Acute Otitis Externa

Diffuse inflammation of the external auditory canal skin, usually bacterial, with symptoms present for less than six weeks. It is distinct from furunculosis (localised follicular abscess), otomycosis (fungal overgrowth) and necrotising otitis externa (osteomyelitis of the skull base).

Anatomy that governs the clinical picture

• The lateral third is cartilaginous, carries hair follicles, sebaceous and ceruminous glands, and has a subcutaneous layer. The medial two thirds is bony, lined by thin skin adherent to periosteum with almost no subcutaneous tissue, so minimal oedema produces severe pain and rapid canal occlusion.
• Sensory supply is shared by the auriculotemporal nerve (V3), the auricular branch of the vagus (Arnold nerve, hence reflex cough on instrumentation), the great auricular nerve (C2, C3) and a contribution from the facial and glossopharyngeal nerves. This explains referred otalgia from pharynx, larynx, temporomandibular joint and dentition.
• The fissures of Santorini in the cartilaginous canal and the bony cartilaginous junction are the anatomical routes by which infection escapes into the parotid space, retromandibular tissues and skull base. Granulation at that junction is the sentinel finding for necrotising disease.

Pathophysiology

The canal defends itself through an acidic pH of roughly 5.0 to 5.7, hydrophobic cerumen containing lysozyme and immunoglobulin, and lateral epithelial migration that carries debris outward. Water exposure raises pH and washes out cerumen. Instrumentation with cotton buds abrades the stratum corneum and drives debris medially. Occlusion by hearing aids, earplugs, exostoses or a narrow canal traps moisture. Once the barrier fails, keratin becomes hydrated, bacteria colonise, and oedema of a non compliant canal produces disproportionate pain and obstruction of drop delivery.

Microbiology

• Pseudomonas aeruginosa accounts for roughly 40 to 60 percent of isolates.
• Staphylococcus aureus for roughly 10 to 20 percent, including methicillin resistant strains in hospital exposed or recurrently treated patients.
• Polymicrobial growth is common; anaerobes and Proteus occur in chronic or previously treated canals.
• Fungi account for approximately 10 percent overall but dominate after repeated antibacterial drops, principally Aspergillus niger and Candida albicans.

Predisposing factors

Swimming and humid climates, cotton bud use, hearing aid and earphone occlusion, eczema, psoriasis, seborrhoeic dermatitis, acne, diabetes mellitus, HIV and other immunosuppression, prior radiotherapy to the temporal bone, exostoses in cold water swimmers, canal stenosis, and radiotherapy induced xerosis.

Severity spectrum and natural history

Preinflammatory pruritus progresses to mild inflammation with a patent canal, then moderate disease with partial occlusion, then severe disease with complete occlusion, periauricular cellulitis and systemic features. Adequately treated disease resolves within 7 to 10 days. Untreated or inadequately debrided disease progresses to chronic otitis externa with fibrotic canal stenosis, or in the diabetic and immunocompromised to skull base osteomyelitis with cranial neuropathy and appreciable mortality.

Symptoms

• Otalgia that is severe and out of proportion to visible findings, aggravated by chewing, yawning, lying on the ear and any traction on the pinna.
• Pruritus, usually the earliest symptom and the dominant one in eczematous and fungal disease.
• Aural fullness and conductive hearing loss proportional to canal occlusion, typically 10 to 30 dB.
• Otorrhoea that is scant, watery and later purulent. Profuse mucoid discharge suggests a middle ear source through a perforation, since the canal has no mucous glands.
• Tinnitus and autophony are uncommon and suggest an alternative or coexisting middle ear problem.

Signs

• Tragal tenderness and pain on pinna traction, the most discriminating bedside signs.
• Diffuse canal erythema and oedema, keratin and purulent debris, and a tympanic membrane that is normal when visible.
• Regional lymphadenopathy in preauricular, postauricular and upper deep cervical nodes.
• Periauricular cellulitis, pinna erythema, and an auricle displaced laterally and inferiorly in severe disease. Postauricular swelling with a forward and downward displaced pinna and loss of the postauricular sulcus indicates mastoiditis rather than otitis externa.
• Trismus when inflammation involves the temporomandibular region.

Severity grading by canal patency

• Mild: pruritus and minor discomfort, minimal oedema, canal patent, drops enter freely.
• Moderate: partial canal occlusion, moderate pain, debris obscuring the drum, drops unlikely to reach the medial canal without toilet.
• Severe: complete occlusion, intense pain, periauricular extension, fever, lymphadenopathy. Requires a wick and reassessment.

Red flags demanding escalation

• Granulation tissue or exposed bone at the bony cartilaginous junction on the floor of the canal.
• Pain persisting or worsening despite adequate topical therapy and toilet, particularly nocturnal deep boring pain and temporal headache.
• Any cranial nerve palsy. The facial nerve fails first at the stylomastoid foramen; involvement of IX, X and XI at the jugular foramen and of XII in the hypoglossal canal indicates advanced skull base disease.
• Fever, systemic sepsis, or facial and neck cellulitis.
• Diabetes, HIV, chemotherapy, long term corticosteroids, or elderly patients with any of the above.
• Bleeding, a friable canal mass, or ulceration that fails to heal, which requires biopsy to exclude squamous cell carcinoma.

Presentation in specific groups

• Elderly diabetics: modest canal findings with severe pain and normal or minimally raised white cell count. Assume necrotising disease until excluded.
• Children: acute otitis externa is less common. Exclude a retained foreign body, acute otitis media with perforation and discharge, and eczema.
• Immunocompromised patients: fungal and polymicrobial disease, faster progression, higher risk of necrotising disease at younger age and with normal glucose.
• Hearing aid users and swimmers: recurrent disease, often with contact dermatitis to neomycin or to the mould material superimposed on infection.

Acute otitis externa is a clinical diagnosis. The purpose of investigation is to identify the patients who do not have simple otitis externa and those whose infection will not respond to standard topical therapy.

Bedside assessment

• Otoscopy with the largest speculum that will pass, followed by microscopy where available. Microscopy is the single most useful diagnostic and therapeutic step because it allows debris removal and visualisation of the drum.
• Determine tympanic membrane integrity before prescribing. This decides whether aminoglycoside containing drops are permissible.
• Palpate for parotid and mastoid tenderness, examine the temporomandibular joint, oropharynx, larynx and dentition when the canal appearance does not explain the pain.
• Test all cranial nerves when pain is disproportionate, in every diabetic and in every immunocompromised patient.
• Capillary glucose in all patients with severe or refractory disease, and HbA1c where diabetes is newly suspected.

Microbiology

Swab for culture and sensitivity when there is failure of first line topical therapy after 48 to 72 hours, severe or recurrent disease, immunocompromise, prior instrumentation or surgery, suspected necrotising disease, or hospital acquired infection. Take the specimen under direct vision from the medial canal after removing surface debris, since a superficial swab grows colonising skin flora.

Laboratory and imaging when necrotising disease is suspected

• Erythrocyte sedimentation rate is characteristically high, frequently above 60 mm per hour, and is used to track response. C reactive protein falls faster and is useful for early response. White cell count is often normal and its normality does not exclude the diagnosis.
• High resolution computed tomography of the temporal bone demonstrates cortical bone erosion and soft tissue involvement of the skull base, but requires around one third of mineral loss before changes appear, so a normal scan early does not exclude disease.
• Magnetic resonance imaging is superior for marrow signal change, dural involvement, cavernous and sigmoid sinus thrombosis and intracranial extension.
• Technetium 99m bone scintigraphy is highly sensitive for early osteoblastic activity but remains positive long after cure, so it cannot be used to judge treatment endpoint. Gallium 67 scintigraphy or white cell labelled imaging normalises with resolution and is used to guide duration of therapy.
• Biopsy of granulation tissue is mandatory when the response is atypical, to exclude squamous cell carcinoma, and to obtain deep tissue culture including fungal culture.

Audiological assessment

Pure tone audiometry is not required acutely. Perform it when hearing loss persists after canal clearance, when a perforation is found, or when there is any suspicion of sensorineural loss from prior ototopical exposure.

Differential diagnosis and the finding that separates each

• Otomycosis: pruritus dominates over pain, with white or grey fluffy hyphae, black conidiophores of Aspergillus niger, or curdy white Candida debris, typically after antibacterial drops.
• Furunculosis: exquisitely tender localised swelling confined to the hair bearing cartilaginous canal, staphylococcal, may point and discharge.
• Acute otitis media with perforation: preceding upper respiratory illness, deep pain relieved by the onset of discharge, mucoid or pulsatile discharge, and a visible perforation once the canal is cleaned.
• Chronic suppurative otitis media and cholesteatoma: long standing malodorous discharge, attic or marginal defect, granulation, conductive loss disproportionate to canal oedema.
• Necrotising otitis externa: granulation at the bony cartilaginous junction, disproportionate pain, cranial neuropathy, raised inflammatory markers, diabetic or immunocompromised host.
• Contact dermatitis: intense itch, weeping erythema extending onto the concha and lobule, temporally related to neomycin, gentamicin, benzalkonium or propylene glycol exposure. It worsens rather than improves on continued drops.
• Herpes zoster oticus: severe pain preceding vesicles on the concha, canal or palate, with facial palsy and possible vestibulocochlear involvement.
• Squamous cell carcinoma of the canal: chronic non healing ulceration, bleeding on toilet, friable mass, deep pain, facial weakness. Biopsy any tissue that does not resolve with treatment.
• Referred otalgia with a normal canal: temporomandibular dysfunction, dental disease, tonsillar or hypopharyngeal malignancy, cervical spine disease. A completely normal ear examination with persistent otalgia in a smoker over 45 years requires upper aerodigestive tract endoscopy.

Treatment rests on four actions: clear the canal, deliver a high concentration topical agent to the medial canal, control pain properly, and eliminate the moisture or trauma that caused it. Topical concentrations exceed achievable serum levels by a factor of one hundred or more, which is why systemic antibiotics add nothing in uncomplicated disease and drive resistance and fungal superinfection.

Aural toilet

• Microsuction under the microscope is the preferred method and should be repeated at each review until the canal is clean.
• Dry mopping with a cotton wisp on a Jobson Horne probe is acceptable where microscopy is unavailable.
• Avoid syringing when the tympanic membrane status is unknown, when perforation is present, and in all diabetic and immunocompromised patients, because forced irrigation seeds the middle ear and deeper soft tissues.

Topical therapy

Choose the agent according to tympanic membrane integrity, suspected organism and dermatitis component.

Safe with a perforated or uncertain tympanic membrane

• Ciprofloxacin 0.3 percent with dexamethasone 0.1 percent, 4 drops into the affected ear twice daily for 7 days. The steroid shortens time to pain resolution and reduces canal oedema.
• Ofloxacin 0.3 percent, 10 drops once daily for 7 days in adults, or 5 drops once daily in children aged 6 months to 13 years.

Only where the tympanic membrane is intact

• Neomycin sulphate with polymyxin B and hydrocortisone, 3 to 4 drops three or four times daily for 7 days. Effective and inexpensive, but neomycin causes contact sensitisation in roughly 15 percent of exposed patients and both components are cochleotoxic and vestibulotoxic if they reach the middle ear.
• Gentamicin 0.3 percent with hydrocortisone, 2 to 3 drops three or four times daily for 7 days. Same ototoxicity restriction.
• Acetic acid 2 percent, 3 drops three times daily for 7 days. Reasonable for mild disease and for prophylaxis, but inferior to antibiotic steroid combinations in moderate and severe disease and often stings intolerably on inflamed skin.

Practical points that determine success

• Duration is 7 days, extended to 10 to 14 days when resolution is incomplete. Treatment beyond 14 days without reassessment invites fungal superinfection and contact allergy.
• Instil with the affected ear uppermost, remain in that position for 3 to 5 minutes, then pump the tragus to displace air and drive the solution medially. Warm the bottle in the hand to avoid caloric vertigo.
• Do not prescribe drops for a canal that is occluded. They will not reach the disease.
• Water precautions for the whole treatment period and for a week afterwards. A petroleum jelly coated cotton ball for showering; no swimming.
• Remove hearing aids and earphones until re epithelialisation is complete.

Wick insertion

Indicated whenever the canal is sufficiently oedematous that drops cannot reach the medial third.

• Use a compressed cellulose expandable wick or a 1 to 2 cm ribbon gauze impregnated with the chosen preparation.
• Saturate the wick after insertion and instruct the patient to keep it moist with the drops as prescribed. A dry wick is an obstruction, not a treatment.
• Review at 48 to 72 hours. Remove or replace the wick, repeat microsuction, and reassess. Most wicks extrude spontaneously as oedema settles, which is a favourable sign.

Analgesia

Pain in severe otitis externa is frequently underestimated and is often the reason patients present. Prescribe adequately from the outset.

• Paracetamol 1 g orally every 6 hours, maximum 4 g in 24 hours. Reduce to a maximum of 3 g in 24 hours in adults under 50 kg, in significant hepatic impairment, chronic alcohol use or malnutrition.
• Ibuprofen 400 mg orally every 8 hours with food, maximum 2.4 g in 24 hours. Avoid in significant renal impairment, active peptic ulceration, uncontrolled heart failure and in patients on anticoagulants without gastroprotection.
• For severe pain, add codeine phosphate 30 to 60 mg orally every 6 hours for 48 to 72 hours, or oxycodone immediate release 5 mg every 4 to 6 hours in opioid naive adults. Codeine is unreliable in ultrarapid and poor metabolisers and is contraindicated in children under 12 years.
• Paediatric dosing: paracetamol 15 mg/kg every 6 hours, maximum 60 mg/kg in 24 hours; ibuprofen 10 mg/kg every 8 hours, maximum 40 mg/kg in 24 hours.
• Pain that escalates rather than settles within 48 hours of correct topical therapy is a diagnostic finding, not an analgesic failure. Re examine for necrotising disease.

Systemic antibiotics

Restrict oral or intravenous therapy to defined indications, since they do not improve outcome in uncomplicated disease.

Indications

• Cellulitis extending beyond the canal onto the pinna, face or neck.
• Fever or systemic upset.
• Uncontrolled diabetes or significant immunosuppression with moderate or severe disease.
• Failure of adequate topical therapy plus toilet after 72 hours.
• Inability to deliver topical therapy, such as a canal that cannot be opened.
• Suspected necrotising otitis externa.

Regimens

• Ciprofloxacin 500 to 750 mg orally twice daily for 7 to 10 days when Pseudomonas is the presumed pathogen. Reduce to 250 to 500 mg twice daily when creatinine clearance is below 30 mL/min.
• Flucloxacillin 500 mg orally four times daily for 7 days when staphylococcal perichondritis or cellulitis dominates. Clindamycin 300 to 450 mg orally four times daily is the alternative in penicillin allergy and adds anaerobic cover.
• Co amoxiclav 625 mg orally three times daily is reasonable for mixed periauricular cellulitis but lacks reliable pseudomonal cover, so it is not a substitute when Pseudomonas is likely.
• Fluoroquinolone cautions: tendinopathy and tendon rupture, aortic aneurysm and dissection risk, QT prolongation, seizure threshold reduction, dysglycaemia, and reduced absorption when taken with calcium, magnesium, iron, zinc or antacids. Separate those by at least two hours. Ciprofloxacin inhibits CYP1A2 and raises theophylline and tizanidine levels.
• Narrow therapy to culture results as soon as they are available and stop the empirical agent that is not required.

Necrotising otitis externa

When granulation at the bony cartilaginous junction, disproportionate pain, cranial neuropathy or a markedly raised erythrocyte sedimentation rate is present, treat as skull base osteomyelitis.

• Admit, obtain deep tissue biopsy for culture including fungal culture and for histology, and image with computed tomography and magnetic resonance imaging.
• Ciprofloxacin 400 mg intravenously every 8 to 12 hours, or ceftazidime 2 g intravenously every 8 hours, or piperacillin with tazobactam 4.5 g intravenously every 6 to 8 hours, adjusted to renal function and to culture.
• Total duration 6 to 8 weeks, frequently longer, with transition to oral ciprofloxacin 750 mg twice daily once clinically improving and the organism is susceptible. Track response with symptoms, cranial nerve examination, C reactive protein and erythrocyte sedimentation rate, with gallium scintigraphy or magnetic resonance imaging before stopping.
• Aggressive glycaemic control, usually with an insulin regimen during the acute phase.
• Consider fungal aetiology, principally Aspergillus, in the patient failing appropriate antipseudomonal therapy and in profound immunosuppression. Voriconazole is the agent of choice in that setting and requires liver function and drug interaction review.
• Surgery is limited to debridement of sequestrum and granulation, abscess drainage and biopsy. Radical temporal bone resection has no routine role.

Fungal disease

• Meticulous repeated microsuction is the essential step; antifungals fail on an uncleaned canal.
• Clotrimazole 1 percent solution, 2 to 3 drops three times daily for 10 to 14 days, continued for at least one week beyond visible clearance.
• Acetic acid 2 percent drops are a reasonable low cost alternative and useful for maintenance.
• Oral itraconazole 200 mg daily is reserved for extensive or refractory disease in immunocompromised patients, with attention to hepatotoxicity, negative inotropy and CYP3A4 interactions.
• Stop the antibacterial drops that precipitated the overgrowth.

Failure to improve at 48 to 72 hours

Re examine rather than re prescribe. Work through the following causes in order.

• Wick displaced, extruded or dry, or drops not physically reaching the medial canal.
• Non adherence, usually from technique or pain.
• Retained debris requiring further microsuction.
• Fungal superinfection.
• Contact dermatitis to neomycin, gentamicin or a vehicle component. The clue is worsening itch and weeping despite treatment. Stop the drug, switch to a quinolone preparation and use topical corticosteroid alone for the dermatitis.
• Retained foreign body, particularly in children and in patients with cognitive impairment.
• Resistant organism, including methicillin resistant Staphylococcus aureus.
• Underlying necrotising otitis externa or canal malignancy. Both require imaging and biopsy.

Complications and their recognition

• Canal stenosis from repeated or chronic inflammation, presenting as persistent conductive loss and recurrent trapped debris. Management begins with topical corticosteroid and regular toilet; established fibrotic stenosis requires canalplasty with meatoplasty and split skin grafting.
• Perichondritis and chondritis of the pinna, indicated by a swollen tender erythematous auricle with lobule sparing. Requires antipseudomonal systemic therapy and drainage of any subperichondrial collection to prevent cauliflower deformity.
• Periauricular cellulitis and parotitis from spread through the fissures of Santorini.
• Myringitis and tympanic membrane thickening with residual conductive loss.
• Necrotising otitis externa with cranial neuropathy, sigmoid sinus thrombosis, meningitis and intracranial abscess.
• Iatrogenic sensorineural hearing loss and vestibular injury from aminoglycoside drops used in a perforated ear. Any new vertigo or hearing deterioration on such drops requires immediate cessation and audiovestibular assessment.

Prevention and follow up

• Acetic acid 2 percent or a 1 to 1 mixture of isopropyl alcohol and white vinegar, 3 to 5 drops after every swim, is effective prophylaxis in recurrent disease with an intact drum. Alcohol containing preparations are contraindicated with a perforation.
• Stop cotton bud use entirely. Wax should be removed by microsuction, not by instrumentation at home.
• Treat underlying eczema, psoriasis or seborrhoeic dermatitis of the canal with a topical corticosteroid such as betamethasone valerate 0.1 percent drops, tapered to the lowest effective frequency.
• Review hearing aid mould fit and material, and consider vented or hypoallergenic moulds in recurrent cases.
• Routine follow up is unnecessary in mild disease that resolves. Review at 48 to 72 hours in severe disease, in all wicked ears, in diabetics and in the immunocompromised. Refer to otolaryngology for recurrent disease, persistent stenosis, suspected necrotising disease, a canal mass, or hearing loss that persists after the canal is clear.