Chronic Inflammations of Larynx

1. Chronic Laryngitis

Chronic laryngitis is a persistent inflammation of the larynx, primarily affecting the mucosa and submucosa. Unlike acute laryngitis, which resolves quickly, this condition leads to long-term voice changes, significantly impacting a patient’s quality of life. It can be broadly classified into two types: chronic laryngitis without hyperplasia (chronic hyperaemic laryngitis) and chronic hypertrophic laryngitis (chronic hyperplastic laryngitis). Each type has distinct characteristics, causes, and treatment approaches.

Chronic Laryngitis Without Hyperplasia

This form involves diffuse, symmetrical inflammation across the entire larynx, including the vocal cords, ventricular bands, interarytenoid region, and the base of the epiglottis.

Causes: The condition arises from multiple factors, including:

1. 1. Smoking and Alcohol – Both irritate the laryngeal mucosa, leading to chronic inflammation.
   2. Persistent Cough – Chronic lung diseases, such as bronchitis or asthma, cause repeated trauma to the larynx.
   3. Vocal Abuse – Excessive shouting, singing, or speaking for long periods strains the vocal cords.
   4. Allergies – Upper respiratory allergies often extend to the larynx, worsening irritation.
   5. Infections – Fungal infections like candidiasis are common in immunocompromised individuals.
   6. Reflux Diseases – GERD (gastroesophageal reflux) and LPR (laryngopharyngeal reflux) contribute significantly.
   7. Chronic Infections – Sinusitis, dental infections, and tonsillitis can spread inflammation to the larynx.
   8. Occupational Hazards – Exposure to dust, fumes, or chemicals (common in mining, metalwork, and chemical industries) aggravates the condition.

Symptoms: Patients typically experience:

• • Hoarseness – The voice becomes rough and tires easily, sometimes leading to complete loss of voice by the end of the day.
  • Constant Throat Clearing – Dryness and irritation cause frequent hawking.
  • Throat Discomfort – A persistent feeling of scratchiness or soreness.
  • Difficulty Swallowing – Some patients report a sensation of a lump in the throat.
  • Chronic Dry Cough – Often irritating and non-productive.
  • Bitter Taste or Halitosis – Due to postnasal drip or reflux.
  • Referred Ear Pain – Some patients experience mild ear discomfort.

Diagnosis: A fibreoptic laryngoscopy reveals:

• • Generalized redness of the larynx.
  • Swollen, rounded vocal cords with a dull red appearance.
  • Sticky mucus coating the cords and interarytenoid region.

Treatment

1. 1. Treat Underlying Infections – Sinusitis, tonsillitis, or chest infections must be addressed.
   2. Avoid Irritants – Smoking cessation programs (including counseling and nicotine replacement) are essential. Alcohol and polluted environments should also be avoided.
   3. Voice Rest and Therapy – Prolonged voice rest (weeks to months) helps healing. Speech therapy improves vocal techniques.
   4. Steam Inhalation – Moistens the throat and loosens mucus.
   5. Expectorants – Help clear thick secretions, reducing throat clearing.
   6. Reflux Management – Proton pump inhibitors (PPIs) and antacids control acid irritation.

Chronic Laryngitis with Hyperplasia

This more severe form involves thickening of the laryngeal tissues, either diffusely or in localized growths like polyps or nodules.

Causes: The triggers are similar to chronic laryngitis without hyperplasia but lead to tissue overgrowth.

Pathology

• • Early stages involve swelling, redness, and cellular infiltration.
  • Over time, the respiratory epithelium changes to squamous type, and vocal cords thicken.
  • Mucous glands first enlarge but later shrink, causing dryness.
  • In advanced cases, muscle and joint damage may occur.

Symptoms

• • Severe Hoarseness – Voice becomes rough and weak.
  • Chronic Throat Clearing – Due to dryness and irritation.
  • Voice Fatigue – Speaking for long periods becomes exhausting.
  • Throat Discomfort – Worse with prolonged voice use.

Diagnosis: Fibreoptic laryngoscopy (sometimes with stroboscopy) reveals:

• • Dusky red, thickened laryngeal mucosa.
  • Swollen, rounded vocal cords with irregular edges.
  • Red, bulging ventricular bands.
  • Reduced cord mobility due to swelling or joint stiffness.

Treatment

1. 1. Conservative Measures – Same as chronic laryngitis (voice rest, reflux control, avoiding irritants).
   2. Surgical Intervention – In severe cases, vocal cord stripping removes excess tissue. Surgeons must avoid damaging the vocal ligament. Only one cord is operated on at a time to prevent voice loss.

 

2. Reinke’s Oedema (Smoker’s larynx)

Reinke’s oedema, commonly known as “smoker’s larynx,” is a chronic condition characterised by bilateral symmetrical irreversible oedema of the whole of the membranous part of the true vocal cords (from the anterior commissure to the vocal process). This oedema is caused by the accumulation of fluid in the subepithelial space (Reinke’s space) of the vocal cords. The sub-epithelial space is a potential space between the vocal ligament and the overlying mucosa.

While bilateral Reinke’s oedema is typically benign, unilateral presentation warrants investigation to rule out underlying malignancy. Without treatment, the condition progressively worsens voice quality and may rarely undergo malignant transformation.

Causes and Risk Factors. The condition primarily affects middle-aged adults (40-60 years), with smoking being the predominant cause. Other contributing factors include chronic voice abuse, laryngopharyngeal reflux (LPR), chronic sinusitis with postnasal drip, and myxoedema (hypothyroidism). These factors cause persistent irritation and inflammation of the vocal cord tissues.

Clinical Presentation and Symptoms. Patients most commonly present with progressive hoarseness and a characteristically low-pitched, rough voice. This occurs as patients unconsciously compensate by using their false vocal cords for phonation. The voice quality typically worsens throughout the day with continued use.

Diagnosis. Indirect laryngoscopy or 90-degree telescope examination or flexible laryngoscopy examination reveals distinctive features:

• There is a symmetrical, pale, translucent swelling of both vocal cords
• There is ballooning of the membranous part of the vocal folds
• Vocal cord mobility is preserved
• Hyperaemia of the ventricular bands

Treatment. Management requires a multimodal strategy:

1. Surgical intervention is the primary treatment, aiming to remove the fluid and reduce the excessive mucosa without damaging the underlying vocal ligament. Reduction glottoplasty is done, in which the superior aspect of the vocal cord is incised, the Reinke’s space is entered, the submucosal fluid contents are aspirated, and the excess mucosa is trimmed. It can be done with Cold instrument microsurgery or LASER (CO2 or KTP).
2. Adjunct therapies:
   • Strict smoking cessation
   • Voice therapy to address vocal misuse
   • Postoperative voice rest and rehabilitation
   • Management of contributing factors like LPR

 

3. Arytenoid Granuloma (Pachydermia Laryngis/ Contact ulcer/Granuloma/ Intubation Granuloma/ Peptic Granuloma)

Pachydermia laryngis is a benign chronic inflammatory condition affecting the back of the larynx, particularly the interarytenoid region and posterior vocal cords. Typically symmetrical, this disorder results from mechanical trauma, either following intubation or prolonged vocal abuse, where repeated friction between the vocal processes leads to thickened, granulation tissue at the posterior commissure area (the posterior commissure area includes the vocal process of arytenoids along with the anterior surface of the body of arytenoids).

Aetiology. While the exact cause remains unclear, key contributing factors include:

• Excessive smoking and alcohol use
• Chronic vocal abuse(e.g., shouting, excessive talking)
• Acid reflux (GERD), which irritates the larynx with stomach acid

Symptoms. Patients usually experience hoarseness, a husky voice, pain in the throat and irritation (constant desire to clear the throat).

Diagnosis involves indirect laryngoscopy, revealing reddish or greyish tissue buildup (granulation tissue) in the affected areas.

Treatment.

1. Voice rest and speech therapy to reduce strain.
2. Microlaryngeal biopsy confirmation to rule out cancer or tuberculosis (though this condition is benign).
3. Surgical removal of persistent granulation tissue under microscopic guidance (MLS), sometimes requiring repeat surgery.
4. Acid reflux management to prevent further irritation.
5. Avoid smoking.

 

4. Atrophic laryngitis (laryngitis sicca)

Atrophic laryngitis is caused by Klebsiella ozaenae infection. There is atrophy of laryngeal mucosa and crust formation. Typically affecting women with atrophic rhinitis or pharyngitis, it causes hoarseness of voice that briefly improves after coughing out crusts. Patients may also experience dry cough and breathing difficulty if crusts obstruct airways.

On laryngoscopic examination,  shiny, atrophic laryngeal mucosa with foul-smelling crusts is seen. Removing these crusts may reveal raw, bleeding surfaces. Sometimes, crusting extends to the trachea.

Treatment:

1. Elimination of the causative factor
2. Antibiotics targeting the infection.
3. Humidification and soothing sprays (e.g., glucose in glycerine or pine) to loosen crusts.
4. Expectorants (ammonium chloride/iodides) also loosen the crusts.
5. Managing nasal/pharyngeal conditions to prevent recurrence.

 

5. Tuberculosis of larynx

Laryngeal tuberculosis, nearly always developing from active pulmonary TB, primarily strikes middle-aged men. The bacteria typically spread through infected sputum (bronchogenic route) or bloodstream, targeting the larynx’s posterior structures first. The infection progresses in a distinct pattern, initially affecting the interarytenoid fold before moving to the ventricular bands, vocal cords, and finally the epiglottis.

Disease Progression:
Once tubercle bacilli penetrate the mucosa, they form small nodules beneath the surface. These may later ulcerate, creating characteristic lesions while causing significant swelling and redness (pseudoedema). Unlike in the past, cartilage inflammation and destruction now rarely occur thanks to modern treatments.

Symptoms evolve through distinct phases:

• Early stages feature voice weakness (dysphonia) progressing to hoarseness, accompanied by pain during speech
• As ulcers form, patients experience sharp pain radiating to the ears
• Advanced cases develop excruciating swallowing pain (odynophagia) when the epiglottis becomes involved
• Systemic TB symptoms like evening fevers, chronic cough, weight loss, and drenching night sweats commonly appear
• Notably, while TB rarely causes pain in the ear or nose, laryngeal TB is exceptionally painful.

On laryngoscopy examination:

1. Diffuse vocal cord redness with loss of complete adduction is the first sign.
2. Diffusely congested and oedematous larynx affecting predominantly the posterior one-third of the glottis.
3. Pebble-like bumps (mamillated appearance) in the interarytenoid area
4. Multiple small ulcers on the vocal cords create a “mouse-nibbled appearance” that mimics squamous cell carcinoma.
5. Swollen, red and enlarged epiglottis due to cellular infiltration (pseudoedema) “turban epiglottis” in late-stage disease.
6. There can be vocal cord fixation in later stages.

Diagnosis:

• Chest X-rays to confirm lung involvement
• Sputum tests to identify active TB infection
• Laryngeal biopsy showing classic TB granulomas with caseous necrotic centres, Langerhans-type giant cells and mycobacterium organisms.

Treatment:

• Antitubercular regimen (typically 6-9 months of therapy)
• Complete voice rest to minimize further irritation
• Pain management given the condition’s extreme discomfort

 

6. Lupus of the Larynx

Laryngeal lupus represents a chronic, indolent form of tuberculous infection that typically accompanies lupus vulgaris of the nose and pharynx. Unlike conventional laryngeal tuberculosis, which predominantly affects posterior structures of the larynx, this condition demonstrates a predilection for anterior laryngeal regions. The epiglottis serves as the primary site of involvement, often undergoing extensive destruction before the disease extends to the aryepiglottic folds and, less frequently, the ventricular bands.

Clinically, laryngeal lupus is a painless condition and progresses insidiously, with most patients remaining asymptomatic until advanced stages. Diagnosis frequently occurs incidentally during laryngeal examination for concomitant nasal lupus. Notably, pulmonary tuberculosis remains absent in these cases. Treatment is antitubercular drugs and the prognosis is good.

Key Features:

• It involves the anterior part of the larynx, in contrast to tubercular posterior involvement.
• Epiglottic destruction as a hallmark feature.
• Absence of pulmonary tuberculosis.
• Favourable response to antitubercular therapy.

 

7. Syphilis of the Larynx

Laryngeal syphilis, now a rare clinical entity, manifests primarily during secondary and tertiary stages of systemic infection. Patients typically present with hoarseness and dysphagia, though pain remains an uncommon feature. Secondary-stage lesions appear as diffuse erythematous papules, while tertiary disease produces nodular infiltrates that coalesce into painless ulcers, predominantly affecting the epiglottis and aryepiglottic folds.

The condition’s gross morphological similarities to tuberculosis and squamous cell carcinoma necessitate serological confirmation through treponemal-specific testing. Gummatous lesions, when present, may develop anywhere in the larynx, initially presenting as smooth swellings before ulceration. Penicillin remains the therapeutic cornerstone, though clinicians must monitor for laryngeal stenosis—a frequent late complication requiring potential surgical intervention.

Diagnosis:

• Serological testing essential for differentiation from malignant processes
• Gummatous lesions demonstrating variable ulceration patterns
• Airway compromise risk due to fibrotic stenosis

 

 8. Leprosy of the Larynx (Hansen’s Disease)

Laryngeal involvement in leprosy occurs exclusively in the context of systemic disease, invariably accompanied by long-standing cutaneous and nasal manifestations. The supraglottic region bears the brunt of pathological changes, with the epiglottis developing characteristic nodular thickening and ulceration. Patients exhibit progressive dysphonia, adopting a muffled vocal quality as the disease advances.

Diagnostic confirmation requires histopathological identification of Mycobacterium leprae within biopsied lesions. Multidrug therapy incorporating diaminodiphenylsulfone, rifampicin, and clofazimine forms the treatment mainstay, often extending over several years. Despite microbiological cure, healed lesions frequently result in laryngeal deformity and stenosis, occasionally necessitating tracheostomy for airway preservation.

Clinical Progression:

• Supraglottic predominance with epiglottic distortion
• Chronic granulomatous infiltration leading to structural compromise
• Fibrotic sequelae requiring long-term airway surveillance

 

9. Scleroma of the Larynx

Rhinoscleroma, caused by Klebsiella rhinoscleromatis, represents a chronic granulomatous process with particular prevalence in endemic regions such as India. While nasal involvement predominates, laryngeal disease manifests through subglottic swelling, producing hoarseness, wheezing, and progressive dyspnea. The condition evolves through three theorized stages: catarrhal (purulent rhinorrhea), granulomatous (nodule formation), and sclerotic (fibrotic stenosis).

Histopathological examination reveals pathognomonic Mikulicz cells and Russell bodies, while bacterial culture confirms the diagnosis. Antimicrobial therapy with streptomycin or tetracycline, combined with corticosteroids to mitigate fibrosis, constitutes first-line treatment. Nevertheless, many patients ultimately require surgical correction of subglottic stenosis.

Therapeutic Challenges:

• Antibiotic-steroid combinations to arrests disease progression
• Endoscopic surveillance for early stenosis detection
• Surgical reconstruction for advanced airway compromise

 

10. Amyloidosis of the Larynx

Laryngeal amyloid deposition occurs either as localized disease or within systemic amyloidosis frameworks. These proteinaceous aggregates preferentially accumulate in submucosal and subepithelial locations, progressively impairing vocal cord mobility and potentially compromising the airway. Patients present with persistent dysphonia, occasionally progressing to stridor in advanced cases.

CO₂ laser excision has emerged as the intervention of choice, leveraging its precision in vaporizing fluid-rich deposits while preserving surrounding tissues. Histological diagnosis relies on Congo red staining’s characteristic apple-green birefringence under polarized light.

Management:

• Laser-assisted debulking for symptomatic relief
• Systemic evaluation to exclude generalized disease
• Long-term follow-up for recurrence monitoring

 

 11. Sarcoidosis of the Larynx

Laryngeal involvement develops in fewer than 5% of sarcoidosis cases, typically accompanying pulmonary manifestations. Supraglottic structures demonstrate non-caseating granulomas that mimic tuberculosis or fungal infections histologically. Dysphonia and airway obstruction constitute primary concerns, with treatment strategies prioritizing airway preservation.

While systemic corticosteroids remain fundamental, recent advances support office-based steroid injections as effective alternatives to surgical intervention. Laser excision or tracheostomy proves necessary in select cases with critical stenosis.

Diagnosis:

• Biopsy confirmation of non-necrotizing granulomas
• Radiographic assessment for pulmonary involvement
• Multidisciplinary evaluation given the systemic nature

 

———— End of the chapter ————

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Reference Textbooks.

• Scott-Brown, Textbook of Otorhinolaryngology-Head and Neck Surgery.
• Cummings, Otolaryngology-Head and Neck Surgery.
• Stell and Maran’s, Textbook of Head and Neck Surgery and Oncology.
• Ballenger’s, Otorhinolaryngology Head And Neck Surgery
• Susan Standring, Gray’s Anatomy.
• Frank H. Netter, Atlas of Human Anatomy.
• B.D. Chaurasiya, Human Anatomy.
• P L Dhingra, Textbook of Diseases of Ear, Nose and Throat.
• Hazarika P, Textbook of Ear Nose Throat And Head Neck Surgery Clinical Practical.
• Mohan Bansal, Textbook of Diseases of Ear, Nose and Throat Head and Neck Surgery.
• Hans Behrbohm, Textbook of Ear, Nose, and Throat Diseases With Head and Neck Surgery.
• Logan Turner, Textbook of Diseases of The Nose, Throat and Ear Head And Neck Surgery.
• Arnold, U. Ganzer, Textbook of  Otorhinolaryngology, Head and Neck Surgery.
• Ganong’s Review of Medical Physiology.
• Guyton & Hall Textbook of Medical Physiology.

Author:

Dr. Rahul Bagla
MBBS (MAMC, Delhi) MS ENT (UCMS, Delhi)
Fellow Rhinoplasty & Facial Plastic Surgery.
Renowned Teaching Faculty
Mail: msrahulbagla@gmail.com
India

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Keywords: Chronic Inflammations of the Larynx, Reinke’s oedema, Pachydermia Laryngis, Atrophic laryngitis, Tuberculosis of the larynx, Lupus, Syphilis, Leprosy, Scleromae