CME

EARN CATEGORY I CME CREDIT by reading this article and the article beginning on page 22 and successfully
completing 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 credit
by 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

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

titis externa (OE) is a common ambulatorycare condition. Acute OE manifests from bacterial (90% of cases) or fungal (10% of cases)
infections and affects four in 1,000 persons in
the United States annually.1 Chronic OE is
often the result of dermatologic or allergic etiologies.1-5 The
condition is usually confined to the tissues within the external
auditory canal (EAC); however, systemic antibiotics are prescribed to treat this problem in 65% of cases.2 Early OE is
easily treated with a topical application of an acidifying solution. Untreated infections may progress to a life-threatening
condition known as malignant otitis externa (MOE),1,2 especially
in patients who are immunocompromised or have diabetes.
Thus, the earlier this condition is accurately diagnosed and
treated, the less likely the patient is to suffer severe sequelae
and the earlier the patient can return to normal activity.

PATHOPHYSIOLOGY

Otitis externa results when any one of the above factors fails
to protect the EAC. For example, if the canal is stripped of
all cerumen through excessive water exposure (water activities, perspiration, and high humidity) or mechanical means
(insertion of foreign objects such as cotton swabs, fingers, ear
plugs, or hearing aids), then moisture will be allowed into the
keratin cells beneath the cerumen.1-4 This creates an ideal
pH-elevated environment for bacterial and fungal growth.2,3
Before World War II, fungi were implicated as the primary
cause of OE but US military research in the South Pacific
proved that bacteria were the most common cause.1 Pseudomonas aeruginosa is the predominant bacterial pathogen, followed closely by Staphylococcus aureus and S epidermidis;1,2,4,6,7
External os
Tympanic
membrane

The EAC is a skin-lined 2.5-cm meatus that includes and

extends from the tympanic membrane (TM) to the opening
at the external os1 (see Figure 1). The outer third of the canal
infrastructure is cartilaginous and covered with a layer of
sebaceous and ceruminous glands and hair.1 The inner twothirds of the canal are constructed of an osseous base under a
very thin layer of skin that is tightly connected to the underlying periosteum.4 The EAC has specific defenses against offending organisms. A healthy canal is covered with a thin
layer of acidic, lysozyme-rich cerumen that prohibits bacterial
and fungal growth. Cerumen is also hydrophobic, which prevents the canal from absorbing moisture. Lastly, the migratory pattern of epithelial tissue pushes debris from the TM
toward the external os and out of the ear.

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

External
auditory
canal

FIGURE 1. The external auditory canal extends from the

tympanic membrane to the opening at the external os.

Christy Krames

ANATOMY

Aspergillus and Candida are the most common fungal organisms.2 Only 5% of OE cases can be attributed to herpes
zoster oticus, furunculosis, or bullous myringitis.1
OE can also result from a host of noninfectious conditions
classified as eczematous otitis externa, including acne, lupus
erythematosus, psoriasis, atopic dermatitis, and seborrheic
dermatitis.2 These conditions affect the body as a whole;
therefore, systemic treatments will decrease manifestations in
the ear canal. Eczematous OE manifests as decreased skin
elasticity, atrophy of the ceruminous and sebaceous glands,
loss of protective films and secretions, and a pH higher than
6.3 In addition, dryness and atrophy of the glands promote
chronic and recurrent OE.3

these questions will help determine which method of treatment is most expeditious.
PHYSICAL EXAMINATION

A broader, multisystem approach to the physical examination is necessary, including a dermatologic examination that
looks for disease-specific skin changes, if the history points
toward a systemic cause.1 If there is no history of systemic
disease but one is suspected, the appropriate laboratory tests
for diagnosis must be ordered. For example, the clinician
would order a random blood glucose test if diabetes is suspected. A random glucose or glycosylated hemoglobin test
is also appropriate for a patient with known diabetes in
order to determine disease control. An ESR or antinuclear

PATIENT EVALUATION

The early stage of OE occurs within a few days to a week of

exposure to a causative agent. Early signs and symptoms are
generally mild (minimal discomfort, pruritus, an odorless
secretion, modest erythema, decreased hearing, and a feeling
of fullness in the ear). Beyond the early stage of infection,
1 to 2 weeks after onset, patients will have purulent discharge from the os; marked edema of the EAC; and
increased erythema and pain that is exacerbated by chewing,
tragal pressure, or movement of the auricle.1 Severe symptoms include profound pain and discharge, complete canal
obstruction, and external ear signs, such as preauricular and
postauricular lymphadenopathy, parotitis, fever, and auricular cellulitis.1,2
Evaluation begins with a thorough history of the onset and
current symptoms. The clinician should ask leading questions regarding precipitating activities, such as the use of finger nails, cotton swabs, or bobby pins in the ear or recent
participation in recreational water activities. The history
should also take into account significant medical problems
that are known to cause OE. Patients with diabetes, a compromised immune system, or local circulatory insufficiency
from radiation exposure are particularly vulnerable to rapid
progression from mild to severe OE.1,8
Does the patient suffer from any dermatitides such as
lupus, atopic dermatitis, or psoriasis? If the answer is Yes, is
the patient being treated with a topical or an oral medicine
that may help or hinder OE treatment? Accurate answers to

Full visualization of the TM is

essential because an obscured view
makes differentiating OE from
acute otitis externa quite difficult.
antibody test is appropriate if an autoimmune disorder is
suspected. However, within the context of OE, these tests
should only be ordered when they are strongly indicated, as
unnecessary laboratory tests may lead to unnecessary
patient 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 be
performed. The local lymph nodes, including the pre- and
postauricular and cervical chain lymph nodes must also be
included in the examination. The ear canal is examined for
otorrhea, which varies widely in appearance.
The characteristics of otorrhea can give clues as to the differential diagnosis of OE (see Table 1, page 46). For example, a green, foul-smelling discharge is often the result of a
pseudomonal infection.7 The presence of fluffy and white to
off-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 discharge from the os; marked edema of the EAC; and increased erythema and pain that is exacerbated by chewing, tragal pressure, or movement 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.

www.jaapa.com FEBRUARY 2009 22(2) JAAPA 45

CME Otitis externa

black or white conidiophores on white hyphae is associated
with Aspergillus infection.2
The EAC is often completely blocked, obscuring direct visualization of the TM. The canal must be cleaned of all debris
in order for treatment to be effective. However, flushing the
canal must be avoided unless the TM can be fully visualized
and is found to be intact.2 Small perforations of the TM are
common and often missed on examination. Attempting to
flush the EAC when the TM is perforated can result in disruption of the ossicles, which can cause significant cochlearvestibular damage and result in hearing loss, tinnitus, vertigo,
and dizziness.2 These complications can lead to the need for
surgical intervention.2 Flushing the EAC can also cause damage to the canal itself. Inflammation and maceration make the
EAC more susceptible to trauma; therefore, the clinician must
also avoid using a cerumen spoon or curette to clean out the
canal.2 Lastly, if the EAC cannot be cleared of debris because
of swelling, pain, or a lack of equipment, the debris should be
left in place. Frequent follow-ups are needed until the secretions clear spontaneously or can be removed with greater
ease.2 If the EAC is severely swollen, delivering medication to
the place where it is most needed may be mechanically diffiTABLE 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

perforated tympanic
membrane

Acute: Purulent white to yellow

mucus and deep pain are present.
Serous: Clear mucus is present,
especially in patients with allergies.

Trauma

Bloody mucus is present.

Data from Sander R.2

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

cult. Therefore, a preformed cellulose wick specifically designed to apply medication within the EAC may be inserted
and then left in place to facilitate absorption and delivery of
liquid medications to the inner portions of the EAC.1,2
Irrigation of the EAC in patients with OE is very controversial; however, this procedure is still often performed in
the primary care setting. No outcome studies have been conducted that would lead to specific guidelines for its use.9
Therefore, the clinician must use extreme caution when proceeding with mechanical debris removal, and all possible
adverse outcomes and alternative debris removal options
(such as suctioning under direct visualization) should be
explained to the patient.1-4
Full visualization of the TM is also essential on initial
examination because an obscured view makes differentiating
OE from acute otitis media (AOM) difficult.2 Concomitant
OE and AOM is not unusual.1,2,10 Tympanometry is used to
diagnose AOM if the TM is not obscured and is found to be
red.1,10 After confirming the diagnosis of AOM, appropriate
oral antibiotic therapy should be given.
TREATMENT

Treatment regimens for OE vary widely and are largely

dependent upon clinician specialty and whether the patient is
a child or an adult.2,11 However, in cases of mild disease, topical therapy should be attempted first. Topical therapy, first
described over 3,000 years ago, is still in use today.1
Before any topical agent is applied, the clinician should safely remove any debris from the EAC. In very mild cases, a
combination of 2% acetic acid and 1% hydrocortisone is used
at the onset of symptoms.1,2 Some clinicians report more success with a combination of half acetic acid/hydrocortisone and
half 90% alcohol.1,12 Warming fluids to body temperature before introducing them into the EAC reduces dizziness,1,2 and
gentle tragus manipulation encourages fluid absorption deep
into the canal and tissues. Medications are kept within the
EAC by placing cotton at the os; using a cellulose wick is recommended if edema reduces the diameter of the EAC by
more than 50%. When the swelling goes downusually in 2 to
3 daysthe sponge is no longer needed and can be removed
with forceps.1 Most often, the wick falls out on its own.
Moderate to severe cases of OE require antimicrobial ototopical agents, not just an inhibitor such as acetic acid.1 Table
2 lists commonly used ototopical agents. Ototopicals are not
more effective than systemic antibiotics, but they can provide
localized treatment in concentrations approximately 1,000
times higher than can be provided by systemic antibiotics. In
addition, ototopicals are less likely to cause systemic resistance or side effects.1 Oral antibiotics should be used only
when OE is persistent, when AOM is present, or when infection has spread locally or systemically.2
An oral antimicrobial should be included when the infection extends to external canal structures (the cervical lymph
nodes, parotid glands, or auricle).1 Commonly used antibiotics range from aminoglycosides (neomycin, gentamicin) to
fluoroquinolones, with or without concomitant cortico-

steroids.1 However, aminoglycosides are frequently associated with ototoxicity and allergic dermatitis. In addition,
aminoglycosides should never be used in a patient with a
perforated TM. Fluoroquinolone preparations allow for better patient adherence because of their ease of use (twice-a-day
dosing). Furthermore, these preparations can often be used
even when the TM is perforated.1 The risks and benefits of
combining corticosteroids with an aminoglycoside or fluoroquinolone should be weighed carefully. Although cortico-

Malignant otitis externa results

when infection spreads through
the external auditory canal into
the neighboring tissues.
steroids are known to substantially reduce EAC edema associated with OE, they can also act as a sensitizing agent.1,2
Treatment duration varies somewhat based on severity of
disease and speed of resolution. Recommendations are to
treat symptoms for 3 days beyond resolution (approximately
5-7 days).2 For more severe disease, a 10- to 14-day treatment
course is recommended.2 If symptoms fail to resolve in 5 to 7
days the clinician should consider the possibility of patient
sensitivity. For example, perhaps an aminoglycoside allergy is
preventing full resolution; or perhaps the patient is sensitive
to the preservative (benzalkonium chloride, thimerosal, or
propylene glycol) in the agent being used.1
Ten percent of acute OE cases are secondary to a fungal
infection. Obvious and uncomplicated fungal infections
present with the classic whitish, cottonlike hyphae strands
(Candida), with or without interspersed small black or white
fungal balls at the tips of the hyphae (Aspergillus).1 Simple
fungal infections of the EAC respond to a 2% acetic acid
and/or a 90% to 95% alcohol solution. More established infections respond to topical clotrimazole, tolnaftate, or a compounded solution of nystatin 100,000 U/mL otic suspension.1
If typical OE does not respond to standard topical treatment, the clinician must consider the possibility of a fungal
superinfection. In cases of a fungal superinfection, a topical
antifungal is added to the antibiotic regimen. Recalcitrant
cases of fungal infection may require the use of oral itraconazole or fluconazole, 100 mg daily for 10 to 14 days, especially if the TM is perforated. Irrigation should not be used if
the TM is perforated, the debris should be removed by suctioning under direct visualization. In addition, the EAC must
be kept dry at all times. The patient must be instructed to
use a cotton swab with a petroleum jelly when showering to
prevent 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

need to be optimally treated systemically before full otic benefit can be achieved. Furthermore, simultaneous infectious
and autoimmune etiologies are possible.
COMPLICATIONS

All possible reasons for treatment failure must be considered,

including the accuracy of the initial diagnosis. Recalcitrant
cases of OE often occur in patients with diabetes; patients
who are immunocompromised, such as those with HIV
infection; and patients who use corticosteroids or receive
chemotherapy daily or are undergoing radiation treatment.
Coexisting AOM, malnourishment, and chronic illness can
also hinder resolution of OE.1,8 Paying close attention to a
patients reaction to treatment can avoid potentially lifethreatening complications. Meticulous cleaning of the EAC,
enforcing strict precautions and ear protection for waterrelated activities, identifying potential EAC allergens, and
evaluating nutritional and endocrine status are important
measures for preventing and managing recalcitrant OE.
Malignant otitis externa MOE results when infection
spreads through the canal into the neighboring tissues. MOE
involves the mastoid or temporal bone, cartilage, nerves, and
blood vessels.13 The organism most often implicated in MOE
is Pseudomonas aeruginosa.2,8,13 MOE should be suspected
when pain is disproportionate to symptoms; canal skin necrosis or granulation is present; body temperature exceeds
102.2F (39C); or in the presence of facial paralysis, vertigo,
or meningeal signs.1 MOE is difficult to treat and has a mortality rate of 53% or higher.2 Once MOE is diagnosed, the
patient should be referred to a specialist immediately.
Given their superb antipseudomonal activity and excellent
GI absorption, fluoroquinolones are the first-line treatment for
MOE.2 A combination of beta lactam and aminoglycoside
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

www.jaapa.com FEBRUARY 2009 22(2) JAAPA 47

CME Otitis externa

antibiotics is effective for patients who are either allergic to or
do not respond to fluoroquinolone therapy.2 A 2-week course
of antibiotic therapy is usually necessary. Treatment also
includes surgical removal of all infectious and necrotic debris.2
Furuncle This complication is a superficial abscess. A
furuncle in the lateral third of the EAC occurs when the
apopilosebaceous glands become blocked.2 The treatment
for a furuncle includes drainage, hot compress, and topical
and systemic antibiotics. The most common organism cultured in this condition is Staphylococcus aureus,1,2 and appropriate antibiotic therapy should be given.
CONCLUSION

OE is a common ambulatory-care condition that can present

significant challenges to the clinician if not diagnosed and treated appropriately at its onset. Bacteria are the cause of 90% of
cases of OE, the remaining cases are caused by a fungal infection. However, the clinician must always keep in mind the possibility of concurrent endocrine or immune-mediated disease.
These conditions are often either the primary cause or a complicating factor in OE. The quicker the causative pathogen is
identified, the earlier more focused and appropriate treatment
can be rendered, and the less likely the patient will experience
complications. Some complications, such as MOE, can be life
threatening. Rapid identification of this condition and immediate referral to a specialist can save the patients life. JAAPA

Richard 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 MENTIONED
Acetic acid, hydrocortisone (Vosol HC)
Clotrimazole (Lotrimin)
Fluconazole (Diflucan)
Gentamicin (Garamicin)
Hydrocortisone

Itraconazole (Sporanox)
Neomycin
Nystatin
Polymyxin B
Tolnaftate (Tinactin)

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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.
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12. Isaacson G. Treatment of otitis externa. Pediatr Infect Dis J. 2003;22(8):759-760.
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