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

ANATOMY

• LARYNGEAL CARTILAGINOUS

STRUCTURE:

– Unpaired cartilages:

• Thyroid, cricoid, and epiglottic

– Paired cartilages:

• Arytenoid, corniculate and

cuneiform

ANATOMY

• INTRINSIC MUSCLES

– Responsible for vocal fold motion

– 3 types

• Abductor, adductors, and tensor

➢Abductor

– Posterior cricoarytenoid

• Responsible for glottic airway

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

ANATOMY

➢Tensor

– Cricothyroid

• Tightening and lengthening

ANATOMY

• Mucosa and vocal ligament extend over the vocal process

– Cartilaginous (aphonatory)

• Posterior one-third

– Membranous (PHONATORY)!!!!!!

• Anterior two-thirds

• Most benign lesions

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)

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)

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

LESIONS

• NON-NEOPLASTIC

– Vocal Nodules

– Vocal Polyp

– Vocal Cyst

– Reinke’s edema

– Granuloma

– Leukoplakia

• NEOPLASTIC

– Papilloma

BENIGN NON-NEOPLASTICVOCAL CORD LESIONS

• Majority of vocal fold lesions

• CAUSES

– Vibratory injury

– Multifactorial

▪ Extroverts, talkativeness

▪Occupation

▪ Smoking, acid reflux, allergy and

infection

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, …

– …

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; …

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

Pathogenesis

Prolonged or forceful vibration

Vascular congestion with oedema

Hyalinization of Reinke´s space and overlying epithelium

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

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

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

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

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

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

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

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

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

Management

• SURGICAL

• MEDICAL (hydration, reflux)

• VOICE THERAPY

– Limited role

– Epidermoid type

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

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

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

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)

Pathogenesis

Vascular congestion + poor lymphatic drainage in submucosa

Excessive accumulation of edema

Thickening of the epithelial basement membrane

Connective tissue proliferation

IRREVERSIBLE lesion

Diagnosis

• ENDOSCOPY:

– Fusiform oedema in vocal cord

– “Water balloon” appearance

• VIDEOSTROBOSCOPY

– Asymmetric movement of vocal cord

– Overexpressed mucosal wave

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)

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

Management

• MEDICAL

– Discontinue anticoagulants

– Acid reflux

• VOICE THERAPY

• SURGICAL

– Patients who fail conservative management

– Spot coagulation is an excellent option

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

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

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

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

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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