Otitis externa

Otitis externa (OE) is an inflammation of the external auditory canal (EAC), which is most often the result of a local bacterial infection. Risk factors for OE include exposure to water and injury to the skin of the EAC. OE is primarily a clinical diagnosis. It is characterized by ear pain, fullness, and/or itching, and tenderness of the tragus and/or pinna; otoscopy may show erythema, edema, debris, and/or otorrhea of the EAC. Treatment typically involves analgesia, keeping the EAC dry, and administering antiseptic, antibiotic, or glucocorticoid ear drops. Systemic antibiotic therapy is indicated in select cases, e.g., patients with immunosuppression and/or diabetes who are at risk of a more severe variant, malignant otitis externa. Malignant otitis externa is commonly caused by Pseudomonas aeruginosa, typically manifests with severe ear pain, and may lead to osteomyelitis of the skull base and subsequent complications such as cranial neuropathies. Immediate referral, diagnosis, and treatment with systemic antipseudomonal antibiotics are necessary.

• Acute otitis externa (AOE): inflammation of the EAC lasting < 6 weeks ^[1]
• Chronic otitis externa (COE): inflammation of the EAC lasting at least 6 weeks to 3 months ^[1][2]

Acute otitis externa ^[2][3]

• Infectious causes
  • Bacterial infections (most common cause of otitis externa)
    • Pseudomonas aeruginosa (∼ 40% of cases), commonly from swimming activities
    • Staphylococcus aureus, Proteus mirabilis, Escherichia coli
  • Viral infections (rare): Herpes zoster, influenza viruses
  • Fungal infections (less common): Aspergillus (accounts for 90% of all fungal otitis externa), Candida
• Noninfectious causes (less common)
  • Seborrheic otitis externa (associated with seborrheic dermatitis)
  • Eczematous otitis externa (a hypersensitivity reaction to pathogens or topical antibiotics)
  • Neurodermatitis (caused by compulsive/psychogenic scratching).
• Risk factors
  • Injury to the skin of the EAC (e.g., cleaning, insertion of foreign objects such as hearing aids or earplugs, excessive itching)
  • Increased moisture in the EAC (e.g., swimming, humid climate)
  • Immunosuppression, e.g., diabetes, HIV

Chronic otitis externa ^[4]

• Idiopathic
• Refractory fungal or bacterial infection
• May be associated with autoimmune diseases, e.g.:
  • Sarcoidosis
  • Amyloidosis
  • Granulomatosis with polyangiitis

Symptoms ^[3]

• Severe ear pain, particularly at night
• Otorrhea
• Intense itching in the EAC
• Hearing loss
• Jaw pain ^[2]

Examination findings ^[2][3]

• Tenderness on palpation of the tragus
• Pulling up and back on the auricle causes pain.
• The following may also be present:
  • Crusting of otorrhea at the entrance to the EAC
  • Conductive hearing loss
  • Clinical features of cellulitis
  • Regional lymphadenitis

Otoscopy ^[3]

• Erythematous and edematous EAC
• Otorrhea or debris
• EAC may be occluded by a furuncle, impacted cerumen, or foreign body
• The tympanic membrane may be erythematous but should not bulge.

Severe edema of the EAC may prevent otoscopic examination.

Malignant otitis externa (necrotizing otitis externa) ^[3][5]

Malignant otitis externa (MOE) is a necrotizing inflammation of the EAC that may lead to osteomyelitis of the skull base.

Etiology ^[5][6]

• Pathogens
  • Similar to AOE (see “Etiology of OE”)
  • P. aeruginosa is the most common cause, particularly in patients with diabetes. ^[6][7]
• Risk factors for MOE
  • Older adults (> 60 years of age)
  • Diabetes mellitus
  • Immunosuppression

Clinical features of MOE ^[3][5]

• Severe, persistent ear pain and/or jaw pain ^[5]
• Symptoms of extension of infection, e.g.:
  • Headache ^[5]
  • Facial nerve palsy in osteomyelitis of the skull base ^[3]
• Conductive hearing loss
• Red and swollen; EAC and periauricular soft tissue ^[8]
• Otorrhea
• Otoscopic findings: granulation tissue at the cartilage-bone junction of the EAC ^[3]

Diagnostics of MOE ^[3][5][9]

All patients require laboratory studies and imaging.

• Laboratory studies ^[5]
  • CBC: for WBC ^[5]
  • BMP: for serum glucose and creatinine
  • ESR and CRP ^[5]
  • Culture of ear canal : Obtain a sample prior to initiating empiric antibiotics.
• Imaging: More than one modality is often required. ^[5]
  • Modalities ^[9]
    • CT head with IV contrast: preferred initial study
    • MRI head: best modality for detecting soft tissue extension and intracranial abnormalities
    • Radionuclide scans: may be useful for early detection ^[9][10]
    • PET/CT scan: helpful for diagnosis and monitoring treatment response
  • Findings
    • Bone erosion
    • Soft tissue involvement
    • Intracranial extension
    • Abscess
• Surgical biopsy: Consider if there is diagnostic uncertainty or insufficient response to treatment. ^[5]

A negative CT scan does not exclude early MOE, as changes may not be evident until one-third of bone mineral is eroded. ^[11]

Treatment ^[3][5]

Treatment involves early empiric antibiotic therapy, prompt otolaryngology consult, and the control of risk factors for MOE, e.g., diabetes or immunosuppression.

• Systemic antibiotic therapy: typically lasting for 6–8 weeks ; ^[5][6]
  • Initial empiric therapy: Use two antipseudomonal agents from different classes for ≥ 2 weeks, e.g., ciprofloxacin PLUS one of the following:
    • Ceftazidime ^[5][11]
    • Piperacillin/tazobactam ^[5][11]
    • Cefepime ^[5][11]
  • Once culture results are available, tailor antibiotics to sensitivities and continue for an additional 4–6 weeks.
• Local treatment ^[11]
  • Clean and remove debris from the EAC.
  • Consider topical antimicrobial therapy for AOE. ^[8]
    • Obtain a culture first.
    • Use an antipseudomonal agent plus a glucocorticoid. ^[12]
• Surgery: may be required in select cases, e.g., abscess drainage or debridement of bony sequestra
• Monitoring of treatment response
  • Repeat ESR every few weeks.
  • Consider PET/CT scan. ^[9][10]

Patients unresponsive to antibiotic therapy may require a surgical biopsy to rule out fungal etiology or malignancy. ^[5]

Complications ^[8]

• Osteomyelitis of the skull base manifesting with:
  • Meningitis
  • Facial nerve palsy and, less commonly, other cranial neuropathies (e.g., of IX, X, XI, and XII) ^[5]
  • Cerebral abscess
  • Septic cerebral venous thrombosis
• Relapse in up to 20% of patients ^[5]

Prognosis ^[5]

• Overall mortality: < 10%
• Rates may be higher in patients aged over 80 years or with significant comorbidities.

MOE is a severe infection that can be lethal without prompt treatment. Death is most commonly caused by intracranial complications. ^[11][13]

Localized otitis externa (furunculosis) ^[3]

Localized OE is an infection of a hair follicle in the distal EAC.

Etiology ^[12]

• S. aureus (most common)
• Group A Streptococcus

Diagnostics

• Clinical diagnosis
• In addition to classic clinical features of OE, a pustular lesion may be present.

Treatment

• Local application of heat
• Incision and drainage
• Systemic antibiotics (see “Empiric antibiotic therapy for skin and soft tissue infections”)

Otomycosis (fungal otitis externa) ^[3]

Etiology ^[3]

• Pathogens
  • Aspergillus spp. (most common)
  • Candida spp.
• Risk factors
  • Immunosuppression (e.g., HIV, diabetes)
  • Long-term antibiotic therapy
  • Residence in a hot, humid area

Diagnostics

• Largely a clinical diagnosis; in addition to classic clinical features of OE, patients may additionally have:
  • Thick debris in the ear canal
  • Visible hyphae ^[14]
  • Insufficient response to antimicrobial therapy
• Fungal culture is recommended. ^[2]

Treatment ^[3]

• Debridement and cleaning
• Antifungal therapy ^[15]
  • Usually topical, e.g., clotrimazole
  • Occasionally, systemic (e.g., itraconazole) or combined therapy is required.

General principles ^[3]

• Diagnosis is clinical; AOE is likely if all of the following are present : ^[1][3]
  • Rapid onset of symptoms (typically within 48 hours) within the last 3 weeks
  • Symptoms of EAC inflammation (i.e., otalgia, pruritus, and/or fullness)
  • Examination findings of EAC inflammation (i.e., pinnal and/or tragal tenderness)
• Diagnostic studies are only performed:
  • In suspected comorbid disease
  • To rule out differential diagnoses of otitis externa
  • For refractory disease or suspected subtypes, e.g., MOE

Diagnostic studies ^[3]

• Pneumatic otoscopy and/or tympanometry
  • Perform if there is diagnostic uncertainty between AOE and acute otitis media.
  • Both studies are normal in AOE. ^[3]
• Screening for comorbidities: Consider based on clinical features.
  • AOE: screening for diabetes or screening for HIV
  • COE: screening for autoimmune disease ^[16]
• Culture of ear secretions should be obtained if there is: ^[2]
  • Insufficient response to initial treatment
  • ≥ 1 risk factor for a fungal or antibiotic-resistant pathogen
  • Concern the infection has extended (i.e., beyond the EAC)
• Patients with clinical features of MOE: Laboratory studies and imaging are required (see “Diagnostics of MOE”).

The differential diagnoses listed here are not exhaustive.

The following applies to diffuse AOE. For the treatment of localized OE, otomycosis, and MOE, see “Subtypes and Variants.” COE is treated according to its etiology, e.g., fungal, allergic, or autoimmune. ^[16]

Approach ^[2][3]

• Initiate supportive therapy as needed, e.g., analgesia, ear wick, aural toilet.
• Evaluate for indications for systemic antibiotic therapy in AOE and start if present.
• For uncomplicated AOE, initiate topical therapy for OE. ^[3]
  • Antibiotic (ofloxacin, ciprofloxacin, or gentamicin); or antiseptic ear drops
  • Preparations may be combined with glucocorticoids.
• Reassess at 48–72 hours; if there is no improvement, consider: ^[3]
  • Differential diagnoses of OE or MOE
  • Incorrect use or impaired delivery of ear drops
  • Allergic contact dermatitis from an ototopical agent (commonly neomycin)
• Consider a referral to otolaryngology in severe or refractory AOE.

If patients do not respond to initial topical therapy, consider alternative diagnoses such as allergic contact dermatitis from an ototopical agent, otomycosis, or MOE. ^[3]

Supportive therapy ^[3]

• Start scheduled oral analgesia. ^[17]
  • First-line: ibuprofen or acetaminophen ^[3]
  • Second-line: short course combination opioids, e.g., hydrocodone/ibuprofen or oxycodone/acetaminophen ^[3]
  • For further information including dosages, see “Pain management.”
• Advise patients:
  • How to administer ear drops correctly ^[3]
  • To avoid water exposure during treatment ^[3]
  • To disinfect in-ear devices and avoid wearing them until pain and/or discharge has improved ^[3]
  • On prevention of OE
• Consider performing aural toilet or placing an ear wick to facilitate better topical treatment.
  • Perform aural toilet if there is significant debris in the EAC, unless: ^[2][3]
    • Risk factors for MOE are present.
    • The tympanic membrane is perforated.
  • Insert an ear wick if there is significant edema of the EAC or visualization of the TM is not possible. ^[3]

Aural toilet can be painful for patients with severe inflammation; give analgesia beforehand and consider procedural sedation. ^[3]

Do not perform aural toilet in patients without a confirmed intact TM or with risk factors for MOE (e.g., older adults, patients with diabetes or immunosuppression). ^[3]

Antimicrobial treatment

Systemic antibiotics for OE ^[2][3]

• Indications
  • Topical antimicrobial administration is not possible.
  • Disease extension outside the ear canal, e.g.:
    • Cellulitis of the neck or face
    • Suspected MOE
    • Concomitant AOM
  • Uncontrolled diabetes
  • Immunosuppression
  • Previous local radiotherapy
• Choice of agent: should cover P. aeruginosa and S. aureus, e.g., ciprofloxacin ^[18]

Topical antimicrobials for OE ^[2][3]

• Choice of agent
  • Multiple options are effective; choose based on patient factors, preference, cost, etc.
  • Glucocorticoids (included in some preparations) may speed up symptom improvement.
• Treatment duration ^[3]
  • Typically 7 days; may be extended up to 10–14 days if needed
  • Patients with persistent symptoms at 14 days should be reassessed.

If allergic contact dermatitis secondary to ototopical agents (e.g., neomycin) is suspected, discontinue the agent and treat with a topical glucocorticoid. ^[2]

Use quinolones in patients with nonintact (perforated or tympanostomy tube) TM or if the TM cannot be visualized; use of other topical agents risks iatrogenic hearing loss. ^[3]

Indications ^[19]

• Recurrent episodes of OE
• Immunosuppression
• Chronic dermatological conditions (e.g., atopic dermatitis, psoriasis)
• Frequent participation in water sports

Interventions ^[2][20]

• Avoid manipulation of the ear canal (e.g., use of cotton buds to clean the ear).
• Regularly remove and clean earrings and in-ear devices, e.g., hearing aids.
• Treat underlying chronic dermatological conditions.
• Frequent swimmers: Use a tight-fitting bathing cap or ear plugs. ^[3][21]
• After bathing or swimming:
  • Tilt the head to remove water.
  • Dry the ear with a blow-dryer at the lowest heat setting.
• Consider prophylactic use of acetic acid ear drops. ^[2]