Chapter 29. Otitis Externa

Otitis externa (OE) or “swimmer's ear” is commonly defined as an inflammation of the external auditory canal (EAC).* Up to 10% of all persons may experience an episode of OE during their lifetime.1,2 OE most often besets children during the summer months, and can be painful and difficult to manage because of the confines of the ear canal. Early diagnosis and a stepwise treatment approach, including debridement and ototopical therapy, and on occasion systemic antimicrobials, are critical to expedient management. This chapter will review the epidemiology, pathogenesis, management, and complications of OE to facilitate an expeditious and cost-effective treatment for this common disease.

*While strictly speaking the auricle is part of the external ear, infections of this area are less common and are dealt with below.

The EAC is comprised of a thin lining of sebum containing epithelium over a bony and cartilaginous canal. This warm dark tunnel is a perfect culture medium for bacterial and fungal growth if the protective acidic cerumen or epithelial barrier is violated by aggressive cleaning, soapy water, skin conditions such as eczema or a heavy bacterial load.1,3

Almost all acute otitis externa (AOE) in North America is bacterial (98%). The most common offending organisms in AOE include Staphylococcus aureus, Pseudomonas aeruginosa and other gram-negative organisms; many infections are polymicrobial organisms.1,4,5Candida spp. rarely cause primary AOE, however, they are much more prevalent in chronic OE and in partially treated AOE.1

History

Conditions predisposing to AOE include recent water exposure (e.g., swimming), travel, immunocompromised states (e.g., diabetes mellitus), otologic trauma (from cotton swab use), and dermatologic conditions such as eczema. Affected patients often complain of pain limited to the ear canal which ranges from mild to severe intensity; the pain is exacerbated with auricular traction or tragal pressure. Occasionally, pain occurs with mouth opening because of the motion of the temporomandibular joint, which abuts the anterior EAC. Aural discharge may be present, and may be clear or murky colored, rarely bloody, and can be sweet or foul smelling. Fever is uncommon.

Physical Examination

Because of the exquisite tenderness children may exhibit with OE, physical examination may be best approached initially without instrumenting the ear canal. A magnifying, illuminating loupe or headlight, with the child lying on its contralateral side may allow for external assessment prior to instrumentation of the ear canal. The otologic examination should focus on the external ear for erythema, edema, and tenderness to palpation. Unlike children with mastoiditis in which the pinna may be protruberant, children with OE rarely have a displaced auricle. Skin surrounding the EAC and auricle may reveal cellulitis. The concha may have crusted drainage, which has collected or dried as it drips from the EAC. Many families will not clean this external part prior to a visit to a health care provider, as they want the provider to see the quality of discharge.

EAC examination should be performed with a smaller diameter speculum, taking care to avoid contacting the tender skin lining the EAC, and tragal pressure should be avoided. The external ear canal may be occluded, partially or completely, by a pink to red boggy edema of the EAC skin, and usually will exhibit a flaky or cheesy yellow–white exudate which may be cultured (Figure 29–1).5 EAC edema and tragal pain may limit the view of the tympanic membrane (TM) as well as debridement of the exudate.

If the TM is visible, it may be coated with a thin layer of debris and/or appear thickened. Evaluation for middle ear effusion may therefore be difficult.

Cranial neuropathies should heighten concern for the diagnosis of necrotizing or “malignant” otitis externa (NOE).6 NOE is characterized by granulation tissue in the EAC. NOE must be differentiated from a tuberculous or neoplastic process, or an inflammatory condition such as Langerhans cell histiocytosis, by biopsy with histopathologic analyis and culture (for bacteria, fungi, and mycobacteria).6

Microscopic evaluation of drainage may reveal the causative organism. Gram staining typically detects both bacteria and yeast. Yeast can also be detected by potassium hydroxide preparation or Gomori methenamine silver staining. Such assessments, along with bacterial and fungal culture, are useful when first- or second-line ototopical therapy and debridement as outlined below have been unsuccessful.

Hearing assessment shows a conductive hearing loss in the affected ear, either by tuning fork testing or by formal audiometry. Audiometric evaluation is not required to establish the diagnosis of OE. Audiologic assessment may be difficult to perform because of the tenderness of the external ear, and may show conductive hearing loss caused by the debris and swelling in the EAC. Testing of the auditory nerve for sensorineural hearing levels (the “bone conduction” hearing test) may be uncomfortable because of the tenderness in this region, but should indicate normal auditory nerve function.

There is not a role for routine imaging by computed tomography (CT) or MRI scan for most cases of OE, unless there is concern for spread beyond the ear canal such as intracranial complications. For NOE, gallium scan for diagnosis and thallium scan to follow the disease course may be considered.6

Causes of chronic otorrhea are summarized in Table 29–1. The differential diagnosis of an AOE includes a localized skin infection of the hair bearing lateral portion of the EAC, caused by a furuncle or an infected sebaceous cyst. These infections are usually restricted to an area of the EAC rather than involving the entire length of the EAC as in the case of OE, and are usually staphylococcal rather than pseudomonal in origin.

More extensive infections of the external ear may involve the pinna or auricle. These infections are usually caused by posttraumatic subperichondrial collections of blood which become infected. Infected collections around the cartilage of the auricle may result, if untreated, in the deformity termed “wrestler's” or “cauliflower” ear. Management involves prompt and aggressive incision and drainage, with placement of bolsters to re-appose the skin and cartilage, and an anti-pseudomonal antibiotic.

Embryologic persistence of the first or second branchial arch may result in preauricular cyst or fistulas. An infected branchial remnant would require antibiotic therapy followed by incision and drainage, and/or eventual complete surgical removal of the lesion to prevent recurrence. A pit or fistula in the region of the EAC, or a preauricular cyst, would indicate the possibility of an infected branchial remnant. Imaging with an MRI or CT scan may be required in such cases for diagnosis when infections are not responsive to culture-directed therapy and aural debridment, to assess for the extent and depth of a tract or canal duplication.

Infection from trauma may occur from violation of the dermal barrier by cotton swabs or other paraphernalia, such as “wax spoons” which may be used to instrument the ear. In addition, EAC skin can become inflamed or irritated from iatrogenic causes, such as ototopical solutions which alter the pH and commensal organisms of the EAC. Sensitivity to metals in ear piercings (most commonly nickel) can have a similar effect on the skin. In cases of suspected atopic dermatitis, removal of the offending allergen and topical antibiotic and steroid therapy may be considered.

Chronic myringitis presents with TM granulation (Figure 29–2) and aural discharge. Treatment is difficult and includes ototopical medications and debridement of the granulation tissue.7 Biopsy for tumor and mycobacterial processes may also be considered particularly for a child with a chronic or recurrent process.

Effective initial management of OE involves the “four D's”: Prompt Diagnosis, Debridement, Directed drop and drug therapy, and promoting a Dry environment (water precautions and drying agents) (Table 29–2 and Figure 29–3).

Debridement

Aural debridement is accomplished by curette or suction in the ambulatory setting. Treatment may require several weeks to a month's time. Cleaning may be accomplished through the otoscope, using the illuminated magnifying loupes, or a microscope. Hospitalization may be necessary for disease refractory to outpatient care, for complications, or when pain cannot be managed by oral medications. Pain can be severe, requiring narcotics, particularly in adolescent patients.

Directed Drop and Antimicrobial Therapy

Topical otic drops are useful to change the pH of the EAC and as antimicrobials. Initial cure may begin using dilute white vinegar (3 parts of vinegar to 1 part water) or a 1:1 mixture of vinegar and rubbing alcohol, particularly if a family is not able to readily fill a prescription because of distance (e.g., while on vacation and a “telephone diagnosis” is made). This “camper's cure” is available as a prescription form (Vosol), which permits acidification of the EAC with topical solution of 2% acetic acid. In addition to acetic acid, other ototopicals for which there has been demonstrated clinical efficacy include boric acid, aluminum acetate, silver nitrate, topical steroids without antimicrobials, anitfungals, and N-cholortaurine.1

Antimicrobial therapy focuses on targeting the most common offending organism—P. aeruginosa. This is usually achieved by using topical ofloxacin as a first line, or less commonly by initial use of ciprofloxacin drops.8 Oral ciprofloxacin is indicated for auricular chondritis or cellultitis complicating OE.

Oral antibiotics are not the first line of therapy for uncompliated AOE. Rather, these may be used for cellulitis involving the adjacent cutaneous structures of the pinna, erythema extending beyond the confines of the EAC, in an immunocompromised patient or for children with osteitis, abcess formation, middle ear disease, or recurrent infections.1

Steroid therapy via topical drops reduces canal edema and is advised for children with bloody otorrhea, canal edema which limits the view of the TM, and for OE in which pain and otorrhea are not diminished by a week of nonsteroid drop therapy. Steroid drops are particularly useful when granulation is present. Management of granulation is best accomplished by initial reduction of the bulk of granular tissue by debridement, or complete removal if possible in the office, followed by topical therapy. Topical steroids may be delivered as part of a combination antibacterial–steroid preparation (such as Ciprodex) or as a separate ototopical (e.g., Dexacidin).9 Ototopical therapy is considered to achieve clinical resolution in 65% to 90% of patients within 7–10 days.1

For OE refractory to debridement and drops after approximately 2 weeks, culture and Gram stain for aerobic and fungal organisms may be considered. Fungal OE is strongly suspected when black spores are seen, or when a white fuzzy layer coats the EAC. Suspicion of fungal OE may be aroused as well by the familiar sweet “athlete's foot” odor of fungal dermatitis. Fungal OE is usually managed effectively by debridement and by topical antifungal drops (e.g., Lotrimin), or by a combination antifungal/steroid-containing cream (e.g., Mycolog cream, containing Nystatin and triamcinolone), which may be applied by a small cotton applicator (fashioned in the office or commercially available).

Bacterial and fungal OE that are not responding promptly to debridement and culture-directed drop therapy, may be treated by painting the EAC with a cotton applicator, dipped in Gentian violet. This purple stain is effective against a wide variety of microorganisms. Caution is advised regarding the relative permanence of this stain on office furniture and clothing.

This stepwise approach to treating OE with a logical progression of ototopical agents is advised to limit antimicrobial resistance. Furthermore, topical antimicrobial therapy for OE is less likely than oral treatment to contribute to the emergence of resistant organisms colonizing at distant sites caused by limited systemic absorption of ototopical antimicrobial agents.1

Frequency of drop therapy depends upon tolerance to therapy, and the severity of the OE, and may vary from five drops, twice a day to four times daily. Effective therapy is achieved—regardless of the actual “drop count”—by seeing the drops welling up in the EAC, and by compressing the tragus to medialize the drops. Analgesic premedication is advised because of the extreme tenderness which can characterize OE.

Caution should be exercised in ototopical selection in cases where there is a concern that the TM is not intact (e.g., in a child with a history consistent with a preceding rupture of the TM from AOM caused by fever, and pain relief upon discharge evidencing ruptured TM, or in a child with a recently seen patent tympanostomy tube). Specific agents to avoid in such cases include those preparations which contain alcohol or which are acidifying.

Edema of the EAC may limit examination, cleaning, and entry of ear drops. Occlusive EAC edema may require placement of a wick so that drops can reach the medial EAC. The wick may be composed of tightly rolled cotton or a commercially available cellulose wick (Pope Merocel Wick, Medtronic, Jacksonville, FL, USA). In general, the commercially available wick is easier to place and less likely to shred than cotton upon removal, which may leave a nidus for infection. Merocel Wick placement may be accomplished simply by pushing a dry 1.5 cm length of wick medially using one's thumb. The Wick does not need to contact the TM, in fact, such medial positioning of the wick may be both painful and harmful to the TM.

Drops may be applied after wick placement. The dry wick will expand from its approximately 2 mm diameter to approximately 4 mm diameter, and remain soft. As the EAC edema regresses, the wick may lateralize and be removed by the child, the family, or a provider, or simply fall out. Replacement is not required so long as drops are felt to be reaching the medial EAC.

Dryness

Dry ear precautions prevent further moisture from exacerbating the maceration of the EAC skin and allow for effective topical drop therapy. Lambswool, or more often a cotton ball impregnated by petrolatum jelly, may be placed against the concha to occlude the meatus of the EAC to limit water exposure during bathing or hair washing. Swimming is generally contraindicated since wax and silicone plugs are painful to place and difficult to retain, even with the use of a retentive headband (such as the Ear Band-It®, Jaco Enterprises, Phoenix, AZ, USA). The vicious cycle of moisture begetting inflammation and exudate must be stressed to children and their parents as OE is most frequently seen during the swim season. An expedient return to swimming will be achieved only by curing the OE; water exposure only prolongs the painful condition and need for continued office visits with potentially uncomfortable debridements. The use of a hair dryer to remove moisture from the external canal after swimming and showering will also help in preventing and managing OE although care must be taken as thermal injuries may occur. Avoiding otologic trauma by limiting Q-tip use, and by avoiding the insertion of a hearing aid, may also help by protecting the epithelium of the EAC and allowing for aeration of the EAC.3

Special Consideration: NOE

In diabetic or immunocompromised patients, malignant OE can develop; P. aeruginosa is the usual offending organism in such cases. Severe otalgia, cranial neuropathies, and OE point to a diagnosis of NOE. Otologic findings include friable granulation tissue in the EAC. In the setting of concerning symptoms and signs, an underlying malignancy should be considered, and therefore a biopsy for histopathologic assessment is indicated. Diagnosis of NOE requires CT scan which demonstrates bony erosion. Serial gallium scanning may help to monitor disease resolution, which can take many months.6 The treatment of NOE includes long-term intravenous antibiotic treatment with an antipseudomonal such as ceftazidime or ciprofloxacin (may be administered orally). Debridement of the granulation tissue and bony sequestra must be performed, and adjuvant hyperbaric oxygen therapy may be considered.

OE is a commonly seen disorder in children that can most often be effectively managed by early diagnosis, debridement, a logical progression of ototopical therapy, and maintenance of dry ear precautions.