Otitis externa

• Otitis externa is inflammation of the skin of the external auditory canal. Acute diffuse "swimmer's ear" is usually bacterial, caused most often by Pseudomonas aeruginosa and Staphylococcus aureus.
• The hallmark is severe ear pain, made worse by pressing on the tragus or pulling the pinna. The ear canal looks red, swollen and wet.
• Most uncomplicated cases are treated with topical antimicrobial drops, with or without a steroid, after gently cleaning the canal. Tablets are usually not needed.
• The main dangers are malignant (necrotising) otitis externa in older people with diabetes or immunosuppression, and fungal infection after repeated antibiotic drops.
• Keep water out of the ear, avoid cotton buds, and recheck anyone who is not better within 48 to 72 hours.

By the end of this page you should be able to:

1. Explain how moisture and trauma turn the ear canal from a self-cleaning, acidic tube into an infected one.
2. Recognise acute diffuse, circumscribed, chronic and malignant otitis externa, and list the features that separate each from the others.
3. Tell otitis externa apart from acute otitis media, an infected hair follicle, perichondritis and other look-alikes.
4. Choose and apply topical treatment, including aural toilet, a wick, the correct drug when the eardrum is perforated, and sensible analgesia.
5. Recognise malignant (necrotising) otitis externa early, plan imaging and microbiology, and organise prolonged systemic therapy.
6. Advise on prevention and on care when drops, specialists or imaging are not available.

Otitis externa is an infection of the skin and the tissue just beneath it (the cutis and subcutis) of the external auditory canal. It may also involve the pinna and the tympanic membrane.^[1] Four forms are described.^[1]

• Acute diffuse otitis externa (AOE) is the common "swimmer's ear": a diffuse bacterial inflammation of the whole canal skin. It is defined as rapid onset, generally within 48 hours, of symptoms and signs of ear canal inflammation present for less than 6 weeks.^{[4] [2]}
• Circumscribed otitis externa is a boil (furuncle) in a hair follicle of the cartilaginous part of the canal, usually caused by Staphylococcus aureus.^[1]
• Chronic otitis externa lasts longer than 3 months, or follows more than 4 attacks a year. It is often driven by an underlying skin disease and presents with itch and a blocked, scaly ear rather than pain.^[1]
• Malignant (necrotising) otitis externa is a destructive infection with invasive perichondritis and osteomyelitis of the lateral skull base. It occurs mainly in older people with diabetes or immunosuppression and can be life-threatening.^[1]

Otitis externa has a lifetime prevalence of about 10%.^[1][2] It is common worldwide, but more frequent in tropical than in temperate climates because of heat and humidity.^[1] Annual incidence is about 1% in the Netherlands and the United Kingdom.^[1][3] One study reported 4 cases per 1000 Americans each year,^[3] and in the United States in 2007 there were an estimated 8.1 health care visits per 1000 population for acute otitis externa.^[2] The incidence is increased fivefold in swimmers, hence the name "swimmer's ear".^[1][3] The highest incidence of AOE is in children aged 5 to 14, but 53% of visits are for patients aged 20 or older.^[2] The acute form affects males and females equally and peaks in children aged 7 to 12, but overall it is adults who are most often affected, children only rarely.^[1][3] The acute form usually disables daily life: in one study 36% of patients interrupted normal activities for a median of 4 days, and 21% needed bed rest for a median of 3 days.^[3]

The ear canal is not a bare tube. It has a lateral cartilaginous part, lined by skin with hair follicles, sebaceous glands and ceruminous glands, and a medial bony part covered by thin skin stuck to the bone.^[1] Cerumen, with a pH usually between 5 and 5.7, is acidic and water-repellent, and it inhibits bacterial growth.^[1] The canal also has its own cleansing: epithelial cells migrate outward, carrying debris and microbes with them.^[1]

Anything that removes cerumen, raises the pH, macerates the skin, or scratches it lets infection start.^[1][3]

• Water exposure: swimming, perspiration, high humidity, bathing. Water macerates the skin, washes out cerumen and raises the pH.^[1][3]
• Trauma: cotton buds, fingernails, hearing aids, earplugs, keys, removal of wax, and devices that rub the canal.^[1][3]
• Skin disease: eczema, psoriasis, seborrhoeic dermatitis, atopic dermatitis, acne, and lupus erythematosus all disturb the barrier.^[2][3]
• Anatomy: a narrow canal, bony exostoses ("surfer's ear"), a hairy canal, or excess wax that traps moisture.^[1][3]
• Systemic factors: diabetes mellitus, immunosuppression from drugs or HIV, and prior radiotherapy.^[1][2][4]
• Local irritants: soap, shampoo, alkaline ear drops, hairspray, and prior surgery or radiotherapy of the canal.^[1]
• Ear disease: chronic suppurative otitis media with a perforated drum, recent antimicrobial use, and chronic otitis media.^[1][2][5]

More than 90% of acute cases are bacterial.^[1][2] The two dominant organisms are Pseudomonas aeruginosa (reported in 22 to 62% of cases) and Staphylococcus aureus (11 to 34%).^[1] One-third of cases are polymicrobial.^[2] The normal ear canal is colonised by Staphylococcus and Corynebacterium species and streptococci.^[1] Acute diffuse otitis externa is almost exclusively a bacterial infection.^[4]

Fungi are an uncommon cause of acute otitis externa, accounting for about 10% of acute cases, and a more common cause of chronic cases.^[1] The usual organisms are Aspergillus species (60 to 90% of fungal cases) and Candida species (10 to 40%).^[1] Worldwide, otomycosis has been reported in 5 to 80% of suspected ear infections, and in one Nepalese study 23% (100 of 440) of patients with ear discharge, pain and itch had positive fungal cultures.^[5] Predisposing factors include prolonged antibiotic use, which changes the local flora, diabetes, immunosuppression, an immunocompromised state, and chronic otitis media with a perforated drum.^[1][2][5] Polymicrobial infection is common in the bacterial form.^[1]

The infection starts because the protective system fails. Loss of the acidic, hydrophobic cerumen layer and maceration of the canal skin allow bacteria already present in the canal, or introduced by water, to multiply. Inflammation then swells the canal, obstructs its self-cleaning, and traps debris and discharge. The exudate may itself sustain the process: Pseudomonas exotoxin A, for example, can limit the benefit of topical drops.^[1] Because the skin of the bony canal is thin and stuck to the periosteum, inflammation there is unusually painful.^[1]

Chronic change follows repeated or undertreated episodes: hyperkeratosis, edema, fibrosis and narrowing of the canal, with a persistently alkaline pH and loss of the normal self-cleaning. More than half of patients with chronic otitis externa have bilateral disease.^[1]

The characteristic symptom is severe ear pain (otalgia), often out of proportion to how the ear looks. The pain is worsened by chewing, by pressure on the tragus, or by pulling the pinna.^[1][2] The onset is usually rapid, as water exposure or trauma occurs, then symptoms build over hours.^[2] Other symptoms include:

• itch, especially in chronic or fungal disease
• discharge from the canal, clear, purulent or coloured
• a feeling of fullness or blockage
• reduced hearing from canal swelling or debris
• jaw or neck discomfort
• fever, usually mild (up to 39 degrees C); a higher fever suggests spread beyond the canal.^[1]

Fungal infection often starts with itch and a feeling that drops are not helping, then adds white fluffy debris and ongoing discharge despite completed antibiotic courses.^[2][5]

Look at the pinna, mastoid, lymph nodes, cranial nerves, and surrounding skin as well as the ear.^[2] The classic findings of acute otitis externa are pain on pressure of the tragus and tension on the pinna, with swelling and erythema of the canal, sometimes to total obstruction.^[1][2] The skin may be red or pale from edema.^[1] Discharge is common and can be swabbed.^[1] Hearing, tested by tuning fork or audiogram, shows a conductive loss when the canal is swollen.^[1]

Otomycosis is suggested by otorrhoea, an edematous or erythematous canal, and cotton-like fungal growth on otoscopy.^[2] With necrotising disease there may be granulation tissue or polyps in the floor of the canal, sometimes with exposed bone, and a protruding pinna (pseudomastoiditis) can occur.^[1][2]

A furuncle is a painful, localised, pus-filled swelling of one hair follicle in the cartilaginous canal, usually caused by Staphylococcus aureus. It is tender to touch and may be confused with a foreign body.^[1]

^[1][2] Physically, the key distinguishing feature is that diffuse AOE hurts when the canal is moved: tenderness of the tragus, pinna, or both, often intense and disproportionate to how the ear looks.^[4]

Most patients need no tests at all. Diagnosis is clinical from the history and examination, including the canal, tympanic membrane (if visible), pinna, mastoid, lymph nodes, cranial nerves and surrounding skin.^[2]

• Swab for culture and sensitivity is reserved for refractory, recurrent, or severe cases, for otomycosis, for suspected malignant disease, and when a resistant organism such as meticillin-resistant Staphylococcus aureus is a concern.^[1][3] It helps direct topical and systemic therapy.^[1]
• Hearing test (tuning fork or audiogram) confirms the expected conductive loss.^[1]
• Blood tests: no test diagnoses uncomplicated disease. In suspected malignant otitis externa, a markedly raised ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein) help assess disease progression and response, and blood cultures may be taken.^[2]
• Imaging is used only for suspected malignant disease (see below).

The AAO-HNS guideline defines diffuse AOE as inflammation with rapid onset, generally within 48 hours, in the previous 3 weeks, in a patient aged 2 years or older; it is almost exclusively bacterial.^[4] Because it is a clinical diagnosis, severity is graded by bedside findings rather than by a score:

• Mild: inflamed canal, mild pain, no obstruction.
• Moderate: edematous, very tender canal, partial obstruction, mucopurulent discharge.
• Severe: canal totally obstructed by edema, severe pain, regional cellulitis, fever or periauricular edema, or signs of spread beyond the canal.^[2]

Any patient with a "perforated or open" tympanic membrane should be thought of as having middle ear involvement until proven otherwise.

The aim is to remove debris and infection, relieve pain, and restore the canal's environment. The standard regime is:

1. Clean the canal (aural toilet). Remove wax and exudate. This may itself dramatically relieve pain, because toxins in the discharge sustain inflammation and block drops. In hospital or clinic, use suction or a Jobson Horne probe under direct vision; in primary care a small suction tip inserted less than 1 cm can be used. Oral antibiotics are spared by doing this properly. Patients must not clean their own ears with cotton buds, which cause microtrauma.^[1][2]
2. Topical antimicrobial or antiseptic drops, with or without a steroid. This is the first-line treatment for uncomplicated disease.^[3][4] Topical treatment delivers high local drug concentrations without systemic side effects, and 65 to 90% of patients improve within 7 to 10 days; improvement is usually clear within 72 hours.^[1][2][3] Drug choices include:
   • quinolones (ciprofloxacin, ofloxacin), non-ototoxic and well tolerated;
   • aminoglycosides (neomycin, gentamicin, polymyxin B) combined with a steroid, effective but ototoxic and can cause contact dermatitis in 15 to 30% of patients; ^[1]
   • antiseptics such as 2% acetic acid, which is comparably effective to antibiotic or steroid drops if treatment lasts about 7 days but less effective if treatment is needed for 2 to 3 weeks.^[1][3] Combined antibiotic-steroid drops reduce pain and edema more than an antibiotic alone in the first few days.^[2] Topical corticosteroid monotherapy has only case-report evidence.^[1]
3. A wick if the canal is swollen shut: place a dry compressed cellulose or ribbon gauze wick, expand it immediately with drops, replace it after 24 to 48 hours if the drum is still not visible, then continue drops for 7 to 10 days. Do not use cotton wool, which disintegrates and is hard to remove.^[2]
4. Analgesia: regular ibuprofen or paracetamol (acetaminophen). Topical local anaesthetic drops can help but can mask worsening, so the patient should be reviewed within 48 hours. Opioids are rarely needed because good topical therapy relieves pain substantially within 48 to 72 hours.^[1][2]
5. Education: drops should be instilled with the patient lying with the affected ear uppermost, the canal filled, then held in position for at least 3 to 5 minutes, with gentle tragal or pinna movement to run the drops in; the ear is then left to drain and dry naturally. Patients should continue for the recommended length and stop water entry until resolved.^[1][2]

Systemic antibiotics are reserved for spread of infection beyond the canal, for patients with poorly controlled diabetes or immunosuppression, or when topical treatment is genuinely impossible.^[1][2][4] Despite this, 20 to 44% of patients with AOE receive systemic antibiotics.^[2][3] When given, they must cover Pseudomonas aeruginosa and Staphylococcus aureus; oral quinolones (especially ciprofloxacin) resolve symptoms in about 90% of appropriate cases and reduce hospitalisation.^[2] Reinforce good glucose control in patients with diabetes.^[1][2]

A non-ototoxic preparation (a quinolone) must be used when the drum is perforated or when a tympanostomy tube is in place, because aminoglycosides are ototoxic in that setting.^[3][4] This applies whenever a tympanic membrane perforation is known or suspected, because debris may hide a hole.^[3][4] Treatment is usually given for 7 to 10 days; patients with antibiotic-steroid drops can expect symptoms to last about 6 days.^[3] Acetic acid is adequate for about a week but less effective if treatment must run to 2 or 3 weeks.^[1][3] Overall 65 to 90% of cases resolve in 7 to 10 days whatever agent is chosen.^[1][2]

Chronic disease is diagnosed when symptoms last longer than 3 months or attacks occur more than 4 times a year.^[1] The cause is often an underlying skin condition (atopic dermatitis, psoriasis, seborrhoeic dermatitis) or a dysfunctional canal (alkaline pH, stenosis, excessive wax). Pain is uncommon, but itch, dryness, scaling, moisture and conductive hearing loss are typical.^[1][2] Management is directed at the cause: remove irritants, keep the ear dry, and treat the underlying dermatology. A swab excludes bacterial or fungal infection. Topical steroids suppress chronic inflammation; reported options include 0.1% triamcinolone cream or 0.05% desoximetasone cream twice daily for dermatological forms.^[2] Tacrolimus and short courses of oral steroids are occasionally used for resistant cases, and canaloplasty is considered only for significant stenosis.^[1]

Otomycosis is a superficial fungal infection of the canal, often an itch first, then pain, discharge and sometimes hearing loss. Risk factors mirror bacterial otitis externa plus chronic otitis media with a perforated drum and antimicrobial use, which alters the local flora.^[2][5] On examination the canal is edematous and erythematous with cotton-like fungal growth.^[2]

Treatment is local: toileting and dry mopping to clear debris, plus topical antifungal preparations such as clotrimazole, miconazole, ciclopirox or nystatin, used for about 2 weeks, which is the common practice.^[1][5] Fungal infection in a patient with a perforated drum should be treated parenterally, for example with fluconazole or itraconazole, guided by sensitivity, because dye and ototoxic preparations are no longer recommended.^[1] If a systemic antiseptic is unavailable, a wick impregnated with an antifungal solution is practical. Clotrimazole is widely used and effective, with reported cure rates of 50 to 100%, though randomised evidence for azoles specifically is limited and of low certainty.^[5] The evidence does not show clear superiority of one azole or of azoles over placebo.^[5]

This is the form to recognise early. It is a destructive infection of the canal, perichondrium and lateral skull base, producing osteomyelitis.^[1][2]

• Who gets it: mainly older men who are diabetic or immunosuppressed; it is rare but reported in severely immunocompromised children such as those with acute leukaemia or after bone marrow transplantation.^[1][2]
• Organism: Pseudomonas aeruginosa in about 90% of cases, releasing proteases that destroy tissue and cause vasculitis.^[1][2]
• Presentation: intense, unrelenting otalgia (84 to 100%), conductive hearing loss and foul otorrhoea (17.6 to 100%), with granulation tissue or polyps, often in the floor of the canal, and sometimes exposed bone.^[1][2] There may be cranial nerve palsies: facial nerve palsy is common, and lower cranial nerves (9 to 12) may be affected, producing dysphagia, dysphonia and shoulder weakness.^[2] Further spread can cause inner ear damage, venous sinus thrombosis, meningitis or brain abscess.^[1]
• Imaging: high-resolution CT shows bone erosion and is ideal for later bony change; MRI is best for early soft tissue and skull base changes.^[1][2] The gold standard is combined static and functional imaging, high-resolution CT together with FDG-PET/MRI, and functional imaging can show osteitis before bone erosion appears on CT. Technetium-99 scanning is the most sensitive for early bony disease; gallium-67 or indium-111-labelled leukocyte scans help monitor response. A biopsy is needed to exclude malignancy or cholesteatoma.^[1][2]
• Laboratory: Pseudomonas grows from canal exudate in about 90% of cases.^[1] A markedly elevated ESR or CRP supports diagnosis and tracks response.^[2]
• Treatment: pathogen-directed parenteral or oral antibiotics, guided by culture and sensitivity, for at least 4 to 6 weeks (the time the involved bone needs to revascularise). If cultures are pending, start empirical antipseudomonal therapy based on severity. Topical antiseptic or antimicrobial strips may be used, and topical therapy is an adjunct only.^[1] If disease is protracted or does not respond, remove necrotic tissue and bone sequestra surgically, because they impair antibiotic penetration.^[1] Extensive skull base resection does not improve outcome. Optimise blood glucose control, and consider hyperbaric oxygen as an adjunct (no randomised trials).^[1] Follow up clinically and with imaging, repeated every 2 to 6 weeks until no infection remains. Petrous osteomyelitis carries a mortality of 10 to 21%, higher if two or more risk factors are present: age over 70, diabetes, facial nerve palsy, or a positive CT scan.^[1][2]

• Regional spread: cellulitis of the pinna, perichondritis, mastoiditis, facial cellulitis and systemic toxicity.^[3]
• Chronic otitis externa and canal stenosis from repeated or untreated episodes.^[3]
• Necrotising disease: osteomyelitis, cranial nerve palsy, venous sinus thrombosis, meningitis, brain abscess.^[1]
• Ototoxic injury if aminoglycoside drops are used with a perforated drum.^[3]
• Contact dermatitis after aminoglycoside-containing drops (15 to 30% of patients).^[1][3]

Uncomplicated acute otitis externa resolves in 65 to 90% of patients within 7 to 10 days, whichever agent is chosen, and most patients avoid hospital care if it is managed topically.^[1][2] Symptoms treated with antibiotic-steroid drops last about 6 days.^[3] Necrotising disease, by contrast, has a mortality of 10 to 21% even with treatment, and requires prolonged therapy and follow-up.^[1]

• Keep water out of the ear during swimming or bathing (swim cap, cotton wool with petroleum jelly as a seal), or dry the canal afterwards by tilting and using a hairdryer on a cool setting.^[1][2][3]
• Avoid cotton buds and other objects in the ear; treat underlying skin disease.^[1][3]
• After swimming, acidifying drops (for example 2% acetic acid or a half-and-half white vinegar and water or alcohol solution) may help, though clinical trial evidence for home remedies is lacking.^[2][3]
• Use earplugs with care: they can irritate the canal and increase risk.^[2]
• In swimmers with recurrent disease, arrange physician cleaning of the canal before a swimming holiday.^[1]

• Children: acute otitis externa is uncommon in young children and is most frequent between ages 5 and 14; neonates and infants need careful assessment to exclude anomalies and suppurative otitis media.^[2][3]
• Older adults: more likely to have malignant disease if diabetic or immunocompromised, and to need imaging and prolonged therapy.^[1][2]
• Immunocompromised patients: topical disease often fails, systemic therapy is usually needed, and invasive fungal or bacterial infection must be considered.
• Patients with a perforated drum or tympanostomy tube: use a non-ototoxic quinolone drop.^[3][4]
• Pregnancy: safety data for specific otic preparations are limited; use the lowest effective topical treatment and specialist advice where disease is severe. Drug choices follow the individual product labels.

Where specialists, suction or imaging are unavailable:

• The diagnosis is clinical: pain on tragal or pinna pressure plus a red, swollen, wet canal is usually enough.^[2]
• Clean the canal gently with a small suction tip or dry swab, then use cheap antiseptic drops: 2% acetic acid (or a vinegar and water or alcohol solution) is comparable to antibiotic drops for about a week and is often available.^[1][2][3] Warn patients not to use cotton buds.
• Quinolone drops are the best option if the drum is perforated or the status is unknown; if unavailable, treat based on local availability and risk, recognising that aminoglycosides are ototoxic with a perforation.^[3][4]
• Give simple analgesia (ibuprofen or paracetamol) and educate on drop technique and water precautions.^[1][2]
• Treat otomycosis by toileting plus topical clotrimazole cream or drops for 2 weeks where possible; clotrimazole's reported cure rate is 50 to 100%.^[5]
• Suspect malignant disease in every older, diabetic or immunocompromised patient with severe persistent otalgia, granulation or exposed bone; start empirical antipseudomonal therapy, control blood glucose, and refer urgently for CT or MRI and possible prolonged intravenous therapy.^[1][2]
• Dry the ears carefully and avoid further water entry while travelling or working outdoors.
• In remote areas a general practitioner or paediatrician can perform gentle irrigation and instillation if no specialist is present, provided the drum is known to be intact.^[1]

• Otitis externa is infection of the external ear canal skin, classified as acute diffuse, circumscribed, chronic and malignant forms.
• Lifetime prevalence is about 10%; annual incidence is around 1%, and swimmers have a fivefold higher risk. More than 90% of acute cases are bacterial, most often Pseudomonas aeruginosa and Staphylococcus aureus.
• Pain worsened by tragal pressure or pinna traction is the hallmark.
• Topical antimicrobial (or antiseptic) drops, with or without steroid, after aural toilet are first-line for uncomplicated disease; 65 to 90% resolve in 7 to 10 days.
• Use a non-ototoxic quinolone if the eardrum is perforated or a tube is present.
• Oral antibiotics are for spread beyond the canal, poorly controlled diabetes, immunosuppression, or inability to use drops.
• Reassess within 48 to 72 hours; failure to improve is a risk factor for malignant disease. ^[4]
• Otomycosis is usually treated with toileting plus topical azoles for about 2 weeks; evidence for one agent over another is weak.
• Malignant (necrotising) otitis externa is a skull base osteomyelitis, usually due to Pseudomonas, in older people with diabetes or immunosuppression; mortality is 10 to 21%. Treatment needs 4 to 6 weeks of antipseudomonal therapy, source control, and imaging follow-up.

• Acute otitis media
• Mastoiditis
• Diabetes mellitus
• Otitis externa prevention and water precautions
• Fungal infections of the ear
• Skin disease of the ear canal