Otitis externa is an inflammation of the external ear canal commonly caused by infection. It constitutes one of the most common otolaryngologic encounters in the emergency department. This condition is addressed commonly as swimmer’s ear or tropical ear because it often occurs after a history of repeated water exposure and occurs more commonly in warm and humid environments. This condition became of significant interest during World War II because of its high incidence among the troops in the South Pacific. During World War II, otitis externa accounted for 50% to 70% of the caseload for otolaryngologists in the South Pacific.
Today, otitis externa accounts for 7.5 million annual ototopical prescriptions in the United States and is a significant cause of ear pain and conductive hearing loss. This chapter discusses the basic anatomy of the external canal, different etiologies of otitis externa, and treatment and prevention that are needed by the pediatric practitioner managing this condition.
Epidemiology
According to the Centers for Disease Control (CDC), in 2007, the burden of acute otitis externa in the United States was 2.4 million health care visits (8.1 visits/1000 population), an estimated 1/123 persons affected during that year. Estimated annual rates of ambulatory care visits for acute otitis externa between 2003 and 2007 were highest among children 5 to 9 (18.6%) and 10 to 14 years of age (15.8%). Approximately 3% of emergency department visits for acute otitis externa in 2007 led to hospitalization. Incidence peaked during summer months, and the regional rate was highest in the South. Direct health care costs were approximately $0.5 billion annually and nearly 600,000 hours annually of clinician’s time. In a retrospective analysis of the Nationwide Emergency Department Sample from 2009 through 2011, more than 8.6 million visits were due to an otologic diagnosis, which represented 2.2% of all emergency department and 6.7% of all pediatric emergency department encounters. Otitis externa accounted for 11.8% of all the cases.
Otitis externa was the most common cause of outpatient visits for waterborne disease between 2005 and 2006. Outbreaks of otitis externa have been identified in competitive swimmers in association with insufficiently chlorinated pools, in divers, and in association with swimming in recreational fresh water lakes.
Normal Anatomy
The external ear is composed of the auricle and external auditory canal. The auricle of the ear is a skin-covered cartilaginous structure on the temporal region of the head and is an extension of the external auditory canal. The external auditory canal is divided into two regions: a lateral cartilaginous portion and a medial bony portion that ends at the tympanic membrane.
The cartilaginous portion of the external auditory canal makes up approximately 40% of its 2.5 cm total length and typically is directed slightly upward and backward. This shape and the presence of cerumen help to prevent water and foreign objects from entering the canal. In the anterior portion of the cartilaginous canal are the fissures of Santorini, which provide a route for the spread of infection from the canal into the adjacent parotid and surrounding tissues. The bony canal makes up the remainder of the canal length and is directed slightly downward and anterior. The isthmus, which is the narrowest portion of the canal, corresponds to the bony-cartilaginous junction.
The sensory innervation of the external auditory canal is complex and includes contributions from cranial nerves V, VII, IX, and X. This robust sensory innervation is responsible for the exquisite pain associated with otitis externa. The skin of the entire external auditory canal consists of keratinizing stratified squamous epithelium. It is the only keratinizing epithelium that lacks eccrine sweat glands.
Differences exist in the canal skin of the cartilaginous canal and the skin covering the bony canal. The cartilaginous canal skin is thicker and contains rete pegs, dermis, dermal papillae, hair follicles, and sebaceous and cerumen glands, which are absent in the bony canal. The thinner skin of the bony canal lacks dermal papillae and rete pegs. The lack of subcutaneous tissue in the bony canal allows the tight attachment of the skin to the underlying periosteum, rendering the bony canal wall more vulnerable to trauma.
Protective Mechanisms of the External Ear
Three major defense mechanisms protect the external auditory canal and lateral surface of the tympanic membrane: the tragus and antitragus, the skin with its cerumen coat, and the isthmus of the canal. The tragus and antitragus provide a partial barrier to the entrance of the foreign bodies into the external auditory canal.
The skin of the cartilaginous canal contains many hair cells and sebaceous and apocrine glands, such as cerumen glands. Together, these three adnexal structures are termed the pilosebaceous unit and provide a protective function in the external auditory canal. Migration of the skin of the external auditory canal also helps keep the canal free of debris. The pattern of migration is from the tympanic membrane laterally and radially away from the umbo. Glandular secretions combine with sloughed squamous epithelium to form an acidic coat of cerumen, one of the primary barriers to infection of the canal. Cerumen is composed of lipids that are hydrophobic, and its major function is to waterproof the canal. The acidic nature of cerumen has been shown to inhibit bacterial and fungal growth. This acidic pH also helps maintain the cohesion and integrity of the stratum corneum.
Racial and gender differences that are noted in the characteristics of cerumen do not seem to have major clinical significance. Whites and blacks produce cerumen with higher levels of lipids in contrast to Asians, who produce cerumen with higher levels of proteins. Cerumen in males also has been shown to have a higher pH level than that in females. The canal normally is a self-protecting and self-cleansing structure. The cerumen coat gradually works its way to the lateral part of the canal and sloughs externally. Instrumentation and excessive cleansing of the canal can alter this primary protective barrier and may lead to infection ( Box 15.1 ).
Hot and humid environment
Water exposure
Instrumentation of ear canal
Previous radiation therapy
Draining ear
Contact dermatitis
Normal Bacterial Flora
The normal bacterial flora of the external auditory canal is a combination of aerobic (80%) and anaerobic (20%) organisms. Aerobic bacteria include Staphylococcus epidermidis, Pseudomonas aeruginosa, α-hemolytic streptococci, and diphtheroids.
The bacteriology of the cerumen and the external auditory canal is essentially the same. In a study by Stroman and colleagues of 291 bacteria isolated from cerumen and 302 bacteria isolated from the canal, 99% and 96%, respectively, were gram-positive. Staphylococci accounted for 63% of bacteria. Staphylococcus auricularis is the isolate found most frequently (23% in cerumen and 21% in the canal), followed by S. epidermidis (14% from cerumen and 17% from the canal, respectively). After staphylococci, the coryneform bacteria (diphtheroids) are the organisms most frequently isolated. The third most frequently recovered bacteria belong to the streptococci and enterococci groups. Alloiococcus otitidis was isolated with the greatest frequency (>95%).
In addition, seven species of Bacillus were isolated. From the Micrococcaceae family, Micrococcus luteus was isolated most frequently. Turicella otitidis was the primary coryneform recovered—58% from cerumen and 65% from the canal. Corynebacterium auris was the second most frequently isolated coryneform, accounting for approximately 12% of bacteria. Twenty-one other species of coryneform bacteria (including 10 previously undefined species of Corynebacterium and 4 of Microbacterium ) were isolated as well. Coryneform bacteria represented approximately 20% of the bacteria isolated. Propionibacterium acnes and a variety of Peptococcus spp. make up the anaerobic flora.
Acute Otitis Externa
Acute otitis externa is an infection of the external auditory canal that often is the end result of a combination of factors. Bacterial and fungal infections of the external auditory canal occur when the natural defenses break down, resulting in a significant reduction in the amount of cerumen, an injury to the skin of the canal, or a shift of the normal canal flora. Humidity, heat, and maceration all produce itching, which often leads to manipulation and instrumentation of the canal, which in turn leads to additional trauma. Otitis externa may be caused by insults that result in the removal of the protective lipid film from the canal, allowing the entrance of organism to the apopilosebaceous unit. Rapid proliferation of bacteria occurs as a result of the warm, dark, and moist canal environment.
Inflammation and infection can cause canal edema or complete obstruction of the canal in severe cases, with purulent discharge. If the infectious process goes untreated, it leads to cellulitis of the auricle and surrounding area.
Symptoms of otitis externa, in addition to pruritus and drainage, include pain and tenderness on palpation or manipulation of the external ear. Pain arises as the soft tissues and skin of the canal distract the periosteal lining of the bony canal. Pain is severe and may interfere with daily activities and is the major reason for medical consultation.
History and Physical Examination
Otitis externa is a clinical diagnosis. The evaluation often reveals exposure to water, previous auricular instrumentation, or trauma. The physician should inquire about predisposing factors, such as diabetes, immunosuppression, history of eczema, or previous radiation therapy, all of which may predict a more complicated course.
Symptoms of acute otitis externa include otalgia (70%), itching (60%), fullness (22%), with or without hearing loss (32%) or ear canal pain on mastication.
On physical examination, the pinna may appear swollen or erythematous with eczematization ( Fig. 15.1 ) or may be protruding. Primary care practitioners and emergency department personnel may erroneously consider the diagnosis of mastoiditis based on auricular protrusion. On manipulation of the auricle, the patient often experiences severe pain. Tragal tenderness is another key feature of this disease. A handheld otoscope often suffices to establish the diagnosis, but the microscope is recommended for full cleaning of the ear canal. The canal appears swollen, with various grades of patency, depending on the severity of the infection. Purulent discharge combined with keratin debris usually fills the canal. It is important to attempt to visualize the tympanic membrane if the canal is not completely obstructed. Absence of drainage from the middle ear confirms the diagnosis of otitis externa.
Pathogens in Acute Otitis Externa
Common bacterial pathogens that cause otitis externa include P. aeruginosa, Staphylococcus aureus, Escherichia coli, and Proteus spp. ( Box 15.2 ). Pseudomonas spp. have been found to be the predominant organism in various studies. Historically, Pseudomonas spp. have accounted for 50% to 80% of bacteria isolated from cases of chronic otitis externa. In a study by Roland and Stroman, gram-negative bacteria accounted for 53% of recovered organisms; 45.3% were gram positive. In this study, P. aeruginosa accounted for 37.7% of the total number of isolates, whereas Pseudomonas otitidis accounted for 2.3% of recovered organisms.
Gram-Negative Organisms
Pseudomonas aeruginosa
Pseudomonas spp. Nov. “otitidis”
Proteus mirabilis
Serratia marcescens
Gram-Positive Organisms
Staphylococcus aureus
Staphylococcus epidermidis
Corynebacterium auris
Enterococcus faecalis
Fungi and Yeasts
Aspergillus fumigatus
Candida albicans
Candida parapsilosis
Staphylococci are the most common gram-positive organisms recovered in cases of otitis externa, accounting for 25% of the cases. S. epidermidis is the most common staphylococcal species recovered, followed by S. aureus. Coryneform bacteria are the second largest group of gram-positive bacteria isolated from cases of otitis externa. Reports of methicillin-resistant S. aureus as an increasing pathogen isolated from otorrhea resulting from otitis externa showed variable prevalence: 0.3%, 5.3%, 6.3%, and up to 9.8% of cases.
Other organisms identified as pathogens include Enterobacter, Klebsiella, Serratia, and Proteus spp. and E. coli . Although Microbacterium spp. previously were considered normal flora, more recently they have been identified at a 10 times higher rate in infected ears in contrast to normal controls. Microbacterium also has been the single recovered isolate in treatment failures and reinfections.
Management of Acute Otitis Externa
No consensus exists about the most effective treatment for otitis externa; however, evidence-based guidelines have been published with strong recommendations issued for acute uncomplicated infection in patients older than 2 years of age including pain assessment and appropriate analgesic prescription and avoidance of systemic antibiotics for initial therapy unless there is extension outside the ear canal or the presence of specific host factors that would indicate a need for systemic therapy. In addition there is continued strong support for treatment to include meticulously cleaning the external auditory canal. It is also important to differentiate acute otitis externa from other pathologies with similar symptoms, identify factors that modify management (i.e., nonintact tympanic membrane, tympanostomy tube, diabetes, immunocompromised state, prior radiotherapy), implement strategies to improve the delivery of topical drops (aural toilet, wick placement, drop administration instructions, etc.), consider use of a nonototoxic preparation in patients with known or suspected tympanic membrane perforation or tympanostomy tubes, and reassess if the patient fails to respond to treatment within 48 to 72 hours to either confirm the diagnosis or to exclude other causes of illness.
Treatment usually includes thorough cleaning and suctioning of the purulent debris and application of topical agents. Topical treatment has been shown effective and is the mainstay of treatment. A wick may be placed in the canal to provide adequate delivery of the topical solution when significant swelling of the external auditory canal occurs. Although no clinical trials have assessed the effectiveness of aural toilet alone, without the wick and adequate cleaning of the canal, the topical drops may not achieve adequate penetration and are ineffective. Available options for topical therapy include multiple topical antibiotics, antiseptics, steroids, and combination agents. Topical antimicrobial therapy increased absolute clinical cure rates of acute otitis externa by 46% and bacteriologic cure rates by 61% in contrast to placebo. Freedman compared topical neomycin/colistin/hydrocortisone with topical placebo and found less severe edema and itching by day 3 and less severe edema, itching, redness, scaling, and weeping by day 7. Without treatment, only 15% of patients with acute otitis externa have clinical cure within 10 days; however, the cure rate increases to 65% to 85% when topical antimicrobial therapy is administered.
Rosenfeld and colleagues performed a meta-analysis to assess topical antiseptics and antibiotics and found comparable clinical cures at 7 to 14 days. The most common antiseptics used in the treatment of otitis externa include acetic acid, boric acid/ethyl alcohol and aluminum acetate, and N -chlorotaurine. Acetic acid and aluminum acetate solution at pH 3.0, commonly known as modified Burow solution, has been found to inactivate in vitro Pseudomonas spp., gram-positive organisms (including MRSA, but excluding Enterococcus ), and Candida albicans within 5 minutes and all gram-negative bacteria within 20 minutes.
Topical antibiotic preparations usually are divided into two groups: quinolones and nonquinolone antibiotics. Nonquinolone antibiotics, such as polymyxin, neomycin, gentamicin, tobramycin, and oxytetracycline, have been the mainstay of treatment for otitis externa for several decades. Most of these agents have some degree of ototoxicity, however, which renders them undesirable in the case of a tympanic membrane perforation or a patent pressure-equalizing tube. The introduction of quinolones in the late 1980s for management of otitis externa and necrotizing external otitis provided a nonototoxic alternative treatment. Topical antibiotic therapy allows for the administration of high concentrations of antibiotics, which can overcome organisms with high minimal inhibitory concentrations. Rosenfeld and colleagues reported comparable clinical cure rates for topical quinolone antibiotics compared with nonquinolones at 3 to 4 days, 7 to 10 days, and 14 to 28 days. This same study found no differences in adverse effects between the two antibiotic groups.
One of the most common mistakes in the treatment of otitis externa is not identifying a tympanic membrane perforation and draining middle ear as the source of the infection, which may have treatment implications because of the ototoxicity of some compounds.
Typical duration of topical treatment is 7 to 10 days. Patients with more severe infections may require 10 to 14 days of treatment. It is commonly recommended that drops be given for 3 days beyond the cessation of symptoms.
Oral antibiotics are not routinely indicated for the treatment of otitis externa. A clinical trial by Roland and colleagues comparing oral antibiotic plus antibiotic/steroid drop versus antibiotic/steroid drop showed that a single topical agent is equivalent to combination of topical and oral antibiotic treatment for otitis externa and has similar clinical outcomes.
Indications for systemic antibiotics in acute otitis externa are few and include complicated infection by associated cellulitis of the surrounding skin or other underlying conditions (e.g., diabetes or immunosuppression). In spite of increasing awareness of inappropriate antibiotic use and its implications, prescription of systemic antibiotics in the outpatient setting remains frequent and has experienced only a modest decrease (about 4.9%) over the past few years. Up to 40% of patients are prescribed systemic antibiotics in addition to or instead of topical therapy, many of which are not active against P. aeruginosa or S. aureus, the most common pathogens associated with otitis externa. Use of systemic antibiotics can be only be justified when there is a concomitant diagnosis of otitis media or regional spread of infection. Oral antibiotics, when not appropriately prescribed, increase treatment cost, potential side effects, and likelihood of noncompliance and are more likely to contribute to emergence of antimicrobial resistance than is topical antimicrobial therapy. An evidence-based review concluded that no significant topical antibiotic resistance develops from the use of ototopical antibiotic treatment alone.
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