📋 Key Information Summary
- Hoarseness (dysphonia) affects approximately 6–7% of the Australian population at any given time and accounts for significant primary care presentations annually.
- Acute laryngitis is the most common cause and is usually self-limiting (≤2 weeks); most cases are viral and do not require antibiotics.
- Any hoarseness persisting beyond 4 weeks in an adult warrants specialist ENT referral and laryngoscopy to exclude laryngeal malignancy.
- Red flags include haemoptysis, unexplained weight loss, dysphagia, odynophagia, referred otalgia, a neck mass, stridor, and hoarseness in a smoker aged >40 years.
- Risk factors for laryngeal cancer include tobacco use (strongest association), heavy alcohol consumption, occupational exposures (asbestos, wood dust), and HPV infection.
- Vocal cord nodules, polyps, and cysts are benign lesions managed with voice therapy as first-line; surgical excision is reserved for refractory cases.
- Gastro-oesophageal reflux disease (GORD) and laryngopharyngeal reflux (LPR) are common contributors to chronic hoarseness and should be empirically treated with a PPI trial.
- Vocal cord dysfunction (VCD) / inducible laryngeal obstruction (ILO) mimics asthma and is characterised by paradoxical vocal cord adduction during inspiration, often in young females and athletes.
- Flexible nasendoscopy by an ENT specialist is the gold-standard investigation for persistent hoarseness; stroboscopy adds further detail of mucosal wave abnormalities.
- Voice therapy with a speech pathologist is the cornerstone of management for most benign laryngeal conditions and functional dysphonia.
- Aboriginal and Torres Strait Islander peoples have higher rates of tobacco use and delayed access to ENT services, contributing to later-stage laryngeal cancer diagnosis.
- Occupational voice users (teachers, call-centre workers, singers) have an elevated risk of voice disorders and should receive early referral to speech pathology.
Introduction & Australian Epidemiology
Hoarseness, or dysphonia, is a symptom characterised by an abnormal change in voice quality, pitch, loudness, or effort. It arises from disruption to the laryngeal vibratory mechanism and may reflect pathology at any level — from the mucosal surface of the vocal folds to the recurrent laryngeal nerve, central nervous system, or cricoarytenoid joint. The condition is common in Australian primary care, with an estimated point prevalence of 6–7% and a lifetime prevalence approaching 30%.
The aetiology spans a broad spectrum: acute viral laryngitis accounts for the majority of acute presentations, while chronic hoarseness may be attributable to benign structural lesions (nodules, polyps, cysts), inflammatory conditions (reflux laryngitis, allergic laryngitis), neoplasia (laryngeal squamous cell carcinoma), neurological disorders (recurrent laryngeal nerve palsy, Parkinson disease), or functional / psychogenic causes (muscle tension dysphonia, vocal cord dysfunction).
In Australia, laryngeal cancer accounts for approximately 800–1,000 new diagnoses per year (AIHW data), with a male-to-female ratio of roughly 4:1 and a median age at diagnosis of 65–70 years. Five-year survival is approximately 65%, but this drops substantially for advanced-stage disease. Aboriginal and Torres Strait Islander Australians are disproportionately affected, with higher rates of head and neck cancers and later-stage presentation due to barriers in accessing specialist services in regional and remote areas.
Occupational voice disorders represent a significant cause of work-related health burden. Teachers, singers, call-centre workers, and fitness instructors are overrepresented among those with chronic dysphonia. The Australian workforce includes an estimated 300,000+ professional voice users for whom voice disorders can result in significant economic and psychological impact.
This guideline provides a structured approach to the diagnosis and management of hoarseness in Australian practice, covering diagnostic modelling, red flag identification, benign and malignant laryngeal pathology, and vocal cord dysfunction, with attention to Australian-specific epidemiology, PBS-listed treatments, MBS-rebated investigations, and considerations for underserved populations.
Hoarseness Diagnostic Model & Red Flags
Approach to the Patient with Hoarseness
A systematic approach to hoarseness begins with characterising the onset, duration, progression, and associated features. History-taking should identify risk factors, occupational voice demands, medication use (inhaled corticosteroids, anticholinergics), and comorbidities (reflux, autoimmune disease, thyroid disorders, neurological conditions).
Duration-Based Framework
| Duration | Classification | Likely Aetiologies | Action |
|---|---|---|---|
| < 2 weeks | Acute | Acute viral laryngitis, vocal overuse, laryngopharyngeal reflux flare | Supportive care; reassurance; review at 2 weeks if no improvement |
| 2–4 weeks | Subacute | Prolonged laryngitis, bacterial superinfection, early neoplasm, vocal fold haemorrhage | Trial of voice rest + PPI; if no improvement by 4 weeks → ENT referral |
| > 4 weeks | Chronic | Benign lesions, laryngeal carcinoma, vocal fold paresis, neurological disease, muscle tension dysphonia | Urgent ENT referral with laryngoscopy; exclude malignancy |
Red Flag Features
Urgent ENT referral is required if ANY of the following red flags are present:
- Hoarseness persisting > 4 weeks in an adult
- Haemoptysis or blood-stained sputum
- Unexplained weight loss (>5% body weight in 6 months)
- Progressive dysphagia or odynophagia
- Referred otalgia (ear pain without ear pathology)
- Palpable neck mass (especially level II–IV lymph nodes)
- Stridor or respiratory distress
- Smoker aged > 40 years with new-onset hoarseness
- History of head and neck irradiation
- Rapidly progressive voice change with neurological features
Key History and Examination Points
- Voice character: Breathy (vocal fold paresis, glottic gap), rough/grating (mucosal lesion), strained/strangled (muscle tension dysphonia, adductor spasmodic dysphonia), aphonic (complete cord paralysis or severe oedema)
- Tobacco history: Quantify in pack-years; any smoking history increases malignancy risk
- Alcohol intake: >14 standard drinks/week is a risk factor; synergistic with tobacco
- Voice use: Occupational demands (teacher, singer, call-centre worker, clergy)
- Medications: Inhaled corticosteroids (fluticasone particularly), anticholinergics, ACE inhibitors (cough-related), anticoagulants (haemorrhage risk)
- Reflux symptoms: Heartburn, regurgitation, throat clearing, globus sensation, chronic cough
- Neurological review: Dysarthria, dysphagia, tremor, fasciculations (consider motor neuron disease, Parkinson disease, multiple sclerosis)
- Systemic symptoms: Fatigue, weight gain, cold intolerance (hypothyroidism); dry eyes, dry mouth (Sjögren syndrome)
Inhaled corticosteroids and dysphonia: High-dose inhaled corticosteroids (especially fluticasone propionate) cause dysphonia in up to 30% of users via myopathy of laryngeal muscles and candidiasis. Ensure patients rinse and gargle after use. If hoarseness persists, consider switching device or formulation and refer to ENT if not resolving after cessation.
Primary Care Examination
In the primary care setting, the following should be assessed:
- General inspection: nutritional status, lymphadenopathy (cervical, supraclavicular)
- Neck examination: palpate thyroid gland, anterior and posterior cervical chains
- Oral cavity and oropharyngeal inspection (tongue base, tonsils, posterior pharyngeal wall)
- Auscultation of the neck for stridor
- Cranial nerve examination (especially CN X, XII)
Direct visualisation of the larynx (mirror or flexible nasendoscopy) requires specialist equipment and is not expected in general practice. Referral to an ENT specialist is the appropriate pathway for persistent or concerning hoarseness.
Chronic Laryngitis & Benign Vocal Cord Tumours
Chronic Laryngitis
Chronic laryngitis is defined as laryngeal inflammation persisting beyond 3 weeks. Unlike acute laryngitis (usually viral), chronic laryngitis has identifiable causes that must be systematically sought and addressed.
Aetiologies of Chronic Laryngitis
| Category | Examples | Key Features |
|---|---|---|
| Reflux-related (LPR) | Laryngopharyngeal reflux | Throat clearing, globus, posterior commissure granulomas, arytenoid erythema; often without classic heartburn |
| Infectious | Chronic fungal (Candida), tuberculosis, leprosy | Immunocompromised patients; TB in ATSI communities and migrants from high-prevalence countries |
| Allergic / environmental | Allergic laryngitis, irritant exposure | Occupational exposures, smoking, industrial chemicals |
| Autoimmune | Granulomatosis with polyangiitis, sarcoidosis, rheumatoid arthritis (cricoarytenoid joint) | Systemic symptoms; subglottic stenosis in GPA |
| Iatrogenic | Post-intubation, inhaled corticosteroids, radiation | Temporal relationship to intervention |
Laryngopharyngeal Reflux (LPR)
LPR is a distinct entity from classic GORD. Up to 50% of patients with LPR do not report heartburn. The laryngeal epithelium is more susceptible to acid-pepsin injury than oesophageal mucosa, with fewer protective mechanisms. Diagnosis is primarily clinical, supported by laryngoscopic findings (posterior laryngeal oedema, erythema, pseudosulcus, ventricular obliteration).
Treatment involves a combination of:
- Lifestyle modifications: weight loss, elevation of head of bed, avoidance of late meals, limiting caffeine, alcohol, spicy and acidic foods
- Proton pump inhibitor (PPI) therapy: standard or double-dose for a minimum of 8–12 weeks (e.g., esomeprazole 20–40 mg orally once or twice daily, 30 minutes before meals)
- Alginate-based therapy (e.g., Gaviscon®) after meals and at bedtime for mucosal protection
- Consider H₂ receptor antagonist at bedtime (famotidine 20 mg) if nocturnal breakthrough
PPI trial for LPR: A minimum 8-week trial of double-dose PPI (e.g., esomeprazole 40 mg BD) is recommended before concluding LPR is not contributing to hoarseness. Response rates are approximately 50–70%, lower than for classic GORD. If refractory, consider ambulatory pH monitoring and ENT referral.
Benign Vocal Cord Lesions
Benign lesions of the vocal folds are common causes of chronic dysphonia, particularly in occupational voice users. They are classified by location, morphology, and tissue characteristics.
| Lesion | Pathology | Demographics | Management |
|---|---|---|---|
| Vocal fold nodules | Bilateral, symmetrical calluses at junction of anterior and middle thirds | Teachers, singers, children; voice overuse/misuse | Voice therapy (first-line); >90% respond; surgery rarely needed |
| Vocal fold polyps | Unilateral, usually at anterior–middle third; oedematous or haemorrhagic | Adults; often a single vocal abuse episode (scream, cough) | Voice therapy + voice rest; microsurgical excision if persistent after 3–6 months |
| Vocal fold cysts | Epidermoid or mucus retention; unilateral or bilateral | Adults and children; congenital (epidermoid) or acquired | Microsurgical excision; voice therapy adjunct |
| Reinke oedema | Diffuse gelatinous oedema of the superficial lamina propria (Reinke space) | Smokers, women, voice overuse; associated with reflux and hypothyroidism | Smoking cessation (essential); voice therapy; surgical reduction if airway compromise or severe dysphonia |
| Vocal fold granuloma | Granulation tissue at vocal process of arytenoid | Post-intubation, reflux, voice abuse, intubation injury | Anti-reflux therapy (high-dose PPI); voice therapy; botulinum toxin injection; surgery as last resort (high recurrence) |
| Laryngeal papillomatosis | HPV 6/11 related; recurrent respiratory papillomata | Children (juvenile-onset) and adults | Serial laser/microdebrider excision; adjuvant cidofovir injection; HPV vaccination may reduce recurrence |
Pharmacotherapy for Benign Vocal Cord Lesions
Esomeprazole
Nexium® · PPI
Adult dose
20–40 mg PO daily or BD, 30 min before meals, for 8–12 weeks (LPR trial)
Paediatric dose
≥1 year: 0.5–1 mg/kg/day PO once daily
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Prednisolone
Panafcortelone® · Corticosteroid (short course for acute laryngitis with significant oedema)
Adult dose
25–50 mg PO daily for 3–5 days (short course only; specialist-directed for voice performance emergencies)
Paediatric dose
1–2 mg/kg/day PO for 3–5 days (croup dosing: 0.15–0.6 mg/kg single dose)
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Amoxicillin–Clavulanate
Augmentin® · Antibiotic (bacterial superinfection of larynx)
Adult dose
875/125 mg PO BD for 7 days (if purulent laryngitis suspected)
Paediatric dose
22.5 mg/kg (amox component) PO BD for 7 days
Renal adjustment
eGFR 10–30: 500/125 mg BD; eGFR <10: 500/125 mg OD
PBS status
✔ PBS General Benefit
Voice Therapy
Voice therapy delivered by a certified practising speech pathologist is the first-line treatment for most benign laryngeal conditions. Core components include:
- Vocal hygiene education (adequate hydration, avoidance of throat clearing, limiting caffeine/alcohol)
- Resonant voice therapy and semi-occluded vocal tract exercises (SOVTEs, e.g., straw phonation)
- Laryngeal manual therapy (external laryngeal manipulation)
- Breathing and postural training
- Pitch and loudness modification
- Psychological support for performance anxiety (where relevant)
Medicare rebates are available for allied health services under chronic disease management (CDM) plans (MBS items 10950–10970), allowing up to 5 allied health visits per calendar year. Patients with an ATSI health assessment (MBS item 715) may access additional allied health sessions.
Laryngeal Cancer
Epidemiology
Laryngeal squamous cell carcinoma (SCC) accounts for over 95% of laryngeal malignancies. In Australia, approximately 800–1,000 new cases are diagnosed annually, with an age-standardised incidence of 3.2 per 100,000. The male-to-female ratio has narrowed over recent decades (currently approximately 4:1). Five-year overall survival is approximately 65%, but varies substantially by stage:
| Stage | Location | 5-Year Survival | Typical Treatment |
|---|---|---|---|
| I (T1N0M0) | Confined to one subsite, normal cord mobility | 85–95% | Radiotherapy or endoscopic resection |
| II (T2N0M0) | Extends to adjacent subsite or impaired mobility | 70–80% | Radiotherapy (± concurrent chemotherapy) |
| III | Fixed cord and/or regional node involvement | 45–60% | Concurrent chemoradiotherapy or total laryngectomy + adjuvant |
| IV | Extensive local invasion and/or distant metastases | 20–35% | Total laryngectomy + adjuvant CRT or palliative systemic therapy |
Risk Factors
- Tobacco smoking: Strongest risk factor; relative risk 5–15× for heavy smokers; risk is dose-dependent (pack-years)
- Alcohol: Independent risk factor; synergistic multiplicative effect with tobacco
- Occupational exposures: Asbestos, wood dust, paint fumes, sulphuric acid, formaldehyde, nickel compounds
- HPV infection: Primarily HPV-16; increasingly recognised, particularly for oropharyngeal and supraglottic SCC
- Gastro-oesophageal reflux: Chronic acid exposure to laryngeal mucosa (controversial but epidemiologically supported)
- Immunosuppression: Post-transplant, HIV/AIDS
- Plummer-Vinson syndrome: Iron deficiency, oesophageal webs, postcricoid carcinoma (rare in Australia)
- Prior head and neck irradiation
Subsites
Laryngeal cancer is classified by subsite, which influences presentation, treatment, and prognosis:
- Glottic (60%): Most common; presents early with hoarseness; limited lymphatic drainage → low nodal metastasis rate at presentation
- Supraglottic (30%): Presents later with sore throat, otalgia, dysphagia, neck mass; rich lymphatic drainage → higher nodal metastasis rate
- Subglottic (5%): Rare; presents late with stridor, dyspnoea
Clinical pearl: Glottic carcinoma presents early because even small vocal fold lesions cause hoarseness. The key to early detection is maintaining a low threshold for laryngoscopy in any adult with hoarseness lasting > 4 weeks, particularly those with a smoking history. Supraglottic carcinoma often presents at a later stage because it does not affect the vocal folds initially.
Investigation Pathway for Suspected Laryngeal Cancer
1
Primary Care
History and examination; identify red flags; refer to ENT via fast-track/2-week-wait pathway where available
2
ENT Assessment
Flexible nasendoscopy ± stroboscopy; assessment of vocal fold mobility, mucosal irregularity, mass lesion
3
Biopsy
Direct laryngoscopy under GA with biopsy and examination under anaesthesia (EUA); histopathological confirmation
4
Staging
CT neck/chest, MRI (if cartilage invasion suspected), PET-CT (advanced disease), HPV testing (supraglottic)
5
MDT Discussion
Head and neck MDT: ENT surgeon, radiation oncologist, medical oncologist, speech pathologist, dietitian
Treatment Principles
Treatment of laryngeal cancer follows principles of organ preservation where possible, managed through specialist head and neck multidisciplinary teams (MDTs) at designated cancer centres across Australia.
- Early-stage (I–II): Radiotherapy is the standard of care for T1–T2 glottic carcinoma, offering excellent local control (85–95%) with voice preservation. Transoral laser microsurgery (TLM) is an alternative for selected T1–T2 lesions.
- Locally advanced (III–IV, larynx-preservation eligible): Concurrent chemoradiotherapy (cisplatin-based) allows larynx preservation in approximately 60–70% of patients.
- Advanced (larynx-preservation not feasible): Total laryngectomy with post-operative adjuvant radiotherapy ± chemotherapy. Reconstruction and voice rehabilitation (tracheo-oesophageal puncture, oesophageal speech, electrolarynx).
- Systemic therapy for recurrent/metastatic disease: Platinum-based chemotherapy (cisplatin + 5-FU); immunotherapy with pembrolizumab (PBS authority required for recurrent/metastatic HNSCC progressing on/after platinum-based chemotherapy).
Key Chemotherapy Agents
Cisplatin
Platinex® · Platinum agent
Adult dose
100 mg/m² IV every 3 weeks (concurrent with RT) × 3 cycles
Renal adjustment
Contraindicated if CrCl <60 mL/min; use carboplatin (AUC 1.5 weekly) as substitute
Key monitoring
Renal function (eGFR), electrolytes (Mg²⁺, Ca²⁺, K⁺), audiometry, FBC
PBS status
⚠ PBS Authority Required
Pembrolizumab
Keytruda® · PD-1 inhibitor
Adult dose
200 mg IV every 3 weeks or 400 mg IV every 6 weeks
Indication
Recurrent/metastatic HNSCC with PD-L1 CPS ≥1, progressed on/after platinum-based chemotherapy
Renal adjustment
No adjustment required
PBS status
⛔ PBS Authority Required (Specialist)
Survivorship and rehabilitation: Post-laryngectomy patients require lifelong tracheostomy care, voice rehabilitation (speech pathology), nutritional support, and psychological counselling. Thyroid and parathyroid function should be monitored (hypothyroidism occurs in 30–50% after neck radiotherapy). Referral to a head and neck cancer survivorship clinic is recommended.
Vocal Cord Dysfunction
Definition and Terminology
Vocal cord dysfunction (VCD), also termed inducible laryngeal obstruction (ILO), is characterised by paradoxical adduction (closure) of the vocal cords during inspiration, resulting in variable extrathoracic airflow obstruction. It is a functional disorder of laryngeal coordination rather than a structural or organic pathology. The term "inducible laryngeal obstruction" (ILO) is increasingly preferred by international consensus as it more accurately describes the pathophysiology without implying a psychological origin.
Epidemiology
- Estimated prevalence: 2.5–15% of patients referred for refractory asthma evaluation
- Female-to-male ratio: approximately 2–3:1
- Peak onset: adolescence and young adulthood (15–35 years)
- Overrepresented in athletes (particularly competitive swimmers and runners), healthcare workers, and high-performance individuals
- Up to 50–80% of VCD patients have concurrent asthma, making diagnosis challenging
Pathophysiology
VCD involves inappropriate, transient, involuntary adduction of the true vocal folds (and sometimes supraglottic structures) during the respiratory cycle, predominantly during inspiration. This creates a dynamic upper airway obstruction that mimics asthma. Proposed mechanisms include:
- Laryngeal hyperresponsiveness (analogous to bronchial hyperresponsiveness)
- Enhanced laryngeal chemosensitivity (reflux, post-nasal drip, irritant exposure)
- Central sensitisation and autonomic dysregulation
- Psychological stressors (anxiety, depression, trauma history) — present in 30–70% of cases
- Exercise-induced laryngeal obstruction (EILO) — a specific variant triggered by high-intensity exercise
Clinical Features
| Feature | VCD | Asthma |
|---|---|---|
| Onset/offset | Sudden onset, rapid resolution (seconds–minutes) | Gradual onset, slow resolution (hours–days) |
| Phase of respiration | Predominantly inspiratory; inspiratory stridor | Predominantly expiratory; expiratory wheeze |
| Response to bronchodilators | Poor or absent response despite escalating doses | Usually responsive to SABA |
| Symptom location | Throat / upper chest tightness, voice change during episode | Chest tightness, diffuse wheeze |
| Triggers | Exercise, stress, strong odours, irritants, GERD | Allergens, exercise, cold air, infections |
| Nocturnal symptoms | Rare (usually absent) | Common |
| Flow-volume loop | Flattened inspiratory loop (variable extrathoracic obstruction) | Flattened expiratory loop |
Diagnostic pitfall: VCD frequently coexists with asthma. Up to 50% of VCD patients also have confirmed asthma. The diagnosis of VCD should not be made by exclusion of asthma alone; both conditions should be actively assessed and managed concurrently.
Diagnosis
Essential
Flexible nasendoscopy (during symptomatic episode)
Gold standard. Paradoxical vocal cord adduction on inspiration with a characteristic posterior diamond-shaped glottic chink. Should be performed during provocation if asymptomatic at rest.
Available
Flow-volume loop (spirometry)
Characteristic flattening of the inspiratory limb. Sensitivity is limited (only captured in ~20% during an acute episode). Normal baseline spirometry does not exclude VCD.
Available
Continuous laryngoscopy during exercise (CLE / exercise test)
Gold standard for exercise-induced laryngeal obstruction (EILO). Involves exercising on a treadmill or cycle ergometer while a flexible nasendoscopy remains in situ. Available at select specialist centres in Australia.
Available
Methacholine challenge test
Used to confirm or exclude concurrent asthma. A negative test in the setting of refractory respiratory symptoms should raise suspicion for VCD.
Management
Management of VCD is primarily non-pharmacological and requires a multidisciplinary approach.
Speech Pathology (First-Line)
- Diaphragmatic breathing exercises
- Laryngeal relaxation techniques (e.g., "sniff and sigh," pursed-lip breathing)
- Voice exercises targeting laryngeal control during respiration
- Biofeedback using real-time nasendoscopy or respiratory monitoring
- Trigger identification and desensitisation strategies
- Education: the "laryngeal control breathing" technique for acute attacks (pursed-lip breathing through nose, jaw relaxation, diaphragmatic focus)
Address Contributing Factors
- Reflux management (PPI trial as above)
- Allergic rhinitis optimisation (intranasal corticosteroids, antihistamines)
- Psychological assessment and management (CBT, mindfulness-based stress reduction; consider SSRI if anxiety/depression comorbid)
- Avoidance of known irritant triggers
Pharmacological Adjuncts
Heliox (Helium–Oxygen mixture)
Heliox 70/30 or 80/20 · Acute rescue
Adult dose
Inhaled via non-rebreather mask during acute VCD episode; reduces turbulent flow in upper airway
Setting
ED / hospital (not available for home use)
PBS status
⛔ Not PBS-listed
Sertraline
Zoloft® · SSRI (for comorbid anxiety/depression)
Adult dose
50 mg PO daily, titrate to 100–200 mg daily over 4–6 weeks
Indication
Comorbid anxiety disorder or depression contributing to VCD
Renal adjustment
No adjustment required
PBS status
✔ PBS General Benefit
Acute Management of VCD Episode (ED)
VCD in the emergency department:
- Maintain calm environment; reassure the patient (VCD is not life-threatening)
- Teach pursed-lip breathing or "sniff-and-sigh" technique
- Encourage nasal breathing with jaw relaxed
- Consider heliox (70:30 or 80:20) via non-rebreather mask
- Speech pathology involvement if available
- Do NOT intubate unless absolutely necessary (intubation can worsen laryngeal spasm)
- Avoid unnecessary escalation to ICU for what is a self-resolving upper airway event
Investigations
Primary Care Investigations
Available
Full blood count (FBC)
MBS item 65060. Assess for anaemia (which may exacerbate dyspnoea), leucocytosis (infection), eosinophilia (allergic/atopic)
Available
Thyroid function tests (TFTs)
MBS item 66716. Hypothyroidism causes hoarseness via myxoedematous infiltration of vocal folds; also exclude hyperthyroidism (recurrent laryngeal nerve palsy from thyroid enlargement or surgery)
Available
Spirometry with flow-volume loop
MBS item 11505. Evaluate for flattened inspiratory loop (VCD) vs expiratory obstruction (asthma/COPD). Requires trained operator.
Available
Chest X-ray (CXR)
MBS item 58503. Exclude left recurrent laryngeal nerve palsy secondary to mediastinal pathology (lung cancer, aortic aneurysm, cardiomegaly)
Available
Serology — FBE, ESR, CRP, ANCA, ACE level
If autoimmune aetiology suspected (GPA, sarcoidosis)
Specialist Investigations
Specialist
Flexible nasendoscopy
Gold standard for laryngeal assessment. Performed in ENT outpatient clinic. MBS item 50118 (nasal endoscopy with or without biopsy). Assess vocal fold mobility, mucosal lesions, oedema, erythema, supraglottic structures.
Specialist
Laryngeal stroboscopy
Provides assessment of mucosal wave, vocal fold vibration, and submucosal pathology. Essential for evaluating benign lesions and early glottic carcinoma. Available at major ENT centres.
Specialist
CT neck with contrast
MBS item 56001. Staging of laryngeal carcinoma; assess cartilage invasion, lymph node metastases, extralaryngeal extension.
Specialist
MRI neck
MBS item 63001. Superior soft tissue resolution for assessing cartilage invasion, perineural spread, tongue base involvement.
Specialist
PET-CT
MBS item 61359 (MBS-funded for staging of head and neck SCC under specific criteria). Assess for distant metastases, synchronous primaries, and post-treatment response.
Specialist
Direct laryngoscopy + biopsy under GA
MBS item 41673 (laryngoscopy). Definitive tissue diagnosis for suspected malignancy. Allows EUA, mapping biopsy, and assessment of tumour extent.
Specialist
Continuous laryngoscopy during exercise (CLE)
Diagnostic gold standard for EILO. Available at select centres. Exercise on treadmill/cycle ergometer while flexible scope in situ to capture paradoxical cord movement at peak exercise.
Special Populations
Paediatrics
Persistent hoarseness in children (beyond 2–4 weeks) warrants paediatric ENT referral. Common causes include vocal nodules (most frequent, bilateral, from voice overuse), recurrent respiratory papillomatosis (HPV 6/11), and congenital laryngeal anomalies (laryngomalacia, vocal fold paralysis, subglottic haemangioma).
Croup (acute laryngotracheobronchitis):
Most common infectious cause of acute hoarseness in children. Treat with oral dexamethasone 0.15–0.6 mg/kg single dose (mild to moderate croup) or nebulised budesonide 2 mg if vomiting. Adrenaline nebulisation (1:1000, 4 mL) for severe croup with stridor at rest.
Voice therapy for paediatric vocal nodules should be play-based and age-appropriate. Many nodules resolve spontaneously at puberty as hormonal changes alter the vocal fold mucosa.
Pregnancy
Hormonal changes during pregnancy (oestrogen, progesterone) cause vocal fold oedema and capillary engorgement, leading to mild dysphonia in up to 30% of pregnant women. This is usually self-limiting and resolves postpartum.
GORD and LPR are common during pregnancy due to lower oesophageal sphincter relaxation. Lifestyle modifications are first-line; antacids (calcium carbonate) and Gaviscon® are safe. PPIs: omeprazole and esomeprazole are the preferred options if PPI therapy is required (Category B3).
Avoid:
Bismuth subsalicylate, prolonged corticosteroid courses, and unnecessary radiation exposure. CT neck should be deferred unless malignancy is strongly suspected (use MRI without gadolinium as the preferred alternative).
Elderly
Presbylaryngis (age-related vocal fold atrophy) is common and presents with a breathy, weak voice. It is a diagnosis of exclusion after malignancy has been ruled out. Management includes voice therapy and, in selected cases, injection laryngoplasty (e.g., hyaluronic acid or calcium hydroxylapatite) to medialise the atrophic vocal fold.
Medication review:
Polypharmacy in elderly patients increases risk of drug-induced dysphonia. Common culprits include inhaled anticholinergics, ACE inhibitors (cough), antipsychotics (tardive laryngeal dystonia), and diuretics (laryngeal drying). Review all medications in any elderly patient presenting with hoarseness.
Recurrent laryngeal nerve palsy in the elderly may be the presenting feature of thoracic malignancy (left lung cancer, mediastinal lymphadenopathy) or aortic aneurysm. Chest imaging is mandatory in new-onset vocal fold paralysis.
Renal Impairment
Uraemic laryngitis: advanced chronic kidney disease (CKD stage 4–5) can cause laryngeal oedema, ulceration, and vocal fold dysfunction from uraemic toxins. Improved with adequate dialysis.
Drug considerations:
PPIs: no dose adjustment for esomeprazole/omeprazole. Amoxicillin–clavulanate: dose reduction required (see drug card). Cisplatin: contraindicated if CrCl <60 mL/min — use carboplatin as substitute. Cetirizine/loratadine: no adjustment but use with caution in severe CKD.
Immunocompromised
Consider unusual infectious causes of laryngitis: fungal (Candida, Aspergillus), mycobacterial (TB, atypical mycobacteria), viral (CMV, HSV). HIV-positive patients are at increased risk of laryngeal Kaposi sarcoma, lymphoma, and recurrent respiratory papillomatosis (aggressive course).
Immunosuppressed patients with hoarseness:
Lower threshold for ENT referral and direct laryngoscopy with biopsy. Consider empiric antifungal therapy (fluconazole 200 mg PO daily) if oral candidiasis is present with laryngeal symptoms.
Post-transplant patients on tacrolimus/ciclosporin may develop vocal fold tremor or laryngeal stenosis from chronic rejection. Regular ENT surveillance is advised.
Hepatic Impairment
Hepatic dysfunction affects drug metabolism. PPIs (esomeprazole): use with caution in severe hepatic impairment (Child-Pugh C); maximum 20 mg/day. Paracetamol: maximum 2 g/day in severe liver disease. Corticosteroids: avoid prolonged courses; monitor for hepatotoxicity.
Alcohol-related liver disease is frequently associated with laryngeal pathology due to combined effects of alcohol toxicity and reflux. Assessment of alcohol use (AUDIT-C) is recommended.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander Australians experience a disproportionate burden of head and neck cancers, including laryngeal carcinoma, driven by higher rates of tobacco use and delayed access to specialist ENT services. Culturally safe, responsive healthcare is essential throughout the diagnostic and management pathway.
Key recommendation: All Aboriginal and Torres Strait Islander adults presenting with hoarseness lasting > 2 weeks should receive expedited ENT referral, with a lower threshold for investigation than the general population. Active follow-up and case management through the primary care team (including Aboriginal Health Workers) is strongly recommended to prevent loss to follow-up.
📚 References
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