ENT JC098: Dysphonia: Laryngitis, Voice Abuse, Tumour And Laryngeal Cancer Flashcards

1
Q

Dysphonia, Aphonia, Hoarseness

A

Dysphonia:
- Any impairment of voice

Aphonia:
- Total loss of voice

Hoarseness:
- Rough / Noisy quality of noise

***Voice disorder (Dysphonia) =/= Speech disorder (Fluency disorder (e.g. stuttering) / Dysarthria (articulation problem))

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2
Q

Physiology of Speech

A

5 steps:
1. Airflow generator (Breath support)
- Lungs
- Intercostal muscles
- Diaphragm

  1. Voice production (Vibrator) —> Problem: Voice disorder (Dysphonia)
    - True vocal cords
  2. Resonance (Upper airway) —> Problem: Dysarthria
    - Nasal cavity, sinuses
    - Pharynx
    - Oral cavity
  3. Articulation —> Problem: Dysarthria
    - Tongue
    - Teeth
    - Jaw movement
  4. Speech
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3
Q

Conversion of airflow into sound waves

A

Vocal cord (5 layers):
1. Epithelium

  1. ***Superficial lamina propria / Reinke’s space (transparent gel-like, pliability of VF)
    - provide soft floating layer to support epithelium
    - sound wave can generate on epithelium
  2. Intermediate lamina propria
    - progressive ↑ in consistency
    - elastic rubber band texture
  3. Deep lamina propria
    - collagen layer
  4. Vocalis muscle

Glottic cycle (transform kinetic energy of airflow into sound waves):
Cyclical closure of vocal cord
—> Build up of subglottic pressure
—> Cyclical puffs of air
—> Bernoulli’s effect of exhaled airstream (air pressure between cords ↓ suddenly due to high air velocity)
—> Suck vocal cords together
—> Sound waves

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4
Q

***Causes of Dysphonia

A
  1. Organic (e.g. anatomical change in vocal cord)
    - Poor breathing support
    - Neurological
    - Local vocal cord pathologies
  2. Functional (e.g. muscle tension dysphonia)
  3. Psychogenic (e.g. conversion disorder)
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5
Q
  1. Organic causes of Dysphonia
A
  1. Poor breathing support
    - Poor respiratory condition (e.g. asthma, COPD)
    - Poor coordination (between voice and breath)
  2. Neurological
    - Central (e.g. Parkinsonism)
    - Peripheral (e.g. RLN palsy (***Vocal cord palsy), SLN palsy)
  3. Local vocal cord pathologies
    - Benign
    —> Acute laryngitis
    —> **Vocal cord nodules
    —> **
    Vocal cord polyp
    —> **Reinke’s edema
    —> **
    Recurrent respiratory papillomatosis
  • Malignant (Cancer of larynx)
    —> ***SCC
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6
Q

***Causes of Speech disorders

A

Organic
- Upper airway problem (Resonance)
1. Oropharynx (e.g. Tonsillar hypertrophy: “hot potato” voice)
2. Hyponasality (inadequate airflow through nose during speech)
3. Hypernasality (excessive airflow through nose during speech e.g. cleft palate)

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7
Q

Vocal cord palsy

A

Causes:
1. Idiopathic (e.g. infection of RLN)

  1. Brainstem lesion (RLN is from CN10 which is from brainstem)
  2. Pathology along ***RLN
    - e.g. CA thyroid, esophagus, lung, Ortner’s syndrome (big left atrium —> compress on RLN)
  3. Pathology involving ***Arytenocricoid joint
    - e.g. dislocation after intubation, RA (∵ AC joint a synovial joint), cancer infiltration from larynx / hypopharynx
  4. Iatrogenic (most common)
    - nerve damaged during surgery (HN, thyroid, esophageal, cardiac, thoracic surgery)

Treatment:
1. Unilateral VC palsy
- Voice therapy (strengthen normal VC to push against paralysed VC)
- **Injection laryngoplasty (make paralysed VC more bulky, usually temporary, for VC that have potential to recover later)
- **
Medialisation thyroplasty (permanent, place a piece of synthetic material to push paralysed VC to midline)

  1. Bilateral VC palsy
    - ***Tracheostomy as airway protection
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8
Q

Vocal cord nodule***s

A

Always come in **pairs (∵ VC hitting each other too much e.g. overuse of voice ~ callus in hand)
- Bilateral + Symmetrical
- Junction of **
Anterior + Middle 1/3 of vocal folds (only anterior / middle 1/3 is membranous (soft + vibrating + hitting each other), posterior 1/3 is Arytenoid cartilage)

Cause:
- Chronic vocal trauma —> **Localised edema (reversible) —> **Fibrosis (irreversible) —> Nodules

S/S:
- ***Breathy voice (nodules preventing complete closure of VC)

Treatment:
- ***Speech therapy +/- Excision (will recur if no speech therapy)

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9
Q

Vocal polyp

A

***Unilateral protrusion (vs nodules)

Cause:
- **Acute vocal trauma —> Burst of capillaries —> **Haemorrhagic cyst (red in colour) —> Fibrosis —> Polyp (pale in colour)

S/S:
- Breathy voice

Treatment:
- Excision

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10
Q

Reinke’s edema

A

Fluid collection in Reinke’s space (i.e. Superficial lamina propria) (~2 bags of water)

Causes:
1. ***Smoking (Smokers’ voice)
2. Laryngeal reflux
3. Hypothyroidism

S/S:
- **Effortful (need great exhalation effort to build up subglottic pressure)
- **
Low-pitch (∵ VC cannot vibrate very fast)
- Rough

Treatment:
- Correct underlying causes (e.g. stop smoking) + Excision (~ liposuction of arm)

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11
Q

Recurrent respiratory papillomatosis (RRP)

A
  • Cauliflower disease of VC
  • ***HPV 6, 11 infection
    —> In-utero transfer, Birth tract contact (Children)
    —> Oral sex (Adult)

S/S:
- Hoarseness
- **Airway obstruction
- **
Malignant transformation (CA larynx)
- Tracheobronchial spread

Treatment:
- Chance of spontaneous regression upon puberty
- Surgical debulking +/- Adjuvant medical therapy (e.g. IFN, Chemotherapy —> not very effective)
—> ***NO complete cure (∵ HPV DNA embedded everywhere in larynx)

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12
Q

Neoplastic lesions of Vocal cord

A
  1. Leukoplakia
    - whitish plaque (local thickening of epithelium due to water absorption) —> ↑ risk of malignancy (5-15%)
  2. Erythroplakia
    - reddish plaque (local thickening + attracting blood vessels to bring in blood supply) —> ***high risk of malignancy

BOTH need ***Biopsy!!!

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13
Q

Cancer of Larynx

A

Risk factors: Smoking

Commonest pathology: ***SCC

S/S:
- **Hoarseness (VC no longer flat —> cannot close completely + **Bulky / Stiff VC)
- Airway obstruction
- Cervical LN metastasis

Treatment:
Early stage
1. **RT
2. **
Surgery: Laser excision, Partial laryngectomy

Advanced stage (Multimodal treatment)
1. Surgery: Total laryngectomy
2. Adjuvant RT + Chemotherapy (to control LN metastasis)

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14
Q

***Approach to Hoarseness

A

History taking:
1. Smoking

  1. Onset / Pattern of Hoarseness
    - Acute / Chronic
    - Episodic / Progressive
  2. Occupation / Vocal demand
  3. ***Red flag symptoms for CA larynx
    - Bleeding (blood-stained sputum / saliva)
    - SOB
    - Dysphagia
  4. ANY hoarseness ***>2 weeks —> refer ENT for examination!!!

P/E, Investigations:
1. Cervical lymphadenopathy

  1. Inspection of larynx
    - Indirect laryngoscopy (vision through reflected light by dental mirror —> difficult ∵ gag reflex)
    - **Flexible laryngoscopy
    - **
    Rigid laryngoscopy with Stroboscopy
    (Direct laryngoscopy: not for clinical examination, direct vision without reflection, only for intubation / foreign body removal)
  2. TNM staging
    - T: Local tumour stage (Endoscopy, CT / MRI to see infiltration)
    - N: Regional LN (USG neck + FNAC to determine whether lymphocyte / carcinoma cells)
    - M: Distant metastasis (CXR, Blood test, PET)
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15
Q

Flexible / Rigid laryngoscopy + Stroboscopy

A
  1. Trans-nasal flexible endoscope
    - advantage: Less gag reflex (∵ no need to go through mouth)
    - disadvantage: Inferior quality of vision (∵ limited diameter of scope —> carrying less light)
  2. Trans-oral rigid
    - advantage: Allow use of stroboscope, Better quality of image (∵ larger diameter to carry more light)
    - disadvantage: Gag reflex issue

Stroboscopy:
- Voice of patient picked up by microphone —> determine **fundamental frequency (i.e. vibrating frequency of vocal cord)
- Light source emitting at / near fundamental frequency of voice (閃閃下)
—> Generate **
Illusion of slow motion of VC vibration
—> Detect subtle VC lesions

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16
Q

Approaches to HNSCC

A

Investigations:
1. Flexible endoscopy + Biopsy
- assess **extent of tumour
- biopsy for **
histological diagnosis

  1. Upper **panendoscopy (bronchoscopy + esophagoscopy)
    - detect **
    synchronous lesions (i.e. >=2 cancers at the same time) in upper aerodigestive tract
    - nasopharynx, oropharynx, hypopharynx, larynx (down to level of main bronchus + carina), esophagus (down to EGJ level)
    - risk of synchronous cancer: 8-10%
    - ***field change effect (large areas of cells at a tissue surface or within an organ are affected by carcinogenic alterations)
  2. USG neck +/- FNAC
    - 30% subclinical cervical lymphadenopathy (i.e. cannot be palpated)
  3. CT / MRI neck with contrast
    - assess extent of tumour
17
Q

Voice rehabilitation after Total laryngectomy

A
  • Mouth only connects to Esophagus only
  • Larynx removed —> no vibrator to convert airflow into sound
  • Airway not connected to mouth / nose —> no articulation
  1. Electrolarynx
    - easy to use
    - unnatural robotic sound
  2. Pneumatic device (“Taiwan” tube)
    - requires greater manual dexterity + coordination
    - rubber band within tube (mimic vocal cord) —> air go through —> vibrate
    - able to articulate (alter vibration from pneumatic device)
    - need to cover tracheostome fully to prevent air leak
  3. Tracheo-esophageal speech
    - good intelligibility
    - no extra devices needed (an indwelling device (NOT a vibrator) already connecting esophagus and trachea —> esophagus vibrate to make sounds ~burp)
    - requires ***greatest manual dexterity + coordination
    - one-way valve device may become dirty / infected with time —> need to clean by patients using a brush
  4. Esophageal speech
    - very difficult to learn
    - need to swallow air in esophagus —> release air back out in a controlled fashion