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Patient Story
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An 11-year-old girl with a history of psoriasis presented to her pediatrician with a 2-day history of ear pain and drainage from her right ear canal. On physical examination, she is well appearing and afebrile. She has exquisite pain on movement of her right pinna and dried drainage visible at the opening of her external auditory canal (EAC). Her EAC is erythematous and mildly edematous, but the tympanic membrane is visualized and appears normal. She also has psoriatic lesions around her ear and scalp as currently her psoriasis is not under control (Figure 21-1). The pediatrician makes the diagnosis of otitis externa and prescribes once daily ofloxacin drops for 7 days. The girl has a prompt response and recovers completely.

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FIGURE 21-1

Dried drainage at the opening of the external ear canal in a girl with otitis externa. Note the psoriatic lesions, which predisposed this girl to otitis externa. (Used with permission from Richard P. Usatine, MD.)

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Introduction
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Otitis externa (OE) is common in all parts of the world. OE is defined as inflammation, often with infection, of the EAC.1

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Synonyms
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Swimmer’s ear.

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Epidemiology
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  • Incidence of OE is not known precisely; its lifetime incidence was estimated at 10 percent in one study.2

  • In temperate climates, it is more common in the summer.

  • Associated with head immersion in water.

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Etiology and Pathophysiology
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  • Common pathogens, which are part of normal EAC flora, include aerobic organisms predominantly (P. aeruginosa and Staphylococcus aureus) and, to a lesser extent, anaerobes (Bacteroides and Peptostreptococcus). Up to 1/3 of infections are polymicrobial. A small proportion (2% to 10%) of OE is caused by fungal overgrowth (e.g., Aspergillus niger usually occurs with prolonged antibiotic use).1

  • Pathogenesis of OE includes the following:

  • Trauma, the usual inciting event, leads to breach in the integrity of EAC skin.

  • Skin inflammation and edema ensue, which, in turn, leads to pruritus and obstruction of adnexal structures (e.g., cerumen glands, sebaceous glands, and hair follicles).

  • Pruritus leads to scratching, which results in further skin injury.

  • Consequently, the milieu of the EAC is altered (i.e., change in quality and quantity of cerumen, increase in pH of EAC, and dysfunctional epithelial migration).

  • Finally, the EAC becomes a warm, alkaline, and moist environment—ideal for growth of different pathogens.

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Risk Factors3
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  • Environmental factors:

    • Moisture—Macerates skin of EAC, increases pH, and washes away protective cerumen layer (e.g., swimming, sweating, humid environments).

    • Trauma—Leads to injury of EAC skin (e.g., cotton buds, fingernails, hearing aids, ear plugs, paper clips, match sticks, mechanical removal of cerumen).

    • Warm environments.

  • Host factors:

    • Anatomical—Buildup of wax and debris that lead to retained moisture (e.g., ...

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