Infections of the Head and Neck

Acute otitis externa (AOE) is defined as a diffuse inflammation of the external ear canal, which may also involve the pinna or tympanic membrane (1). This condition is also known as “swimmer’s ear” or “tropical ear” due to a higher prevalence in individuals with prolonged water exposure during swimming or who live in warm and humid climates (2). The annual incidence of AOE is about 1:100 to 1:250 within the general population (3). The external ear comprises the auricle and external ear canal. The medial 60% of the external auditory canal is osseous and contains thin skin densely adherent to the underlying periosteum (Fig. 109.1). The lateral 40% of the external auditory canal is cartilaginous and contains a thin layer of subcutaneous tissue between the skin and cartilage. This subcutaneous layer contains hair follicles and sebaceous and apocrine glands. The skin of the auditory canal has a property of migrating from the tympanic membrane outward, resulting in self-cleansing. Cerumen is formed by glandular secretions and sloughed epithelium and provides both a chemical and mechanical protective barrier to infection. Cerumen is slightly acidic, maintaining a canal pH of 5 to 6.5, which helps inhibit bacterial and fungal growth. The lipid content of cerumen prevents maceration and breakdown of the epithelium. It is the breakdown in this natural defense mechanism that allows for opportunistic infections, giving rise to otitis externa (4). The risk factors for acute otitis externa are prolonged exposure to water from swimming; dermatologic conditions such as seborrhea, psoriasis, eczema; trauma from ear cleaning, and foreign objects; use of assistive devices such as earplugs or hearing aids; anatomic abnormalities such as exostoses and narrow ear canals; immunocompromising systemic conditions such as diabetes, HIV; concomitant ear diseases such as cholesteatoma, suppurative otitis media; and a history of cancer radiotherapy (1,5). Symptoms and signs of ear canal inflammation usually have rapid onset. Some of the presenting symptoms may be otalgia, itching, aural fullness, decreased hearing, and pain with chewing. Patients with AOE will often have disproportionately severe pain and will have significant tenderness when pushed on the tragus, or with manipulation of the pinna. Otoscopic exam usually reveals ear canal cellulitis and edema. Depending on the severity of the ear canal swelling, the tympanic membrane may or may not be visualized. The ear canal is often filled with purulent discharge and debris. Inflammation may spread to involve the entire auricle and adjacent skin. Regional lymphadenopathy may be present on the exam (1). Most cases of AOE are bacterial. Pseudomonas aeruginosa and Staphylococcus species have been found to be the most common pathogens (6). Fungal involvement is uncommon in primary AOE. It is more often seen in chronic otitis externa or as secondary overgrowth following the treatment of bacterial infection. Initial treatment of otitis externa involves removal of debris from the external ear canal, pain control, use of topical medications, acidification of the ear canal, and control of predisposing factors. Debridement of the external ear canal removes infectious material and allows for better penetration of topical medications. Topical medications can usually be administered directly into the ear canal. However, in many cases marked edema of the ear canal will prevent proper penetration of the medicated drop down into the canal. In this situation, placement of a cotton wick directly into the ear canal for several days will facilitate delivery of the medication (1). Currently recommended topical preparations consist of antibiotics and steroid combinations. Quinolone antibiotic preparations may have broader microbial coverage and a low risk of contact dermatitis. Caution should be used when treating with neomycin-containing topical preparations due to a potential for neomycin to cause contact sensitivity and in turn lead to worsening of symptoms. Neomycin-containing preparations also have a low risk of causing permanent sensorineural hearing loss and should be used with caution in patients with perforated tympanic membranes. Acetic acid, boric acid, aluminum acetate, and silver nitrate have also been found to be effective. When treating immunocompromised patients, or if otitis externa infection has spread beyond the ear canal, consideration should be given to the use of systemic antibiotics as well. The choice of antibiotics should be based on their antipseudomonal and antistaphylococcal properties (1).