Chronic Laryngitis

Persistent laryngeal inflammation lasting beyond 3 weeks, producing chronic dysphonia. It is not a single disease but a final common pathway for a set of distinct causes, and the diagnostic task is to identify which of them is operating, since the treatments differ entirely.

Pathophysiology

Sustained irritation produces chronic inflammatory infiltration, squamous metaplasia with replacement of the normal respiratory epithelium, thickening of the epithelium and lamina propria, glandular hyperplasia with altered mucus, and eventually submucosal fibrosis. The mucosal wave becomes stiff and asymmetric, producing persistent roughness. Chronic irritation with tobacco carries the additional risk of dysplasia and malignant transformation, which is the reason chronic laryngitis in a smoker is never simply a benign diagnosis.

Causes

Irritant and behavioural:

• Tobacco smoking, which is the single most important cause and which also drives dysplasia.
• Alcohol.
• Occupational irritants: dusts, solvents, welding fumes, chemicals.
• Vocal misuse and abuse in teachers, singers, call centre workers, clergy, sports coaches and market traders.
• Chronic cough and throat clearing.
• Mouth breathing and dry environments.

Reflux:

• Laryngopharyngeal reflux, which is a major cause and which produces a characteristic posterior laryngitis with interarytenoid thickening, arytenoid erythema, pseudosulcus and ventricular obliteration.

Infective and inflammatory:

• Fungal laryngitis, principally Candida, in inhaled corticosteroid users, diabetics and the immunocompromised.
• Tuberculosis, which classically affects the posterior larynx with granulation and ulceration, and which is the great mimic of laryngeal carcinoma. It typically accompanies pulmonary disease but may be isolated. Any patient from a high prevalence area or with HIV and a laryngeal lesion requires mycobacterial investigation before being labelled with carcinoma or with simple laryngitis.
• Syphilis, leprosy, actinomycosis, histoplasmosis, blastomycosis and rhinoscleroma.
• Granulomatosis with polyangiitis, which causes subglottic stenosis.
• Sarcoidosis, which classically produces a pale oedematous turban shaped epiglottis and supraglottis.
• Amyloidosis, producing submucosal nodules.
• Relapsing polychondritis, which threatens the airway through cartilage collapse.
• Rheumatoid arthritis with cricoarytenoid joint involvement.

Iatrogenic:

• Inhaled corticosteroids, directly and through candidal infection.
• Radiotherapy, producing oedema and fibrosis.
• Intubation injury and chronic tracheostomy.

Postnasal drip and chronic rhinosinusitis contribute through irritant secretions and through the cough and throat clearing they provoke.

• Persistent hoarseness, typically of gradual onset and fluctuating in severity, often worse in the morning where reflux is the cause and worse at the end of the day where vocal overuse is the cause. This temporal pattern is a useful discriminator.
• Vocal fatigue and reduced vocal endurance.
• Reduced pitch range, with loss of the upper register.
• Increased effort to phonate.
• Chronic throat clearing and a sensation of mucus in the throat.
• Globus sensation.
• Dry irritating cough.
• Throat discomfort and dryness.
• Occupational impact, which may be severe in voice dependent occupations and which should be quantified.

Red flags

• Hoarseness persisting beyond 3 weeks in any patient, and particularly in a smoker.
• Progressive rather than fluctuating dysphonia.
• Odynophagia, dysphagia, referred otalgia, haemoptysis, weight loss or a neck mass.
• Stridor or exertional dyspnoea, indicating airway narrowing.
• Aspiration.
• Constitutional symptoms, night sweats, or a history of tuberculosis exposure.
• Systemic features suggesting vasculitis or connective tissue disease.
• Immunosuppression.

Examination

• Voice assessment with a validated instrument such as the Voice Handicap Index or the GRBAS scale, grading grade, roughness, breathiness, asthenia and strain.
• Flexible nasolaryngoscopy in every patient with chronic hoarseness, without exception.
• Findings: diffuse erythema, thickening and oedema of the vocal folds, loss of the pearly white appearance, mucus stranding, dilated vessels, keratosis, and in reflux disease posterior interarytenoid thickening and cobblestoning, arytenoid and posterior commissure erythema, ventricular obliteration and pseudosulcus vocalis.
• Assess vocal fold mobility, glottic closure and supraglottic hyperfunction.
• Look specifically for a discrete lesion, leukoplakia, ulceration or asymmetry, since these change the diagnosis entirely.
• Examine the neck, oral cavity and chest.

• Flexible nasolaryngoscopy, which is mandatory.
• Videostroboscopy, which assesses the mucosal wave, glottic closure pattern, amplitude and symmetry, and which detects subtle scarring, sulcus and submucosal lesions invisible on standard laryngoscopy. It also distinguishes structural from functional dysphonia.
• Direct microlaryngoscopy under general anaesthesia with biopsy for any suspicious lesion, leukoplakia, ulceration, asymmetry, or disease not responding to treatment. Biopsy is the only way to exclude dysplasia, carcinoma, tuberculosis and granulomatous disease.
• Send biopsy material for histology, mycobacterial culture and stain, fungal culture and, where indicated, immunohistochemistry and Congo red staining for amyloid.
• Fungal swab or biopsy for candidal laryngitis.
• Chest radiography and, where indicated, computed tomography of the chest, in every patient with chronic laryngitis and risk factors, both for tuberculosis and for a bronchial primary causing recurrent laryngeal nerve palsy.
• Sputum for acid fast bacilli and Xpert testing where tuberculosis is possible, together with HIV testing.
• Antineutrophil cytoplasmic antibody, urinalysis, renal function, angiotensin converting enzyme, and autoimmune screen where granulomatous or vasculitic disease is suspected.
• Full blood count, glucose and HbA1c, thyroid function, since hypothyroidism causes a low pitched hoarse voice through myxoedematous infiltration of the folds and is readily corrected.
• Twenty four hour dual probe pH impedance monitoring or oropharyngeal pH monitoring where reflux is suspected and empirical treatment has failed. In practice a therapeutic trial is more often used than testing.
• Assessment for chronic rhinosinusitis and allergy.

Treatment is directed at the identified cause. Prescribing a proton pump inhibitor to every hoarse patient without laryngoscopy is both ineffective and dangerous, since it delays the diagnosis of malignancy.

Eliminate irritants, which is the foundation

• Complete smoking cessation with structured support and pharmacotherapy. This is the single most effective intervention and is disease modifying, since continued smoking sustains the inflammation and drives dysplasia.
• Alcohol reduction.
• Removal from occupational irritant exposure, with occupational health involvement.
• Adequate hydration and environmental humidification.
• Avoidance of dehydrating agents including caffeine and antihistamines.

Voice therapy, which is central and frequently underused

• Referral to a speech and language therapist for every patient with a behavioural component, which is most of them.
• Vocal hygiene education: hydration, avoidance of throat clearing with substitution of a hard swallow or sip of water, avoidance of whispering, avoidance of shouting and speaking over noise, and use of amplification.
• Resonant voice therapy, semi occluded vocal tract exercises such as straw phonation and lip trills, and confidential voice therapy, which reduce vocal fold impact stress and improve efficiency.
• Reduction of supraglottic hyperfunction and muscle tension.
• Vocal warm up and cool down routines for professional voice users.
• Occupational modification: reduced speaking hours, amplification for teachers, scheduled voice rest.

Reflux management

• Lifestyle: weight loss, smaller meals, no eating within 3 hours of lying down, avoidance of alcohol, caffeine, chocolate, mint, fatty and spicy food, and elevation of the head of the bed by 15 to 20 cm.
• Proton pump inhibitor: omeprazole 20 mg twice daily, or lansoprazole 30 mg twice daily, or esomeprazole 40 mg once or twice daily, taken 30 to 60 minutes before meals, since these drugs require an activated proton pump to work and taking them with or after food substantially reduces efficacy. This dosing detail is regularly omitted and is a common cause of apparent treatment failure.
• Duration of at least 8 to 12 weeks, with response taking 2 to 3 months. Patients who stop at 2 weeks because nothing has changed should be warned in advance.
• Alginate preparations after meals and at bedtime, which form a raft and are particularly effective for the non acid and gaseous reflux that contributes to laryngeal symptoms.
• H2 receptor antagonist at night as an adjunct.
• Consider that the evidence for proton pump inhibitors in laryngopharyngeal reflux is weaker than commonly assumed, with several trials showing no benefit over placebo. Prolonged empirical treatment without response should prompt reassessment rather than dose escalation, given the association of long term use with fracture, hypomagnesaemia, vitamin B12 deficiency and enteric infection.
• Fundoplication in selected patients with documented reflux, objective testing and a partial response to medical therapy.

Fungal laryngitis

• Fluconazole 100 to 200 mg daily for 3 weeks.
• Review inhaler technique, add a spacer, reduce the corticosteroid dose to the minimum effective, and reinforce rinsing and spitting.
• Confirm the diagnosis where possible, since fungal laryngitis and dysplasia can look similar and treating blindly delays diagnosis.

Inhaled corticosteroid related laryngitis

• Use a spacer, rinse and spit after every dose, step down to the lowest effective dose in discussion with the respiratory team, and consider switching device or drug.

Specific inflammatory and infective diseases

• Tuberculosis: standard antituberculous therapy with rifampicin, isoniazid, pyrazinamide and ethambutol for 2 months followed by rifampicin and isoniazid for 4 months, under specialist supervision, with contact tracing and notification. Laryngeal tuberculosis is highly infectious and requires respiratory isolation until treatment has been established.
• Granulomatosis with polyangiitis: induction with corticosteroid plus rituximab or cyclophosphamide under rheumatology care, with airway intervention such as intralesional steroid injection and dilation for subglottic stenosis. Avoid unnecessary tracheostomy where medical control can be achieved.
• Sarcoidosis: systemic corticosteroid, intralesional corticosteroid injection, and steroid sparing agents.
• Relapsing polychondritis: systemic immunosuppression with urgent airway assessment, since laryngotracheal collapse is life threatening.
• Amyloidosis: endoscopic laser or microsurgical debulking, with systemic assessment for systemic amyloidosis.
• Rheumatoid cricoarytenoid arthritis: systemic disease control, with airway assessment since fixation in the adducted position causes obstruction.

Management of dysplasia

• Where biopsy shows dysplasia, the management is complete smoking cessation, excision or laser resection of the lesion, and intensive surveillance with repeat laryngoscopy at 3 monthly intervals initially. Mild dysplasia may be observed with habit cessation; moderate and severe dysplasia require excision. Progression to carcinoma occurs in a significant proportion, and these patients require long term follow up.

Follow up

• Review at 6 to 12 weeks after initiating treatment with repeat laryngoscopy.
• Failure to improve requires microlaryngoscopy and biopsy rather than a further course of medical therapy.
• Long term surveillance in smokers, in patients with dysplasia, and in those with granulomatous or systemic disease.
• Any change in the character of the dysphonia, or the development of any red flag, requires immediate reassessment.