary intention healing
2. Intracordal HA/collagen injection
3. Medialization thyroplasty
4. Fat implant via microflap or Gray’s minithyrotomy
5. Mucosal slicing technique of Pontes
6. Bipedicle flap with submucosal division of scar

Kevan Page 28
Vancouver 191

82
Q

What are 4 surgical options to treat sulcus vocalis? Describe them.

A
  1. Fat implantation via microflap or Gray mini thyrotomy
  2. Collagen injection into lamina propria
  3. Microflap and dissection
  4. Mucosal sliding technique of Ponte’s

Ponte’s Mucosal Sliding Technique:
- Attempts to reorganize lines of stress through scarred and damaged lamina propria
- Done by making a series of parallel mucosal slices of varying length perpendicular to the vocal fold as well as an incision alongside the lower side of the sulcus to create multiple mucosal flaps
- Not widely utilized, prolonged recovery period of 9-12 months

Gray Minithyrotomy:
- Involves creating a small thyrotomy (smaller than with a medialization thyroplasty) and performing a subepithelial dissection
- Can be used to create a pocket for fat implantation

83
Q

How do you differentiate between a true sulcus vocalis and a pseudosulcus?

A

Pseudosulcus = caused by infraglottic edema due to laryngeal reflux

Differentiating features:
1. Sulcus vocalis involves the membranous vocal folds only
2. Pseudosulcus will extend beyond the vocal process

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84
Q

Discuss vocal process granulomas

  1. What are they? What is the pathophysiology?
  2. What are the causes and epidemiology? List 6 ways that intubation may be at risk for it.
  3. What are the endoscopy and stroboscopy findings? 3
  4. What are the treatment options? 8
A

Pathophysiology:
- Repetitive trauma leads to mucosal ulceration over vocal processes of arytenoids, causes cartilage exposure and inflammation
- Inflammation of the mucosa and perichondrium of the vocal process due to forceful apposition or chronic inflammation

Causes:
1. Voice overuse/abuse
2. GERD
3. M > F preponderance
4. Chronic coughing or throat clearing
5. Prolonged intubation
6. Traumatic intubation
7. Multiple tube exchanges
8. Incorrectly sized ETT
9. Tube movement while intubated
10. Unilateral VF immobility (increased straining)

Endoscopy/Stroboscopy:
1. Classically appears on the vocal process
2. May have a contralateral reactive lesion
3. Mature granulomas may become pedunculated and ball-valve

Management:
1. Voice hygiene
2. Adequate hydration
3. Antireflux strategies - cut out coffee, dietary modifications
4. PPI long-term
5. Voice therapy
6. Inhaled steroids (Fluticasone 50mcg BID x12 weeks)
7. Botox injection - 1-2U on side of lesion and some consider 1-2U contralaterally to prevent overcompensation
8. May consider steroid injection vs. PO steroids (controversial)
7. Surgery should be considered only as a last resort: Microlaryngeal surgery - Cold steel vs. endoscopic CO2 excision (only if very symptomatic; may still recur) - DO NOT expose underlying cartilage or the granuloma will recur
8. Biopsy not indicated due to its classic appearance

85
Q

What is the most common benign neoplasm of the larynx in children?

A

Recurrent Respiratory Papillomatosis (RRP)

86
Q

What is RRP caused by? Which one is more associated with aggressive disease?

A

HPV 6 and 11 infection

HPV11 is associated with more aggressive disease

87
Q

What are the different types of RRP and how do they differ? List 3 differences

A

Juvenile Onset RRP (JoRRP)
- Tends to be more aggressive
- Diagnosis before the age of 18
- Children diagnosed < 3yo are more likely to require >4 surgeries per year (3.6x) and to have multiple anatomic sites affected (2x)
- Generally improves around puberty

Adult onset RRP (AoRRP)
- Tends to be less aggressive
- Diagnosis after age 18 (peak 20-40)
- M>F
- Higher risk in immunocompromised

88
Q

List 5 risk factors for RRP

A
  1. Vaginal delivery
  2. First born
  3. Prolonged labour
  4. Active condyloma at the time of delivery
  5. Immunosuppression
89
Q

What are the clinical features of RRP? 3

A
  • Often misdiagnosed for asthma or group

Classic triad for JoRRP:
1. Progressive hoarseness
2. Stridor
3. Respiratory distress

Any child with these features should undergo laryngoscopy

90
Q

What is the histopathology of RRP?

A

Classic features of a papillary structure: Fingerlike projection of stratified squamous epithelium with a fibrovascular core

Ciliated epithelium undergoes squamous metaplasia when exposed to repeated trauma and is replaced with non-ciliated epithelium, which creates an iatrogenic squamociliary junction

91
Q

Discuss extralaryngeal spread of RRP. In what patient population does it usually occur - 3 risks? What are the most common sites? What is the prognosis? What is the % of malignant transformation?

A

Epidemiology:
1. 30% of children
2. 16% of adults

Risk factors:
- More common in HPV-11 associated disease
- < 3 at age of diagnosis (2x)
- Presence of tracheostomy

Most common sites in order:
1. Oral cavity
2. Trachea
3. Bronchi

Prognosis:
- Death usually occurs from surgical complications or due to respiratory failure from disease progressive
- Malignant transformation is uncommon (1.6%)

92
Q

What is the mainstay of management for RRP? What score can be used to document the course of RRP?

A
  1. Surgery is mainstay of therapy, but not a cure
  2. Family counselling and setting expectations is key

Derkay Score is used to document the course of RRP (moreso in research setting). Rates 0 to 3 (0 = none, 1 surface lesion, 2 raised lesion, 3 bulky lesion) for 25 different anatomical locations.

Kevan Page 31

93
Q

What are 5 surgical options for RRP?

A
  1. Cold steel excision
  2. CO2 laser
  3. KTP/PDL laser
  4. Microdebrider
  5. Tracheostomy ONLY if absolutely necessary - should be avoided if at all possible due to increased risk of extralaryngeal spread
94
Q

What on physical exam can be used to help identify papillomatous lesions in RRP?

A

Narrow Band Imaging

95
Q

What are the indications for adjuvant therapy in RRP? 4

A
  1. More than 4 surgeries a year
  2. Extralaryngeal spread
  3. Tracheostomy
  4. Other - patient factors (e.g. comorbidities not fit for surgery, complications from surgery)
96
Q

What are 7 types of adjuvant treatment options for RRP? What are some of their risk factors?

A
  1. PPI - inflammation is thought to cause metaplasia which creates more squamociliary junctions that can cause spread
  2. Indole-3-carbinol (negative regulator of estrogen)
  3. Intralesional Cidofovir (antiviral)
  4. Intralesional or systemic Bevacizumab (Avastin) - VEGF inhibitor (modulates angiogenesis)
  5. HPV vaccination - reduces frequency of interventions needed
  6. Interferon - blocks viral replication of RNA and DNA; alters cell membranes and makes them less susceptible to viral penetration.
    - Risks if given systemically: N/V, elevated liver enzymes, alopecia, leukopenia, thrombocytopenia
  7. Cox-2 inhibitors - anecdotal evidence, but multi-institutional double blinded RCTs did not reveal a therapeutic advantage
97
Q

What HPV strains does the Gardasil-9 cover?

A

6, 11, 16, 18, 31, 33, 45, 52, 58

98
Q

What are 15 complications of endotracheal intubation? Categorize them into early and late complications

A

Early:
1. Laryngeal/pharyngeal trauma
2. Cricoarytenoid joint dislocation
3. Subglottic cyst
4. Ventilator associated pneumonia
5. Pneumothorax
6. Post-extubatiion pulmonary edema

Late:
1. Neuropraxia (lingual, hypoglossa, laryngeal)
2. Pressure necrosis (especially post commiissure)
3. Perichondritis
4. Interarytenoid scarring/posterior glottic stenosis –> VC fixation
5. Bilateral Vocal fold paralysis
6. Intubation granulomas –> VC fixation
7. Subglottic stenosis
8. Glottic web
9. Vocal fold immobility - fixation or paralysis

99
Q

What is the chance of risk of complications from endotracheal intubation? What factors increase the risk of complications - List 5.

A
  • 10% of patients show signs of laryngeal injury after 1 day of intubation
  • Adults: 90% show signs of injury at >7 days
  • Infants/Children: 90% show signs of injury at >3 weeks

Risk of complications increases with:
1. Size of endotracheal tube (related to height of patient - not weight! Chubbier does not mean bigger ETT)
2. Length of intubation (more than 7d adult, more than 3wks child)
3. Traumatic intubation
4. Increased cuff pressures
5. Systemic vasculopathy (e.g. diabetes)

Per Bailey’s: Postintubation or post-tracheostomy stenosis is not uncommon, ranging from 10-19%, but typically only is symptomatic in less than 1% of cases

100
Q

What is a safe length of time for intubation in adults, children, and neonates?

A

Adults = 5-10 days
Children = up to 50 days
Neonates = up to 6 months

101
Q

What is the differential diagnosis for subglottic stenosis?

A
  1. Idiopathic
  2. Iatrogenic (e.g. prolonged intubation)
  3. Inflammatory (e.g. GPA, relapsing polychondritis, etc.)
  4. Infection (e.g. laryngitis, tracheitis)
  5. Neoplastic (SCC, chondrosarcoma, etc.)
102
Q

List a complete differential for the etiology of upper airway stenosis

A

Trauma:
1. Intubation injury
2. External blunt trauma
3. Penetrating trauma
4. Chemical injury

Systemic:
1. Wegener’s
2. Sarcoid
3. Amyloidosis
4. Relapsing polychondritis
5. Pemphigoid/pemphigus
6. Laryngopharyngeal reflux

Infectious:
1. Tracheitis
2. Ulcerative laryngitis
3. Tuberculosis
4. Diphtheria

Other:
1. Congenital
2. Neoplastic
3. Idiopathic
4. Post radiation

103
Q

Discuss the classification systems for glottic stenosis.

A

Glottic stenosis is divided into:
1. Anterior glottic stenosis (anterior glottic web)
2. Posterior glottic stenosis
3. Compelte glottic stenosis

Cohen Classification (AGS)
1. Grade 1 = 0-35%
2. Grade 2 = 36-50%
3. Grade 3 = 51-75%
4. Grade 4 = 76-100%

Bogdasarian and Olson Classification (PGS)
1. Grade 1 = Interarytenoid scar band not involving the posterior commissure
2. Grade 2 = Extension to the posterior commissure
3. Grade 3 = Fixation of one cricoarytenoid joint
4. Grade 4 = Bilateral cricoarytenoid joint fixation

104
Q

Discuss the classification of subglottic stenosis (list 2 classification systems)

A

Subglottic stenosis can be classified by:
1. Degree of luminal obstruction (Cotton-Myer)
2. Length/structures of airway involved (McCaffrey) - adds to diagnostic and therapeutic planning by helping predicting prognosis after surgery

Cotton Myer Classification (SGS)
1. Grade 1 - 0-50% obstruction
2. Grade 2 - 51-70% obstruction
3. Grade 3 - 71-99% obstruction
4. Grade 4 - 100% obstruction with no detectable lumen

McCaffrey Classification
1. Stage 1 - confined to the subglottis, < 1cm long
2. Stage 2 - confined to subglottis, >1cm long
3. Stage 3 - SGS extending to the trachea but not glottis
4. Stage 4 - SGS involving glottis with unilateral or bilateral vocal fold paralysis

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105
Q

Regarding glottic webs, discuss:

  1. How do they affect the fundamental frequency?
  2. Management strategies for anterior glottic web. Name 7
A

GLOTTIC WEBS:
- Can be a normal variant

FUNDAMENTAL FREQUENCY:
1. Increases fundamental frequency

MANAGEMENT:
1. Observation
2. CO2 laser excision
3. Cold steel excision
4. Steroid injection
5. Mitomycin C injection (antineopalstiic agent that prevents scar formation by inhibiting fibroblast proliferation)
6. Endoscopic keel placement
7. Laryngofissure and keel placement

106
Q

Describe the different surgical techniques for anterior glottic web. Name 7

A

ENDOSCOPIC: CO2 LASER / COLD STEEL DIVISION
1. Division + endoscopic microflap to cover one side + mitomycin C injected in the other side (only suiitable for smaller web)

  1. Division + endoscopic keel placement (larger webs)
    - Trach not required, use an endo-extralaryngeal needle passer and suture the keel
    - Requires a second procedure for keel removal
  2. Division + microsutures on the edge of the divided folds (one procedure, but technically difficult)
  3. Division alone
    - Hiigh rate of restenosis
    - Requires secondary procedures (balloon dilation, re-lysis)

OPEN: LARYNGOFISSURE WITH TRACH (Required if there is a significant cartilaginous component)
1. Division with keel placement
2. Division with resurfacing the folds (labial skin, split thickness skin graft)
3. Division and resection/reconstruction of subglottic stenosis with LTR/CTR

Vancouver 198

107
Q

How does Mitomycin C work?

A

Mitomycin C:
- Antibiotic derivative from Streptomyces Caespitosus
- Preferentially inhibits fibroblasts
- Useful for stenosis management in both adults and pediatrics

108
Q

What are ways to prevent anterior glottic webs? Name 2

A

Prevention = Avoid injury to the anterior glottis
- If surgery at the anterior commissure is required, there are two options:

  1. Stage the procedure with operating on one side of the commissure, let it heal, come back and operate on the other side
  2. Operate on both sides of the anterior commissure, but place a keel afterwards
109
Q

What are 2 types of keels?

A
  1. Teflon
  2. Silastic
110
Q

What are risk factors / etiologic factors for adult acquired subglottic stenosis? Name 10

A

A. IDIOPATHIC

B. INFECTIOUS
1. Bacterial
2. Fungal

C. INFLAMMATORY
1. Wegener’s
2. SLE
3. Sarcoid
4. Relapsing polychondritis
5. GERD

D. IATROGENIC
1. Surgical
2. Laser surgery
3. High tracheostomy
4. Cricothyrotomy

E. TRAUMATIC
1. Intubation (>90%): Oversized, repeated, shearing motion (agitation), route, duration
2. External laryngeal trauma
3. Airway burns (inhalationa, thermal, chemical, radiation)

F. OTHER
1. Endocrine (e.g. hypothyroidism)
2. Neoplastic (benign / malignant, intrinsic or extrinsic)

111
Q

What are 5 features of intubation that increases risk of subglottic stenosis?

A
  1. Prolonged (> 7 days)
  2. Repeated
  3. Traumatic
  4. Tube too big
  5. Cuff overinflated
112
Q

What is the differential diagnosis of non-neoplastic, non-traumatic, non-infectious subglottic stenosis in adults? 6

A

AW PISS

  1. Amyloidosis
  2. Wegener’s Granulomatosis (GPA)
  3. Relapsing Polychondritis
  4. Idiopathic
  5. Sarcoidosis
  6. Systemic lupus erythematosus
113
Q

What are preventative measures for avoiding subglottic stenosis? 3

A
  1. Smaller ETT without compromising safe ventilation (air leak at < 25cm H2O)
  2. Diagnosing and treating LPR (pH probe)
  3. Prophylactic antibiotics when tracheotomy is performed following prolonged/traumatic intubation

Note: Prolonged intubation up to 6 months preferred over tracheostomy in neonates

114
Q

Regarding idiopathic subglottic stenosis, discuss:
1. What is it?
2. Risk factors? 1
3. Treatment? 2

A

IDIOPATHIC SUBGLOTTIC STENOSIS (ISS):
- Rare inflammatory process of unknown cause
- Limited to subglottis and upper 2 tracheal rings

Risk Factors:
1. Young female > 85% (estrogen may be involved with wound healing response)

Treatment:
1. Surgery is main treatment modality
- Endoscopic laser with mitomycin-c for < 1cm
- Open laryngotracheal surgery (CTR) for thicker complex scar

115
Q

What are the possible investigations and ancillary tests for the work-up of subglottic stenosis? 9

A

Examination:
1. Flexible nasolaryngoscopy
2. Bronchoscopy (rigid and flexible)
3. Biopsy (TB, Wegerner’s, Sarcoidosis, etc.)

Imaging:
1. CT - helps determine length of stenotic segment
2. Echocardiogram - rule out vascular ring
3. Angiogram (Exclude vascular ring)
4. Fluoroscopy

Other:
1. cANCA (assess for GPA)
2. PFTs - flow volume loops - determine degree of obstruction and pattern of obstruction
3. Reflux testing - 24 hour dual probe pH monitor or MII-pH monitoring

Kevan Page 39

116
Q

How do you test and grade for subglottic stenosis intraoperatively?

A
  1. Assess using cuffless pediatric ET tube
  2. Assess air leak ventilation pressure
    - If leak at < 10cm H2O –> upsize tube
    - If between 10-25cm H2O (compare to expected ETT)
    - If > 25 cm H2O leak –> downsize tube
  • Comparing to expected ET tube size for patient age deduction
  • % of lumen obstruction from the above
  • Useful for prognosis of decannulation, and number of operations required to decannulation
117
Q

Discuss the treatment options for subglottic or tracheal stenosis.

5 non-op treatments
7 surgical options

A

Observation:
1. Grade I-II with minimal symptoms and reliable follow up (Especially congenital)
2. Repeat bronchoscopy every 3-6 months

Non-Operative Management:
1. Control of reflux
2. Management of rheumatologic disease
3. Avoidance of chronic irritants
4. Small caliber tube if chronic tracheostomy
5. Acute exacerbations: Supplemental O2, humidified air, systemic steroids, antibiotics when appropriate, heliox

Surgical options:
1. Tracheostomy
2. Endoscopic procedures
3. Balloon dilation
4. Cold steel
5. Laser

Endoscopic Management: Balloon Dilatation
1. ± Steroid injection
2. ± Mitomycin C injection
3. ± laser incisions

Open Management
1. Cricotracheal resection
2. Laryngotracheoplasty (anterior cricoid split ± cartilage graft, posterior cricoid split ± cartilage graft, both - four quadrant technique) - note any procedure with a graft is a laryngotracheal reconstruction (LTR)
3. Slide tracheoplasty (complete tracheal rings)
4. Tracheal Stenting:
- Rarely done unless in a palliative setting
- Can be bare metal or silastic
- Allografts have had mixed results
- Tissue engineering is an emerging modaliity
- Montgomery T-tube stent = combined tracheal and subglottic stent with a tracheostomy tube

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118
Q

What are five types of tracheal stenting?

A
  1. Aboulker or Cotton-Lorenz stent (rigid Teflon - polytef II, hollow lumen)
  2. Montgomery T tube (hollow silicone)
  3. Montgomery laryngeal stent (solid silicone)
  4. Single Stage LTR (ETT used as alternative to stenting)
  5. Silastic sheet / Swiss roll

Vancouver 197

119
Q

What are 4 indications for laser use in subglottic stenosis?

A
  1. Grade I, II stenosis
  2. Granulation tissue
  3. Thin webs
  4. Crescent-shaped bands
120
Q

What are predictors of failure in endoscopic CO2 laser for SGS?

A
  1. Circumferential thick (cicatricial scarring)
  2. Length > 1cm
  3. Involved/Exposure of cartilage during CO2 laser excision predisposing to chondritis
  4. Posterior glottic stenosis with arytenoid fixation
  5. Previous failure
  6. Previous severe bacterial infection associated with tracheostomy
  7. Loss of cartilaginous framework (“not enough”)
  8. Glottic involvement

CLIPPING

121
Q

What is one main contraindication of Cricotracheal resection?

A

Subglottic scarring within 3mm of vocal folds

122
Q

What are four advantages of cricotracheal resections and thyrotracheal anastomosis compared to an LTR?

A
  1. Safe effective treatment for severe SGS
  2. Results are superior to similar cases done by LTR techniques
  3. Voice quality results are better (preserves voice)
  4. No interference with normal growth of larynx
123
Q

What are 2 disadvantages of cricotracheal resections & thyrotracheal anastomosis?

A
  1. Possibility of injury to the recurrent laryngeal nerve (lateral cricoid dissection is performed in subperichondrial plane & lateral resection is anterior to the cricothyroid joint)
  2. Possible partial dehiscence at anastomotic site resulting in restenosis (laryngeal release only if > 5 tracheal rings resected)
124
Q

What are 3 options for post-operative airway support for glottic edema following cricotracheal resections & thyrotracheal anastomosis?

A
  1. Short term ET intubation
  2. Montgomery T tube stenting for older child (4-6 weeks)
  3. Distal tracheostomy (4-6 weeks)
125
Q

What are 2 indications for four quadrant cricoid split?

A
  1. Grade III + IV
  2. Congenital elliptical cricoid

Procedure:
- Division of anterior and posterior walls (± grafts) + lateral walls of cricoid (anterior to inferior cornu of thyroid & extraperichondrial externally to avoid RLN)
- Aboulker or Cotton-Lorenz stent for 6 months (very unstable airway)

126
Q

What is the definition of congenital subglottic stenosis? (compared to acquired subglottic stenosis)

A
  1. No history of ETT or laryngeal trauma

Caused by failure or incomplete recanalization of the laryngeal lumen at 10 weeks gestation

127
Q

Which has worse symptoms and prognosis: congenital vs. acquired Subglottic stenosis?

A

Acquired
- Congenital tends to improve with growth of the child

128
Q

How much of the adult trachea can you resect surgically?

A
  • 6cm with releasing procedures (ie. up to 50% of the length of the adult trachea)
  • 3.5cm without releasing procedures

*When neck is extended, approximately 1/3 of the trachea is extrathoracic (no need for thoracotomy in upper 1/3)

129
Q

Discuss the management strategies for tracheal re-approximation

A
  1. Tension free closure
  2. Preservatiion of blood supply (bloos supply is LATERAL, so minimize lateral dissection)
  3. Grillo stitch (internal or external) - suture from chin to sternum

Releasing procedures:
1. Suprahyoid release
- Most commonly used
- Suprahyoid musculature is released
- Hyoid cartilage is divided medial to the digastric tendon separating the body from the greater cornu (essentially a Sistrunk)

  1. Infrahyoid (aka. Thyrohyoid release)
    - Transection of the thyrohyoid membrane
    - Mobilization of the greater cornu of the thyroid to allow the larynx to drop inferiorly
    - Largely fallen out of favour due to post-operatiive swallowing dysfunction
  2. Intrathoracic Techniques
    - Not routinely done in ENT
    - Examples include mobilization of the hilum, dividing the left mainstem bronchus or freeing the pulmonary artery from the pericardium

Suprahyoid release: https://ars.els-cdn.com/content/image/1-s2.0-S1043181023000325-gr6.jpg

130
Q

What are 5 factors that increase risk of anastomotic failure for tracheal re-approximation?

A
  1. Stenotic segment >4cm
  2. Diabetes
  3. Age < 17 years old
  4. Laryngotracheal resection
  5. Presence of a tracheostomy
  6. Infection

4 PLAID

Greater than 4cm stenotic segment
Presence of trach
Laryngotracheal resection
Age < 17
Infection
Diabetes

131
Q

What are 8 direct factors that lead to presbylarynx?
What are 6 indirect factors that lead to presbylarynx?

A

DIRECT FACTORS:
1. Fatty degeration of laryngeal muscles –> atrophy/weakness
2. Calcification of laryngeal cartilages –> decreased compliance
3. Ossification of arytenoids –> decreased compliance
4. Decreased elasticity, increased fibrosis of laryngeal muscles
5. Mucosal atrophy –> prone to injury
6. Salivary atrophy –> decreased lubrication
7. Edentulous –> decreased articulation
8. Pulmonary disease –> reduced amplification, breath support, vocal stamine

INDIRECT FACTORS:
1. Hearing loss –> poor articulation, reduced speech
2. Anxiety/depression –> reduced speech
3. Dehydration –> decreased lubrication
4. Mucosal irritants –> GERD, smoking
5. Hypothyroidism –> VC edema
6. Neuromuscular disorder (e.g. PD, ALS, Tremor, DM) –> weak, tremulous laryngeal muscles

132
Q

Describe the symptoms of presbylarynx (6).
What are 7 endoscopic findings?

A

Symptoms:
1. Breathy voice
2. Vocal aesthenia
3. Aspiration, weak cough
4. Vocal fatigue
5. Pitch change - in men become higher, in women lower
6. Tremor

Endoscopic findings:
1. Bowed vocal folds
2. Vocal fold atrophy (ie. prominent vocal processes, arrowhead configuration)
3. Gray/yellow discoloration (fibrofatty accumulation)
4. Chronic glottal incompetence
5. Incomplete Spindled closure pattern
6. Prominent laryngeal ventricles (secondary to TA atrophy)
7. Mucosal dryness

Vancouver 204

133
Q

What are the 3 different types of laryngeal cysts?
What is the most common type?
How are they typically treated?

A
  1. Supraglottic cysts
    - If congenital, most frequently occurs in supraglottis
    - Superficial arytenoid or laryngeal/lingual surface of epiglottis
    - Treatment: excision, marsupialization; low recurrence rate
  2. Glottic cysts
  3. Subglottic cysts
    - Most common site of larygngeal cysts
    - Frequently acquired (intubation, suctioning)
    - Congenital = mucous gland hyperplasia
    - Recurrence is common
    - Large obstructive cysts may present during acute infection
    - Treatment: Marsupialization/unroof (using laser, electrocautery, or instruments)
134
Q

What is the saccule?
Discuss Saccular Disorders. What are the two main types? What is the pathophysiology of a saccular cyst?
What is the classification of a saccular cyst? 3
What are the treatment options? 3

A

Saccular disorders includes Saccular Cysts and Laryngoceles.
- Both saccular cysts and laryngoceles arise due to abnormal dilatation of the saccule to form a mass
- The saccule is a mucous gland appendage that lies between the false VF and the thyroid cartilage (deep within the ventricle)
- Ends as a blind ended pouch near the posterolateral aspect of the laryngeal surface of the epiglottis

  • Saccular cysts are fluid filled only
  • Laryngoceles have air within the lumen

SACCULAR CYSTS:
- Fluid filled only
- Can become infected to form an infected saccular cyst
- Thought to be formed due to obstruction of the saccular orifice
- More common in children
- Clinical presentation: CONSTANT symptoms (e.g. stridor, hoarseness, cough, feeding difficulty) that may expand rapidly causing obstruction

Classified as either (1) anterior/superior or (2) lateral/posterior based on location
- Anterior/Superior: Emanates from anterior ventricle and extends into laryngeal lumen (protrudes medially into ventricle)
- Lateral/Posterior: Expand within the paraglottic space and are submucosal. Appear similar to internal laryngocele. Protrudes into false VC and AE folds (more commonly recur)

Treatment options: Secure airway, endoscopic marsupialization (e.g. cold steel, microdebrider, CO2 laser), Open approaches (e.g. Trans-thyrohyoid membrane, lateral thyrotomy with resection of thyroid cartilage ala)
- Prognosis: Recurrent and multiple procedures common

Kevan Pediatrics Qusetion 149

135
Q

What is a laryngocele?
Name 2 risk factors/suspected causes
How does it typically present?
Discuss the classification (3)
Complications 3
Treatment options (3)

A

LARYNGOCELES:
- Air within the lumen (sometimes has an air-fluid level)
- Can become infected to form a laryngopyocele (filled with pus)
- Contain air due to communication with the laryngeal lumen (not seen in saccular cysts)
- More common in adults/older population
- Thought to be formed due to dilation from high transglottic pressures (brass/woodwind players, glass blowers) or obstructed by neoplasm; or congenital or idiopathic
- Clinical presentation: INTERMITTENT symptoms (due to influx/outflux of air) - stridor, hoarseness, cough, feeding difficulty; intermittent balloon-like compressible neck mass; borborygmi (gurgling with auscultation over neck mass - Bryce’s sign)

Classified as (1) internal, (2) external, or (3) combined based on location
- Internal: Exclusively within the thyroid cartilage, confined to interior of larynx, extends posterosuperiorly into area between false VC and AE fold
- External: Exclusively outside the cartilaginous larynx - pass through thyrohyoid membrane, presents at neck mass
- Combined: Both inside of and outside the thyroid cartilage

Diagnosis: FNL, CT neck

Complications: Secondary infection, rare malignancy, airway obstruction

Treatment options:
- Secure airway if necessary, bronchoscopy to r/o other airway anomalies, biopsy to r/o cancer
- Internal options: Endoscopic marsupialization (e.g. cold steel, microdebrider, CO2 laser)
- External options: Open approaches - Trans-thyrohyoid membrane approach; lateral thyrotomy approach with resection of thyroid cartilage ala

136
Q

What is the DeSanto clinical classification of epithelial laryngeal cysts?

A
  1. Ductal (synonymous with mucous retention cyst): Arise from obstruction of glandular ducts, they can occur at any site, < 1cm majority of the time
  2. Saccular cyst: Fluid-filled dilation of the saccule without communication with the laryngeal lumen, subclassified as:
    - Anterior (60%): Cyst tends to bulge medially, obscures anterior portion of VF
    - Lateral (40%): Larger, extends superiorly and laterally (AE/false VF); can bulge through thyrohyoid membrane
137
Q

What is the Newman (histological) classification of laryngeal cyst? 3

A
  1. Epithelial (subclassified as)
    - Ductal
    - Saccular (further classified as anterior vs. lateral)
  2. Tonsillar
    - Resemble tonsillar crypts with an abundantly follicular lymphoid lining
    - No data to suggest they are clinically different from epithelial cysts
  3. Oncocytic
    - Cystic lesions lined by oncocytes
    - Resemble Warthin’s tumor
    - Oncocytes originate from metaplasia of seromucinous gland ductal epithelium due to chronic inflammation (e.g. smoking)
138
Q

What are 3 systemic diseases that should be considered in the differential of a vocal fold lesion?

A
  1. Hypothyroidism
  2. Acromegaly
  3. Rheumatoid arthritis
139
Q

What should be ruled out in a patient with laryngeal amyloidosis? How should this be done?

A

Multiple Myeloma

  1. Bone marrow biopsy
  2. SPEP & UPEP for M protein
  3. CXR
140
Q

What is a laryngeal chordoma?
What is the treatment? 1
Sex predilection? 1

A

LARYNGEAL CHORDOMA:
- Hyaline cartilage growth of posterior cricoid on endolaryngeal surface
- Slow growing but requires debulking or complete excision
- 4:1 male preponderance

141
Q

What are 3 benign tumors that arise from Schwann cells of the larynx? What is their origin that they arise from?

A
  • Neurogenic tumors occur in the aryepiglottic fold or false VF, usually submucosal

Origin: Internal branch of the superior laryngeal nerve

Types:
1. Schwannoma: Benign, encapsulated, slow growing, rare malignant sarcomatous degeneration
2. Neurofibroma: Proliiferation of sheath cells and fibers, nonencapsulated, nodular and diffuse
3. Granular cell tumor: Slow, painless growth, well circumscribed

142
Q

Regarding Granular cell tumors of the larynx, discuss:
1. What are the other names?
2. Clinical presentation? 5 symptoms and where are they most commonly found
3. Diagnosis?
4. Where do they arise from?
5. Histology and stains? 5
6. Complications? 2
7. Types? 3
8. Treatment? 1

A

Aka. Abrikossoff tumor

CLINICAL PRESENTATION:
- Slow, painless growth
- Well circumscribed
- Most commonly occurs on the tongue
- Can also be commonly found at the posterior aspect of the true VC
- Typically solitary, polypoid, sessile, papillary or cystic

DIAGNOSIS:
1. Endoscopy with biopsy

CAUSE:
1. Arise from Schwann cells

HISTOLOGY:
1. Large polygonal cells iin nests/strands/sheets
2. Infiltrative, no distinct capsule
3. Defining characteristic = abundant eosinophilic cytoplasm filled with granules of varying sizes (lysosomes in varying stages of fragmentation)
4. Keratin pearl formation in some cases (pseudoepitheliomatous hyperplasia)
5. Stains: S100 and PAS positive, Synaptophysin, NSE, Chromogranin

COMPLICATIONS:
1. Recurrence (8%)
2. Malignant transformation (5%)

TYPES:
1. Congenital
2. Mucosal
3. Gingival

TREATMENT:
1. Complete excision (Endoscopic or open via laryngofissure or conservative resection

143
Q

What are seven pseudoepitheliomatous lesions of the larynx?

A
  1. Granular cell tumors
  2. Rhinoscleroma
  3. Necrotizing sialometaplasia
  4. Pachydermia laryngitis
  5. Histoplasmosis
  6. Blastomycosis
  7. Aspergillus/Candida
144
Q

What are 6 contraindications to airway surgery?

A

ABSOLUTE:
1. Tracheostomy dependent (aspiration, severe bronchopulmonary dysplasia)
2. Severe GERD refractory to surgical and medical therapy
3. Unfit for general anesthesia

RELATIVE:
1. Chronic steroid use
2. Uncontrolled diabetes
3. Cardiac, renal or pulmonary disease

145
Q

Regarding Puberphonia, discuss:
1. What is it?
2. What is the pathophysiology of male voices during puberty? 2
3. Treatment? 2

A

Puberphonia = Mutational Falsetto
- A functional voice disorder that is characterized by the habitual use of a high-pitched voice after puberty
- Often seen in males, ± with emotional distress

Pathophysiology during puberty:
- Testosterone effect causes VF thickening, lengthening, and rotation, decreased tone and decreases fundamental frequency
- Thyroid cartilage enlarges and the angle becomes more acute

TREATMENT:
1. Voice therapy
2. ± Psych

146
Q

What is Functional dysphonia?
1. Who does it typically present in?
2. Differential? 3
3. Treatment? 3

A

FUNCTIONAL DYSPHONIA
- Aka. Psychogenic dysphonia
- Related to psychologic issues causing severe decrease in voice output

Presentation:
1. Women > Men

Differential:
1. Spasmodic dysphonia
2. Secondary MTD
3. Tremor

Treatment:
1. Speech therapy
2. Psychiatry
3. Pharmacotherapy

147
Q

How do you differentiate spasmodic dysphonia from functional dysphonia? 2

A
  1. SD will not respond to speech therapy, but functional will
  2. SD improves with whispering, singing, laughing
148
Q

Regarding Oculopalatolaryngopharyngeal myoclonus, discuss:
1. What is it?
2. What is the pathophysiology? 3
3. Clinical presentation 2
4. Treatment? 5

A

WHAT IS IT?
- Uncommon, consisting of rhythmic contraction of the soft palate, pharynx, and larynx at a rate of 1-2/second

Pathophysiology:
1. Lesion in the central tegmental tract (need MRI)
2. Can be seen in French Canadians (consanguinity Lac St. Jean)

Lesions in the GUILLAIN-MOLLARET TRIANGLE:
1. Contralateral Dentate nucleus
2. Red nucleus
3. Inferior olivary nucleus
“Guillain has red olives in his lower opposite teeth”

Clinical Presentation:
1. SLow rhythmic adduction and abduction of VF at the same time as the palatal and pharyngeal contractions –> choppy voice and intermittent hypernasality
2. Pendular Nystagmus

Treatment:
1. Baclofen
2. Carbamazepine
3. Clonazepam
4. Serotonin
5. Botox injections

149
Q

What are all the different types of indications for botox for laryngopharyngeal pathology? 11
Where do you inject for each?

A
  1. Adductor SD (into TA)
  2. Abductor SD (into PCA)
  3. Stuttering (into TA)
  4. Vocal Tic (into TA) - or tremors can be injected into supra/infrahyoid musculature
  5. Mutational dysphonia/puberphonia (into Cricothyroid)
  6. Ventricular dysphonia/dysphonia plica ventricularis (injection into false fold/AE muscle)
  7. Dysphagia due to Cricopharyngeal dysfunction (into cricopharyngeus)
  8. TEP speech failure due to cricopharyngeal spasm (into cricopharyngeus)
  9. Vocal fold granulation and prevention of posterior glottic stenosis (into TA - decrease strength of vocal fold closure, tends to take a more abducted position at rest)
  10. Arytenoid rebalancing (post-dislocation, into adductor muscles on that side)
  11. Bilateral true vocal fold paralysis (into adductors)
150
Q

What are the overall side effects of botox injections for laryngopharyngeal pathology? 7

A
  1. Dysphagia with liquids (most common)
  2. Aspiration
  3. Weak breathy voice/hypophonia
  4. Sore throat
  5. Blood tinged sputum
  6. Hyperventilation and dizziness
  7. Airway obstruction
151
Q

What is the grading system for Reinke’s edema?

A

Grade 1: Minimal polypoid degeneration of the vocal fold up to 25% of the glottic airway.
Grade 2: Expanded polypoid lesion occupying 25% to 50% of the glottic airway.
Grade 3: Expanded polypoid lesion, 50% to 75% of the glottic airway.
Grade 4: Obstructive lesion regardless of laterality, occupying beyond 75% of the glottic airway.

Laryngology (8 decks)

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