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BENIGN VOCAL FOLD DISORDERS
M I G U E L G . W A G N E R
R 1 E N T
H U S E 2 0 1 8
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ANATOMY
• LARYNGEAL CARTILAGINOUS
STRUCTURE:
– Unpaired cartilages:
• Thyroid, cricoid, and epiglottic
– Paired cartilages:
• Arytenoid, corniculate and
cuneiform
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ANATOMY
• INTRINSIC MUSCLES
– Responsible for vocal fold motion
– 3 types
• Abductor, adductors, and tensor
➢Abductor
– Posterior cricoarytenoid
• Responsible for glottic airway
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ANATOMY
➢Adductors
– Thyroarytenoid
• Two muscles:
– Lateral – shortens and adducts
– Medial – shortens and thickens
– Lateral cricoarytenoid
• Lengthening and adduction
– Interarytenoids (oblique and transverse)
• Only unpaired intrinsic muscles
• Closure of posterior glottis
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ANATOMY
➢Tensor
– Cricothyroid
• Tightening and lengthening
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ANATOMY
• Mucosa and vocal ligament extend over the vocal process
– Cartilaginous (aphonatory)
• Posterior one-third
– Membranous (PHONATORY)!!!!!!
• Anterior two-thirds
• Most benign lesions
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HISTOLOGY
• Stratified squamous EPITHELIUM
• LAMINA PROPRIA:
– Superficial (Reinke’s space)
• Loose fibrous matrix
– Intermediate
• Elastin
– Deep
• Fibroblast and collagen (dense)
• MUSCLE:
– vocalis muscle (medial portion of the
thyroarytenoid muscle)
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HISTOLOGY• Stratified squamous EPITHELIUM
• LAMINA PROPRIA:
– Superficial (Reinke’s space)
• Loose fibrous matrix (few fibroblast) MW
– Intermediate
• Elastin
– Deep
• Fibroblast and collagen (dense)
• MUSCLE:
– vocalis muscle (medial portion of the
thyroarytenoid musle)
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PHONATION
• Adducted position of vocal folds
• Mucosa undulates freely over the ligament and muscle
• “Body-Cover” theory:
– The “body” is relatively static + wave is propagated in the mucosal “cover”
1. Increase subglottic pressure until it overcomes the glottal closure force
2. Air pass between the vocal folds:
I. The wave begins infraglottically and is propagated upward to the free edge of the cord;
II. As the superior edges of the vocal fold begin to separate, the lower edges close
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LESIONS
• NON-NEOPLASTIC
– Vocal Nodules
– Vocal Polyp
– Vocal Cyst
– Reinke’s edema
– Granuloma
– Leukoplakia
• NEOPLASTIC
– Papilloma
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BENIGN NON-NEOPLASTICVOCAL CORD LESIONS
• Majority of vocal fold lesions
• CAUSES
– Vibratory injury
– Multifactorial
▪ Extroverts, talkativeness
▪Occupation
▪ Smoking, acid reflux, allergy and
infection
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EVALUATION
• CLINICAL HISTORY
– Age
– Vocal symptoms: dysphonia, voice change, discomfort, …
– Onset and duration of symptoms
– Activities: singers, teachers, football fan, …
– Risk factors: smoking, reflux, alcohol, drying medication, allergies, …
– …
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EVALUATION
• ENDOSCOPY:
– Laryngeal structure, arytenoid and vocal fold
motion, mucus, vascularity, supraglottal activity and
vocal fold edge shape
– NO vibratory patterns
• VIDEOSTROBOSCOPY
– To assess vocal fold vibration patterns
– Evaluates the glottal closure, mucosal wave,
symmetry and regularity
– To characterize stiffness, scar or submucosal injury;
to detect small vocal fold lesions; to identified
asymmetric mass or tension; …
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VOCAL NODULE
• Children and women
• CHRONIC injury
• BILATERAL
• CAUSE:
– Voice misuse or abuse
• CLINICAL:
– Permanent or intermittent dysphonia +
coughing + need for throat clearing
– Lower and breathy voice
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Pathogenesis
Prolonged or forceful vibration
Vascular congestion with oedema
Hyalinization of Reinke´s space and overlying epithelium
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Diagnosis
• ENDOSCOPY:
– Bilateral + shiny white + wide base
– Anterior/mild third of both vocal folds
➢Acute oedematous, translucent
➢Chronic fibrotic, white
• VIDEOSTROBOSCOPY
– Hourglass appearance
– Relatively symmetrical mucosal wave
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Management
• VOICE THERAPY
– Primary treatment
• MEDICAL
– Reflux, stop smoking, good
hydration,…
• SURGICAL if:
– Nodule of any size with an
unacceptable voice
– After an adequate therapy of 3
months
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VOCAL POLYPS
• > ♂
• UNILATERAL
• CAUSES:
– Acute severe voice abuse
– Anticoagulant
• CLINICAL:
– Abrupted dysphonia after a vocal abuse
– Normal speaking voice + intermittent aberrant sounds
– Difficulty to achieve high-pitched tones
• STAGES:
1. Submucosal hemorrhage
2. Hemorrhagic polyp
3. Fibrotic polyp
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Pathophysiology
Shearing forces
Capillary rupture and hematoma
Superficial capillaries
Thin, superficial and widely spread hematoma
– Little effect on mucosa oscillation
– Resolution within 2 weeks
Deeper capillaries
Alters margin and stiffens of the mucosa
POLYP
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Diagnosis
• ENDOSCOPY:
– Anterior/middle third along free margin
– Broad based or pedunculated
– Moving in and out of the glottis (if pedunculated)
– Contact lesion in contralateral vocal cord
• VIDEOSTROBOSCOPY:
– Usually have intact mucosal waves
– Phase asymmetry with impaired glottic closure
– Decreased amplitude of vibration on the affected
side
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Management
➢Management different based on polyp size
– Small polyps Conservative management
– Bigger polyps/ Surgical approach
uncomfortable dysphonia
• MEDICAL
– Stop anticoagulants
– Reflux treatment
• VOICE THERAPY
– Small polyps
– Postsurgical rehabilitation
• SURGICAL
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VOCAL CORD CYST
• Congenital or acquired
• UNILATERAL or BILATERAL
• Spherical and subepithelial lesions located in the
middle third of the vocal cord
• CLINICAL:
– Same as the nodule (dysphonia, throat clearing,
…)
• The cyst content can be serous, mutinous or
keratin
• Spontaneous rupture SULCUS VOCALIS
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Pathogenesis
• EPIDERMOID cyst:
– Epithelial cells buried congenitally or healing mucosa
– > Voice misuse
– > Bilateral
– > effect on voice
• MUCOUS RETENTION cyst:
– Plugging of the mucous glands
– Spontaneous
– > Unilateral
– < effect on voice
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Diagnosis
• ENDOSCOPY:
– Epidermoid: yellow + larger + bilateral
– Mucous: white + smaller + unilateral
• VIDEOSTROBOSCOPY
– Decreased amplitude of vibration on the
affected side
– Absent mucosal wave over the lesion
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Management
• SURGICAL
• MEDICAL (hydration, reflux)
• VOICE THERAPY
– Limited role
– Epidermoid type
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VOCAL GRANULOMA
• + ♂
• CARTILAGINOUS portion of the vocal cord
• CAUSE:
– Vocal cord trauma: acid reflux, chronic cough, throat clearing, intubation, …
• PATHOPHYSIOLOGY
– Inflammation of the mucosa and the perichondrium of the cartilaginous glottis
• CLINICAL:
– Unilateral discomfort/pain over midthyroid cartilage
– Normal or held-back vocal quality
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Diagnosis
• ENDOSCOPY
– Ulcerated area with a whitish
exudate
– Bilobed lesion
• VIDEOSTROBOSCOPY
– Mucosal wave present
– Location in cartilaginous posterior
vocal cord
– Large lesions can effect closure
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Management
➢SPONTANEOUS resolution in 3-6 months
• MEDICAL
– Anti-reflux regimen
• VOICE THERAPY
– To abolish throat clearing
• SURGICAL
– Last resort:
• Spontaneous resolution
• Recurrence is common
– Reserved for lesions
• Enlarging
• Affecting the voice
• Suspicion for malignancy
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REINKE’S EDEMA
• Polypoid corditis, Reinke’s oedema or smoker’s polyps
• Middle aged + talkative women + long-term history of smoking
• Unilateral or bilateral
• CAUSE:
– Chronic irritant exposure (> tobacco)
• CLINICAL:
– Dysphonia
– Lower pitch (masculine range)
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Pathogenesis
Vascular congestion + poor lymphatic drainage in submucosa
Excessive accumulation of edema
Thickening of the epithelial basement membrane
Connective tissue proliferation
IRREVERSIBLE lesion
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Diagnosis
• ENDOSCOPY:
– Fusiform oedema in vocal cord
– “Water balloon” appearance
• VIDEOSTROBOSCOPY
– Asymmetric movement of vocal cord
– Overexpressed mucosal wave
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Management
• MEDICAL
– STOP smoking or any irritant
• VOICE THERAPY
– Reduce size of the oedema and improve vocal functioning
• SURGERY
– Voice remains unacceptable to the patient
➢Risk of malignance: 1.7% patients with potentially malignant lesions (atypical
hyperplasia, and IEN I and II)
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CAPILLARY ECTASIA
• + ♀ singers
• CLINICAL:
– Hoarseness after short periods of singing
• PATHOPHYSIOLOGY
– Vibratory microtrauma lead to capillary angiogenesis
• ENDOSCOPY:
– Abnormal dilation of capillaries, can also present as clusters
• Predisposes to:
– Increased vulnerability to mucosal swelling
– Vocal fold haemorrhage
– Haemorrhagic polyp formation
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Management
• MEDICAL
– Discontinue anticoagulants
– Acid reflux
• VOICE THERAPY
• SURGICAL
– Patients who fail conservative management
– Spot coagulation is an excellent option
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LEUKOPLAKIA
• White hyperkeratotic plaque which represents a change in the
epithelium
– 10.2 per 100,000 (Males)
– 2.1 per 100,000 (Females)
• PATHOPHYSIOLOGY:
– Unknown
– Chronic irritation (smoking)
• 3 STAGES:
1. No dysplasia
2. Mild to moderate dysplasia
3. Severe dysplasia
• 8-14% chance of malignant transformation
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LEUKOPLAKIA
• VIDEOSTROBOSCOPY
– From normal to sluggish
mucosal wave
– Can vary in severity but a
mucosal wave should be present
• MANAGEMENT
– SURGICAL
– Tissue diagnosis is necessary to rule
out malignancy
– Excision or laser
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VOCAL CORD PAPILLOMA
• Most common benign neoplasm (84%)
• Alteration of mucosal immunosurveillance
• + Recurrent
• Prevalence
– 4.3 per 100,000 children
– 1.8 per 100,000 adults
• HPV (type 6 and 11 most common)
– Type 11 associated with more aggressive disease
– Types 16 and 18 higher risk of malignant
transformation
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VOCAL CORD PAPILLOMA
• JUVENILE:
– Type 6 and 11
– Papillomatosis diffuse
– > Aggressive and rapidly recurrent
– Exuberant tissues (“clusters of grapes”)
• ADULT-ONSET:
– Localized, solitary lesion
– Carpet variant: velvety appearance + little
projection from the surface
– < Aggressive
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VOCAL CORD PAPILLOMA
• VIDEOSTROBOSCOPY
– Mass effect with decreased mucosal wave
• MANAGEMENT
– SURGERY
• It´s NOT curative
• CO2 laser, pulse Dye and KTP, microdebrider
– Adjuvant treatment
• Interferon
• Cidofovir (antiviral)
• Bevacizumab (trials)
– Vaccine (Gardasil)
• Incidence of RRP
• Herd immunity
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