Etiology and Pathogenesis

The lateral two-thirds of the ear canal is composed of epithelium with glands producing cerumen; in the medial third, the epithelium is tightly adherent to the periosteum and there are no glands. Uniquely, the cells and cerumen migrate laterally to self-cleanse. Cerumen has antimicrobial activity with a low pH and lysozymes; therefore, insufficient cerumen may predispose to AOE. With a combination of moist conditions (from swimming, humidity, sweating, and so on) and local trauma to the ear canal, organisms invade the epithelium, causing cellulitis.

In the United States, between 90% and 98% of cases of AOE are bacterial in origin. The most common bacterium by far is Pseudomonas aeruginosa. The second most common bacteria are Staphylococcus species, including S. aureus. Other gram-negative and -positive bacteria are often cultured. Fungi, either Candida or Aspergillus spp., and some other organisms cause the remaining cases of canal inflammation. It is common to have polymicrobial infections.

Clinical Presentation

The patient presents with symptoms that are rapid in onset over days, including ear pain and pruritus, or “fullness” in the ear canal. Some families may also note redness, discharge, or even hearing loss if the condition has progressed sufficiently to block the ear canal.

The peak incidence of AOE occurs in children age 7 to 12 years. There has often been significant water exposure, and even if swimming pool water quality is high, causative organisms are generally still present. Some parents or patients may admit to canal trauma with cotton swabs or bobby pins when questioned on history.

In AOE, the physical examination is critical in diagnosis. Debris and cerumen must be cleared from the canal to ensure accurate otoscopy of the TM as well as to improve the ability of topical treatment to reach the area of infection. The hallmark sign of AOE is tenderness of the tragus or the pinna when manipulated. The clinician will see diffuse edema and erythema of the canal, possibly with otorrhea or other debris present (Figure 31-2). The TM may be erythematous, but this should not imply a definite diagnosis of otitis media. On pneumatic otoscopy, if there is normal movement of the TM without visible effusion, the erythema may be attributed to the AOE.

Figure 31-2 Acute otitis externa.

On differential diagnosis, other conditions that should be considered include otitis media with perforation, malignant otitis externa (necrotizing osteomyelitis), furunculosis, contact otitis of the ear canal (largely from nickel jewelry, but also topical antimicrobials, chemicals, plastics, and so on), and other generalized dermatologic conditions occurring in or around the ear canal.

Evaluation and Management

After the diagnosis of AOE has been made by history and physical examination, it is rare that further evaluation is warranted. Only if an initial presentation has not resolved with prescribed therapy should a culture be taken for bacterial and fungal identification. On suspicion that the patient could have malignant otitis externa, further imaging may be needed to clarify the diagnosis. This serious condition should be suspected if the patient has a high temperature or necrotic tissue, facial paresis, meningeal signs, or mastoid involvement.

Appropriate management of AOE includes treating the causative organism as well as the debilitating pain. Topical therapy should be the initial treatment for uncomplicated AOE, and systemic antibiotics are not warranted. No studies have reliably proven one topical agent to work better than another. Acetic acid (2.0%) and alcohol (90%-95% isopropyl) solutions work as well as antimicrobial drops to clear AOE; however, they may be irritating. Aminoglycosides and fluoroquinolones with and without steroids have been approved for treatment of AOE. Examples include combinations of ciprofloxacin and hydrocortisone or dexamethasone, the combination of neomycin, polymyxin B, and hydrocortisone, and ofloxacin.

Because none of these treatments has proven best, an important consideration is the side effect profile. With a perforated TM or a myringotomy tube present, agents with ototoxicity should be strictly avoided, including the aminoglycosides and alcohol-based products. Contact dermatitis commonly (5%-15% prevalence) occurs with aminoglycoside otic drops. Other factors to consider include cost and compliance. Currently, fluoroquinolone drops are much more costly than other preparations. Conversely, patients may be more compliant with the fluoroquinolone drops because they need only be administered twice daily compared with four times daily for aminoglycosides.

Systemic oral antimicrobials should be reserved for cases in which cellulitis is extending onto the external ear or face, necrotizing disease is discovered, a concomitant middle ear infection exists, or the patient has an underlying immunodeficiency that makes him or her more susceptible to disease progression.

If a fungal cause of AOE is suspected, the clinician will see white strands with or without black or white fungal balls. Mild fungal infections respond to acid or alcohol solutions, but more advanced infections may require a topical antifungal such as clotrimazole.

Appropriate drug delivery is paramount. If the canal debris cannot be cleared by the physician, a wick should be inserted so that topical treatment can reach the infection. The parents should be instructed on how to correctly administer drops with the patient lying down, drops applied until filling the ear canal, and the patient maintaining this position for 3 to 5 minutes. Children should avoid submerging their heads underwater for 7 to 10 days while being treated, and beneficial effects from treatment should be seen in 48 to 72 hours.

Pain should be evaluated and treated for each patient. Most patients will benefit simply from a nonsteroidal antiinflammatory drug (NSAID). Topical anesthetic agents such as benzocaine may be used, but the relief they provide may mask progression of disease.