• Acute laryngitis is extremely common — it is part of the spectrum of upper respiratory tract infections (URTIs), which are the most frequent infectious diseases worldwide
• Estimated lifetime prevalence approaches nearly 100% (virtually everyone experiences at least one episode)
• Accounts for approximately 15–20% of all respiratory disease presentations where hoarseness is the chief complaint
• In children, viral laryngotracheitis (croup) has a peak incidence of ~6 per 100 children per year in those aged 6 months to 3 years ^[2]

• Adults: Acute viral laryngitis is common across all ages; chronic laryngitis is more prevalent in middle-aged and older adults
• Children: Peak incidence at 6–36 months (3 years old) for croup; male predominance (M:F = 1.5:1) ^[2]
• Occupational laryngitis (voice abuse): more common in teachers, singers, salespeople, call centre workers — those who use their voice professionally

• Seasonal influence: peaks in autumn and early winter (corresponding to respiratory virus seasons — parainfluenza, RSV, influenza) ^[2]
• In Hong Kong specifically, influenza peaks are bimodal (Jan–Mar and Jul–Aug), so laryngitis from influenza can occur in summer as well

• Dense urban living and air pollution (PM2.5, NO₂) contribute to chronic laryngeal irritation
• High rates of GERD-related laryngopharyngeal reflux (LPR) — partly attributable to dietary factors and high prevalence of H. pylori (though H. pylori's direct role in reflux is debated)
• Nasopharyngeal carcinoma (NPC) is highly prevalent in southern China/Hong Kong — always consider NPC in the differential of chronic hoarseness with neck mass ^[4]
• Laryngeal carcinoma risk factors — smoking and alcohol — remain prevalent in Hong Kong's male population ^[5]

• Exposure to respiratory viruses: close contacts, crowded environments (schools, MTR in Hong Kong)
• Immunocompromised states: HIV, post-transplant immunosuppression, chemotherapy, diabetes
• Malnutrition ^[2][6]
• Underlying chronic illness ^[6]
• Lack of vaccination: unvaccinated children at risk for diphtheria (rare but devastating cause)

• Smoking — direct thermal and chemical irritant to laryngeal mucosa; also a risk factor for laryngeal carcinoma ^[1][5][7]
• Alcohol — desiccates laryngeal mucosa and is a co-carcinogen with tobacco ^[5][7]
• Voice abuse/misuse — shouting, singing without proper technique, prolonged speaking → mechanical trauma to vocal cords (vocal nodules, polyps) ^[1]
• Gastroesophageal reflux disease (GERD) / Laryngopharyngeal reflux (LPR) — acid and pepsin cause chemical laryngitis of the posterior glottis ^[1][8]
• Environmental irritants: occupational dust, chemical fumes, air pollution, dry air
• Irradiation (history of radiotherapy to head/neck) ^[5]
• Allergies: allergic laryngitis (atopic individuals)
• Medications: inhaled corticosteroids (without rinsing mouth → fungal laryngitis from Candida), anticholinergics (dry mucosa), bisphosphonates (reflux-related)
• Chronic laryngitis is a risk factor for laryngeal carcinoma ^[5]

• The larynx is a cartilaginous structure in the anterior neck at the level of C3–C6 vertebrae
• It connects the pharynx (above) to the trachea (below)
• The larynx extends from the epiglottis superiorly to the cricoid cartilage inferiorly ^[5]

This is critical for understanding pathology localisation (especially tumours):

The larynx is divided into 3 anatomical regions ^[1][5]:

1. Supraglottis — from the epiglottis to the junction of the ventricle floor with the true vocal cords

   • Includes: epiglottis, aryepiglottic folds, false vocal cords (vestibular folds), laryngeal ventricle
   • Rich lymphatics → higher incidence of lymph node metastasis (30–50%) ^[5]
   • Presents as advanced disease due to paucity of early symptoms ^[5]

2. Glottis — the true vocal cords and the anterior and posterior commissures

   • Most common site of laryngeal cancer ^[5]
   • Presents early with hoarseness because even tiny lesions on the vocal cord disrupt phonation ^[5]
   • Sparse lymphatics → LN metastasis is rare in early glottic cancer

3. Subglottis — from 1 cm below the free edge of the true vocal cords to the lower border of the cricoid cartilage

   • Presents as advanced disease; propensity for local extension; higher recurrence rates; poorer survival ^[5]
   • Higher rate of lymphatic spread (40%) ^[5]
   • In children, the subglottic space is the narrowest part of the airway (in adults, it is the glottis)

The vocal cords are the functional core of the larynx for phonation:

• True vocal cords: paired folds of mucous membrane overlying the vocalis muscle and vocal ligament
  • Covered by stratified squamous epithelium (designed to withstand mechanical trauma of vibration)
  • The free edge vibrates when air passes through — this produces sound
  • Reinke's space: a potential subepithelial space on the vocal cord where oedema collects (Reinke's oedema — seen in smokers and voice abusers)
• False vocal cords (vestibular folds): superior to the true cords; lined by pseudostratified ciliated columnar epithelium (respiratory epithelium); do not normally vibrate

Two branches of the vagus nerve (CN X):

• The left RLN loops under the aortic arch, making it vulnerable to pathology in the mediastinum (lung cancer, aortic aneurysm, mediastinal lymphadenopathy)
• The right RLN loops under the right subclavian artery (shorter course, less vulnerable)
• RLN injury → vocal cord paralysis → hoarseness (unilateral) or airway obstruction (bilateral)

• Superior laryngeal artery (branch of superior thyroid artery from external carotid) — supplies supraglottis
• Inferior laryngeal artery (branch of inferior thyroid artery from thyrocervical trunk) — supplies glottis and subglottis
• Supraglottic lymphatic drainage: pierces thyrohyoid membrane with the superior laryngeal artery → drains to subdigastric and superior jugular nodes ^[5]
• Glottic and subglottic drainage: exits via cricothyroid ligament → prelaryngeal node (Delphian node), paratracheal nodes, and deep cervical nodes along the inferior thyroid artery ^[5]

The larynx serves three primary functions:

1. Phonation (voice production) — vocal cord vibration modulated by airflow from the lungs
   • This is why hoarseness (dysphonia) is the cardinal symptom of laryngitis
2. Airway protection — the epiglottis and vocal cords close during swallowing to prevent aspiration
   • Impaired laryngeal function → risk of aspiration
3. Respiration — the vocal cords abduct during inspiration to allow airflow
   • Laryngeal oedema or vocal cord paralysis → stridor (especially inspiratory, because during inspiration, negative intraluminal pressure tends to collapse a partially obstructed extrathoracic airway)

A critical concept for understanding paediatric laryngitis/croup:

• In children, the subglottic space is the narrowest point of the airway (bounded by the rigid cricoid ring — the only complete cartilaginous ring)
• The paediatric larynx is more cephalad (higher, at C3–C4 level) and funnel-shaped
• Poiseuille's Law (applied clinically): airway resistance is proportional to 1/r⁴
  • Even 1 mm of mucosal oedema dramatically increases resistance in a small airway
  • In a neonate with ~4 mm subglottic diameter, 1 mm oedema reduces cross-sectional area by ~75% and increases resistance 16-fold
  • In an adult with ~12 mm diameter, the same 1 mm oedema reduces area by only ~30%
• This is why the same viral infection that causes "just hoarseness" in an adult can cause life-threatening stridor in a toddler

Chronic laryngitis (≥ 3 weeks) has a broader differential:

The pathophysiology follows the same general URTI pathway, adapted for the larynx ^[6]:

1. Viral inoculation: Virus (e.g., parainfluenza, rhinovirus) deposits on the laryngeal mucosa via droplet/contact transmission
2. Epithelial invasion: Virus attaches to receptors on respiratory epithelial cells of the larynx and enters cells
3. Innate immune response: Infected cells release cytokines (IL-1, IL-6, TNF-α) and chemokines → recruitment of polymorphonuclear leukocytes (PMNs) and lymphocytes
4. Inflammation: Vascular permeability increases → oedema of the laryngeal mucosa (especially the submucosal layer, Reinke's space on the vocal cords, and the subglottic region)
5. Mucosal swelling → the vocal cord edge becomes irregular and stiffened → impaired vibration → hoarseness
6. Mucus hypersecretion: Goblet cells and submucosal glands overproduce mucus → cough, throat clearing
7. Mucociliary clearance impaired → accumulation of secretions

The symptoms of common cold (and by extension, laryngitis) are primarily due to the host's innate immune response rather than direct viral cytopathic damage ^[6]. This is why anti-inflammatory treatments (e.g., corticosteroids in croup) work — they dampen the immune-mediated oedema.

Normal phonation requires:

• Smooth, regular vocal cord edges for uniform vibration
• Adequate mucosal wave (the superficial lamina propria, "Reinke's space," must have appropriate viscosity)
• Appropriate vocal cord tension (controlled by cricothyroid and vocalis muscles via SLN and RLN)
• Adequate subglottic pressure from expiratory airflow

In laryngitis:

• Mucosal oedema → irregular vocal cord edges → turbulent vibration → rough, breathy voice
• Increased mass of vocal cords (from oedema/exudate) → lower pitch (voice sounds deeper)
• Stiffened mucosa → reduced mucosal wave → voice sounds "tight" or "strained"
• Severe oedema → vocal cords cannot adduct properly → aphonia (complete voice loss)

As explained in the anatomy section:

• In children, the subglottic region (narrowest part of the paediatric airway, bounded by the inflexible cricoid ring) swells → lumen critically narrows
• Poiseuille's law: resistance ∝ 1/r⁴ → even 1 mm oedema causes dramatic resistance increase
• Inspiratory stridor predominates because the extrathoracic airway collapses further during the negative intraluminal pressure generated on inspiration (Bernoulli effect)
• In adults, the larger airway diameter means the same degree of swelling does not cause critical narrowing → hoarseness predominates without stridor (except in severe cases such as allergic angioedema)

1. Duration — acute vs chronic (the single most important discriminator)
2. Onset and progression — sudden (allergic, spasmodic croup) vs gradual (viral, chronic)
3. Voice use — occupation, recent shouting/singing
4. Smoking and alcohol — quantify pack-years and units/week
5. GERD symptoms — heartburn, regurgitation, throat clearing, globus (but remember LPR can occur WITHOUT classic heartburn ^[8])
6. Associated URTI symptoms — rhinorrhea, sneezing, sore throat
7. Respiratory symptoms — stridor, dyspnoea, cough character
8. Dysphagia / odynophagia / drooling — alarm features
9. Weight loss, night sweats, haemoptysis — TB, malignancy
10. Medications — inhaled corticosteroids, ACE inhibitors, anticholinergics
11. Past medical history — intubation history (intubation trauma), autoimmune disease, previous RT
12. Allergies — allergic rhinitis, history of angioedema
13. In children — vaccination status (diphtheria, Hib, measles), age, fever character

1. Listen to the voice — hoarseness, muffled quality ("hot potato"), aphonia
2. Listen for stridor — inspiratory, expiratory, biphasic
3. Assess respiratory status — RR, SpO₂, accessory muscle use, retractions (in children)
4. Examine oropharynx — tonsillar size, pharyngeal erythema, membrane (diphtheria), drooling
5. Examine neck — lymphadenopathy, thyroid, laryngeal crepitus ^[9]
6. Do NOT examine the throat in a child with suspected epiglottitis — risk of complete airway obstruction
7. Laryngoscopy (indirect mirror / flexible nasendoscopy / direct laryngoscopy) — the definitive examination for any significant or chronic hoarseness

There are no formal validated diagnostic criteria. The diagnosis is made clinically when:

• Hoarseness (dysphonia) is present as the predominant symptom
• Duration is < 3 weeks
• There is a plausible acute cause (URTI symptoms, recent voice abuse, irritant exposure)
• No red flag features are present

Confirmation of etiological diagnosis is NOT necessary for most patients since acute laryngitis is a self-limited disease that usually requires symptomatic treatment ^[11][12].

Croup is a clinical diagnosis ^[11]. The diagnostic triad is:

1. Barking ("seal bark" / "sea lion") cough — due to subglottic/tracheal oedema
2. Inspiratory stridor — turbulent airflow through narrowed subglottic airway
3. Hoarseness — vocal cord oedema

With or without:

• Preceding coryzal symptoms (present in viral croup, absent in spasmodic croup) ^[11]
• Low-grade fever
• Respiratory distress

Imaging (Neck XR) is NOT indicated if clinically suggestive ^[11] — only performed if the diagnosis is uncertain or to differentiate from epiglottitis/foreign body.

For croup specifically, the Westley Croup Severity Score ^[11] guides management intensity:

Score interpretation ^[11]:

• ≤ 2 points → mild: home treatment with symptomatic care ± PO dexamethasone
• 3–7 points → moderate: outpatient treatment with PO dexamethasone + nebulised adrenaline
• 8–11 points → severe: hospitalisation with same treatment
• ≥ 12 points → ICU admission with IM/IV dexamethasone ± repeated nebulised adrenaline

Most cases of acute laryngitis do not require blood tests. However, investigations are warranted when the presentation is atypical, chronic, or has red flags.

Mandatory when laryngoscopy reveals:

• Any suspicious mass, ulcer, or leukoplakia — to exclude SCC or dysplasia
• Granulomatous-appearing lesion — to differentiate TB vs GPA vs sarcoidosis vs carcinoma
• TB can mimic carcinoma on gross appearance → always send tissue for both histopathology AND AFB culture/PCR ^[5]

Performed via direct laryngoscopy under GA (microlaryngoscopy) — allows operating microscope for precise biopsy.

Histopathological findings to expect:

When laryngopharyngeal reflux (LPR) is suspected as the cause of chronic laryngitis:

Relevant when upper airway obstruction is suspected:

• Flattened inspiratory limb on flow-volume loop → variable extrathoracic obstruction (e.g., unilateral vocal cord paralysis, laryngomalacia)
• Flattened expiratory limb → variable intrathoracic obstruction
• Both limbs flattened (box-shaped loop) → fixed obstruction (e.g., bilateral vocal cord paralysis, subglottic stenosis, tracheal tumour)
• Inducible laryngeal obstruction (ILO / vocal cord dysfunction): flattened inspiratory loop during exercise challenge but normal at rest; laryngoscopy during exercise shows paradoxical vocal cord adduction

Acute viral laryngitis is self-limiting and requires only supportive management ^[6].

• Minimise distress — a crying, agitated child generates more turbulent airflow → worsens stridor. Keep the child calm, on parent's lap, avoid unnecessary examinations or procedures
• Monitor — pulse oximetry, respiratory rate, work of breathing, level of consciousness
• Corticosteroids are the cornerstone — they reduce laryngeal/subglottic mucosal inflammation and oedema (takes 2–6 hours to work)
• Nebulised adrenaline is the rescue therapy — provides rapid but temporary relief (works within minutes, lasts 1–2 hours)

• No stridor at rest for at least 2–4 hours after last nebulised adrenaline
• Comfortable at rest, not distressed, feeding well
• Parents educated on warning signs (return if stridor at rest, increased work of breathing, drooling, unable to feed, colour change)
• Consult ENT for recurrent or slow-to-resolve croup → may be associated with underlying subglottic stenosis ^[11]

Post-laryngectomy voice rehabilitation:

• Tracheo-oesophageal puncture (TEP) with voice prosthesis — most common method; air from trachea passes through prosthesis into oesophagus, vibrating the pharyngo-oesophageal segment to produce voice
• Oesophageal speech — swallowing air and releasing it to vibrate the pharyngo-oesophageal segment (no prosthesis needed, but difficult to learn)
• Electrolarynx — handheld device pressed against neck that generates sound

• Total duration: 6 months (standard regimen)
• Why laryngeal TB must be treated: it is highly infectious (patients are often sputum-positive), and untreated it causes progressive destruction, fibrosis, and potential airway compromise
• Always biopsy suspicious laryngeal lesions because TB mimics carcinoma ^[5] — you do not want to irradiate a patient who actually has TB

Management depends on the cause and whether it is unilateral vs bilateral, acute vs chronic:

This is the most feared acute complication and the reason laryngitis in children (croup) is taken seriously.

Asthma exacerbation ?due to ↑ airway hyperreactivity with local inflammation ^[6][18].

• Viral URTI (including laryngitis) is the most common trigger for acute asthma exacerbations in children
• Mechanism: viral infection upregulates inflammatory mediators in the airway → increased eosinophilic inflammation → bronchial hyperresponsiveness → bronchospasm
• Clinical implication: If wheezing persists after resolution of laryngitis (especially with RSV or parainfluenza), prompt investigation for asthma ^[6][18]

This is the most important long-term complication of chronic laryngitis from a clinical perspective.

The field carcinogenesis concept explains why:

• Smoking and alcohol are the dominant risk factors for CA larynx ^[5][7] — they provide the chronic mucosal irritation
• CA larynx most commonly presents as SCC ^[7] — because the vocal cords are lined by stratified squamous epithelium, and chronic irritation drives squamous carcinogenesis
• Glottic cancer (most common laryngeal cancer) presents EARLY with hoarseness ^[5] — even tiny lesions on the vocal cord disrupt vibration, providing an early warning sign. This is actually a "helpful" complication in a sense — it allows early diagnosis

Radiotherapy is the mainstay of laryngeal preservation treatment ^[7], but it comes with its own complications:

Total laryngectomy is a major procedure with significant impact on function:

Since thyroid surgery is a common cause of iatrogenic laryngitis/vocal cord paralysis, its complications are relevant here [18a]^[20]: