hoarseness year-4

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HOARSENESS

ANATOMY OF LARYNX Location:

related posteriorly to C3‐C6 vertebral bodies in adult, ends at lower border of C6

Moves vertically and anteroposteriorly during swallowing and phonation

Can be moved passively from side to side producing laryngeal crepitus.

LARYNGEAL CARTILAGES 3 unpaired and 3 paired cartilages

Unpaired: Thyroid, cricoid and epiglottis Paired: Arytenoid, corniculate and cuneiform

LARYNGEAL MEMBRANE Extrinsic membrane

Thyrohyoid membrane – pierced by superior laryngeal nerve & internal laryngeal nerve

Cricothyroid membrane Cricotracheal membrane

Intrinsic membrane Cricovocal membrane Quadrangular membrane

LARYNGEAL INLET The boundary is formed by the:

superior border of the epiglottis aryepiglottic folds cuneiform tubercles corniculate tubercles interarytenoid notch

interarytenoid notch

INTERIOR LARYNGEAL CAVITY

Laryngeal cavity extends from laryngeal inlet to the inferior border of cricoid cartilage.

3 compartments: Laryngeal vestibule Laryngeal ventricle Infraglottic cavity

EXTRINSIC MUSCLE OF LARYNX• Move the larynx as a whole

INTRINSIC MUSCLE OF LARYNX Move the laryngeal parts – change the length and

tension of the vocal folds & size and shape of the rima glottides.

BLOOD SUPPLY & LYMPHATIC DRAINAGE Arterial supply:

Superior and inferior laryngeal aa. (from sup. & inf. thyroid aa.)

Venous drainage: Superior and inferior laryngeal veins

Lymphatic drainage: Superior to VF – superior deep cervical l/n Inferior to VF – inferior deep cervical l/n

SENSORY INNERVATION ( VAGUS NERVE )

FUNCTION OF LARYNX Protection of lower airway

Sphincteric closure of laryngeal opening ( laryngeal inlet, false cord and true cord )

Cessation of breathing Cough reflex

Phonation Respiration Fixation of the chest

PHONATION Glottal vibration is a result of an interaction between

aerodynamic forces and vocal fold muscular forces. Aerodynamic myoelasic theory of voice production:

Vocal cords are kept adducted Infraglottic air pressure generated by exhaled air Air forces the cords opening and air is released as small puffs

which vibrate the vocal cords. Produced sound is amplified by mouth, pharynx, nose and chest.

Sound is converted into speech by action of lips, tongue, palate, pharynx and teeth.

INTRODUCTION TO HOARSENESS

Hoarseness is defined as roughness of voice resulting from variations of periodicity and/or intensity of consecutive sound waves.

For production of normal voice, vocal cords should:Be able to approximate properly with each other.Have a proper size and stiffness.Have an ability to vibrate regularly in response to air column. Any condition that interferes with the above functions causes

hoarseness.Loss of approximation may be seen in vocal cord paralysis or

fixation or a tumour coming in between the vocal cords.Size of the cord may increase in oedema of the cord or a

tumour; there is a decrease in partial surgical excision or fibrosis.

Stiffness may decrease in paralysis, increase in spastic dysphonia or fibrosis.

Cords may not be able to vibrate properly in the presence of congestion, submucosal haemorrhages, nodule or a polyp.

ACUTE LARYNGITIS AetiologyThe infectious type is more common and usually follows

upper respiratory infection.

To begin with, it is viral in origin but soon bacterial invasion takes place with Strept. pneumoniae, H. influenzae and haemolytic streptococci or Staph. aureus. Exanthematous fevers like measles, chickenpox and whooping cough are also associated with laryngitis

The non-infectious type is due to vocal abuse, allergy, thermal or chemical burns to larynx due to inhalation or ingestion of various substances, or laryngeal trauma such as endotracheal intubation.

Clinical Features Symptoms are usually abrupt in onset and consist of:Hoarseness which may lead to complete loss of voice.Discomfort or pain in throat, particularly after talking.Dry, irritating cough which is usually worse at night.General symptoms of head, cold, rawness or dryness of

throat, malaise and fever if laryngitis has followed viral infection of upper respiratory tract.

Laryngeal appearances vary with severity of disease. In early stages, there is erythema and oedema of epiglottis,

aryepiglottic folds, arytenoids and ventricular bands, but the vocal cords appear white and near normal and stand out in contrast to surrounding mucosa.

Later, hyperaemia and swelling increase. Vocal cords also become red and swollen. Subglottic region also gets involved.

Sticky secretions are seen between the cords and interarytenoid region.

In case of vocal abuse, submucosal haemorrhages may be seen in the vocal cords.

TreatmentVocal rest. This is the most important single factor. Use of

voice during acute laryngitis may lead to incomplete or delayed recovery.

Avoidance of smoking and alcohol.Steam inhalations with oil of eucalyptus or pine are soothing

and loosen viscid secretions.Cough sedative. To suppress troublesome irritating cough.Antibiotics. When there is secondary infection with fever and

toxaemia or purulent expectoration.Analgesics. To relieve local pain and discomfort.Steroids. Useful in laryngitis following thermal or chemical

burns,

ACUTE LARYNGO-TRACHEO-BRONCHITIS(CROUP) It is an inflammatory condition of the larynx, trachea and

bronchi AetiologyMostly, it is viral infection (parainfluenza type I and II)

affecting children between 6 months to 3 years of age.Male children are more often affected. Secondary bacterial infection by Gram positive cocci soon

supervenes.

PathologyThe loose areolar tissue in the subglottic region swells up

and causes respiratory obstruction and stridor. This, coupled with thick tenacious secretions and crusts, may

completely occlude the airway.

SymptomDisease starts as upper respiratory infection with hoarseness

and croupy cough. There is fever of 39-40C. This may be followed by difficulty in breathing and

inspiratory type of stridor. Respiratory difficulty may gradually increase with signs of

upper airway obstruction, i.e.suprasternal and intercostal recession.

TreatmentHospitalisation is often essential because of the increasing

difficulty in breathing.Antibiotics like ampicillin 50 mg/kg/day in divided doses is

effective against secondary infections due to gram-positive cocci and H.influenzae.

Humidification helps to soften crusts and tenacious secretions which block tracheobronchial tree.

Parenteral fluids are essential to combat dehydration.Steroids, e.g. hydrocortisone 100mg i.v. may be useful to

relieve oedema.Adrenaline racemic adrenaline administered via a respirator

is a bronchodilator and may relieve dyspnoea and avert tracheostomy.

Intubation/tracheostomy is done, should respiratory obstruction increase in spite of the above measures.

Tracheostomy is done if intubation is required beyond 72 hours. Assisted ventilation may be required.

LARYNGEAL DIPHTHERIA AetiologyMostly, it is secondary to faucial diphtheria affecting

children below 10 years of age. Incidence of diphtheria in general is declining due to wide-

spread use of immunisation .

Pathology Effects of laryngeal diphtheria are due to:Formation of a tough pseudomembrane over the larynx and

trachea which may completely obstruct the airway.Exotoxin liberated by bacteria leading to myocarditis and

various neurological complications.

Clinical Features

General symptoms. Onset is insidious with low grade fever, sore throat and malaise but patient is very toxaemic with tachycardia and thready pulse.

Laryngeal symptoms. Hoarse voice, croupy cough, inspiratory stridor, increasing dyspnoea with marked upper airway obstruction.

Greyish white membrane is seen on the tonsil, pharynx and soft palate. It is adherent and its removal leaves a bleeding surface . Similar membrane is seen over the larynx and trachea.

Cervical lymphadenopathy. Characteristic "bull-neck” may be seen.

FAUCIAL DIPHTHERIA

DiagnosisLaryngeal diphtheria is mostly secondary to faucial diphtheria.Diagnosis is always clinical but confirmed by smear and culture of

corynebacterium diphtheriae. Treatment is started on clinical suspicion.Diphtheria antitoxin. Dose depends on clinical severity and

duration of illness, and varies from 20,000 to 100,000 units i. v. route as saline infusion after a test dose. It neutralises free toxin circulating in the blood.

Antibacterials. Benzylpenicillin, 500,000 units i.m. every 6 h ours for 6 days, is effective against diphtheria bacilli. Erythromycin can be given to those who are allergic to penicillin.

Maintenance of airway. Tracheostomy may become essential. Direct laryngoscopy, removal of diphtheritic membrane and intubation can be done. Intubation relieves respiratory obstruction and can make subsequent tracheostomy easy.

Complete bed rest. Complete bed rest for 2-4 weeks is essential to guard against effects of myocarditis

ComplicationsAsphyxia and death due to airway obstruction.Toxic myocarditis and Circulatory failure.Palatal paralysis with nasal regurgitation.Laryngeal and pharyngeal paralysis.

CHRONIC LARYNGITISA. CHRONIC LARYNGITIS WITHOUT HYPERPLASIA(CHRONIC HYPERAEMIC LARYNGITIS)

It is a diffuse inflammatory condition symmetrically involving the whole larynx, i.e. true cords, ventricular bands, interarytenoid region and root of the epiglottis.

AetiologyIt may follow incompletely resolved acute simple

laryngitis or its recurrent attacks.Presence of chronic infection in paranasal sinuses, teeth

and tonsils and the chest are important contributory causes.

Occupational factors, e.g. exposure to dust and fumes such as in miners, and workers in chemical industry

Smoking and alcohol.Persistent trauma of cough as in chronic lung diseaseVocal abuse.

Clinical features

Hoarseness. This is the commonest complain. Voice becomes easily tired and patient becomes aphonic by the end of the day.

Constant hawking. There is dryness and intermittent tickling in the throat and patient is compelled to clear the throat repeatedly.

Discomfort in the throat.Cough. It is dry and irritating.Laryngeal examination. There is hyperaemia of

laryngeal structures. Vocal cords appear dull red and rounded. Flecks of viscid mucus are seen on the vocal cords and interarytenoid region.

Treatment

Eliminate infection of upper or lower respiratory tract. Infection in the sinuses, tonsils, teeth or chronic chest infection (bronchitis, bronchiectasis, tuberculosis, etc.) should be treated.

Avoidance of irritating factors, e.g. smoking, alcohol or polluted environment, dust and fumes.

Voice rest and speech therapy. Voice rest has to be prolonged for weeks or months. Patient should receive training in proper use of voice.

Steam inhalations. They help to loosen secretions and give relief.

Expectorants. They help to loosen viscid secretions and give relief from hawking.

B. CHRONIC HYPERTROPHIC LARYNGITIS(SYN. CHRONIC HYPERPLASTIC LARYNGITIS) It may be either a diffuse and symmetrical process or a localised

one, the latter appearing like a tumour of the larynx. Localised variety presents as dysphonia plica ventricularis, vocal nodules, vocal polyp, Reinke's oedema and contact ulcer

AetiologySame as discussed under chronic laryngitis without hyperplasia. PathologyPathological changes start in the glottic region and later may

extend to ventricular bands, base of epiglottis and even subglottis. Mucosa, submucosa, mucous glands and in later stages intrinsic

laryngeal muscles and joints may be affected. Initially, there is hyperaemia, oedema and cellular infiltration in the

submucosa. The pseudostratified ciliated epithelium of respiratory mucosa

changes to squamous type, and squamous epithelium of the vocal cords to hyperplasia and keratinisation.

The mucous gland suffers hypertrophy at first but later undergo atrophy with diminished secretion and dryness of larynx.

Clinical featuresThis disease mostly affects males (8: 1) in the of 30-50 years.Hoarseness, constant desire to clear the cough, tiredness of voice,

dry cough and discomfort in throat when the voice has been used for an extended period of time are the common presenting symptoms.

Examination. On examination, changes are diffuse and symmetrical.

Laryngeal mucosa, in general, is dusky red and thickened.Vocal cords appear red and swollen. Their edges lose sharp

demarcation and appear rounded. In late stages, cords become bulky and irregular giving nodular appearance.

Ventricular bands appear red and swollen and may be mistaken for prolapse or eversion of the ventricle

Mobility of cords gets impaired due to oedema and infiltration, and later due to muscular atrophy or arthritis of the cricoarytenoid joint.

TreatmentConservative. Same as for chronic laryngitis without hyperplasia.

Surgical. Stripping of vocal cords, removing the hyperplastic and oedematous mucosa, may be done in selected cases. Damage to underlying vocal ligament should be carefully avoided. One cord is operated at a time.

POLYPOID DEGENERATION OF VOCAL CORDS (REINKE'S OEDEMA) It is bilateral symmetrical swelling of the whole of

membranous part of the vocal cords, most often seen in middle-aged men and women. This is due to oedema of the subepithelial space (Reinke's space) of the vocal cords.

Chronic irritation of vocal cords due to misuse of voice, heavy smoking, chronic sinusitis and laryngopharyngeal reflex are the probable aetiological factors. It can also occur in myxoedema.

Clinical FeaturesHoarseness is the common symptom. Patient uses false cords for voice production and this gives him a low pitched and rough voice.

On indirect laryngoscopy, vocal cords appear as fusiform swellings with pale translucent look. Ventricular bands may appear hyperaemic and hypertrophic and may hide the view of the true cords.

TreatmentDecortication of the vocal cords, i.e. removal of strip of epithelium, is done first on one side and 3-4 weeks later on the other.

Voice rest.Speech therapy for proper voice production.

PACHYDERMIA LARYNGIS It is a form of chronic hypertrophic laryngitis affecting posterior part of

larynx in the region of interarytenoid and posterior part of the vocal cords.

Clinically, patient presents with hoarseness or husky voice and irritation in the throat.

Indirect laryngoscopy reveals heaping up of red or grey granulation tissues in the interarytenoid region and posterior thirds of vocal cords; the latter some times showing ulceration due to constant hammering of vocal processes as in talking, forming what is called the 'contact ulcer'.

The condition is bilateral and symmetrical. It does not undergo malignant change. However, biopsy of the lesion is essential to differentiate the lesion from

carcinoma and tuberculosis. Aetiology is uncertain. It is mostly seen in men who indulge in excessive

alcohol and smoking. Other factors are excessive forceful talking and gastro-oesophageal reflux disease where posterior part of larynx is being constantly bathed with acid juices from the stomach.

Treatment is removal of granulation tissue under operating microscope which may require repetition, control of acid reflux and speech therapy.

ATROPHIC LARYNGITIS(LARYNGITIS SICCA) It is characterised by atrophy of laryngeal mucosa and crust

formation. Condition is often seen in women and is associated with atrophic rhinitis and pharyngitis.

Common symptoms include hoarseness of voice which temporarily improves on coughing and removal of crusts.

Dry irritating cough and sometimes dyspnoea is due to obstructing crusts .

Examination shows atrophic mucosa covered with foul smelling crusts.

When crusts have been expelled, mucosa may show excoriation and bleeding. Crusting may also be seen in the trachea.

Treatment is elimination of the causative factor and humidification. Laryngeal sprays with glucose in glycerine or oil of pine are comforting and help to loosen the crusts. Associated nasal and pharyngeal conditions will require attention. Expectorants containing ammonium chloride or iodides also help to loosen the crusts.

BENIGN LESION OF LARYNX

BENIGN TUMORS OF LARYNX

Non-neoplastic Neoplastic

Solid :-Vocal nodules-Vocal polyps-Contact ulcer-Intubation granuloma-Leukoplakia-Amyloid tumors-Reinke’s oedema

Cystic :-Ductal cyst-Saccular cyst-Laryngocoele

Squamos papilloma:-Juvenile type-Adult-onset type

ChondromaHemangiomaGranular cell tumorGlandular tumorRhabdomyosarcomaLipomaFibroma

VOCAL CORD NODULE VS VOCAL CORD POLYP

Vocal cord nodule Vocal cord polyp

- Growth of epithelium that covers the mucosa membrane.

- Polyp growth at vocal cord.

- Callous thickening of vocal cord lining over time.

- Blistering of vocal cord lining.

- Occurs due to vocal abuse or vocal misuse.

-Occurs due to :i) Vocal abuseii) Chronic laryngeal allergic

reactioniii) Chronic inhalation of irritants

(industrial fumes & cigarette smoke)

- The size is smaller, harder and callous-like growth.

- The size is larger, appear swelling or bump, stalk-like growth or blister-like lesion.

- Bilateral of vocal cord. - Mostly unilateral but can be bilateral of vocal cord.

TREATMENTS FOR NODULES AND POLYPS Medical therapy: - Treat the primary cause (smoking, GERD, hypothyroid). - Voice rest, voice therapy (hygiene, reducing vocal

abusive behavior, alter pitch etc).

Surgical therapy: - To remove if the mass is large or have existed for long

time (>6 months & didn’t improve with voice therapy).

BENIGN LARYNGEAL PAPILLOMASEtiology• human papilloma virus (HPV) types 6, 11 infected during childbirth passage through the cervix or from

oral-genital sexual activities. 

Epidemiology often referred to as recurrent respiratory papillomatosis

(RRP) because of their propensity to recur after surgical removal.

• biphasic distribution - birth to puberty (juvenile RRP) - adult onset (20-40 y/o)

MOST COMMONLY FOUND AT COLUMNAR AND SQUAMOUS JUNCTION

SINGLE PAPILLOMA MULTIPLE PAPILLOMA

JUVENILE RECURRENT RESPIRATORY

PAPILLOMATOSIS (RRP) Postulated to be vertically transmitted during the

process of childbirth. Almost all papillomas in the throat are caused by

HPV subtypes [HPV- 6, HPV-11, HPV-16 & HPV-18]. These same subtypes that appear in the cervix.

Researchers believe that the throat can be infected during childbirth passage through the cervix or from oral-genital sexual activities. 

Signs and symptoms of Juvenile RRP :

Symptomatic after age 6 months. Stridor. Worsening of the airway obstructive features as the papilloma

grows. Other clinical presentations include cough, pneumonias, and dysphagia.

Hoarseness without airway obstruction may indicate the small lesion. Aphonia or breathy voice larger glottic lesion. A low-pitched, coarse, fluttering voice subglottic lesion.

Extra notes : Signs of severe airway obstruction include tachypnea, stridor,

retractions (suprasternal, substernal, intracostal), flaring of the nasal ala, and use of accessory neck or chest muscles.

Children are often misdiagnosed with asthma, croup, allergies, vocal nodules, or bronchitis. Recurrent respiratory papillomatosis (RRP) is misdiagnosed because of its rarity and the slowly progressive nature of the disease.

ADULT ONSET RECURRENT RESPIRATORY PAPILLOMATOSIS (RRP)

Factors: i)Oroanal or orogenital contact is considered a possible mode

of virus transmission. ii)a latent virus becoming active.

more localized, single, smaller in size, less aggressive and can recur after surgical removal but not as aggressive as juvenile.

common in males in age group of 30-50 years Usually arises from anterior half of the vocal cord or

anterior commissure.

Clinically appear as glistening white irregular growths, pedunculated or sessile, friable and bleeding easily

TREATMENTS Medical treatments: Acyclovir - To treat herpes virus infection. Interferon (IFN)- The produced enzymes block viral

replication of RNA and DNA, thus making less susceptible to viral penetration & prevent recurrence.

Surgical treatments: Carbon dioxide laser Surgical microdebrider - The surgical microdebrider has

recently been used for laryngeal and tracheal papillomas.

MALIGNANT LESION OF

LARYNX

Laryngeal Carcinoma

Undifferentiated carcinoma

Miscellaneous carcinomas

Adenocarcinoma

Sarcomas

Squamous cell

carcinoma (85-95%) Carcinoma in

situ

Verrucous, spindle cell and

basaloid SCC

LARYNGEAL CARCINOMARisk factors:- Prolong use of tobacco and alcohol- Men : female = 2 : 1, increase in women who smoke- Secondhand smoker- Laryngeal papillomatosis due to infection with human papilloma virus subtypes 16 & 18.

- Previous radiation to neck for benign lesions or laryngeal papilloma.

- Chronic gastroesophageal reflux (GERD).

- Genetic factors.

- Occupational exposure to asbestos, mustard gas and other chemical or petroleum products.

INCIDENCE OF LARYNX CA BY SITESquamous Cell Carcinoma

• Glottic - 59%, involves the true vocal folds

• Supraglottic - 40%, confined to the supraglottic area (free border of the laryngeal epiglottis, false vocal folds and laryngeal ventricles)

• Subglottic - 1%, extend or arise more than 10mm below the free margin of the true vocal fold up to the inferior border of the cricoid cartilage.

PRESENTATIONS IN SUPRAGLOTTIC & GLOTTIC TUMORS

Supraglottic Tumor Glottic Tumor

Supraglottic tumors may not alter laryngeal function until they reach a relatively large size, at which time airway obstruction may be the first symptom. 

Glottic tumors alter voice quality early in their development and are thus often discovered at an early stage.

The mechanism of swallowing is altered when tumors invade and alter the physiology of the swallowing muscles. This may lead to either dysphagia or aspiration.• hoarseness – progressive & continuous• stridor• sore throat • ear pain• airway compromise• aspiration• persistent cough

Indirect laryngoscopy : • friable fungating ulcerative masses• changes in the mucosal color•multiple areas of central necrosis and exudate surrounding areas of hyperemia

TREATMENTS 1) Radiotherapy – Reserved for early lesion.

2) Surgical treatments : Transoral laser microsurgery Open partial laryngectomy Total laryngectomy

Neurological lesion of larynx

LARYNGEAL PARALYSIS It can be unilateral or

bilateral

Involved: 1. Recurrent laryngeal nerve2. Superior laryngeal nerve3. Both (combined or complete

paralysis)

ETIOLOGY Surgical iatrogenic injuries - thyroid surgery, anterior

cervical disc surgery, carotid surgery, or chest surgery. Malignant invasion of either the vagus or recurrent

laryngeal nerve -skull base tumors, thyroid cancer, lung cancer, esophageal cancer, and metastases to the mediastinum (often observed with lung cancer primaries)

Blunt trauma to the neck or chest. Idiopathic -When a clear-cut etiology for the unilateral vocal

fold paralysis (UVFP) is not found, it is classified as.

CAUSES Supranuclear: Rare Nuclear: involvement of nucleus ambiguus in medulla,

usually associated with other lower cranial nerve paralysis High vagal lesions: may be involved at the level of jugular

foramen or parapharyngeal space Low vagal trunk or RLN Idiopathic: in about 30% of cases

CAUSES OF RLN PARALYSIS (LOW VAGAL TRUNK OR RLN)

Right Left Both-Neck trauma-Benign or malignant thyroid disease-Thyroid surgery-Carcinoma cervical oesophagus-Aneurysm of subclavian artery-Carcinoma apex right lung-Tuberculosis of cervical pleura-Idiopathic

i) Neck- Accidental trauma- Thyroid disease- Thyroid surgery- Carcinoma cervical

oesophagus- Cervical

lymphadenopathy

ii) Mediastinum- Bronchogenic cancer- Carcinoma aortic

oesophagus- Aortic aneurysm- Mediastinal

lymphadenopathy- Enlarged neck

auricle- Intrathoracic surgery- Idiopathic

-Thyroid surgery-Carcinoma thyroid-Cancer cervical

esophagus-Cervical

lymphadenopathy

UNILATERAL VOCAL FOLD PARALYSIS•occurs from a dysfunction of the recurrent laryngeal or vagus nerve - results in ipsilateral paralysis of all intrinsic muscles except cricothyroid•Vocal cord assumes a median or paramedian position and does not move laterally on deep inspiration

glottal incompetence

weak or absent vocal fold vibration

Dysphonia

Dysphagia (liquids)

significant air wasting

sensation of shortness of breath

and running out of air during speech

Weak cough

Clinical Features

• Significant muscle tension is often seen in the larynx as a compensatory mechanism for the glottal gap – patient complaint of pain in the throat after voice use.

aspiration

• 1/3 of patients asymptomatic

Medical therapy: - muscle-nerve transplant - medialization thyroplasty (moving the paralyzed vocal cord toward midline)

- injection of a substance to increase the size of the paralyzed vocal cord

Voice therapy - pitch alteration - increase breath support and loudness

- find the correct position for optimal

voicing 

TREATMENTS

Surgical therapy : i) Temporary treatment involves endoscopic injection of a

resorbable material into the affected vocal fold. (Cymetra, hyaluronic acid, gelfoam)

ii) Permanent vocal fold surgical treatment can be divided into vocal fold injection (permanent materials ie fat, fascia, or the semipermanent calcium hydroxylapatite) and laryngeal framework surgery.

Preoperatively, the arrow demonstrates the paralyzed vocal fold, which is characteristically foreshortened, lateralized, and flaccid.

Postoperatively, the image shows the same vocal fold following laryngeal framework surgery. The left vocal fold is now midline and has improved length.

CONGENITAL ANOMALIES Congenital anomalies of the larynx that cause

hoarseness : 1) Laryngeal webs, 2) Laryngeal clefts, 3) Laryngeal cysts

LARYNGEAL WEBS Caused by failure of resorption of the epithelial layer

that obliterates the laryngeal opening in normal development results in incomplete separation of the vocal folds.

Laryngeal webs also can result from trauma to the airway (eg, because of intubation, traumatic injury, or prior surgical manipulation.

Diagnosis : - modified barium swallow - laryngopharyngoscopy

LARYNGEAL CLEFTSEmbryologic failure of fusion of the cricoid cartilage and tracheoesophageal septum.

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