Acute Otitis Externa (AOE)

from – https://www1.racgp.org.au/ajgp/2024/december/approach-to-otitis-externa-in-australian-general-p

Abbreviations (expanded):

• AOE: Acute otitis externa
• AOM: Acute otitis media
• CSOM: Chronic suppurative otitis media
• EAC: External auditory canal
• TM: Tympanic membrane
• TMJ: Temporomandibular joint
• SCC: Squamous cell carcinoma

Definition:

• Acute inflammation of the outer ear (external auditory canal, EAC).
• Common in humid/tropical climates (e.g. North Queensland).
• Also referred to as “swimmer’s ear” or “tropical ear“
• Frequently encountered in general practice.

Microbiology:

• 90% of cases are bacterial in origin.
• Common organisms:
  • Pseudomonas aeruginosa
  • Staphylococcus aureus
• ~30% are polymicrobial (mixed bacterial flora).
• Fungal (otomycosis) may occur after prolonged topical antibiotic use or in immunocompromised hosts.

Typical Course:

• Triggered by factors that increase EAC vulnerability.
• Responds well to topical antibiotic drops and ear toileting within 72 hours.
• Untreated or complicated cases, especially in people with diabetes mellitus, risk progression to necrotising otitis externa (NOE).

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Anatomy

• Outer ear = pinna + EAC (S-shaped canal → tympanic membrane).
• EAC composition:
  • Outer ⅓ cartilaginous (hair-bearing skin, fissures of Santorini).
  • Inner ⅔ bony (thin stratified squamous epithelium).
• Anatomical risk factors: narrow, tortuous, collapsing canal or exostoses ↑ risk of AOE.

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History

• Key predisposing factors:
  • Trauma to EAC (cotton buds, instrumentation).
  • Water exposure: swimming, showering, humid climate → promotes bacterial growth.
  • Obstruction/occlusion: hearing aids, earplugs, headphones → poor ventilation, cerumen retention.
  • Self-cleaning attempts: syringing, cotton buds → microtrauma.
• Comorbid conditions:
  • Diabetes mellitus: microangiopathy, impaired immunity, delayed wound healing → susceptibility to AOE and necrotising otitis externa (NOE).
  • Immunosuppression: reduced host defence (e.g. corticosteroid or chemotherapy use, HIV infection).
  • Dermatological disease: eczema, psoriasis, seborrhoeic dermatitis → weakens canal skin.
  • Prior radiotherapy: compromises blood flow, skin integrity, may cause EAC stenosis.

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Risk Factors for AOE

Category	Examples
Water/Moisture exposure	Swimming, spas, showers, humidity (wet season/summer)
Local injury	Cotton buds, foreign bodies, syringing, instrumentation
Canal obstruction	Hearing aids, earplugs, earphones, canal stenosis, exostoses, excess hair
Comorbidities	Diabetes, immunosuppression, chronic otitis media, cerumen impaction, prior radiotherapy
Dermatological	Atopic/contact dermatitis, psoriasis, eczema, seborrhoeic dermatitis, keratosis obturans

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Aboriginal & Torres Strait Islander Population

• Higher prevalence of ENT conditions and diabetes (2.8× higher mortality cause).
• NT data: 6/9 NOE cases were Indigenous, diabetic, ~16 yrs younger onset.
• Clinical vigilance warranted for acute otalgia in Indigenous patients → consider NOE.

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Symptoms

Onset:

• Usually within 48 hours of cerumen barrier disruption or water exposure.

Key Symptoms:

• Unilateral ear pain (otalgia) — may radiate to jaw or temporal region.
• Itching (pruritus) in the ear canal.
• Aural fullness or “blocked ear” sensation.
• Hearing loss (conductive, due to canal edema or debris).
• Jaw pain — worsens with chewing or pinna manipulation.

Examination Findings

General:

• Tenderness of pinna or tragus (pain on traction).
• EAC edema and erythema (red, swollen canal).
• Reduced or absent cerumen.
• Otorrhoea (ear discharge) — may be clear, purulent, or serosanguinous.
• Regional lymphadenitis (preauricular or postauricular nodes).
• Tympanic membrane: erythematous but usually intact (unless secondary perforation).
• Surrounding skin: cellulitis of pinna or adjacent face/neck.

Severe Cases:

• Intense otalgia (often disproportionate to examination findings).
• Marked EAC edema causing canal obstruction.
• Purulent otorrhoea.
• Periauricular edema and erythema.
• Cervical or postauricular lymphadenopathy.

Otoscopy:

• EAC: erythematous, swollen, moist ± otorrhoea/debris.
• Bacterial: nonspecific debris.
• Fungal:
  • Aspergillus – white hyphae + black spores.
  • Candida – off-white sebaceous debris.

• Swab if empirical treatment fails.
• Assess TM integrity (guides safe topical therapy; secondary perforation possible).

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Diagnosis & Differentials

Diagnostic Criteria (per 2014 American Academy of Otolaryngology–Head and Neck Surgery, AAO-HNS, guideline)

• Essential features:
  1. Rapid onset (<48 hours) of external auditory canal (EAC) inflammation.
  2. Symptoms:
     • Ear pain (otalgia)
     • Itching (pruritus)
     • Aural fullness or blocked sensation
  3. Signs:
     • Tenderness (particularly tragal tenderness — pathognomonic)
     • Erythema and oedema of the EAC.
• Causative organisms:
  • Predominantly bacterial:
    • Pseudomonas aeruginosa
    • Staphylococcus aureus
  • Fungal (otomycosis):
    • Aspergillus and Candida species
    • Often co-pathogens, seen in immunocompromised patients or following prolonged antibacterial drop use.
• Overlap of bacterial and fungal features:
  • Otalgia, otorrhoea (discharge), pruritus, erythema.
  • Diagnosis confirmed by:
    • Otoscopy findings
    • Ear swabs (if recurrent or refractory)
    • Clinical history (water exposure, trauma, device use, diabetes, etc.)

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Differential Diagnoses of Otitis Externa

Category	Condition	Distinguishing Clinical Features
Otological	Acute otitis media (AOM) / Chronic suppurative otitis media (CSOM)	– Middle ear effusion visible as dull/yellow tympanic membrane (TM). – TM may bulge; immobile on pneumatic otoscopy. – If TM intact → EAC and pinna not inflamed. – If TM perforated → secondary EAC inflammation from discharge.
	Mastoiditis	– Usually complication of AOM. – Bulging posterior EAC wall. – Mastoid tenderness, erythema, swelling, fluctuance. – Pinna displaced anteriorly.
	Furunculosis (infected hair follicle in EAC)	– Localised, fluctuant, erythematous nodule in distal EAC (“pimple-like”). – Focal source of infection rather than diffuse canal inflammation.
	Perichondritis	– Marked inflammation of pinna cartilage with lobule sparing (lobule lacks cartilage). – EAC not involved.
	Neoplasm / abnormal growth (e.g. cholesteatoma, squamous cell carcinoma, basal cell carcinoma, melanoma)	– May mimic chronic or treatment-resistant AOE. – Consider if persistent or unresponsive to therapy. – May have constitutional symptoms or cranial nerve findings (e.g. facial nerve palsy).
Inflammatory	Contact dermatitis	– Triggered by materials (metals, plastics), chemicals (soap), or medications (topical antibiotics). – Predominant symptom: itching (pruritus) ± mild otalgia. – Symptoms resolve after removal of offending agent.
	Ramsay Hunt syndrome (herpes zoster oticus)	– Reactivation of varicella-zoster virus affecting facial nerve. – Vesicular rash on EAC, pinna, or tongue. – Neuropathic otalgia + facial nerve paresis (droop, loss of taste).
Dermatological	Eczema (atopic dermatitis)	– Predominant itching. – EAC erythematous with crusting/exudate but little oedema. – Fissures in infra-auricular/retroauricular folds.
	Seborrhoeic dermatitis	– Due to Malassezia yeast overgrowth. – Scaly, erythematous plaques around scalp, pinna, face, and trunk. – EAC inflammation absent.
	Psoriasis	– Bilateral erythematous, sharply demarcated scaly plaques on EAC and pinna. – Pruritus common; otalgia often absent.
Other	Temporomandibular joint (TMJ) disorder	– No EAC or pinna inflammation. – History of TMJ injury (trauma, bruxism, dental procedure, malocclusion) or repetitive jaw movement (e.g. gum chewing). – Masticator muscle tenderness; TMJ crepitus on movement.

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Acute vs Chronic Otitis Externa

Duration

• Acute Otitis Externa (AOE):
  • Lasts < 6 weeks.
• Chronic Otitis Externa (COE):
  • Persists > 3 months.
  • May include intermittent acute flare-ups of AOE.

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Chronic Otitis Externa (COE) – Clinical Features

• Symptoms:
  • Mild, painless discomfort.
  • Itching (pruritus) is common.
  • Often chronic or relapsing course.
• Examination findings:
  • Dry, flaky, erythematous (red) skin of the external auditory canal (EAC).
  • Clear otorrhoea (discharge).
  • May show skin thickening or hyperkeratosis.
  • Otoscopic findings can resemble AOE.
• Investigations:
  • Swab and culture chronic or recurrent infections to guide antibiotic/antifungal choice.
• Clinical note:
  • COE can coexist with or alternate with acute flare episodes of AOE.

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Management of Acute Otitis Externa (AOE)

1. General Principles

• Goals:
  • Eradicate infection and inflammation.
  • Relieve pain.
  • Restore the normal external auditory canal (EAC) environment.
  • Prevent recurrence.
• Key measures:
  • Avoid water exposure (no swimming, use ear plugs or cotton with Vaseline during shower).
  • Cease ear instrumentation (no cotton buds or ear cleaning).
  • Provide analgesia (e.g. paracetamol or NSAIDs).
  • Address predisposing factors (eczema, diabetes, hearing aids, dermatitis).

2. First-Line Therapy — Topical Antibiotic Ear Drops

• Topical antibacterial therapy is the mainstay of treatment for AOE.
• Swab is not required initially — empiric therapy appropriate as most cases are bacterial.
• Clinical response: 65–90% of patients improve within 7–10 days with topical treatment alone.
• Topical agents provide drug concentrations 100–1000× higher than oral antibiotics at the site of infection.

3. Choice of Topical Agent

Class	Examples (brand)	Indication	Key Considerations
Quinolone-based (non-ototoxic)	Ciprofloxacin 0.3% (Ciloxan) Ciprofloxacin 0.2% + hydrocortisone 1% (Ciproxin HC)	AOE ± tympanic membrane (TM) perforation	– Preferred if TM integrity uncertain or perforated. – Non-ototoxic; safe for middle ear exposure. – Slightly higher cost. – Usually 5 drops twice daily for up to 2 weeks, until a few days after symptoms have cleared
Non-quinolone-based (potentially ototoxic)	Framycetin (Soframycin) Framycetin + gramicidin + dexamethasone (Sofradex) Neomycin + gramicidin + triamcinolone (Kenacomb/Otocomb)	AOE with intact TM	– Not safe if TM perforated. – Less expensive and equally effective if TM intact. – 3 drops 2–4 times daily until a few days post-symptom resolution.
Antifungal / anti-inflammatory	Clioquinol + flumetasone (Locacorten-Vioform) Clotrimazole 1% (Canesten)	Otomycosis	– Indicated for fungal AOE. – Avoid in TM perforation. – 3 drops twice daily until a few days after clearance.
Non-antibiotic acidic agents \(for prevention)	Acetic acid 1.73% + isopropyl alcohol 63.4% (Aqua Ear)	Post-swimming prevention	– Reacidifies EAC; prevents recurrence. – Not for active infection or TM perforation. – May sting on application.
Cerumenolytics	Docusate sodium (Waxsol) Carbamide peroxide (Ear Clear)	Cerumen clearance (not for infection)	– Used to soften wax pre-toileting. – Avoid in TM perforation.

Treatment duration:

• Continue 2–3 days beyond symptom resolution, generally ≤14 days total.

Clinical pearl:

• In general practice, tympanic membrane integrity can be difficult to confirm due to pain, swelling, or debris.
• In such cases, default to quinolone-based drops to avoid potential ototoxicity.

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4. Systemic (Oral or IV) Antibiotics

• Not indicated for uncomplicated AOE.
  • topical agents already provide concentrations 100- to 1000-fold higher than their systemic counterparts
  • They also do not expedite clinical resolution or pain relief compared to topical treatment
• Indications for systemic therapy:
  • Infection extending beyond EAC (periauricular cellulitis).
  • High-risk populations:
    • Diabetes mellitus.
    • Immunocompromised states (HIV, chemotherapy, corticosteroid use).
  • Necrotising otitis externa (NOE) suspicion.
• Consult infectious diseases (ID) specialist for systemic regimen — few effective anti-pseudomonal oral options and rising resistance.
  • Typical agents: ciprofloxacin or ceftazidime (guided by culture and local guidelines).

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Drug Delivery and Technique

Ear Drop Administration

• Position:
  • Patient should lie with the affected ear facing upward.
  • The external auditory canal (EAC) should be completely filled with drops.
  • Ideally, instillation is done by another person for accuracy.
• Technique:
  • Maintain position for ≈5 minutes for optimal penetration.
  • Perform tragal pumping (pressing on the tragus several times) to expel trapped air and enhance medication spread.
• Rationale:
  • Ensures full drug contact along the EAC and tympanic membrane (TM).
  • Enhances local efficacy, particularly where swelling or debris is present.

Ear Toilet (Microsuction and Debridement)

• Microsuction:
  • Preferred method of ear toilet.
  • Clears otorrhoea (discharge) and debris to improve topical antibiotic penetration.
  • Multiple sessions may be required alongside topical therapy.
• Alternative:
  • Gentle tissue spear dabbing (avoid twisting to prevent shearing injury and pain).
• Avoid:
  • Ear irrigation/syringing — contraindicated in suspected acute otitis media (AOM), diabetic, or immunocompromised patients → ↑ risk of necrotising otitis externa (NOE).

Wick Insertion

• Indication:
  • When EAC oedema prevents medication penetration.
• Type:
  • Pope Wick – expandable hydrocellulose sponge (~15 mm length; average EAC ≈25 mm).
• Method:
  • May pre-moisten with an otic agent such as Kenacomb Otic, though not essential.
  • Once inserted, apply prescribed ear drops to impregnate and expand the wick.
  • Ensure the lateral tip remains visible to confirm correct placement.
• Follow-up:
  • Clinical improvement expected within 72 hours.
  • Wick should be removed at 72 hours and EAC reassessed.

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Pain Management

First-line:

• Paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) (e.g. ibuprofen).
• Use regular dosing rather than “as needed” for sustained relief.

Second-line (rare):

• Opioids – reserved for severe pain or procedural use (e.g. suction), but seldom required as symptoms usually improve within 72 hours.

Topical analgesics:

• Not recommended – limited efficacy and may interfere with antibiotic absorption.

Topical corticosteroid combinations:

• Dual-action drops (e.g. ciprofloxacin + hydrocortisone) reduce local inflammation and pain and may reduce systemic analgesic requirements.

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Follow-up

• Review after 48–72 hours:
  • Assess pain, hearing, and EAC appearance.
  • If no improvement → consider:
    • Fungal infection.
    • Incorrect drop technique.
    • Canal obstruction (no drug penetration).
    • Alternative diagnosis (see differential list).
• Re-examine after completion of therapy to ensure full resolution and rule out chronic otitis externa or neoplasm in non-resolving cases.

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Prevention / Patient Education

• Moisture avoidance:
  • Ear plugs for swimming or bathing; coat with petroleum jelly for a watertight seal.
  • Use hair dryer (low heat, 30 cm away) to dry the canal after water exposure.
  • Acetic acid/alcohol prophylactic drops (e.g. Aqua Ear) post-swimming if TM intact.
• Device hygiene:
  • Hearing aid users should remove devices regularly to ventilate canal and clean earpieces frequently.
• Cerumen management:
  • Use cerumenolytics (e.g. Waxsol, Ear Clear) as needed.
  • Avoid instrumentation (cotton buds, pins).
• Control systemic risk factors:
  • Optimise diabetes mellitus management.
  • Address eczema, psoriasis, seborrhoeic dermatitis.
  • Consider specialist consultation for underlying comorbidities.

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Indications for ENT Referral

• Persistent or worsening infection:
  • Symptoms persist > 2 weeks or worsen despite appropriate therapy.
• Debris or otorrhoea obstructing treatment:
  • When microsuction not available or cannot be performed safely in general practice.
• Severe EAC oedema preventing drop or wick insertion.
• Systemic extension:
  • Periauricular cellulitis, fever, or lymphadenitis.
• Neurological involvement:
  • Facial nerve palsy or other cranial nerve deficits (suggestive of NOE).
  • Urgent ENT and emergency department referral required; prompt imaging (MRI/CT) indicated.
• Immunocompromised or diabetic patients not responding to treatment should be referred early.

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Necrotising Otitis Externa (NOE)

Definition

• Necrotising otitis externa (NOE): also known as malignant otitis externa, is an invasive skull-base osteomyelitis originating from severe or untreated AOE.
• Historical mortality up to 67%, now 2–15% with modern anti-pseudomonal therapy.

At-Risk Populations

• Older adults (>65 years).
• Predominantly in diabetic and immunocompromised populations.(e.g. on corticosteroids, chemotherapy, HIV infection).

Microbiology

• Pseudomonas aeruginosa – responsible for >90% of NOE cases.

Pathophysiology

• Infection spreads medially via fissures of Santorini into the bony EAC, stylomastoid foramen (cranial nerve VII), mastoid tip, and jugular foramen (cranial nerves IX–XI).
• Leads to osteomyelitis, granulation tissue formation, and cortical bone erosion.

Clinical Features

• Early stage:
  • Persistent otalgia, otorrhoea, granulation tissue in EAC.
• Advanced disease:
  • Cranial nerve involvement:
    • Facial nerve (VII): facial palsy (most common).
    • Lower cranial nerves (IX–XII): dysphagia, dysphonia, shoulder weakness.
  • Periauricular cellulitis, severe pain, persistent discharge.
  • skull base osteomyelitis (SBO)
  • May progress to meningitis or brain abscess.

Investigations

• Imaging:
  • Magnetic Resonance Imaging (MRI): early soft-tissue and skull-base involvement.
  • Computed Tomography (CT): later bony erosion.
  • Technetium-99m bone scan: highly sensitive for early bony disease.
• Laboratory tests:
  • Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP): elevated and useful for monitoring disease activity.
  • Culture and biopsy: confirm infection and exclude squamous cell carcinoma (SCC) (which may mimic NOE with pain and otorrhoea).

Clinical Importance

• High morbidity and mortality if not identified early.
• Requires urgent ENT referral and intravenous antipseudomonal therapy (e.g. ciprofloxacin, ceftazidime).
• Close monitoring of high-risk groups (especially elderly diabetic patients).

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Otomycosis (Fungal Otitis Externa)

Definition

• Fungal infection of the external auditory canal (EAC).
• Often follows antibacterial drop use or prolonged moisture exposure.

Causative Pathogens

• Candida albicans.
• Aspergillus species (especially A. niger, A. fumigatus).

Risk Factors

• Same as AOE (water exposure, trauma, occlusion).
• Additional factors:
  • Chronic otitis media with tympanic membrane perforation.
  • Prolonged antibiotic drop use (disrupts flora and pH).

Clinical Features

• Symptoms:
  • Pruritus (itching) – hallmark.
  • Otalgia (ear pain).
  • Hearing loss.
  • Otorrhoea (discharge).
• Examination findings:
  • EAC erythema and edema.
  • Cotton-like fungal growths visible on otoscopy:
    • Aspergillus → fuzzy white hyphae with black dots.
    • Candida → creamy, sebaceous debris.
• Investigations:
  • Swab or culture for mycological confirmation.