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Laryngology > VFP, Cough, Reflux > Flashcards

VFP, Cough, Reflux Flashcards

1
Q

√What are 9 types of medications that can cause dysphonia/hoarseness, and how?

A
  1. ACE Inhibitors (cough)
  2. Anticoagulants (hemorrhage)
  3. Anticholinergics (dessicating/cause drying)
  4. Antipsychotics (dystonias)
  5. Bisphosphonates (chemical laryngitis)
  6. Diuretics (dessicating/cause drying)
  7. Inhaled steroids (mucosal irritation, fungal laryngitis)
  8. Testosterone/Danocrine (alters sex hormone levels, alters VF shape)
  9. Chemotherapy (Vincristine/Vinblastine - VF paralysis)

ITs AAAABCD

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2
Q

√List a complete differential for vocal fold paresis/parlaysis

A

IATROGENIC (24-26%)
- Cardiac Surgery
- PDA ligation
- Thyroid surgery
- Esophageal or thoracic surgery
- Prolonged intubation

TRAUMA
- Penetrating neck injury

AUTOIMMUNE/SYSTEMIC
- Sarcoidosis
- Rheumatoid arthirtiis
- Amyloidosis
- SLE
- Diabetes mellitus

INFECTIOUS
- Viral inflammation
- TB
- Sarcoidosis
- Lyme disease
- Syphillis
- EBV

NEOPLASTIC (Malignancy 25% - primary pulmonary and mediastinal adenopathy most commonly)
- Laryngeal malignancy
- Thyroid malignancy
- Lung carcinoma
- Anything along the course of the RLN

NEUROLOGIC
- Systemic: Stroke, MS, ALS, GBS
- Peripheral: Charcot-marie-tooth, Myasthenia Gravis
- Poliomyelitis
- Pseudobulbar palsy
- Wallenberg
- Arnold Chiari Malformation (most common in child)

MEDICATIONS:
- Neurotoxic medications: Vinka alkaloids (vincristine/vinblastine), streptomycin, quinine, lead

IDIOPATHIC (20%) - 70% will recover but may take 12 months
- Usually post-viral

OTHER:
- Thoracic aneurysm of cardiomegaly (Ortner syndrome)

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3
Q

What are possible surgical/iatrogenic causes of vocal fold paralysis? Name 7

A
  1. Thyroidectomy (5-10% RLN injury, 30% in revision)
  2. Skull base surgery
  3. Anterior cervical discectomy and fusion (R>L)
  4. Carotid endarterectomy
  5. Coronary artery bypass grafting
  6. Esophagectomy
  7. Pulmonary resection
  8. Mediastinoscopy
  9. Intubation (pressure-induced neuropraxia from cuff in proximal subglottis)
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4
Q

What is Ortner’s Syndrome?

A

Cardiovocal Syndrome

Vocal fold paresis or paralysis caused by compression of the RLN due to a cardiovascular disorder.

Classically, this is a left RLN palsy due to compression of the nerve between the thoracic aorta and pulmonary arteries, due to left atrial dilation.

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5
Q

What are 6 FNL features of unilateral vocal fold paralysis secondary to RLN injury?

Changes that occur to the vocal fold after severing the RLN

A
  1. Variable fixed position (medial, paramedian, lateral) and/or immobile
  2. Jostle sign = passive medial movement of the affected cord during adduction due to absence of lateral tension from the denervated musculature
  3. Decreased length
  4. Decreased height
  5. Vocal fold atrophy and bowing (spindle)
  6. Ipsilateral arytenoid rotated/displaced anteriorly (prolapsed)
  7. Yellowing discoloration
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6
Q

What are long term changes in the paralyzed vocal fold? 4

A
  1. Muscle atrophy
  2. Anterior arytenoid displacement
  3. Pooling of secretions
  4. Shortened fold with lower position

MAPS

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7
Q

What is the Jostle Sign?

A

Jostle sign = passive medial movement of the affected cord during adduction due to absence of lateral tension from the denervated musculature

(And, lateral movement of the arytenoid on the immobile side during glottic closure due to contact from the mobile arytenoid)

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8
Q

If RLN is transected in surgery, why does it appear that the vocal fold is still moving on endoscopy?

A
  • Bilateral innervation of inter-arytenoid muscle, but absence of lateral tension from the denervated musculature, causing slight medialization of the paralyzed fold on adduction
  • SLN has neural input to the anterior 1/3 of the vocalis
  • Jostle sign - brief lateral movement of the arytenoid on the immobile side during glottic closure due to contact from the mobile arytenoid
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9
Q

Outline a complete workup for vocal fold paralysis - 9

A
  1. Complete H&P
  2. Flexible laryngoscopy ± videostroboscopy
  3. Labs: CBC, fasting glucose, TSH, FTA-ABS (syphillis), Lyme titers, toxin screen (lead, arsenic)
  4. MBS and/or FEES (if suspicion of aspiration)
  5. Barium swallow (exclude esophageal mass, vascular compression, or aspiration)
  6. High resolution CT larynx (if suspicious of endolaryngeal pathology)
  7. CT or MRI skull base to upper chest
  8. CXR ± CT chest (rule out lung mass)
  9. Laryngeal EMG (only useful between 4-6 months for prognosticating recovery, but can be used earlier if suspect the arytenoid is stuck) - paralysis vs. fixation, RLN vs. SLN, myopathy vs. neuropathy
  10. MRI Brain and Neuro consult (if suspicion of central/neurologic cause)
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10
Q

What are 5 symptoms and 9 signs of unilateral Superior laryngeal nerve injury?

A

Symptoms:
1. Unstable pitch
2. Unable to reach higher pitches
3. Decreased range
4. Dysphagia/Aspiration (loss of laryngeal sensation to the supraglottis and glottis via internal branch)
5. Vocal fatigue

Signs:
1. Guttman’s Sign
2. Deviation of petiole to the side of weakness (60%)
3. Phase asymmetry between vocal folds
4. Axial rotation of the posterior commissure toward the normal side in 50% of patients with rapidly alternating “eee” and sniff maneuver
5. Asymmetric VF tension (bowed vocal folds)
6. Asymmetric VF height (inferior displacement)
7. “PPP” rule = posterior commissure points to paralyzed side in unilateral SLN paralysis
8. Pooling of secretions on ipsilateral side
9. Ipsilateral false VF adducted (compensatory)

Current literature provides no consensus for diagnosis of SLN paralysis based on laryngoscopy alone

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11
Q

What is the Guttman Test for testing Superior laryngeal nerve paralysis?

A

Normal Patient:
1. Frontal pressure on thyroid lowers
2. Lateral pressure raises pitch

Paralyzed Cricothyroid (e.g. SLN paralysis):
1. Frontal pressure raises pitch
2. Lateral pressure lowers pitch
*Presumably due to unopposed action of other normal cricothyroid deviating the larynx (no known explanation)

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12
Q

What are 3 factors that determine what a vocal fold position would be after vocal fold paralysis?

A

Generally the position in unpredictable and is dependent on the following factors:
1. Reinnervation/synkinesis
2. Residual innervation
3. Atrophy/fibrosis of the denervated muscle and not due to the level of the lesion

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13
Q

How can you differentiate RLN injury from vagal injury (RLN+SLN)? List endoscopic differences; what special tests (2) could you and what are their findings?

A

Endoscopic findings:
1. RLN injury: paramedian vocal fold position (cricothyroid action maintained, which helps adduct vocal fold) - implies lesion below the nodose ganglion
2. RLN + SLN injury: Lateral vocal fold position (loss of cricothyroid adduction)

Objective tests:
1. Laryngeal EMG
2. FEEST (Functional endoscopic evaluation of swallowing with sensory testing)

FEEST:
- During FEEST, a puff of air is delivered to the supraglottic mucosa via a side port, and the presence of the laryngeal adductor reflex (LAR) is observed
- LAR: Glottic closure reflex, a mechanism of laryngeal protection, preventing material from inappropriately entering the upper airway

Degree of sensory impairment based on LAR:
1. Normal = LAR elicited at 3mmHg
2. Mild impairment: 6mmHg
3. Moderate impairment: 9mmHg
4. Severe impairment: No LAR at 9mmHg

Left and right sides are examined separately to determine the side of the lesion

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14
Q

What is the nerve or loop of Galen? What is the prevalence and what are 3 different ways it can present?

A

Galen’s Anastomosis is a connection between the internal branch of the SLN and RLN.

Occurs in 76.7% (n=890 hemilarynges)
- 92.3% single trunk
- 4.2% double trunk
- 3.5% plexus

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15
Q

What are 9 uses for laryngeal EMG?

A
  1. Intraoperative nerve monitoring
  2. Diagnose neurologic disorders (MG, ALS)
  3. Localization of lesion (RLN vs SLN, central vs. peripheral)
  4. Establish prognosis (correlate in 60-70% after 4 weeks)
  5. Biofeedback (e.g. injections for botox)
  6. Differentiate between paralysis and arytenoid fixation
  7. Evaluation of synkinesis
  8. Muscle localization for botox injections
  9. Help choose VC with worse neuromotor status for destructive procedures in bilateral VF palsy
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16
Q

What are common muscles tested in routine laryngeal EMG and their innervations?

A

Cricothyroid - SLN
Thyroarytenoid - RLN
Posterior cricoarytenoid - RLN

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17
Q

What are 3 different types of electrical activity seen on EMG?

A
  1. Insertional
  2. Spontaneous (fibrillation potentials or positive sharp waves = muscle irritability as it is denervating)
  3. Voluntary
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18
Q

In a patient with vocal fold immobility, what is the significance of the following findings on laryngeal EMG:
1. Normal
2. Fibrillation
3. Polyphasic potentials

A
  1. Normal - joint fixation
  2. Fibrillation - denervation (begins about 3 weeks)
  3. Polyphasic potentials (reinnervation and synkinesis - TA to PCA, or vise versa)
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19
Q

What are 3 elements of Laryngeal EMG analysis?

A
  1. Spontaneous activity - present or absent
  2. Recruitment - normal, reduced, or absent
  3. Motor unit morphology - normal/bi/triphasic, low amplitude, polyphasic, fibrillation
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20
Q

What are good prognostic laryngeal EMG findings?

A
  1. No spontaneous activity
  2. Some recruitment
  3. Normal/bi/triphasic or low amplitude polyphasic motor unit potentials
    - First sign of regeneration
    - Count the number of times the line crosses the baselines, >4 = abnormal polyphasic
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21
Q

What are poor prognostic laryngeal EMG findings? 5

A
  1. Presence of spontaneous activity
  2. No recruitment
  3. Fibrillation potentials
  4. Sharp waves
  5. Electrical silence
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22
Q

What is the optimal timing for laryngeal EMG?

A

Early use (< 3 months) has debatable prognostic benefit

4-6 months: Most helpful for prognostication of nerve injury recovery

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23
Q

Describe the classification of laryngeal EMG findings in laryngeal paralysis

A

CLASS I:
- Spontaneous activity: Absent
- Recruitment: Normal
- Motor unit morphology: Normal
- Interpretation: Normal

CLASS II:
- Spontaneous activity: Absent
- Recruitment: Reduced
- Motor unit morphology: Low-amplitude polyphasics
- Interpretation: Reinnervation

CLASS III:
- Spontaneous activity: Absent
- Recruitment: Reduced
- Motor unit morphology: Giant polyphasic units
- Interpretation: Old injury

CLASS IV:
- Spontaneous activity: Present
- Recruitment: Reduced
- Motor unit morphology: Polyphasic units
- Interpretation: Equivocal

CLASS V:
- Spontaneous activity: Present
- Recruitment: None
- Motor unit morphology: Fibrillations, positive sharp waves
- Interpretation: Denervation

Vancouver Pg 178

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24
Q

If on laryngeal exam you discover VF immobility but EMG shows normal voluntary electrical activity, discuss 3 possibilities

A
  1. Cricoarytenoid joint fixation (ankylosis)
  2. Fibrous scar formation
  3. Laryngeal synkinesis
  4. (or too early after injury)
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25
Q

List 6 different treatment options for unilateral vocal fold paralysis.

A
  1. Observation (chance of spontaneous recovery up to 12 months)
  2. Voice therapy
  3. Compensatory swallowing strategies if needed
  4. Injection laryngoplasty (percutaneous, transoral, laryngoscopy)
  5. Medialization thyroplasty (+/- arytenoid adduction)
  6. Laryngeal reinnervation (e.g. ansa to RLN, or hypoglossal transfer; neuromuscular pedicle - LCA/TA (tone) or PCA (improve airway))
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26
Q

What drug can be used in acute uniliateral vocal fold paralysis?

A

Nimodipine (calcium channel blocker that prevents vasospasm)
- Thought to reduce cellular apoptosis after neuronal injury and promote axonal sprouting at the nodes of Ranvier
- Meta-analysis showed increased odds of vocal fold motion recovery and facial motion recovery when used perioperatively

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27
Q

What are the 4 types of thyroplasty / classification of laryngeal framework procedures ? What is the name of this classification?

A

Isshiki Classification of Laryngeal Framework Surgery:
1. Type 1: Medialization thyroplasty
2. Type 2: Vocal fold lateralization (e.g. in BVFP, adductor SD)
3. Type 3: VF shortening/relaxing (ie. decreasing pitch)
4. Type 4: VF Lengthening/tensing (ie. increasing pitch, such as in M to F gender affirmation)

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28
Q

What are the indications for Type I Isshiki medialization thyroplasty? (5)

A
  1. Paralysis - glottic incompetence with dysphonia, poor cough, and aspiration
  2. Skull base surgery - high vagal paralysis
  3. Atrophy - presbyphonia
  4. Sulcus (difficult to treat)
  5. Scarring
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29
Q

What are the contraindications for Type I Isshiki medialization thyroplasty? (9)

A
  1. Immunodeficiency
  2. Coagulopathy
  3. Neoplasm
  4. Previous teflon
  5. Previous surgery or trauma (relative)
  6. Previous XRT
  7. Potential for recovery
  8. Poor contralateral abduction
  9. Poor pulmonary function

“I C Nadia Pee x 6”

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30
Q

What are 3 temporary and 5 permanent vocal fold implant material options

A

Temporary:
1. Hyaluronic acid (Restylane)
2. Carboxymethylcellulose (Prolaryn, Radiesse Voice Gel)
3. Calcium Hydroxyapatite (Prolaryn Plus, Radiesse Voice)

Permanent:
1. Silastic
2. Dense Hydroxylapatite (VoCoM = “Vocal cord Medialization” brand)
3. Gore-Tex
4. Teflon (no longer used due to granuloma formation)
5. Fat
6. Titanium
7. Prefabricated implamts (montgomy silicone implant)

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31
Q

How do you place your thyroid cartilage window for a Type 1 Thyroplasty?

A

7-5-3 Mnemonic:
7 = 7mm from midline in men
5 = 5mm from midline in women
3 = 3mm above the inferior border of the thyroid cartilage (parallel to border)
*Along a plane parallel to a line between the inferior border of the thyroid artilage and the upper notch of the inferior cornu
*At most up to midpoint of thyroid cartilage

Window size = 6 x 13mm
a. Hydroxylapatite (VoCoM) 6x10mm
b. Silastic (Montgomery) 6x13mm

Kevan Page 15
Ross Lecture

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32
Q

What are the Top 3 reasons for failure of TYpe I Isshiki medialization thyroplasty? What is most common? Can you name 3 others?

A
  1. Implant too high (most common)
  2. Implant too anterior
  3. Under-correction of the glottic gap posteriorly (consider arytenoid adduction with a posterior gap >4mm)

Others:
1. Extrusion of implant
2. Infection of implant
3. Hematoma

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33
Q

When is an arytenoid adduction typically performed and how does it work? List 5 physiologic effects that result from arytenoid adduction.

A

Performed in conjunction with medialization thyroplasty - suture from the muscular process of the arytenoid (do it anteriorly through the thyroplasty window)

Function:
- Traction on arytenoid at muscular process
- Mimics action of lateral cricoarytenoid (LCA)

Physiologic effects:
1. Lowers position of vocal process (decreases difference in height)
2. Medializes and stabilizes vocal process
3. Stiffens the vocal process
4. Lengthens vocal fold
5. Rotates arytenoid cartilage (decreases the abnormal rotation)

“LOWERS”
S: Stiffness
M: Medializes
A: Abnormal rotation decrease
L: Lengthens
L: Lowers

Vancouver 178

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34
Q

What are the indications for an arytenoid adduction? What are the contrainindications?

A

Indications:
1. Large posterior glottic gap (if not corrected with Type 1 thyroplasty, usually necessary if ≥4mm)
2. Lateralized vocal fold during phonation (jostle)
3. Vertical height mismatch
4. Severely shortened vocal fold
5. Inability to achieve good voice intra-operatively with thyroplasty alone

Contraindications:
1. Mobile vocal fold
2. Early vocal fold paralysis with chance of recovery
3. Limited abduction of contralateral vocal fold

35
Q

List 6 factors that may influence the choice of procedure or treatment for unilateral vocal fold paralysis, and how do they do so?

A

ACCCED
Aspiration, cause, compensation, comorbidities, emg results, Demands

Presence of clinical aspiration
- Favours early surgical intervention

  1. Nature of nerve injury (transection, stretch, or unknown)
    - Nerve cut: favours early treatment
    - Intact or stretch: favours observation or temporizing injection laryngoplasty
  2. Vocal demands of patient
    - Non-vocal professional or limited voice favours observation
  3. Medical comorbidity
    - Comorbid favours procedures with local anesthetic
  4. Laryngeal EMG findings
    - Good prognosis: Favours observation or temporizing
    - Poor prognosis: Favours early medialization laryngoplasty or permanent injection
  5. Compensation (what is the status of the contralateral VF?)
    - Poor contralateral abduction = poor medialization candidate
36
Q

List 8 complications of type 1 thyroplasty

A
  1. Bleeding (including hematoma)
  2. Infection
  3. General Anesthesia
  4. Airway obstruction
  5. Implant extrusion
  6. Inadequate medialization
  7. Height mismatch
  8. Granuloma formation
37
Q

List 7 complications of vocal fold medialization injections

A
  1. Under injection - requires multiple procedures
  2. Over injection - airway compromise
  3. Improper placement
  4. Migration of injection material
  5. Intrachordal injection - impairs vibratory ability
  6. Granuloma formation (polytef)
  7. Persistent edema
38
Q

What materials can be used for injection thyroplasty, and how long do they last? List 7 materials

A

VERY SHORT LASTING:
1. Gelfoam (4-6 weeks) - saline resorption so over inject ~30%
2. Radiesse voice gel = Average 1-2 months - carrier gel from Radiesse without calcium hydroxyapatite

INTERMEDIATE LASTING:
1. Alloderm (2-4 months) - acellular dermis, no allergy testing needed, expensive
2. Bovine collagen (Zyplast) - 4-6 months, risk of host reaction - must get allergy testing first
3. Hyaluronic acid (e.g. Restylane, Juvederm, Perlane) - 6-10 months, no antigenic properties
4. Carboxymethylcellulose (Prolaryn) - 3-6 omnths

LONG ACTING:
1. Calcium Hydroxyapatite (Prolaryn Plus/Radiesse Voice) = 12-18 months (some say 2+ years)
2. Fat (≥ 6 months) - 50% resorption so over inject by 40%, morbidity of harvest site
3. Polytef - Teflon (permanent) if no recovery expected; discontinued due to granuloma formation, irreversibility, risks of migration, stiffening of mucosal wave

39
Q

List 5 approaches for injection thyroplasty

A
  1. Transoral
  2. Transnasal (with working channel scope)
  3. Percutaneous/Trans-cervical:
    a/ Thyrohyoid membrane
    b/ Trans-thyroid cartilaginous
    c/ Cricothyroid membrane
40
Q

What are general tips for injection laryngoplasty - where do you inject and how deep? Where should you avoid injecting?

A
  1. Inject laterally, lateral to the vocal ligament, into vocalis muscle, approximately 3-5mm deep (goal is to push vocalis muscle belly medially)
  2. Inject near the vocal process, at the junction between the posterior 1/3 of the VF and anterior 2/3

Percutaneous injection technique:
1. Aim needle 30 degrees for females and 45% for males

Avoid injecting into:
1. The anterior 1/3 of the VF (will result in strained voice)
2. Submucosal/SLP injection (will impair mucosal wave and worsen voice)

Vancouver Page 180

41
Q

What are 6 contraindications to injection thyroplasty (especially awake ambulatory approach)?

A
  1. Bilateral vocal fold paralysis (will worsen airway), or any other reason for tenuous airway
  2. Anticoagulated (relative contraindication)
  3. Infection over injection site
  4. Difficult to appreciate landmarks
  5. Uncooperative patient
  6. Allergy to injection material

U BADIA

Uncooperative
Bilateral VFP or tenuous airway concern
Anticoagulation
Difficult anatomy
Infection over injection site
Allergy to components

42
Q

Why has teflon fallen out of favour for thyroplasty?

A

Teflon Granuloma

43
Q

When doing a RLN reinnervation procedure, what is the median time to first sign of successful re-implantation? Within what time frame between nerve injury to repair are better outcomes seen? What population is the procedure less successful in?

A

Often an initial improvement can be seen as early as 3-4 months following surgery. Improvement, however can continue for several years

Better outcomes if performed within 2 years of nerve injury.

Less successful in elderly patients.

44
Q

List a differential diagnosis of bilateral vocal fold immobility

A
  1. Iatrogenic
  2. Malignancy
  3. Neurologic
  4. Endotracheal intubation
  5. Idiopathic/infectious

Note: Important to differentiate bilateral VC paralysis from posterior glottic stenosis

45
Q

What are 8 treatment options for bilateral vocal fold paralysis? What are 2 experimental treatment options? What are the indications for each, pros, and cons?

A
  1. Tracheostomy
    - Indications: acute dyspnea, temporary management of BVFP
    - Pros: Immediate airway obstruction relief, improvement in ventilation, no revisions required
    - Cons: Destructive of normal tissue, psychosocial impairment, scar, decreased QOL and trach care
  2. Arytenoidectomy
    - Methods: Endolaryngeal, extralaryngeal (E.g. woodman lateral approach, anterior thyrotomy approach)
    - Indications: Permanant management, to avoid decannulation or tracheostomy
    - Pros: Quick, no dyscosmesis, can be combined with cordotomy, more cost-effective than trach
    - Cons: Irreversible, worse voice, scar or granuloma, aspiration, possible need for revision
  3. Cordotomy or Cordectomy
    - Laser cordotomy = transverse cut between vocal process and vocal fold
    - Indications: Permanant management, to avoid decannulation or tracheostomy
    - Pros: same as arytenoidectomy, but also less tendency for aspiration than arytenoidectomy
    - Cons: same as arytenoidectomy
  4. Isshiki Type 2 Thyroplasty (lateralization thyroplasty)
    - Indications: Temporary with expectation of recovery of laryngeal function
    - Pros: Reversible, better voice quality, less revision rate than the above, can be performed endoscopically
    - Cons: Dysphonia, need for adjustment, repeat procedures, dysphagia or aspiration
  5. Suture lateralization
  6. Laryngotracheoplasty
  7. Arytenoid abduction
    - PLicating vocal process to external laryngeal framework (Woodman lateral approach, or anterior thyrotomy approach)
  8. Laryngeal reinnervation (e.g. phrenic/neuromuscular pedicle transposition to PCA)
    - Indications: Non-atrophic viable muscles maintained through synkinetic reinnervation

Experimental:
1. Laryngeal pacing
- Indications: Non-atrophic viable muscles maintained through synkinetic reinnervation
- Pros: Greater ventilatory improvement, no compromise of voice or swallowing
- Cons: 2 human trials, complicated procedure, expensive, device has to be replaced 5-10 years

  1. Stem cell therapy
    - Indications: BVFP caused by neurodegenerative diseases
    - Pros: Could promote nerve regeneration and prevent muscle atrophy
    - Cons: Experimental, no human trial, not effective in preventing synkinesis, issues associated with isolation/culture and survival of stem cells
  2. Gene therapy:
    - Indications: BVFP caused by neurodegenerative diseases
    - Pros: Less invasive, could promote nerve regeneration and prevent muscle atrophy
    - Cons: experimental, no human trials, not effective in preventing synkinesis, neuronal damage by viral vectors
  3. Neuromodulation:
    - Indications: Recently injured RLN, muscles still denervated and nerve regenerating prior to synkinetic reinnervation
    - Pros: Canine studies, electrical neuromuscular conditioning promotes selective reinnervation of muscles, minimizes synkinesis and restores ventilation to normal
    - Cons: Experimental, no human trials
  4. Botox injection
    - Indications: Temporary management of synkinetic larynx
    - Pros: Less invasive, short term for improving ventilation, little effect on voice/swallowing
    - Cons: Repeated injections required, human trials limited

Vancouver pg 180

46
Q

What are four open approaches to the larynx?

A
  1. Laryngofissure
  2. Transthyrohyoid membrane
  3. Minithyrotomy - a term used any time a window is taken out of the cartilage, or a partial incision into the cartilage is made
  4. Woodman procedure - approaching the larynx around the thyroid ala cartilage (from behind) - initially designed to assist with arytenoidectomy for bilateral VC paralysis - see Ross lecture 2023

https://pubmed.ncbi.nlm.nih.gov/23119426/#:~:text=Woodman’s%20External%20Arytenoidectomy%20technique%20is,limited%20exposure%20of%20arytenoid%20cartilage.

47
Q

What are 3 airway protection mechanisms?

A
  1. Swallowing mechanism
  2. Laryngeal sphincters
  3. Cough reflex/mucociliary clearance (FVC is the main contributor to increased airway pressure in cough)
48
Q

Discuss 5 factors that increase risk of aspiration in the aging adult

A
  1. Increased oral transit time
  2. Increase time to trigger the pharyngeal phase
  3. Decreased laryngeal elevation
  4. Increased laryngeal penetrance but no true aspiration
  5. Glottic gap (spindle closure pattern)
49
Q

Describe the cough reflex pathway

A
  1. Receptors: Larynx and carina and all respiratory epithelium
  2. Afferents to medulla cough centre - via CNX and lesser from V and IX
  3. Efferents: Phrenic to diaphragm, spinal motor in intercostals
50
Q

List a complete differential for chronic cough

A
  1. Environmental - smoke, pollutants, alelrgens
  2. Inflammatory - pharyngitis, laryngitis, rhinitis, PND (paroxysmal noctural dyspnea), PNA, GERD
  3. Neoplastic - any upper or lower airway
  4. Cough variant asthma
  5. Central (physiologic)
  6. Drugs - ACEi, Sitagliptin
  7. Peripheral - stimulation from ear, pleura, pericardium, stomach
51
Q

What is the definition of acute vs. chronic cough?

A
  • Acute < 3 weeks
  • Chronic > 8 weeks
52
Q

What are the top 5 most common causes of chronic cough?

A
  1. CRS/rhinitis (25-50%)
  2. Asthma/Allergy (15-40%)
  3. GERD (5-40%)
  4. Upper airway cough syndrome
  5. ACEi
53
Q

What is the mechanism of action of chronic cough? 2

A
  1. Peripheral sensitization - increased peripheral nerve excitability
  2. Central - increased midbrain activity, decreased control over afferent descending processes
54
Q

What are 3 different treatment options for non-responders after treating underlying cause of cough?

A
  • > 80%
  1. Suppressants:
    - Central: Codeine
    - Peripheral: Topical anesthetics (lidocaine)
  2. Expectorants:
    - Promote drainage of respiratory secretions (Guaifenesin)
  3. Mucolytics (e.g. Guaifenesin - decrease viscosity)
55
Q

What is the medical management of chronic cough? 8

A
  1. Lifestyle modifications is the primary treatment
  2. SLP (cough suppression therapy)
  3. Gabapentin (CHEST guidelines recommend 300mg PO OD to start, up to 1800mg divided BID) - first line
  4. Amitriptyline
  5. Treat GERD if present but do not treat if no signs or symptoms present
  6. Morphine
  7. Baclofen
  8. Tramadol
56
Q

What are the anatomic/mucosal defenses against reflux? List 5.

A
  1. Upper esophageal sphincter
  2. Lower esophageal sphincter
  3. Esophageal peristalsis
  4. Esophageal buffers (salivary bicarbonate)
  5. Esophageal mucous secretions (prevents reflux from penetrating epithelium)
57
Q

What are the 3 stages of gastric acid production in the stomach? What does the intragastric pH generally range from?

A

Intragastric pH range from 1-3

CGI:

  1. Cephalic Phase:
    - 30% of gastric acid secretions
    - Stimulated by anticipation of eating and smell/taste of food
  2. Gastric Phase:
    - 60% of gastric acid secretions
    - Stimulated by stomach distension and by proteins produced by digestion
  3. Intestinal Phase:
    - 10% of gastric acid secretions
    - Triggered by small intestine distension once chyme enters
58
Q

What is the Belafsky Reflux Symptom Index (RSI)?
How many questions, what is the score out of?
What score suggests reflux?
What are the domains of questions?

A
  • Most widely used clinical validated QOL instrument related to LPR
  • 9 questions, scored out of 0-5, total out of 45
  • Score > 13 suggests the presence of laryngopharyngeal reflux

Within the last month, how did the following problems affect you? 0 = No problem, 5 = Severe problem
1. Hoarseness or a problem with your voice
2. Clearing your throat
3. Excess throat mucous or postnasal drip
4. Difficulty swallowing food, liquids, or pills
5. Coughing after you ate or after lying down
6. Breathing difficulties or choking episodes
7. Troublesome or annoying cough
8. Sensations of something sticking in your throat or a lump in your throat
9. Heartburn, chest pain, indigestion, or stomach acid coming up

“HE BELCHED”
Hoarseness
Excess mucous
Breathing difficulty
Excess throat clearing
Lying down cough
Cough (annoying/troublesome)
Heartburn
Excess sensations of something sticking
Dysphagia

59
Q

What is the Belafsky Reflux Finding Score (RFS)?
8 features of the score
What score suggests LPR? What is the maximum score?

A
  • Validated endoscopic checklist for features of LPR

8 Features on the RFS:
1. Subglottic edema (0 absent; +2 present)
2. Thick endolaryngeal mucous (0 absent; +2 if present)
3. Granuloma/Granulation tissue (0 absent; +2 if present)
4. Ventricular obliteration (+2 if partial, +4 if complete)
5. Posterior commissure hypertrophy (+1 mild, +2 moderate, +3 severe, +4 obstructing)
6. Vocal fold edema (+1 mild, +2 moderate, +3 severe, +4 polypoid)
7. Diffuse laryngeal edema (+1 mild, +2 moderate, +3 severe, +4 obstructing)
8. Erythema/hyperemia

Maximum score = 26
A score of >7 suggests LPR

“EPIGLOTTis”
Erythema
Posterior commissure hypertrophy
Infraglottic/subglottic edema
Granuloma
Laryngeal edema
Obliteration of ventricles
True vocal fold edema
Thick endolaryngeal mucous

Kevan Page 32

60
Q

What are ways (anatomically and physiologically) that the body protects itself from GERD? 8

A
  1. LES closed at rest
  2. UES closed at rest
  3. Esophageal peristalsis
  4. Esophageal mucous
  5. Carbonic anhydrase isoenzyme 3
  6. Laryngeal adductor reflex
  7. Metaplasia to stratified squamous epithelium
  8. Gravity
61
Q

What are 5 risk factors for globus sensation?

A
  1. Hiatal hernia
  2. EtOH
  3. Tobacco
  4. Asthma (50% have GERD)
  5. OSA

OH TEA

62
Q

What are 4 theories of the pathophysiology of globus sensation?

A
  1. Direct inflammation of laryngopharynx by acid, pepsin (produced by chief cells) and digestive enzymes
  2. Vasovagal reflex hypertonicity of cricopharyngeus triggered by acidification or distention of the distal esophagus
  3. Upper esophageal sphincter functional abnormality and esophageal dysmotility
  4. Micro-aspiration
63
Q

What are 5 risk factors for globus sensation?

A
  1. Hiatal hernia
  2. EtOH
  3. Tobacco
  4. Asthma (50% have GERD)
  5. OSA
64
Q

What are some conditions that are associated from laryngopharyngeal reflux? What is the most common? Name 10

A
  1. Laryngotracheal stenosis (SGS most common association - 92%)
  2. Laryngomalacia
  3. Laryngospasm/cough/asthma/recurrent croup/SIDS
  4. Vocal fold nodules
  5. Vocal fold polyps
  6. Otitis media
  7. Vocal process (contact) ulcers/granulation/granulomas
  8. Carcinoma
  9. Chronic laryngitis/mucosal thickening/pachyderma laryngitis
  10. Dental caries and erosion
  11. Barrett’s esophagus
  12. Esophageal ulcers
  13. Increasing age - increased abdominal volume, lax sphincters
65
Q

What are the 8 endoscopic findings of laryngopharyngeal reflux?

A

Mnemonic - Think anatomically + GEM
OR use the EPIGLOTTis mnemonic for the reflux finding score

  1. (Entire) Diffuse laryngeal edema
  2. (Supraglottis + Hypopharynx) Posterior commissure hypertrophy
  3. (Between supraglottis and glottis) Ventricular obliteration
  4. (Glottis) Vocal fold edema
  5. (Subglottis) Subglottic edema - can result in pseudosulcus
  6. (G) Granulation/granuloma
  7. (E) Erythema/hyperemia - cobblestoning
  8. (M) Mucous/thick endolaryngeal mucous
66
Q

What are the indications for further testing for patients with GERD? 4
What would this further testing include?

A
  1. Recurrent symptoms
  2. Poor response to treatment (Still symptomatic after 3 months of empiric treatment)
  3. Atypical symptoms - cough, asthma
  4. Weight loss or dysphagia

Generally further testing may include 24 hour double probe pH monitoring or MII-pH testing

67
Q

Discuss the diagnostic methods for LPR - 6

A
  1. Scope
  2. 24 hours pH probe / MII-pH probe
  3. Esophageal manometry
  4. Acidification test
  5. Barium swallow
  6. BAL for lipid-laden macrophages (=aspiration)
68
Q

What is the gold standard investigations for GERD?

A

Dual probe ambulatory 24 hour pH monitoring

  • MII-pH monitoring may supplant this in the future (multichannel intraluminal impedence monitoring)
69
Q

Discuss 6 investigations for reflux. What/when are they used for, what do they measure, and how is it done?

A
  1. Esophagoscopy ± Biopsy
    - Rule out pathology that may mimic LPR
    - Identify reflux associated pathology (e.g. Barrett’s)
  2. Ambulatory 24hour pH monitoring
    - Single probe = esophageal probe (at distal LES)
    - Dual probe = esophageal (distal LES) and pharyngeal (cricopharyngeus) probe
    - Coated wire is placed transnasally after calibration to the desired levels in the esophagus
    - General probe locations (for 3 probe): (1) Distal probe ~5cm above LES, (2) Proximal probe ~20cm above LES (just below UES), and (3) pharynx
  3. Multichannel Intralumiinal Impedence pH monitoring
    - aka. MII-pH monitoring
    - Combination of a pH probe with an impedence monitor
    - Both the content (acid, weakly acidic, non acidic) and direction (anterograde and retrograde) can be identified
    - Impedence system with multiple impedence electrodes along the length of the catheter.
    – Gas has a high impedence
    – Mucosa has lower impedence
    – Liquids like saliva or reflux has lowest impedence. Multiple probes allows for direction of impedence delta to be ascertained (anterograde = swallow, retrograde = reflux)
  4. Barium Swallow, MBS/VFSS
    - Not as sensitive as pH probe monitoring (25-33% sensitive)
  5. Sputum Pepsin Testing
    - Pepsinogen is synthesized only by the chief cells of the gastric fundus and is converted to pepsin in the acidic environment of the stomach
    - Specific to refluxate
    - Not commercially available at present
  6. Esophageal Manometry
    - Measures intraluminal pressures and coordination at 3 functional regions: LES, Esophageal body, UES; with pressure inducers 5cm apart
    - Mainly used in the diagnosis of motility disorders
    - Also used to rule out esophageal peristalsis prior to anti-reflux surgery
    - Involves a catheter placed into the esophagus that measures esophageal contractions
  7. Lipid Laden Macrophage test - Bronchoalveolar lavage
  8. Radionuclide T-99 Reflux scan (pediatrics)
  9. Acidification Tests
    - Rarely used
    - Bernstein Test: Instills NS for 15 minutes via NGT, then 0.1M HCI @ 6cc/min until symptomatic or for 45 minutes
    - Tuttle test in children is similar, uses age-dependent HCl instillation, pH < 3 x 2 occasions is positive
70
Q

How is 24 hour pH monitor results interpreted?
What is considered a reflux event?
What are the 6 components to the Demeester score?

A

Reflux event = pH < 4

Distal esophageal events:
- Reflux events are scored based on positioning and number of episodes
- This results in a Johnson-Demeester Score
- A Demeester score of >14.72 is considered abnormal (special calculation) – ONLY EVALUATES DISTAL ESOPHAGEAL PROBE

Scoring System (Demeester Score):
1. % total time pH < 4
2. % upright time pH < 4
3. % Percent Supine time pH < 4
4. Number of reflux episodes
5. Number of reflux episodes ≥ 5 min
6. Longest reflux episode (15 minutes)

Pharyngeal Events:
- No similar scoring system
- Some consider any reflux episode to be pathologic
- Others suggest a pH of <4 of >0.1% of the study as a threshold

71
Q

What is defined as a reflux episode on pH monitoring?
Differentiate the difference between distal and proximal esophagus, and hypopharynx

A

Reflux episode = pH < 4

Distal esophagus:
- pH < 4 for >4% of the time is abnormal on 24 hour esophageal pH monitoring
- Demeester score > 14.72

Proximal Esophagus:
- pH < 4 for >1% of the time is abnormal

Hypopharynx:
- ANY reflux event (pH < 4) over 24 hours (in the hypopharynx) is sufficient for the diagnosis of LPR in the hypopharynx
- Some suggest pH < 4 for >0.1% of test as threshold

72
Q

Describe the principle behind impedance monitoring

A
  • Small current through two electrodes within a probe
  • Bolus passes by the probe –> decreased impendence (= decreased resistance) between the electrodes = bolus detected
  • Having several impedance probes along the esophagus allows to determine the direction of movement

Anterograde = bolus
Retrograde = reflux

73
Q

What are 3 advantages of multichannel intraluminal impedence pH monitoring, over manometry and dual pH probe?

A
  1. Can identify non-acid reflux
  2. Can identify anterograde and retrograde flow
  3. Compared to manometry, provides information on the functional component of manometrically detected contracts (ie. bolus transit) - Manometry cannot detect passage of bolus, just changes in pressure (similar to anterograde/retrograde point)
74
Q

What is normal esophageal UES and LES tone pressure?

A

UES = 12-24mmHg (up to 100?)
LES = 40 mmHg

75
Q

Discuss treatment options for reflux.
List at least 8 conservative non-medical options

A

Lifestyle Changes:
1. Weight loss
2. Reduce meal size
3. Reduce caffeine and alcohol intake
4. Reduce intake of spicy foods and chocolate - elimination diet
5. Avoid eating before bedtime (3 hours)
6. Avoid lying flat within 3 hours of a meal
7. Stop smoking
8. Avoid tight-fitting clothing
9. Elevate head of bed

76
Q

For reflux
List 7 medical options
List one surgical option.

A

Medical Management:
1. Proton Pump inhibitors (e.g. Pantoprazole)
2. H2 receptor antagoniists (e.g. famotidine, ranitidine)
3. Bicarbonate gum
4. Sodium/Calcium bicarbonate buffers (tums)
5. Cytoprotectants (e.g. Sucralfate - reacts with Hcl to form a cross-linking viscous material that acts as a mechanical acid buffer)
6. Alginate (e.g. Gaviscon Advance - sodium alginate from seaweed)
7. Prokinetics (e.g. Maxeran/Metoclopramide - fallen out of favour due to cardiac arrhythmias and side effect profile)

Surgical management:
1. Fundoplication (most common = laparoscopic NIssen fundoplication)

77
Q

How do you prescribe and taper PPIs?

A

AAO = BID PPI for no less than 6 months “for most patients with LPR”
- Optimal effect takes place 30-60mins before meals; max activation (70%) of proton pumps occur at breakfast

Indications to Taper:
- If patient develops symptomatic benefit, begin taper at 6 months.
- If no benefit, begin taper at 3 months
- Failure = gastric pH < 4 for >85%, non-acid reflux, or non-compliance

TAPER PROTOCOL:
1. PPI daily in AM x 8 weeks
2. PPI once every other morning x 8 weeks
3. If symptoms still controlled, then discontinue

78
Q

What if medical therapy for GERD does not work or only partial response? List 5 options

A

Considerations:
- Consider increasing dose of PPI
- Consider supplemental H2RAs once daily at bedtime to help reduce overnight production, or other therapies (e.g. alginate)
- Assess patient compliance to medication
- Consider other conditions that manifest with similar symptoms: EtOH, asthma, smoking, allergy, voice abuse
- pH probe monitoring/endoscopy/GI referral

79
Q

Discuss 2 reasons for PPI failure in laryngopharyngeal reflux

A
  1. Poor patient compliance
  2. Non-acid reflux (some bile salts and pepsin remain stable at non-acidic pH and are thought to contribute to non-acid reflux)
80
Q

What is the surgical treatment for LPR?
List 2

A
  1. Nissen fundoplication is the last resort
    - Encircling the esophagus with the gastric fundus to tighten the LES
    - 75% improvement in symptoms for patients with LPR
  2. Linx (bariatric banding) or Stretta procedure (radiofrequency ablation os LES) can be considered

Nissen fundoplication: https://www.mayoclinic.org/-/media/kcms/gbs/patient-consumer/images/2013/08/26/10/24/ds00967_hq00312_im03999_mcdc7_fundoplicationthu_jpg.jpg

81
Q

Discuss 10 potential risks and side effects of PPIs

A
  1. GI - bloating, constipation, diarrhea
  2. Pneumonia (due to alteration of bacterial flora)
  3. Increased risk of C. Difficile infection (enteric infections and microscopic colitis that can occur in absence of antibiotic use)
  4. Renal: Chronic kidney disease, acute interstitial nephritis
  5. Drug interactions (Decreases activity of clopidogrel)
  6. ??Possible association with early onset dementia (controversial)

Mineral Malabsorption:
2. B12 malabsorption
3. Calcium malabsorption (Ca needs acid to dissolve; increased risk of bone fracture, osteoporosis) - supplement with calcium citrate
4. Magnesium malabsorption
5. Iron malabsorption

82
Q

What are 4 vitamins/minerals that are likely to be deficient in patients taking long-term PPIs?

A
  1. Calcium
  2. Magnesium
  3. Iron
  4. B12
83
Q

How does reflux cause extra-esophageal pathology? List 3 theories

A
  1. Microaspiration theory: Direct contact of pepsin and acid to the epithelium
  2. Trauma theory: Exposure of the laryngeal epithelium itself to acid/pepsin is not sufficient. Another factor, such as vocal abuse or concomitant viral infection, is needed to induce mucosal injury
  3. Esophageal-Bronchial reflex theory: Acid in the distal esophagus stimulates vagally mediated refluxes that causes chronic cough, which then causes laryngeal symptoms and lesions

Laryngology (8 decks)

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