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Assessment and management of chronic otitis externa Kesser 343

such as Wegener’s granulomatosis certainly suggests an autoimmune process. The causative epitopes remain elusive, although fungal antigens, including those else where in the body such as a low-grade onychomycosis, have been suggested [11]. In some patients, those with nickel or neomycin allergy, the obvious causative agent is obviously the contact aller gen [9]. Epicutaneous patch test positivity was statistically higher in patients with chronic eczematous external otitis than in healthy controls, and those patch test positive external otitis patients had a higher recurrence rate (attack rate) than those who were patch test negative [10]. In most patients, however, the agent (if one at all) remains a mystery. Some patients with COE exhibit food hypersen sitivity; both epicutaneous prick test positivity and IgE seropositivity were statistically higher in patients with COE compared with controls in one study [12]. Food hypersensitivity may also play a role in those patients exhibiting the dermatophytid reaction (see below; [11]). Nevertheless, even if the agent is not readily apparent, a careful historical search may reveal the inciting factor. Whereas exogenous causes certainly play a role in COE, some investigators have examined endogenous factors – are the ears of patients with COE fundamentally different? Cerumen has been found to be bactericidal against strains of Pseudomonas , Staphylococcus , and Candida but with low activity against Escherichia coli [13 ]. Yet, when the bac tericidal activity of cerumen against Staphylococcus aureus , S. epidermidis , E. coli , Pseudomonas aeruginosa , and Enter ococcus of otitis externa patients was comparedwith that of healthy volunteers, only the activity against E. coli was statistically different; the authors concluded that theywere not able to confirm that cerumen from patients with recurrent otitis externa had less bactericidal activity than that from a healthy population [14]. What the authors did not address was a quantitative analysis – do patients with COE make less cerumen than healthy patients, and, if so, why? Relative humidity was found to be higher in abnor mal ears (mastoid cavities, ears with tympanic membrane perforation, as well as ears with COE) compared with normal ears [15], and pH was found to be higher in ears with COE compared with control ears [16]. Lowering the pH of the external canal to create an inhospitable environ ment for pathogenic organisms is the foundation for treat ment with topical acetic acid (e.g. acetasol, vosol). Q-tip use can most certainly incite inflammation in the canal skin.Whether an incitingagent or exacerbatingagent, Q-tip use cessation must be a strong recommendation.

Clinically, otomycosis behaves more like COE than acute otitis externa. Hallmark symptoms include intense prur itis, aural fullness, and drainage, often clear. Debris can be so abundant as to cause a conductive hearing loss. Hyphae are often seen on the superficial layer of the debris. Aspergillus and Candida species are the most fre quently isolated fungi. Otomycosis can appear after a course of ototopical antibiotic eardrops, as the bacteri cidal activity of the drops allows fungal overgrowth; it can appear in a patient with a longstanding tympanic mem brane perforation that begins to drain; or it can occur de novo . Otomycosis in the presence of a mastoid cavity is harder to eradicate [17]. Otomycosis can also be a com ponent of a more systemic fungal inflammatory process, fungal allergy, or autoimmune disorder, or a dermatophy tid reaction. Treatment of fungal otitis externa relies on meticulous cleaning of the canal under binocular microscopy. The key to the cleaning is the elevation of the dead skin layer under all the fungal debris. The skin is carefully elevated with a small right angle hook laterally and a plane of dissection is established between the dead skin layer and the healthy (although generally erythematous) skin underneath. The elevation proceeds down the medial canal, and many times a dead skin layer can be elevated off the tympanic membrane. Once all the fungal debris has been removed, the canal can be powdered with a mixture consisting of chloromy cetin 50mg, sulfanilamide 50mg, fungizone 50mg, and hydrocortisone 1mg (‘CSF-HC’). Alternatively, cresylate can be used, but not in the ear with a tympanic membrane perforation. Gentian violet is also an excellent antifungal and drying agent (the vehicle is alcohol) and can be painted throughout the canal skin with a small ‘home made Q-tip’, a straight pick wrapped by cotton. With careful and complete cleaning and a single application of one of these medications coupled with compulsive dry ear precautions and Q-tip cessation, otomycosis can generally be brought to resolution without further treat ment. Antifungal preparations such as clotrimazole, fluconazole, miconazole, or tolnaftate can be used for more recalcitrant patients. These formulations come in creams, gels, oint ments, and solutions. Drug vehicle is an important con sideration, especially in patients with a tympanic mem brane perforation; creams are preferred. Ototoxicity is another consideration; clotrimazole, miconazole, bifona zole, and tolnaftate have a broad spectrum of activity against molds, yeasts, fungi, and dermatophytes, high cure rates, low ototoxicity, greater compliance, and commercial availability as a solution [18 ]. One study found topical ketoconazole to have a higher resolution rate and lower recurrence rate than cresylate drops or aluminum acetate

Otomycosis Fluffy, cotton-like debris in the external auditory canal (EAC) is classic for otomycosis, fungal otitis externa.

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