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44 JAAPA FEBRUARY 2009 22(2) www.jaapa.com

EARN CATEGORY I CME CREDIT by reading this article and the article beginning on page 22 and successfullycompleting the posttest on page 49. Successful completion is defined as a cumulative score of at least 70%correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME creditby the AAPA. The term of approval is for 1 year from the publication date of February 2009.

LEARNING OBJECTIVES Discuss the anatomy and pathophysiology of otitis externa (OE) Describe the evaluation of OE including the history, presenting symptoms, and physical findings Outline treatment options for OE including topical agents and systemic antibiotics

Review the complications associated with failed initial therapy

CME

Otitis externa: Treatment is easy,but a missed diagnosis can be fatal

Acute OE rarely requires systemic antibiotic therapy. However, early indentification of the

causative pathogen and expedient care are needed for effective resolution.

Richard T. Handley, MPAS, PA-C

Otitis externa (OE) is a common ambulatory-care condition. Acute OE manifests from bac-terial (90% of cases) or fungal (10% of cases)infections and affects four in 1,000 persons inthe United States annually.1 Chronic OE is

often the result of dermatologic or allergic etiologies.1-5 Thecondition is usually confined to the tissues within the externalauditory canal (EAC); however, systemic antibiotics are pre-scribed to treat this problem in 65% of cases.2 Early OE iseasily treated with a topical application of an acidifying solu-tion. Untreated infections may progress to a life-threateningcondition known as malignant otitis externa(MOE),1,2 especiallyin patients who are immunocompromised or have diabetes.Thus, the earlier this condition is accurately diagnosed andtreated, the less likely the patient is to suffer severe sequelaeand the earlier the patient can return to normal activity.

ANATOMY

The EAC is a skin-lined 2.5-cm meatus that includes andextends from the tympanic membrane (TM) to the openingat the external os1 (see Figure 1). The outer third of the canal

infrastructure is cartilaginous and covered with a layer ofsebaceous and ceruminous glands and hair.1 The inner two-thirds of the canal are constructed of an osseous base under avery thin layer of skin that is tightly connected to the underly-ing periosteum.4 The EAC has specific defenses against of-fending organisms. A healthy canal is covered with a thinlayer of acidic, lysozyme-rich cerumen that prohibits bacterialand fungal growth. Cerumen is also hydrophobic, which pre-vents the canal from absorbing moisture. Lastly, the migrato-ry pattern of epithelial tissue pushes debris from the TMtoward the external os and out of the ear.

FIGURE 1. The external auditory canal extends from the

tympanic membrane to the opening at the external os.

C

hristyKrames

PATHOPHYSIOLOGY

Otitis externa results when any one of the above factors failsto protect the EAC. For example, if the canal is stripped ofall cerumen through excessive water exposure (water activi-ties, perspiration, and high humidity) or mechanical means(insertion of foreign objects such as cotton swabs, fingers, earplugs, or hearing aids), then moisture will be allowed into thekeratin cells beneath the cerumen.1-4 This creates an idealpH-elevated environment for bacterial and fungal growth.2,3

Before World War II, fungi were implicated as the primarycause of OE but US military research in the South Pacificproved that bacteria were the most common cause.1 Pseudo-monas aeruginosais the predominant bacterial pathogen, fol-lowed closely by Staphylococcus aureusand S epidermidis;1,2,4,6,7

External osTympanic

membrane

Externalauditory

canal

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Aspergillu sand Candidaare the most common fungal organ-isms.2 Only 5% of OE cases can be attributed to herpeszoster oticus, furunculosis, or bullous myringitis.1

OE can also result from a host of noninfectious conditions

classified as eczematous otitis externa, including acne, lupuserythematosus, psoriasis, atopic dermatitis, and seborrheicdermatitis.2 These conditions affect the body as a whole;therefore, systemic treatments will decrease manifestations inthe ear canal. Eczematous OE manifests as decreased skinelasticity, atrophy of the ceruminous and sebaceous glands,loss of protective films and secretions, and a pH higher than6.3 In addition, dryness and atrophy of the glands promotechronic and recurrent OE.3

PATIENT EVALUATION

The early stage of OE occurs within a few days to a week ofexposure to a causative agent. Early signs and symptoms aregenerally mild (minimal discomfort, pruritus, an odorlesssecretion, modest erythema, decreased hearing, and a feelingof fullness in the ear). Beyond the early stage of infection,1 to 2 weeks after onset, patients will have purulent dis-charge from the os; marked edema of the EAC; andincreased erythema and pain that is exacerbated by chewing,tragal pressure, or movement of the auricle.1 Severe symp-toms include profound pain and discharge, complete canalobstruction, and external ear signs, such as preauricular andpostauricular lymphadenopathy, parotitis, fever, and auricu-lar cellulitis.1,2

Evaluation begins with a thorough history of the onset andcurrent symptoms. The clinician should ask leading ques-tions regarding precipitating activities, such as the use of fin-ger nails, cotton swabs, or bobby pins in the ear or recentparticipation in recreational water activities. The historyshould also take into account significant medical problemsthat are known to cause OE. Patients with diabetes, a com-promised immune system, or local circulatory insufficiencyfrom radiation exposure are particularly vulnerable to rapidprogression from mild to severe OE.1,8

Does the patient suffer from any dermatitides such aslupus, atopic dermatitis, or psoriasis? If the answer is Yes, isthe patient being treated with a topical or an oral medicinethat may help or hinder OE treatment? Accurate answers to

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these questions will help determine which method of treat-ment is most expeditious.

PHYSICAL EXAMINATION

A broader, multisystem approach to the physical examina-tion is necessary, including a dermatologic examination thatlooks for disease-specific skin changes, if the history pointstoward a systemic cause.1 If there is no history of systemicdisease but one is suspected, the appropriate laboratory testsfor diagnosis must be ordered. For example, the clinicianwould order a random blood glucose test if diabetes is sus-pected. A random glucose or glycosylated hemoglobin testis also appropriate for a patient with known diabetes inorder to determine disease control. An ESR or antinuclear

antibody test is appropriate if an autoimmune disorder issuspected. However, within the context of OE, these testsshould only be ordered when they are strongly indicated, asunnecessary laboratory tests may lead to unnecessarypatient expense.After systemic disorders have been accounted for, a more

focused head and neck examination that includes the sinuses,nose, mastoids, temporomandibular joints, mouth, pharynx,ear canal, tympanic membrane, and the auricle should beperformed. The local lymph nodes, including the pre- andpostauricular and cervical chain lymph nodes must also beincluded in the examination. The ear canal is examined forotorrhea, which varies widely in appearance.

The characteristics of otorrhea can give clues as to the dif-ferential diagnosis of OE (see Table 1, page 46). For exam-ple, a green, foul-smelling discharge is often the result of apseudomonal infection.7 The presence of fluffy and white tooff-white, black, gray, or bluish green discharge or small

KEY POINTS Otitis externa (OE) is usually confined to the tissues within the external auditory canal (EAC), yet systemic antibiotics are prescribed to treat

this problem in 65% of cases. Early OE is easily treated with a topical application of an acidifying solution; however, untreated infections may

progress to a life-threatening condition known as malignant otitis externa.

Early signs and symptoms are generally mild. Beyond the early stage of infection, 1 to 2 weeks after onset, patients will have purulent dis-

charge from the os; marked edema of the EAC; and increased erythema and pain that is exacerbated by chewing, tragal pressure, or move-

ment of the auricle.

The EAC is often completely blocked in patients with OE, obscuring direct visualization of the tympanic membrane (TM). The canal must be

cleaned of all debris for treatment to be effective. Flushing the canal must be avoided unless the TM can be fully visualized and is found to

be intact.

Treatment regimens for OE vary widely and are largely dependent upon clinician specialty and whether the patient is a child or an adult.

However, in cases of mild disease, topical therapy should be attempted first.

Full visualization of the TM is

essential because an obscured viewmakes differentiating OE fromacute otitis externa quite difficult.

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black or white conidiophores on white hyphae is associatedwithAspergil lus infection.2

The EAC is often completely blocked, obscuring direct vis-ualization of the TM. The canal must be cleaned of all debris

in order for treatment to be effective. However, flushing thecanal must be avoided unless the TM can be fully visualizedand is found to be intact.2 Small perforations of the TM arecommon and often missed on examination. Attempting toflush the EAC when the TM is perforated can result in dis-ruption of the ossicles, which can cause significant cochlear-vestibular damage and result in hearing loss, tinnitus, vertigo,and dizziness.2 These complications can lead to the need forsurgical intervention.2 Flushing the EAC can also cause dam-age to the canal itself. Inflammation and maceration make theEAC more susceptible to trauma; therefore, the clinician mustalso avoid using a cerumen spoon or curette to clean out thecanal.2 Lastly, if the EAC cannot be cleared of debris becauseof swelling, pain, or a lack of equipment, the debris should beleft in place. Frequent follow-ups are needed until the secre-tions clear spontaneously or can be removed with greaterease.2 If the EAC is severely swollen, delivering medication tothe place where it is most needed may be mechanically diffi-

46 JAAPA FEBRUARY 2009 22(2) www.jaapa.com

CME Otitis externacult. Therefore, a preformed cellulose wick specifically de-signed to apply medication within the EAC may be insertedand then left in place to facilitate absorption and delivery ofliquid medications to the inner portions of the EAC.1,2

Irrigation of the EAC in patients with OE is very contro-versial; however, this procedure is still often performed inthe primary care setting. No outcome studies have been con-ducted that would lead to specific guidelines for its use.9

Therefore, the clinician must use extreme caution when pro-ceeding with mechanical debris removal, and all possibleadverse outcomes and alternative debris removal options(such as suctioning under direct visualization) should beexplained to the patient.1-4

Full visualization of the TM is also essential on initialexamination because an obscured view makes differentiatingOE from acute otitis media (AOM) difficult.2 ConcomitantOE and AOM is not unusual.1,2,10 Tympanometry is used todiagnose AOM if the TM is not obscured and is found to bered.1,10After confirming the diagnosis of AOM, appropriateoral antibiotic therapy should be given.

TREATMENT

Treatment regimens for OE vary widely and are largelydependent upon clinician specialty and whether the patient isa child or an adult.2,11 However, in cases of mild disease, topi-cal therapy should be attempted first. Topical therapy, firstdescribed over 3,000 years ago, is still in use today.1

Before any topical agent is applied, the clinician should safe-ly remove any debris from the EAC. In very mild cases, acombination of 2% acetic acid and 1% hydrocortisone is usedat the onset of symptoms.1,2 Some clinicians report more suc-cess with a combination of half acetic acid/hydrocortisone andhalf 90% alcohol.1,12Warming fluids to body temperature be-fore introducing them into the EAC reduces dizziness,1,2 andgentle tragus manipulation encourages fluid absorption deepinto the canal and tissues. Medications are kept within theEAC by placing cotton at the os; using a cellulose wick is rec-ommended if edema reduces the diameter of the EAC bymore than 50%. When the swelling goes downusually in 2 to3 daysthe sponge is no longer needed and can be removedwith forceps.1 Most often, the wick falls out on its own.

Moderate to severe cases of OE require antimicrobial oto-topical agents, not just an inhibitor such as acetic acid.1 Table2 lists commonly used ototopical agents. Ototopicals are notmore effective than systemic antibiotics, but they can providelocalized treatment in concentrations approximately 1,000times higher than can be provided by systemic antibiotics. Inaddition, ototopicals are less likely to cause systemic resist-ance or side effects.1 Oral antibiotics should be used onlywhen OE is persistent, when AOM is present, or when infec-tion has spread locally or systemically.2

An oral antimicrobial should be included when the infec-tion extends to external canal structures (the cervical lymphnodes, parotid glands, or auricle).1 Commonly used antibi-otics range from aminoglycosides (neomycin, gentamicin) tofluoroquinolones, with or without concomitant cortico-

TABLE 1. Differential diagnosis for otorrhea

Diagnosis Manifestation

Cerebrospinal fluid leak Clear, thin, and watery discharge

is present.

Chronic otorrhea Pain is absent.

Presence of purulent mucus is

intermittent.

Fungal infection Discharge is typically fluffy and

white to off-white, but may be

black, gray, bluish green, or yellow.

Presence of small black or white

conidiophores on white hyphae is

associated with Aspergillus.

Osteomyelitis Pain is present.

Purulent mucus with odor is present.

Otitis externa Acute: White mucus is scant but

may be thick.

Chronic: Bloody discharge is present,

especially in granulation tissue.

Otitis media with Acute: Purulent white to yellow

perforated tympanic mucus and deep pain are present.

membrane Serous: Clear mucus is present,

especially in patients with allergies.

Trauma Bloody mucus is present.

Data from Sander R.2

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steroids.1 However, aminoglycosides are frequently associat-ed with ototoxicity and allergic dermatitis. In addition,aminoglycosides should never be used in a patient with aperforated TM. Fluoroquinolone preparations allow for bet-

ter patient adherence because of their ease of use (twice-a-daydosing). Furthermore, these preparations can often be usedeven when the TM is perforated.1 The risks and benefits ofcombining corticosteroids with an aminoglycoside or fluoro-quinolone should be weighed carefully. Although cortico-

steroids are known to substantially reduce EAC edema asso-ciated with OE, they can also act as a sensitizing agent.1,2

Treatment duration varies somewhat based on severity ofdisease and speed of resolution. Recommendations are totreat symptoms for 3 days beyond resolution (approximately5-7 days).2 For more severe disease, a 10- to 14-day treatmentcourse is recommended.2 If symptoms fail to resolve in 5 to 7days the clinician should consider the possibility of patientsensitivity. For example, perhaps an aminoglycoside allergy ispreventing full resolution; or perhaps the patient is sensitiveto the preservative (benzalkonium chloride, thimerosal, orpropylene glycol) in the agent being used.1

Ten percent of acute OE cases are secondary to a fungalinfection. Obvious and uncomplicated fungal infectionspresent with the classic whitish, cottonlike hyphae strands(Candida), with or without interspersed small black or whitefungal balls at the tips of the hyphae (Asperg illus).1 Simplefungal infections of the EAC respond to a 2% acetic acidand/or a 90% to 95% alcohol solution. More established infec-tions respond to topical clotrimazole, tolnaftate, or a com-pounded solution of nystatin 100,000 U/mL otic suspension.1

If typical OE does not respond to standard topical treat-ment, the clinician must consider the possibility of a fungalsuperinfection. In cases of a fungal superinfection, a topicalantifungal is added to the antibiotic regimen. Recalcitrantcases of fungal infection may require the use of oral itracona-zole or fluconazole, 100 mg daily for 10 to 14 days, especial-ly if the TM is perforated. Irrigation should not be used ifthe TM is perforated, the debris should be removed by suc-tioning under direct visualization. In addition, the EAC must

be kept dry at all times. The patient must be instructed touse a cotton swab with a petroleum jelly when showering toprevent water entering the EAC.When treating acute OE, the clinician should also take into

consideration the possibility of a noninfectious etiology.Underlying disorders such as psoriasis, atopic dermatitis,acne, or seborrhea can be the cause of OE. These diseases

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TABLE 2. Common ototopical treatments

ACUTE BACTERIAL OE

Aminoglycosides

Fluoroquinolones, with or without corticosteroids

Hydrocortisone

Neomycin

Polymyxin B

FUNGAL OE (ACUTE OR CHRONIC)

Clotrimazole (Lotrimin)

Tolnaftate (Tinactin)

MILD ACUTE OE (BACTERIAL OR FUNGAL)

2% acetic acid

2% acetic acid with hydrocortisone (Vosol)

2.75% boric acid

95% isopropyl alcohol

Key: OE, otitis externa

Data from Osguthorpe JD and Nielsen DR.1

Malignant otitis externa resultswhen infection spreads throughthe external auditory canal intothe neighboring tissues.

need to be optimally treated systemically before full otic ben-efit can be achieved. Furthermore, simultaneous infectiousand autoimmune etiologies are possible.

COMPLICATIONSAll possible reasons for treatment failure must be considered,including the accuracy of the initial diagnosis. Recalcitrantcases of OE often occur in patients with diabetes; patientswho are immunocompromised, such as those with HIVinfection; and patients who use corticosteroids or receivechemotherapy daily or are undergoing radiation treatment.Coexisting AOM, malnourishment, and chronic illness canalso hinder resolution of OE.1,8 Paying close attention to apatients reaction to treatment can avoid potentially life-threatening complications. Meticulous cleaning of the EAC,enforcing strict precautions and ear protection for water-related activities, identifying potential EAC allergens, andevaluating nutritional and endocrine status are importantmeasures for preventing and managing recalcitrant OE.

Malignant otitis externa MOE results when infectionspreads through the canal into the neighboring tissues. MOEinvolves the mastoid or temporal bone, cartilage, nerves, and

blood vessels.13 The organism most often implicated in MOEis Pseudomonas aeruginosa.2,8,13 MOE should be suspectedwhen pain is disproportionate to symptoms; canal skin necro-sis or granulation is present; body temperature exceeds102.2F (39C); or in the presence of facial paralysis, vertigo,or meningeal signs.1 MOE is difficult to treat and has a mor-tality rate of 53% or higher.2 Once MOE is diagnosed, thepatient should be referred to a specialist immediately.

Given their superb antipseudomonal activity and excellentGI absorption, fluoroquinolones are the first-line treatment forMOE.2A combination of beta lactam and aminoglycoside

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antibiotics is effective for patients who are either allergic to ordo not respond to fluoroquinolone therapy.2A 2-week courseof antibiotic therapy is usually necessary. Treatment alsoincludes surgical removal of all infectious and necrotic debris.2

Furuncle This complication is a superficial abscess. Afuruncle in the lateral third of the EAC occurs when theapopilosebaceous glands become blocked.2 The treatmentfor a furuncle includes drainage, hot compress, and topicaland systemic antibiotics. The most common organism cul-tured in this condition is Staphylococcus aureus,1,2 and appro-priate antibiotic therapy should be given.

CONCLUSION

OE is a common ambulatory-care condition that can presentsignificant challenges to the clinician if not diagnosed and treat-ed appropriately at its onset. Bacteria are the cause of 90% ofcases of OE, the remaining cases are caused by a fungal infec-tion. However, the clinician must always keep in mind the pos-sibility of concurrent endocrine or immune-mediated disease.These conditions are often either the primary cause or a com-plicating factor in OE. The quicker the causative pathogen isidentified, the earlier more focused and appropriate treatmentcan be rendered, and the less likely the patient will experiencecomplications. Some complications, such as MOE, can be lifethreatening. Rapid identification of this condition and immedi-ate referral to a specialist can save the patients life. JAAPA

CME Otitis externaRichard Handley practices at SCV Quality Care, an urgent care/occupational

medicine group in Valencia, California. He has indicated no relationships to

disclose relating to the content of this article.

DRUGS MENTIONEDAcetic acid, hydrocortisone (Vosol HC) Itraconazole (Sporanox)Clotrimazole (Lotrimin) NeomycinFluconazole (Diflucan) NystatinGentamicin (Garamicin) Polymyxin BHydrocortisone Tolnaftate (Tinactin)

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2006;74(9):1510-1516.2. Sander R. Otitis externa: a practical guide to treatment and prevention. Am Fam Physician.

2001;63(5):927-936.3. Schapowal A. Otitis externa: a clinical overview. Ear Nose Throat J. 2002;81(1):21-22.4. Rutka J. Acute otitis externa: treatment perspectives. Ear Nose Throat J. 2004;83(9 suppl 4):20-22.5. Corwell BN, Boyls-White B. Otitis externa or swimmers ear. Atlantic Coast Conference Web site.

http://www.theacc.com/sports/c-swim/spec-rel/010406aad.html. Published January 4, 2006.Accessed January 6, 2009.

6. Roland PS, Stroman DW. Microbiology of acute otitis externa. Laryngoscope. 2002;112(7 pt 1):1166-1177.

7. Sundstrom J, Jacobson K, Munck-Wikland E, Ringertz S. Pseudomonas aeruginosain otitis exter-na. A particular variety of the bacteria? Arch Otolaryngol Head Neck Surg. 1996;122(8):833-836.

8. Selesnick SH. Otitis externa: management of the recalcitrant case. Am J Otol. 1 994;15(3):408-412.9. Evans P. Treatment of otitis externa. J Am Board Fam Pract. 1999;12(3):262.

10. American Academy of Pediatrics Subcommittee on Management of Acute Otitis Media.Diagnosis and management of acute otitis media. Pediatrics. 2004;113(5):1451-1465.

11. Halpern MT, Palmer CS, Seidlin M. Treatment patterns for otitis externa. J Am Board Fam Pract.1999;12(1):1-7.

12. Isaacson G. Treatment of otitis externa. Pediatr Infect Dis J. 2003;22(8):759-760.13. Soudry E, Joshua BZ, Sulkes J, Nageris BI. Characteristics and prognosis of malignant external

otitis with facial paralysis. Arch Otolaryngol Head Neck Surg. 2007;133(10):1002-1004.