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).
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.
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.