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.

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

Swimmer’s ear.

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

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

  
  
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  Associated with head immersion in water.

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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

  
  
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  Pathogenesis of OE includes the following:

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

  
  
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  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).

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

  
  
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  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).

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

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  Environmental factors:

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

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

    
    
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    Warm environments.

  
  
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  Host factors:

  
  
  
  
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    Anatomical—Buildup of wax and debris that lead to retained moisture (e.g., a narrow ear canal, hairy ear canal).

    
    
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    Cerumen—Paucity of or excessive production of cerumen (results in disappearance of the protective layer and retained moisture, respectively).

    
    
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    Chronic skin disorder—for example seborrheic dermatitis, psoriasis, atopic dermatitis (Figures 21-1 and 21-2).

    
    
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    Immunocompromise—for example HIV/AIDS, chemotherapy, diabetes, neutropenia.

Clinical Features

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  OE can either be localized, like a furuncle, or generalized (Figures 21-1 to 21-3). The latter is known as “diffuse OE,” or simply OE. Seborrheic dermatitis of the external ear and EAC can be diffuse or generalized (Figures 21-1 and 21-2).

  
  
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  Forms of (diffuse) OE:¹

  
  
  
  
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    Acute (<6 weeks; Figures 21-3 and 21-4).

    
    
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    Chronic (>3 months)—May cause hearing loss and stenosis of the EAC (Figure 21-5).

    
    
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    Necrotizing or malignant form—Defined by destruction of the temporal bone, usually in diabetics or immunocompromised people; often life-threatening (Figure 21-6).

  
  
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  Key historical features include:

  
  
  
  
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    Otalgia, including pruritus.

    
    
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    Otorrhea (Figures 21-3 to 21-5).

    
    
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    Mild hearing loss.

  
  
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  Key physical findings include:

  
  
  
  
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    Pain with tragal pressure or pain when the auricle is pulled superiorly; this may be absent in very mild cases.

    
    
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    Signs of EAC inflammation (edema, erythema, aural discharge) (Figures 21-3 to 21-5).

    
    
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    Fever, periauricular erythema, and lymphadenopathy point to severe disease.

    
    
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    Complete obstruction of EAC occurs in advanced OE.

  
  
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  Establishing the integrity of the tympanic membrane (TM) (through direct visualization) and the absence of middle-ear effusion (through pneumatic otoscopy) is crucial in differentiating OE from other diagnoses (e.g., suppurative otitis media, cholesteatoma).