Inflammatory disorders of the larynx include a wide range of conditions:

• Acute laryngitis: Inflammation of the larynx that usually lasts up to 7 days.
• Fungal laryngitis: A fungal infection affecting the larynx.
• Epiglottitis: Acute inflammation of the epiglottis.
• Epiglottic abscess: A localized collection of pus due to epiglottic tissue necrosis. It usually affects the lingual surface of the epiglottis.
• Subacute laryngitis: Laryngeal inflammation lasting between 1 and 3 weeks.
• Chronic laryngitis: Persistent inflammation of the larynx exceeding 3 weeks.
• Chronic hyperplastic laryngitis: A subtype of chronic laryngitis marked by mucosal thickening and tissue overgrowth.
• Reflux laryngitis: Laryngeal inflammation caused by the retrograde flow of gastric contents into the laryngopharynx (laryngopharyngeal reflux).
• Vocal cord nodules: Bilateral thickenings of the true vocal fold margins at the junction of the anterior and middle thirds. This condition is usually associated with overuse of the vocal cords.
• Chondritis and perichondritis: Inflammation of the cartilage and perichondrium.

Classification

• Acute Laryngitis:
  • Catarrhal acute laryngitis
  • Edematous (infiltrative) acute laryngitis
  • Acute fungal laryngitis
  • Epiglottitis
  • Epiglottic abscess

• Chronic Laryngitis:
  • Chronic catarrhal laryngitis
  • Atrophic laryngitis
  • Reflux laryngitis
  • Chronic fungal laryngitis

• Chronic Hyperplastic Laryngitis:
  • Diffuse hyperplastic laryngitis
  • Chronic edematous-polypoid laryngitis (Reinke's edema)
  • Vocal nodules
  • Vocal fold polyp
  • Laryngeal pachydermia
  • Contact granuloma of the larynx

• Specific Inflammatory Conditions of the Larynx:
  • Laryngeal diphtheria
  • Laryngeal syphilis
  • Scleroma
  • Laryngeal tuberculosis

• Laryngitis Associated with Systemic Diseases:
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Amyloidosis
  • Granulomatosis with polyangiitis (Wegener’s granulomatosis)

• Inflammation of Laryngeal Cartilages:
  • Chondritis and perichondritis of the thyroid cartilage
  • Chondritis and perichondritis of the cricoid cartilage
  • Chondritis and perichondritis of the arytenoid cartilage
  • Chondritis and perichondritis of the epiglottis

Acute Laryngitis

Etiology

Acute laryngitis is most commonly caused by viruses, such as influenza, parainfluenza, respiratory syncytial virus (RSV), adenoviruses, rhinoviruses, Coxsackie, and coronaviruses. These viruses typically lead to catarrhal or edematous (infiltrative) forms of laryngitis.

Bacteria, on the other hand, tend to cause purulent forms of acute laryngeal inflammation, most notably epiglottitis or an epiglottic abscess. Among the most common bacterial pathogens are Streptococcus pneumoniae, Haemophilus influenzae type B, and Moraxella catarrhalis, as well as other streptococci and staphylococci.

Fungal forms of laryngitis are caused by fungi such as Candida and Aspergillus and often become chronic. These conditions are most common in patients who regularly use inhaled corticosteroids, such as those with bronchial asthma.

In addition to the direct damaging effects of pathogens on the laryngeal mucosa, inflammation may also spread from the upper respiratory tract infection. In cases of acute or chronic sinusitis or adenoiditis, mucus drains down the posterior pharyngeal wall, reaching the vocal folds and causing mechanical irritation.

Anatomic Pathology

Viral infections are typically accompanied by systemic symptoms and catarrhal inflammation of the nasopharynx and oropharynx. Similar inflammatory changes are observed in the mucosa of the larynx as well.

In catarrhal laryngitis, the laryngeal mucosa appears inflamed. The vocal folds are markedly hyperemic with pronounced vascular engorgement. Phonation is impaired due to incomplete closure of the vocal folds. Additionally, mucous secretions may accumulate on the vocal folds and within the piriform sinuses.

In the infiltrative form, pronounced edema of the vocal folds and the interarytenoid region is observed against hyperemic laryngeal mucosa. The vocal folds become gelatinous and irregular, failing to achieve complete closure during phonation. As a result, the glottis appears narrowed. In severe cases, edema may extend to the vestibular folds, which can partially or completely cover the true vocal folds. In some patients, the swelling spreads further into the subglottic mucosa. In addition, copious mucous secretions may be observed along the laryngeal walls and within the piriform sinuses.

Fungal laryngitis is characterized by thick, white, curd-like plaques covering the hyperemic mucosa.

When the epiglottis is inflamed, it becomes swollen and thickened, with pronounced hyperemia of its mucosa. As a result, the underlying structures of the larynx are often not visible during examination.

In cases of epiglottic abscess, a yellow focus of purulent exudate is typically seen on the lingual surface of the edematous, inflamed epiglottis. This condition is commonly associated with abundant mucous discharge.

Clinical Manifestations

The milder forms of laryngitis, such as catarrhal and infiltrative, typically present with the sudden onset of hoarseness. In some cases, patients may experience aphonia (complete loss of voice). These symptoms are often accompanied by sore throat, tickling in the throat, and paroxysmal coughing. In addition to these local manifestations, signs of an upper respiratory tract infection are usually present, including fever, cough, nasal congestion, and rhinorrhea. On average, symptoms of acute laryngitis resolve within 1 to 3 days.

Fungal laryngitis presents somewhat differently. Patients often report dryness and a scratchy sensation in the throat, as well as itching and persistent hoarseness.

Epiglottitis and epiglottic abscess, by contrast, are marked by more severe symptoms. These include drooling, difficulty swallowing, and intense throat pain that worsens during swallowing. Because of the rapid development of laryngeal stenosis, inspiratory stridor is common. In such cases, patients often adopt a characteristic posture: sitting upright and leaning forward, with the neck extended and arms bracing the body on the seat. Suprasternal and intercostal retractions may be visible, indicating increased work of breathing. Patients may also have a fever, and their general condition is severely impaired.

If the disease progresses unfavorably, infection may spread to the cervical fascial spaces, leading to complications such as deep neck infection (cervical cellulitis), mediastinitis, or sepsis. In children, this condition may be life-threatening due to the rapid onset of airway obstruction.

Diagnosis

The diagnostic process begins with taking a thorough medical history. It is essential to evaluate the patient’s general condition and, in particular, to assess for signs of respiratory distress.

A physical examination is followed by an ENT examination, which includes indirect laryngoscopy. However, it's important to note that in children with suspected epiglottitis, indirect laryngoscopy can provoke acute airway obstruction and should be avoided.

When feasible, flexible laryngoscopy may be performed. In patients with laryngitis, stroboscopy may reveal impaired mobility of the true vocal folds.

In cases where an epiglottic abscess is suspected, a lateral neck X-ray may be helpful. It typically reveals the pathognomonic “thumbprint sign” (marked epiglottic swelling).

In epiglottitis or epiglottic abscess, microbiological cultures obtained from the epiglottic mucosa are essential for pathogen identification.

In diagnostically challenging situations or when deep tissue involvement is suspected, ultrasound or computed tomography (CT) of the neck may be required.

Treatment

In all cases where signs of airway obstruction are present, urgent airway management must be the main priority.

For most patients with uncomplicated acute laryngitis, symptomatic treatment is sufficient. Voice rest is recommended, including avoidance of whispering, as well as smoking cessation and adequate hydration. Moreover, humidification of air and inhalation of alkaline mineral water (e.g., using bicarbonate or naturally alkaline mineral waters) may provide symptom relief. If significant edema is present, inhaled corticosteroids may be indicated.

In cases with pronounced systemic symptoms, anti-inflammatory medications may be administered.

If bacterial laryngitis is suspected, topical antibiotics (e.g., sprays) are typically prescribed. Should there be no improvement, systemic antibiotic therapy may be necessary.

For fungal laryngitis, systemic antifungal agents are indicated. Please note that during antifungal treatment, temporary discontinuation of inhaled corticosteroids is recommended when possible.

Epiglottic abscess and epiglottitis require emergency hospitalization and inpatient management. If an abscess is confirmed, surgical incision and drainage is performed, often via indirect laryngoscopy. Patients are also prescribed anti-inflammatory and systemic antibacterial therapy.

In cases of grade 4 laryngeal stenosis, a cricothyrotomy or emergency tracheotomy must be performed to secure the airway.

Chronic Laryngitis

Etiology

The most common causes of chronic catarrhal laryngitis are chronic smoking and voice overuse. Inflammation may also spread from adjacent structures such as the nasopharynx, oropharynx, or lower respiratory tract. In addition, recurrent sinusitis, rhinitis, tonsillitis, tracheitis, or bronchitis can predispose individuals to chronic inflammation of the larynx.

Atrophic laryngitis is more frequently seen in elderly individuals, particularly during hormonal changes such as menopause. It can also be associated with long-term exposure to occupational hazards, including airborne dust and chemical irritants.

Reflux laryngitis occurs due to gastroesophageal reflux, where gastric acid and its vapors reach the upper airways as a result of lower esophageal sphincter insufficiency.

Chronic fungal laryngitis typically represents the progression of inadequately treated or recurrent acute fungal infections, most commonly caused by Candida or Aspergillus species. It is more frequent in immunocompromised patients or in those who are on long-term inhaled corticosteroid therapy.

Anatomic Pathology

Chronic laryngitis develops as a mucosal response to repeated irritation or inflammation.

In chronic catarrhal laryngitis, there is epithelial hyperplasia, submucosal edema, and excessive mucus production. The mucosa appears inflamed and smooth. The vocal folds are thickened and hyperemic and may not close completely during phonation. Moreover, mucus often accumulates in the piriform sinuses.

Atrophic laryngitis is characterized by a marked reduction in the number of mucous glands. The mucosa loses its normal appearance and becomes thin, dry, and parchment-like. Additionally, thick, viscous secretions build up. The vocal folds undergo similar thinning, frequently leaving a characteristic oval-shaped glottic gap during phonation.

Reflux laryngitis typically presents with hyperemia and edema in the interarytenoid region, along with mucus collection in the piriform sinuses.

Fungal laryngitis is marked by white plaques overlying a bright red, inflamed mucosa. These changes typically involve the epiglottis.

Clinical Manifestations

The hallmark of chronic inflammatory laryngitis is persistent hoarseness or voice changes. Patients often complain of early vocal fatigue, dry cough, and a scratchy sensation in the throat.

Atrophic laryngitis presents with a dry, hacking cough and variable degrees of hoarseness, which may progress to aphonia. A feeling of a lump in the throat (globus sensation) is also frequently reported.

Reflux laryngitis is associated with hoarseness, globus sensation, retrosternal discomfort, and sometimes heartburn, although the latter is not a reliable indicator. The symptoms usually worsen at night or during sleep.

Fungal laryngitis may present with dysphagia and persistent hoarseness.

Diagnosis

Diagnosis is based on clinical history and examination. Depending on available equipment, either indirect laryngoscopy or flexible video laryngoscopy is performed.

In cases of suspected reflux laryngitis, referral to a gastroenterologist is required. Further investigations include esophagogastroduodenoscopy (EGD) and 24-hour esophageal pH monitoring.

Treatment

The cornerstone of treatment for catarrhal laryngitis is the identification and elimination of the underlying cause. Smoking cessation and reduction of vocal strain are strongly recommended.

If the inflammation originates from upper or lower respiratory tract infections, appropriate management of the primary focus is essential.

In atrophic laryngitis, regular humidification of the mucosa is advised. This can be achieved with saline inhalations or oil-based sprays. Application of iodine-containing solutions may also be beneficial, as they stimulate mucus production in response to local irritation.

Reflux laryngitis should be managed in collaboration with a gastroenterologist. The aim of the treatment is to reduce gastric acidity. Inhalations with saline, topical antibiotics, and, when indicated, glucocorticoids may be used to reduce laryngeal inflammation.

Fungal laryngitis is managed with topical or systemic antifungal medications, depending on the severity and response.

Chronic Hyperplastic Laryngitis

Etiology

This group of inflammatory disorders of the larynx is most commonly observed in individuals whose professions rely heavily on voice use, especially when voice technique is poor and vocal strain is excessive.

Vocal nodules are most commonly observed in public speakers, singers, and teachers. In addition, smoking and heavy alcohol consumption are major contributing factors. Less commonly, exposure to occupational hazards such as dust, paint fumes, textiles, and leather production can lead to similar changes.

Reinke’s edema is strongly associated with chronic tobacco use and is typically seen in female smokers.

Vocal fold polyps and pachydermia often arise as complications of chronic laryngopharyngeal reflux.

Contact granulomas of the larynx are usually found in patients who have experienced prolonged or traumatic endotracheal intubation, either during general anesthesia or mechanical ventilation.

Anatomic Pathology

Diffuse hyperplastic laryngitis is marked by extensive hyperplasia of the laryngeal mucosa. The most commonly affected areas include the free edges of the vocal folds, the arytenoid cartilages, and the interarytenoid region. The mucosa appears erythematous and uneven.

In edematous–polypoid laryngitis, there is bilateral, gelatinous swelling along the entire free edge of the vocal folds. These folds fail to close completely during phonation, and the glottic airway may become narrowed due to mucosal overgrowth.

Vocal nodules always appear at a characteristic location — the junction between the anterior and middle thirds of the true vocal folds on both sides.

These lesions are broad-based and usually match the surrounding tissue in color. Vocal nodules interfere with complete glottic closure, producing the classic “hourglass” configuration during phonation. Importantly, they may regress on their own with adequate voice rest and reduced vocal load.

A vocal fold polyp represents a localized epithelial edema. Polyps may arise at various distances from the anterior commissure and vary in size from a few millimeters to large lesions prolapsing into the lower larynx and interfering with breathing. They may be sessile or pedunculated, pale pink in color, and typically unilateral. Some polyps are hemorrhagic and may bleed.

Laryngeal pachydermia involves uneven, nodular epithelial overgrowths on the vocal folds or interarytenoid region. These growths are typically pink and broad-based.

Laryngeal granulomas consist of granulation tissue overgrowth at the site of prior trauma (intubation), most commonly the vocal fold. These lesions are usually heterogeneous in color, ranging from pale pink to bright red, and are typically broad-based. Some may resolve spontaneously over time.

Clinical Manifestations

All conditions within this category share common symptoms, including persistent hoarseness, voice changes, chronic dry cough, and the sensation of a lump in the throat (globus sensation). Large polyps may result in aphonia or even laryngeal stenosis.

Diagnosis

Diagnosis is based on clinical history and examination. Depending on available equipment, either indirect laryngoscopy or flexible video laryngoscopy is performed.

Biopsy with histological analysis is an essential component of diagnosis and is usually performed intraoperatively.

Treatment

The first step in treatment is the elimination of causative factors such as smoking, excessive voice use, or exposure to harmful substances in the workplace.

Patients in voice-demanding professions should be referred for voice therapy under the supervision of a phoniatric specialist. In some cases, such as vocal nodules, conservative voice therapy alone may be sufficient for symptom resolution.

Most patients require a combined treatment approach involving both medical therapy and surgical intervention. Conservative therapy includes inhalations with isotonic saline, corticosteroids, and, when appropriate, antiseptic or antibiotic agents. Intralaryngeal instillation of therapeutic agents may also be considered.

Surgical treatment consists of mechanical removal of the lesion. Several methods are available. The so-called “cold” technique involves excision using microinstruments such as forceps, punches, or microdebriders. This approach has the advantage of providing tissue samples for histopathological analysis. However, it carries certain risks, including the potential for excessive tissue removal and damage to the vocal folds, which may result in permanent voice dysfunction.

An alternative technique involves lesion ablation using various types of lasers. The current gold standard is CO₂ laser excision, which minimizes damage to surrounding tissues and supports faster recovery.

After surgery, a period of complete voice rest is essential to facilitate optimal healing and reduce the risk of recurrence.

Specific Inflammatory Conditions of the Larynx

Etiology

Diphtheria is a highly contagious infectious disease that primarily affects children. It is caused by toxigenic strains of the gram-positive bacillus Corynebacterium diphtheriae. The infection typically involves the upper respiratory tract and spreads from the oropharynx downward to the larynx.

Laryngeal syphilis is caused by the gram-negative spirochete Treponema pallidum and usually represents a manifestation of secondary syphilis in the oropharynx following systemic dissemination.

Scleroma results from infection with Klebsiella rhinoscleromatis, which is transmitted via airborne droplets or through direct contact. This condition primarily involves the upper airways.

Laryngeal tuberculosis is almost always secondary to pulmonary tuberculosis. Mycobacterium tuberculosis is introduced into the larynx through infected sputum during coughing. Less commonly, lymphatic or hematogenous dissemination may occur.

Anatomic Pathology

In diphtheria, Corynebacterium diphtheriae releases an exotoxin that causes necrosis of the mucosa, leading to the formation of adherent pseudomembranes. The disease often begins in the tonsillar region and progressively extends toward the larynx. These membranes are typically grayish in color, dense, fibrous, and firmly attached to the mucosal surface. Attempts to remove them result in pinpoint bleeding. Within 3–7 days, spontaneous detachment of the membranes may occur, potentially causing airway obstruction. Systemic absorption of the toxin can lead to damage of internal organs, including the heart and kidneys, resulting in myocarditis and nephritis.

Secondary laryngeal syphilis is characterized by the appearance of gray papules on the mucosa. The vocal folds become hyperemic and thickened. When papules are located on the vocal folds, they may resemble vocal nodules.

Tertiary syphilis presents with gummas (granulomatous lesions) located on the epiglottis or vestibular folds. As these lesions break down, they form deep ulcers with central necrotic debris. Upon healing, stellate scars form, contracting surrounding tissues and potentially leading to airway stenosis.

Scleroma follows a staged progression. Symmetrical infiltrates form at physiologic narrowings of the airway, most commonly the subglottic region in the larynx. The mucosa appears nodular and pale pink, and the airway lumen is mildly narrowed. As the disease advances, infiltrates are replaced by fibrotic scars and adhesions, resulting in progressive stenosis. Other parts of the larynx are much less commonly affected.

In laryngeal tuberculosis, the posterior laryngeal structures, including the interarytenoid region and vocal folds, are most frequently involved. Small nodules develop on an erythematous and infiltrated mucosa. They subsequently ulcerate and transform into tuberculomas. The affected vocal fold becomes thickened and inflamed, with ulceration typically affecting one side. If left untreated, the disease may progress to laryngeal perichondritis.

Clinical Manifestations

Diphtheria presents with both local and systemic symptoms. Patients usually present with fever, headache, malaise, and sore throat. Membranous exudates initially form on the tonsils, later extending to the posterior pharyngeal wall and descending into the larynx. These membranes often have a sweetish odor. Soft tissue swelling and enlargement of regional lymph nodes result in the formation of the so-called "bull neck." As edema and membrane formation extend into the larynx, symptoms such as hoarseness, progressing to aphonia and stridor, may develop. In severe cases, detachment of the membranes may cause acute airway obstruction and asphyxiation. Systemic absorption of large amounts of toxin can damage vital organs, particularly the heart and kidneys. This can precipitate acute heart or kidney failure, potentially resulting in fatal outcomes.

In laryngeal syphilis, symptoms are usually nonspecific and may include hoarseness, aphonia, and sore throat. Progressive scarring may eventually lead to breathing difficulties.

Scleroma is characterized by chronic airway stenosis. Patients typically present with progressive dyspnea, alongside other typical upper airway findings: nasopharyngeal crusting, nasal breathing difficulty, and a distinctive sweet odor.

Tuberculosis of the larynx presents with persistent hoarseness, a prolonged productive cough with copious sputum, sore throat, and low-grade fever.

Diagnosis

Diphtheria is diagnosed based on characteristic symptoms and examination findings. Confirmation of diagnosis involves direct microscopy of swabs, revealing Corynebacterium diphtheriae in a distinctive “club-shaped” arrangement.

The diagnosis of syphilis is confirmed by positive serological testing for Treponema pallidum antibodies.

Scleroma has distinctive features on ENT examination. Serologic testing can confirm the presence of antibodies to Klebsiella rhinoscleromatis. During laryngoscopy or bronchoscopy, biopsies of affected airway tissues are taken for histologic evaluation, which may reveal diagnostic elements such as Mikulicz cells and Russell bodies.

In suspected cases of laryngeal tuberculosis, sputum culture for acid-fast bacilli is performed. A consultation with a tuberculosis specialist is also necessary.

For all the above conditions, close contacts should be examined and monitored.

Treatment

Suspected diphtheria cases must be hospitalized, either in infectious disease units or intensive care settings, depending on clinical severity. Specific therapy involves the administration of diphtheria antitoxin to neutralize circulating exotoxin.

Simultaneously, antibiotics targeting the causative organism are initiated. To prevent diphtheria outbreaks, many countries conduct routine childhood vaccination programs, and close contacts are vaccinated during outbreaks as a precautionary measure.

Patients with syphilis require treatment in specialized venereology centers, as improper self-treatment may lead to latent infection. Penicillin or cephalosporins are the antibiotics of choice.

Scleroma is managed with pathogen-targeted antibiotic therapy. Infiltrative lesions are treated with saline inhalations and topical application of oil-based solutions to soothe the mucosa.

Scar tissue may require surgical excision or endoscopic laryngeal dilation. In cases of decompensated airway stenosis, tracheostomy may be necessary.

The treatment for tuberculosis includes long-term (6–12 months) administration of appropriate antibiotics, such as rifampicin and isoniazid.

Laryngitis Associated with Systemic Diseases

Etiology

This group includes systemic autoimmune diseases. Laryngeal involvement occurs in approximately 25–30% of patients with rheumatoid arthritis (RA) and in about 30% of those with systemic lupus erythematosus (SLE). In granulomatosis with polyangiitis (GPA), previously known as Wegener's granulomatosis, the incidence ranges from 15% to 55%. The prevalence of laryngeal involvement in amyloidosis remains unknown.

Anatomic Pathology

RA is characterized by aseptic joint inflammation. In the larynx, it typically affects the cricoarytenoid joints, resulting in edema and thickening of the joint capsule. In advanced stages, glottic narrowing, sagging of the vocal folds during phonation, and impaired mobility may develop.

Involvement of the true vocal folds may present as yellowish nodules located at the junction of the anterior and middle thirds, resembling bamboo nodes.

In SLE, immune complex deposition leads to damage of vascular, connective, and mucosal tissues. The laryngeal mucosa may appear hyperemic and edematous, with ulcer formation. Cricoarytenoid joint involvement may restrict vocal fold mobility. Healing of mucosal ulcers often results in scar formation, which can contribute to laryngeal stenosis.

Amyloid deposits in the larynx may occur in both primary and secondary amyloidosis. Primary amyloidosis often presents as an isolated disease characterized by submucosal accumulation of amorphous amyloid protein. Secondary amyloidosis develops in the context of underlying systemic diseases, such as rheumatoid arthritis or Crohn’s disease. In the larynx, amyloid may form pale-yellow, polypoid masses covered by smooth, waxy mucosa. The true vocal folds and subglottic space are most commonly affected, and the process may extend into the tracheobronchial tree.

GPA is a necrotizing autoimmune vasculitis that most frequently affects the upper airways and kidneys. In the larynx, subglottic edema and mucosal ulceration with hemorrhagic foci may be seen. Granuloma formation is followed by scarring and progressive stenosis.

Clinical Manifestations

In RA, symptoms may include hoarseness and dyspnea. Severe throat pain that worsens with swallowing and phonation and may radiate to the ear is typical. Ankylosis of the cricoarytenoid joints may cause glottic narrowing and laryngeal stenosis. Vocal fold involvement leads to dysphonia.

During acute flares of SLE, patients may experience intense throat pain, hoarseness, and shortness of breath. Progressive disease can result in chronic laryngeal stenosis.

Amyloidosis often has subtle clinical manifestations. Hoarseness may occur in cases of significant vocal fold involvement, while subglottic amyloid deposits can cause respiratory obstruction.

GPA presents with throat pain, hemoptysis, and hoarseness. As the disease advances, stridor may develop due to subglottic stenosis.

Diagnosis

RA is diagnosed based on laboratory findings, including elevated erythrocyte sedimentation rate (ESR), positive rheumatoid factor, and other markers of autoimmune inflammation.

SLE is confirmed by the presence of serum antinuclear antibodies (ANA) and antibodies against double-stranded DNA (anti-dsDNA) in the serum.

In suspected amyloidosis, a CT scan of the neck may reveal tissue thickening. Definitive diagnosis requires histological confirmation of amyloid deposits in affected areas.

GPA is diagnosed by detecting antineutrophil cytoplasmic antibodies (ANCA) in the blood.

Treatment

These conditions are primarily managed with pharmacotherapy. High doses of corticosteroids, immunosuppressive agents, and anti-inflammatory medications are typically prescribed.

In RA, intra-articular corticosteroid injections into the cricoarytenoid joint may provide symptom relief.

Treatment of amyloidosis differs depending on the type. In primary amyloidosis, corticosteroids are generally ineffective, and surgical excision of the deposits is often required. By contrast, secondary amyloidosis requires treatment of the underlying condition, with high-dose corticosteroids and anti-inflammatory agents being the main therapeutic approaches. Notably, surgical removal of amyloid deposits may paradoxically lead to further accumulation.

Inflammation of Laryngeal Cartilages

Etiology

Chondritis and perichondritis (inflammation of the cartilage and perichondrium) of the larynx may result from a variety of causes. The most common are laryngeal traumas, including iatrogenic injuries during surgical procedures or intubation. Inflammation of the cricoid cartilage frequently occurs following upper tracheostomy.

Recently, aseptic cartilage inflammation has been increasingly observed after radiotherapy for head and neck malignancies. In rare cases, infection may spread from adjacent tissues.

Anatomic Pathology

Cartilaginous inflammation typically leads to mucosal hyperemia and infiltration throughout the larynx, with the most severe luminal narrowing occurring at affected sites. Purulent fistulas may form, opening either into the laryngeal lumen or externally onto the neck. These tracts permit drainage of necrotic cartilage fragments.

In chondritis and perichondritis of the thyroid cartilage, either the internal or external surface may be affected. When the external surface is involved, swelling of the neck’s soft tissues is evident, while no pathological changes are seen within the laryngeal lumen. By contrast, involvement of the internal surface results in mucosal edema and hyperemia over the thyroid cartilage region, thickening of the aryepiglottic folds, and partial obscuration of the glottic opening.

Cricoid chondritis and perichondritis are characterized by subglottic edema, progressing to airway narrowing and eventual cicatricial stenosis.

Involvement of the arytenoid cartilages causes marked enlargement; the vocal folds become immobile during phonation and may adopt a median position.

Inflammation of the epiglottic cartilage presents as globular thickening, stiffness, intense mucosal hyperemia, near-complete laryngeal obstruction, and copious mucus secretion.

Clinical Manifestations

The hallmark symptoms of laryngeal cartilage inflammation are severe throat pain, voice impairment, and varying degrees of respiratory distress.

When the external surface of the thyroid cartilage is involved, the neck may appear visibly enlarged and is tender on palpation.

Chondritis and perichondritis of the cricoid, arytenoid, or epiglottic cartilages may lead to significant respiratory insufficiency.

Epiglottic inflammation can also cause dysphagia with choking during meals and profuse salivation.

Diagnosis

Diagnosis is based on patient history and ENT examination. To determine the extent and precise localization of the lesion, ultrasound or CT of the neck is performed.

Treatment

In the acute phase, broad-spectrum antibiotics and anti-inflammatory medications are indicated.

If fistulas develop, they require debridement and dressing with antiseptic solutions.

Cicatricial stenosis is managed surgically, either through excision or dilation using bougies.

In cases of severe airway obstruction, tracheostomy is performed.