Otitis Externa

Practice Essentials
Otitis externa (OE) is an inflammation or infection of the
external auditory canal (EAC), the auricle, or both.[1, 2, 3] This
condition can be found in all age groups.[4]
Essential update: AAO-HNSF releases updated diagnosis
and management guidelines for acute otitis externa
The American Academy of OtolaryngologyHead and Neck
Surgery Foundation (AAO-HNSF) has released updated
clinical practice guidelines for the diagnosis and treatment of
acute OE. Their recommendations include the following[5] :
Differentiate diffuse acute OE from other possible
causes of otalgia, otorrhea, and inflammation of the
EAC.
Assess patients with diffuse acute OE for factors
that may modify therapeutic management (eg, nonintact tympanic membrane, immunocompromised
state).
Assess for pain in patients with acute OE; base the
analgesia recommendation on the patients pain
severity.
Administer topical medications as initial therapy for
diffuse, uncomplicated acute OE.
Do not administer systemic antimicrobial agents as
initial therapy for diffuse, uncomplicated acute OE;
reserve such treatment for cases in which there is
extension outside of the EAC or there are specific
host factors that require systemic agents.
Instruct patients on how to administer topical drops;
perform an aural toilet, place a wick, or both, when
the ear canal is obstructed.
Use a non-ototoxic topical agent in patients with a
known or suspected perforation of the tympanic
membrane (eg, tympanostomy tube).
Confirm the diagnosis of acute OE and reassess the
differential diagnosis within 48-72 hours in cases
refractory to the initial therapy.
Classification
Acute diffuse OE: Most common form of OE,
typically seen in swimmers
Acute localized OE (furunculosis): Associated with
infection of a hair follicle
Chronic OE: Same as acute diffuse OE but is of
longer duration (>6 wk)
Eczematous (eczematoid) OE: Encompasses various
dermatologic conditions (eg, atopic dermatitis,
psoriasis, systemic lupus erythematosus, and
eczema) that may infect the EAC and cause OE
Necrotizing (malignant) OE: Infection that extends
into the deeper tissues adjacent to the EAC; occurs
primarily in immunocompromised adults (eg,
diabetics, patients with acquired immunodeficiency
syndrome [AIDS])
Otomycosis: Infection of the ear canal from a fungal
species (eg, Candida, Aspergillus)
Signs and symptoms
The key physical finding of OE is pain upon palpation of the
tragus (anterior to ear canal) or application of traction to the

pinna (the hallmark of OE). Patients may also have the

following signs and symptoms:
Otalgia: Ranges from mild to severe, typically
progressing over 1-2 days
Hearing loss
Ear fullness or pressure
Erythema, edema, and narrowing of the EAC
Tinnitus
Fever (occasionally)
Itching (especially in fungal OE or chronic OE)
Severe deep pain: Immunocompromised patients may
have necrotizing (malignant) OE
Discharge: Initially, clear; quickly becomes purulent
and foul-smelling
Cellulitis of the face or neck or lymphadenopathy of
the ipsilateral neck (occasionally)
Bilateral symptoms (rare)
History of exposure to or activities in water
(frequently) (eg, swimming, surfing, kayaking)
History of preceding ear trauma (usually) (eg,
forceful ear cleaning, use of cotton swabs, or water
in the ear canal)
See Clinical Presentation for more detail.
Diagnosis
The patients history and physical examination, including
otoscopy, usually provide sufficient information for the
clinician to make the diagnosis of OE. Note that a patient
who is diabetic or immunocompromised with severe pain in the
ear should have necrotizing OE excluded by an
otolaryngologist.

Laboratory testing

Typically, laboratory studies are not needed, but they may be

helpful if the patient is immunocompromised, if the usual
treatment measures are ineffective, or if a fungal cause is
suspected. Tests may include the following:
Gram stain and culture of any discharge from the
auditory canal
Blood glucose level
Urine dipstick

Imaging studies

Imaging studies are not required for most cases of OE.

However, radiologic investigation may be helpful if an invasive
infection such as necrotizing (malignant) OE is suspected or
if the diagnosis of mastoiditis is being considered.
Imaging modalities may include the following:
High-resolution computed tomography (CT) scanning:
Preferred; better depicts bony erosion[6]
Radionucleotide bone scanning
Gallium scanning
Magnetic resonance imaging (MRI): Not used as
often as the other modalities; may be considered
secondarily or if soft-tissue extension is the
predominant concern[7]
See Workup for more detail.
Management
Most persons with OE are treated empirically. Primary
treatment involves the following:
Pain management

Removal of debris from the EAC

Administration of topical medications to control
edema and infection
Avoidance of contributing factors

Pharmacotherapy
Topical medications (eg, acetic acid in aluminum

acetate, hydrocortisone and acetic acid otic solution,

alcohol vinegar otic mix)
Analgesic agents (eg, acetaminophen, acetaminophen
and codeine)
Antibiotics (eg, hydrocortisone/neomycin/polymyxin
B, otic ofloxacin, otic ciprofloxacin, gentamicin
0.3%/prednisolone
1%
ophthalmic,
dexamethasone/tobramycin, otic ciprofloxacin and
dexamethasone,
otic
ciprofloxacin
and
hydrocortisone suspension)
Oral antibiotics (eg, ciprofloxacin)
Antifungal agents (eg, otic clotrimazole 1% solution,
nystatin powder)

Surgery
Surgical debridement of the ear canal: Usually

reserved for necrotizing OE or for complications of

OE (eg, external canal stenosis); often necessary in
more severe cases of OE or in cases where a
significant amount of discharge is present in the ear;
mainstay of treatment for fungal infections
Incision and drainage of an abscess
See Treatment and Medication for more detail.
Image library

Acute otitis externa. Ear

canal is red and edematous, and discharge is present.
Background
Otitis externa (OE) is an inflammation or infection of the
external auditory canal (EAC), the auricle, or both.[1, 2, 3] It is
a common disease that can be found in all age groups.[4] OE
usually represents an acute bacterial infection of the skin of
the ear canal (most commonly attributable to Pseudomonas
aeruginosa or Staphylococcus aureus[8] ) but can also be
caused by other bacteria, viruses, or a fungal infection (see
Pathophysiology and Etiology).
Several factors can contribute to EAC infection and the
development of OE, including the following[9] :
Absence of cerumen
High humidity
Retained water in ear canal
Increased temperature
Local trauma (eg, use of cotton swabs or hearing
aids)

Aquatic athletes are particularly prone to the development of

OE because repeated exposure to water results in removal of
cerumen and drying of the EAC. Retained water in the ear
canal can cause maceration of the skin and a milieu conducive
to bacterial or fungal proliferation. OE occurs more often in
the summer months, when swimming is more common, [4, 9] and
it is also common in tropical areas.[10] Individuals with allergic
conditions (eg, eczema, allergic rhinitis, and asthma) are also
at significantly higher risk for OE.[11, 12]
Although OE rarely causes prolonged problems or serious
complications, the infection is responsible for significant pain
and acute morbidity (see Presentation). Prompt diagnosis (see
DDx and Workup) and appropriate therapy (see Treatment)
cure the majority of cases without complications; however,
patients who are diabetic, immunocompromised, or untreated
may develop necrotizing (malignant) OE, a potentially lifethreatening infection.
Classification
OE may be classified as follows:
Acute diffuse OE This is the most common form of
OE, typically seen in swimmers; it is characterized
by rapid onset (generally within 48 hours) and
symptoms of EAC inflammation (eg, otalgia, itching,
or fullness, with or without hearing loss or jaw pain)
as well as tenderness of the tragus or pinna or
diffuse ear edema or erythema or both, with or
without otorrhea, regional lymphadenitis, tympanic
membrane erythema, or cellulitis of the pinna[10]
Acute localized OE This condition, also known as
furunculosis, is associated with infection of a hair
follicle
Chronic OE This is the same as acute diffuse OE
but is of longer duration (>6 weeks)
Eczematous (eczematoid) OE This encompasses
various
dermatologic
conditions
(eg,
atopic
dermatitis, psoriasis, systemic lupus erythematosus,
and eczema) that may infect the EAC and cause OE
Necrotizing (malignant) OE This is an infection
that extends into the deeper tissues adjacent to the
EAC; it primarily occurs in adult patients who are
immunocompromised (eg, as a result of diabetes
mellitus or AIDS) and is rarely described in children;
it may result in cases of cellulitis and osteomyelitis
(see
Cellulitis,
Osteomyelitis,
and
Chronic
Osteomyelitis Imaging)
Otomycosis - Infection of the ear canal secondary to
fungus species such as Candida or Aspergillus
Anatomy
The external ear (see the image below) consists of the
auricle and the EAC.

Acute otitis externa. Ear

canal is red and edematous, and discharge is present.
The auricle is composed of elastic cartilage with the
overlying skin attached directly to the perichondrium. It
begins to form during week 6 of gestation through
consolidation of portions of the mesoderm of the first and
second branchial arches, giving rise to the His hillocks. The
first 3 hillocks are derived from the first arch, the second 3
from the second arch. The auricle reaches adult shape by the
week 20 of gestation, but the adult size is not reached until
the age of 9 years.
The EAC begins to form during week 8 of gestation, when the
surface ectoderm of the first pharyngeal groove thickens
and grows toward the middle ear. This core of tissue begins
to resorb by week 21 of gestation to form a channel that is
complete by week 28. The canal reaches adult size by the age
of 9 years and ossifies completely by the age of 3 years. The
EAC is related to the mandibular fossa anteriorly, the
mastoid air cells posteriorly, the middle cranial fossa
superiorly, and the parotid gland inferiorly.
The EAC is lined with squamous epithelium and is
approximately 2.5 cm long in adults. Its function is to
transmit sound to the middle ear while protecting more
proximal structures from foreign bodies and any changes in
environmental conditions. The outer one third of the canal is
primarily cartilaginous and is oriented superiorly and
posteriorly; the inner two thirds of the canal is osseous, is
covered with thinner skin that adheres tightly, and is
oriented inferiorly and anteriorly; this portion of the canal is
devoid of any apocrine glands or hair follicles.
The thicker skin over the outer (cartilaginous) portion of the
EAC contains apopilosebaceous units comprising apocrine and
eccrine glands that secrete their products around the base
of a hair follicle. These secretions combine with sloughed
squamous epithelium (cerumen) to coat the EAC and maintain
an acidic pH (4-5). This cerumen coat migrates from the
isthmus of the EAC to the lateral part, and its waxy nature
protects the underlying epithelium from maceration or skin
breakdown. The quantity of cerumen produced varies widely
among individuals.
The acidity of the cerumen inhibits bacterial or fungal
growth. Whereas a paucity of cerumen allows bacterial
growth, an excess can create an environment ideal for
bacterial invasion by allowing retention of water and debris
(as when the EAC is regularly exposed to water). Localized
trauma from foreign objects placed in the ear can also lead
to direct bacterial invasion in the ear canal. Once an infection
becomes established, localized maceration and inflammation
occur, which lead to symptoms.

Pathophysiology
OE is a superficial infection of the skin in the EAC. The
processes involved in the development of OE can be divided
into the following 4 categories:
Obstruction (eg, cerumen buildup, surfers exostosis,
or a narrow or tortuous canal), resulting in water
retention
Absence of cerumen, which may occur as a result of
repeated water exposure or overcleaning the ear
canal
Trauma
Alteration of the pH of the ear canal
If moisture is trapped in the EAC, it may cause maceration of
the skin and provide a good breeding ground for bacteria.
This may occur after swimming (especially in contaminated
water) or bathinghence the common lay term swimmers
ear. It may also occur in hot humid weather. Obstruction of
the EAC by excessive cerumen, debris, surfers exostosis, or
a narrow and tortuous canal may also lead to infection by
means of moisture retention.
Trauma to the EAC allows invasion of bacteria into the
damaged skin. This often occurs after attempts at cleaning
the ear with a cotton swab, paper clip, or any other utensil
that can fit into the ear.
Once infection is established, an inflammatory response
occurs with skin edema. Exudate and pus often appear in the
EAC as well. If severe, the infection may spread and cause a
cellulitis of the face or neck.
Necrotizing (malignant) OE is a rare complication that occurs
in patients who are immunocompromised or in those who have
received radiotherapy to the skull base. In this condition,
bacteria invade the deeper underlying structures of the soft
tissues and cause osteomyelitis of the temporal bone. This is
a life-threatening disorder with an overall mortality that
historically has approached 50%.
Etiology
OE is most often caused by a bacterial pathogen; other
varieties include fungal OE (otomycosis) and eczematoid
(psoriatic) OE.[13] In one study, 91% of cases of OE were
caused by bacteria.[8] Others have found that as many as 40%
of cases of OE have no primary identifiable microorganism as
a causative agent. The most common causative bacteria are
Pseudomonas species (38% of all cases),[13] Staphylococcus
species, and anaerobes and gram-negative organisms.
Fungal OE may result from overtreatment with topical
antibiotics or may arise de novo from moisture trapped in the
EAC. It is caused by Aspergillus 80-90% of the time; Candida
and other organisms have also been isolated. This condition is
characterized by long, white, filamentous hyphae growing
from the skin surface. Besides otorrhea, erythema and
edema of the EAC are common. In severe cases, soft tissue
stenosis may be present. Extension of the infection may
manifest as cellulitic skin changes involving the concha of the
auricle and the tragus.
Eczematoid (psoriatic) OE is associated with the following
conditions:
Eczema
Seborrhea

Neurodermatitis
Contact dermatitis from earrings or hearing aid use
Purulent otitis media with perforation of the
tympanic membrane and drainage; this may mimic OE
to an extent, but it is usually painless and does not
cause any swelling of the ear canal
Sensitivity to topical medications
Chronic OE is a fairly common condition that is sometimes
the result of incomplete treatment of acute OE.[14] More
often, however, chronic OE is caused by overmanipulation of
the ear canal as a consequence of cleaning and scratching.
Such overmanipulation results in a low-grade inflammatory
response that causes further itching of the skin. Eventually,
the skin thickens, and canal stenosis may occur.
Necrotizing
OE
occurs
in
patients
who
are
immunocompromised and represents a true osteomyelitis of
the temporal bone.
Risk factors for OE include the following:
Previous episodes of OE
Swimming, diving, or participating in aquatic
activities
Use of earplugs or probing of the EAC (possibly
secondary to trauma to the EAC)
Hot, humid weather
Use of a hearing aid
Coexistence of eczema, allergic rhinitis, or asthma
Comorbidities such as diabetes mellitus, AIDS,
leukopenia, or malnutrition
Epidemiology
United States and international statistics
OE is found in all regions of the United States, occurring in 4
of every 1000 people annually.[9, 11] The infection is believed
to be more prevalent in hot and humid conditions such as
prevail during the summer months, presumably because
participation in aquatic activities is higher.[4, 9] Acute, chronic,
and eczematous OE are also common. Necrotizing OE is rare.
The international frequencies of OE have not been fully
determined; however, the incidence is increased in tropical
countries.[10]
Age-, sex-, and race-related demographics
Although the infection can affect all age groups, OE appears
to be most prevalent in the older pediatric and young adult
population, with a peak incidence in children aged 7-12
years.[13] A single epidemiologic study from the United
Kingdom found a similar 12-month prevalence for individuals
aged 5-64 years and a slight increase in prevalence for those
older than 65 years.[4] This was postulated to occur
secondary to an increase in comorbidities, as well as an
increase in the use of hearing aids, which may cause trauma
to the EAC.
OE affects both sexes equally. No racial predilection has
been established, though people in some racial groups have
small ear canals, which may predispose them to obstruction
and infection.
Prognosis
Most incidents of OE resolve without difficulty. The majority
of patients improve within 48-72 hours of antibiotic
administration. Failure to improve within 2-3 days should call

the diagnosis into question and prompt the physician to

reevaluate the patient. OE usually resolves fully in 7-10 days.
Resolution of eczematoid OE occurs with control of the
primary skin condition. In some patients with OE, the ear
must be debrided for full resolution. Surgical incision and
drainage are sometimes necessary.
In some patients, OE can cause severe otalgia necessitating
administration of narcotic pain relievers. Pain usually
improves 2-5 days after initiating therapy. Temporary
hearing loss is common secondary to canal occlusion. Severe
infections may cause lymphadenitis or cellulitis of the face or
neck.
If left untreated, the infection may invade the deeper
adjacent structures and progress to necrotizing (malignant)
OE, a serious condition that requires prolonged treatment
and often results in severe morbidity or mortality. This
complication is almost exclusively seen in immunocompromised
patients, such as those with diabetes, AIDS patients, those
undergoing
chemotherapy,
and
patients
taking
immunosuppressant
medications
(eg,
glucocorticoids).
Pseudomonas is the inciting organism in the vast majority of
cases.
When necrotizing OE develops, mortality is in the 20% range
among adults, mostly because of the associated comorbidities
and the rapid extension of the infection to include sepsis or
intracranial extension. If left untreated, necrotizing OE has
a mortality approaching 50%. This complication should be
suspected if the patients pain and tenderness seem out of
proportion to clinical appearance or if granulation tissue is
seen in the ear canal.
Patient Education
OE is a common problem, with risk factors that are easily
avoided. Education regarding ways of keeping the ear dry is
helpful. Preventive use of acidifying drops is encouraged in
patients with recurrent OE. Avoidance of the use of cottontipped swabs to remove ear cerumen should be discussed with
patients. Improper use of cotton-tipped applicator sticks
simply packs cerumen into the canal and can cause trauma to
the tympanic membrane.
Patients should be made aware that when OE does strike, it
can usually be resolved in a short time, with few if any
complications.
History
Patients with otitis externa (OE) may complain of the
following:
Otalgia, ranging from mild to severe, typically
progressing over 1-2 days
Hearing loss
Ear fullness or pressure
Tinnitus
Fever (occasionally)
Itching (especially in fungal OE or chronic OE)
Severe deep pain If this is experienced by a
patient who is immunocompromised or diabetic, be
alerted to the possibility of necrotizing (malignant)
OE

Discharge Initially, the discharge may be clear and

odorless, but it quickly becomes purulent and foulsmelling
Bilateral symptoms (rare)
Frequently, a history of exposure to or activities in
water (eg, swimming, surfing, and kayaking)
Usually, a history of preceding ear trauma (eg,
forceful ear cleaning, use of cotton swabs, or water
in the ear canal)
Physical Examination
The key physical finding of OE is pain upon palpation of the
tragus (anterior to ear canal) or application of traction to the
pinna (the hallmark of OE). Examination reveals erythema,
edema, and narrowing of the external auditory canal (EAC),
and a purulent or serous discharge may be noted (see the
image below). Conductive hearing loss may be evident.
Cellulitis of the face or neck or lymphadenopathy of the
ipsilateral neck occurs in some patients.

Acute otitis externa. Ear

canal is red and edematous, and discharge is present.
The tympanic membrane may be difficult to visualize and may
be mildly inflamed, but it should be normally mobile on
insufflation. Eczema of the pinna may be present. By
definition, cranial nerve (CN) involvement (ie, of CNs VII and
IX-XII) is not associated with simple OE.
Fungal OE results in severe itching but typically causes less
pain than bacterial OE does. A thick discharge that may be
white or gray is often present. Whereas pseudomonal
infection produces purulent otorrhea that may be green or
yellow, Aspergillus otomycosis looks like a fine white mat
topped by black spheres. Upon close examination, the
discharge may contain visible fungal elements (eg, spores or
hyphae) or have a fuzzy appearance.
The sine qua non of necrotizing OE is pain that is out of
proportion to the clinical findings. Upon close examination,
granulation tissue may be present in the ear canal.
In severe cases, the infection may spread to the surrounding
soft tissues, including the parotid gland. Bony extension may
also occur into the mastoid bone, temporomandibular joint,
and base of the skull, in which case cranial nerves VII
(facial), IX (glossopharyngeal), X (vagus), XI (accessory), or
XII (hypoglossal) may be affected.
Complications
Complications of OE are rare and may include the following:
Necrotizing OE (the most significant complication)
Mastoiditis
Chondritis of the auricle (from spread of acute OE
to the pinna, particularly in patients with newly
pierced ears)

Bony erosion of the base of the skull (skull base

osteomyelitis[15] )
Central nervous system (CNS) infection
Cellulitis or lymphadenitis
Diabetic ketoacidosis is often present in diabetics with this
condition.
Herpes zoster may initially present with symptoms similar to
those of OE, and vesicular eruption may occur 1-2 days after
the initial symptoms. Ramsey Hunt syndrome is a rare
complication of herpes zoster and presents with peripheral
unilateral facial palsy. Patients should be counseled on this
possible presentation and advised to seek medical care if it
occurs.[16]
Diagnostic Considerations
Failure to recognize necrotizing (ie, malignant) otitis externa
(OE) is a significant pitfall. A patient who is diabetic or
immunocompromised with severe pain in the ear should have
necrotizing OE excluded by an otolaryngologist.
Problems to be considered include the following:
Ear canal trauma
Ear canal carcinoma
Otitis media with a perforation or ventilation tube
present
Chondritis
Cranial nerve palsy
Hearing loss
Wisdom tooth eruption
Intracranial abscess
Cavernous sinus thrombosis
Ramsay Hunt syndrome
Furuncle
Skull base osteomyelitis
Preauricular cyst and fistula
Lacerations
Atopic dermatitis
Cerumen impaction
Exostosis and osteoma
Foreign body
Acute (bullous) and chronic (granular) myringitis
Although malignant tumors of the ear canal are rare, they do
occur and sometimes are misdiagnosed as OE.[17] If the
condition does not respond to treatment as expected, an
otolaryngologist should evaluate the patient.
Ramsay Hunt syndrome, more accurately known as herpes
zoster oticus, is caused by varicella-zoster virus (VZV)
infection. It is characterized by facial nerve paralysis and
sensorineural hearing loss, with bullous myringitis and a
vesicular eruption of the concha of the pinna and the
external auditory canal (EAC). Painful OE may be present as
well. Treatment includes use of an antiviral agent (eg,
valacyclovir) and systemic steroids. The role of facial nerve
decompression remains controversial.
A furuncle is usually caused by staphylococcal infection of a
hair follicle. This infection occurs in the lateral cartilaginous
hair-bearing portion of the EAC. On otoscopic examination, a
furuncle appears as a localized process, which may develop
into an abscess, rather than as a diffuse inflammatory
process, as is characteristic of OE.

Skull base osteomyelitis occurs most often in patients who

are diabetic or immunocompromised. The usual bacterial
pathogen is Pseudomonas aeruginosa. Other predisposing
conditions include arteriosclerosis, immunosuppression,
chemotherapy, steroid use, and other immunodeficient
states. The diagnosis is strongly suggested by a history of
diabetes mellitus, severe otalgia, cranial neuropathies, and
characteristic EAC findings.
The EAC may be filled with friable granulation tissue, which
is primarily found inferiorly. Because this presentation may
be identical to that of a soft tissue malignancy, prudence
dictates a tissue biopsy even if a history of diabetes mellitus
is present. Bare bone of the EAC floor may be exposed; small
bony sequestra may be observed as well.
Computed tomography (CT) demonstrates bone erosion, and
gallium scanning can be performed at points throughout
treatment to monitor resolution. Treatment consists of
administration of an antipseudomonal intravenous (IV)
antibiotic such as ceftazidime (in some cases) or oral
ciprofloxacin (in less dramatic cases). Extended treatment
for at least 6 weeks is most appropriate. Hyperbaric oxygen
therapy may also be effective. Surgical debridement is
reserved for granulation tissue and bony sequestra.
A preauricular cyst or fistula may form as the result of
abnormal development of the first and second branchial arch
and may manifest as persistent discharge or recurrent
infection. A draining sinus may be present anterior to the
tragus; when infected, the cyst distends with pus, and the
overlying skin is erythematous. Complete excision is indicated
if these lesions become repeatedly infected. The facial nerve
is at risk for injury during excision because of the close
relation of the cyst or fistula to the superior branches of
the nerve within the parotid gland.
First branchial cleft anomalies have a more complex
embryologic origin than preauricular cysts and fistulas do.
These lesions may not have an obvious sinus tract on the skin
and may manifest as an abscess extending deeply into the
EAC, the parotid, or the neck.
Full-thickness auricular lacerations may be observed after
blunt or sharp trauma. These injuries are managed surgically
by closing both the perichondrium and the skin. In contrast,
external canal lacerations may occur after attempts to clean
the ear canal with cotton-tipped applicators. These
lacerations are usually managed by microscopically placing any
skin flaps in their normal position, packing the ear canal, and
administering topical antibiotic drops.
Atopic dermatitis resulting from sensitivity to topical
antibiotic solutions is well known. Neomycin allergy occurs in
as many as 5% of patients treated with the medication.
Suspect drug sensitivity if worsening of symptoms associated
with skin excoriation and weeping occurs in the distribution
of the topical medication exposure after the application of
drops.
Metal sensitivity also manifests as excoriation, erythema,
and edema around the exposure site (eg, a piercing hole). A
common allergen is nickel, an impurity that may be present in
precious metals. Atopic dermatitis is managed by removal of
the allergen (eg, an earring) and beginning topical steroids

and antibiotics if the wound is secondarily infected. The

diagnosis of metal sensitivity is confirmed by performing a
skin patch test.
Cerumen impaction is the most common abnormality found on
otoscopic examination, yet only a small proportion of the
general population requires regular disimpaction because the
EAC has the innate ability both to produce and to clear itself
of cerumen. Cerumen may vary in color and consistency, and
cerumen impaction may coexist with other pathologic
conditions.
Debris in the EAC from cholesteatoma or tumors may be
confused with cerumen; accordingly, considerable care is
required when debridement of the EAC is attempted.
Debridement may be accomplished by using microinstruments
or by aspirating ear canal contents with a No. 5 or No. 7
Barton suction device under direct vision through the
otoscope or microscope. Irrigation of the ear canal is another
option, but use of a pressurized irrigation system entails the
risk of trauma.
Exostoses and osteomas, the 2 most common bony lesions of
the EAC, differ both histologically and clinically. Exostoses
tend to arise from the anterior or posterior floor of the
medial EAC (or from both simultaneously), have a sessile
base, and are covered with normal-appearing skin. Osteomas
may arise from any region of the bony EAC, are often
pedunculated, may be single or multiple, and are covered by
normal skin. Exostosis and osteomas require surgical
treatment only if they are so large that they lead to a
conductive hearing loss or intractable OE.
Foreign bodies in the EAC are not infrequently encountered.
In children, the appearance of these foreign bodies is
variable; parts of toys or even food may be found in the EAC.
In adults, fragments of cotton swabs are the most common
finding. Erythema and edema surrounding the foreign body
are commonly present. Depending on the patients ability to
cooperate, the foreign body may be removed under a
microscope with the aid of microinstruments.
Acute myringitis is usually caused by a mycoplasmal or viral
infection and has been observed in both adults and children.
It is characterized by hemorrhagic bullae involving the
tympanic membrane and a flulike syndrome. It is self-limiting;
treatment involves pain control and fever management.
Chronic myringitis is defined as deepithelization of the
tympanic membrane, granulation tissue formation, and
discharge. Treatment includes topical application of eardrops,
a caustic solution in unresponsive cases, and mechanical
removal of polypoidal granulations.
Differential Diagnoses
Otitis Media
Approach Considerations
The patients history and physical examination usually provide
sufficient information to allow the clinician to make the
diagnosis of otitis externa (OE). Most persons with OE are
treated empirically.
Thus, laboratory studies typically are not needed. However,
Gram staining and culture of any discharge from the auditory
canal may be helpful if the patient is immunocompromised, if
the usual treatment measures are ineffective, or if a fungal

cause is suspected. However, as many as 40% of all cases of

OE do not produce a dominant pathogen. Adults with OE may
benefit from a blood glucose check or a urine dipstick test to
evaluate for occult diabetes.
Histologic examination of the skin of the external canal
shows acute inflammation with exudate.
CT, MRI, Bone Scan, and Gallium Scan
Imaging studies are not required for most cases of OE.
However, radiologic investigation may be helpful if an invasive
infection such as necrotizing (malignant) OE is suspected or
if the diagnosis of mastoiditis is being considered.
High-resolution computed tomography (CT) is preferred and
better depicts bony erosion.[6] Radionucleotide bone scanning
and gallium scanning have been used to make the diagnosis.
Magnetic resonance imaging (MRI), though not used as often,
may be considered secondarily or if soft tissue extension is
the predominant concern.[7]
Otoscopy
In cases of external ear infection, otoscopic examination
must be performed in conjunction with evaluation of related
structures (eg, the external ear and the head and neck). For
example, the auricle should be examined for swelling,
deformity, and erythema; the face, for evidence of facial
nerve paresis or other cranial neuropathy; and the neck, for
masses.
An otoscope consists of a head and a handle and is used to
examine the external auditory canal (EAC), the tympanic
membrane, and the middle ear. A magnifying lens enhances
the clinicians view. The following 2 types of head are
available for the otoscope:
Diagnostic head This head is fixed to the otoscope
and does not allow the use of microinstruments
through the scope
Working (operating head) This head has a
magnifying lens that can slide to the side, enabling
passage of microinstruments through the speculum
into the EAC and the middle ear
A pneumatic attachment on the diagnostic head allows
assessment of tympanic membrane motion by generating
positive pressure in the EAC, causing the tympanic membrane
to deflect medially. When pressure is released, the tympanic
membrane expands laterally. This technique is an important
tool in the diagnosis of middle ear effusions, vascular lesions,
and inner ear fistulas.
For optimal viewing of the tympanic membrane in an adult,
retract the auricle posteriorly and superiorly to straighten
the EAC; for optimal viewing in a child, pull the auricle
posteriorly. Remove any debris or cerumen to allow an
adequate examination. Proceed with the examination as
follows:
First, examine the EAC for masses, skin changes, and
otorrhea
Next, examine all parts of the tympanic membrane
(eg, pars tensa and pars flaccida)
Next, assess the motion of the tympanic membrane
by means of pneumatic otoscopy
Finally, attempt a thorough examination of the
middle ear contents through the tympanic

membrane, though this examination may be limited

by the opacity of the membrane itself
Approach Considerations
Primary treatment of otitis externa (OE) involves
management of pain, removal of debris from the external
auditory canal (EAC), administration of topical medications to
control edema and infection, and avoidance of contributing
factors.
Most cases can be treated with over-the-counter analgesics
and topical eardrops. Commonly used eardrops include acetic
acid drops, which change the pH of the ear canal;
antibacterial drops, which control bacterial growth; and
antifungal preparations. Eczematoid (psoriatic) OE often
responds to topical steroid drops but may be chronic or
recurrent. The ear may require frequent suction debridement
under a microscope. If significant canal edema develops, an
ear wick may be used to facilitate delivery of topical
medications into the medial canal.
In severe cases, oral or intravenous (IV) antibiotic therapy
and narcotic analgesics may be required.[18] In the case of
necrotizing (malignant) OE, the patient must be admitted to a
hospital for IV antibiotic therapy at the discretion of the
consulting otorhinolaryngologist. The treatment that is
rendered depends on the likely organism, which is best
determined by means of Gram staining of the affected area.
Clinical guidelines are available from the American Academy
of Otolaryngology - Head and Neck Surgery Foundation.[3]
Removal of Debris From Ear Canal
Removal of debris from the ear canal improves the
effectiveness of the topical medication. Gentle cleaning with
a soft plastic curette or a small Frazier suction tip under
direct vision is appropriate. Irrigation with a mix of peroxide
and warm water may be useful for removing debris from the
canal, but only if the tympanic membrane is intact. Any water
instilled must be removed to keep from exacerbating the
condition.
Not uncommonly, children insert a foreign body in their ear
canal and do not mention it to their parents. If any pain
accompanies purulent drainage, the possibility of a foreign
body in the ear canal should be considered. A patient with a
foreign body in place will not improve until it is removed.
Pharmacologic Therapy
Before antibiotic treatment was recommended for OE,
astringents and acetic acid solutions were commonly used to
treat this condition. These solutions can be painful to
inflamed ear canals and are not generally used today. An
aminoglycoside combined with a second antibiotic and a
topical steroid (eg, neomycinpolymyxin Bhydrocortisone)
used to be the most commonly prescribed topical preparation;
however, the neomycin component led to hypersensitivity
reactions and ototoxicity in some patients.
Most physicians prescribe topical antibiotic-containing
preparations. Otic antibiotic and steroid combinations have
shown to be highly successful in treatment, with cure rates
of 87-97%.[19] Other agents used include analgesics for pain
relief, acidifying solutions, and, in some instances,
antipruritics or antihistamines.
Topical medications

Most cases of acute OE respond well to topical treatment.

Antibiotic eardrops, with or without a corticosteroid (given
to decrease inflammation), are the mainstay of therapy.
Topical acidifying and drying agents (given to alter the pH
and to inhibit the growth of microorganisms) may be used in
mild or resolving cases and are useful in fungal infections. An
antifungal agent may be included as necessary.
Mild OE usually responds to the use of an acidifying agent
and a corticosteroid. As an alternative, a 2:1 ratio mixture of
70% isopropyl alcohol and acetic acid may be used. For
moderate OE, consideration should be given to adding
antibacterial and antifungal agents to the acidifying agent
and the corticosteroid.
In a systematic review of therapy for OE, Rosenfeld et al
demonstrated little overall difference among the various
topical agents used to treat this condition[20, 21] ; however,
they found that use of a topical steroid alone increased cure
rates by 20% as compared with a steroid-antibiotic
combination. The combination of oral antibiotics with otic
antibiotic solutions has not been shown to improve treatment
success rates.[22]
Use of aminoglycoside antibiotic eardrops in the presence of
a perforation or ventilation tube may cause problems.
Although this is controversial, many otolaryngologists believe
that aminoglycoside eardrops may be ototoxic if they enter
the middle ear. In these situations, using an alternative,
nonototoxic topical preparation (eg, a fluoroquinolone, with or
without a steroid) may be safer.
Fluoroquinolones are not associated with ototoxicity, and
ofloxacin is safe in cases of a perforated tympanic
membrane. One literature review concluded that OE can be
safely treated with an otic suspension containing 0.3%
ciprofloxacin and 0.1% dexamethasone and that the inclusion
of dexamethasone improves treatment success rates.[19] A
German meta-analysis found a trend suggesting the
superiority of quinolone monotherapy to classic combination
regimens comprising a nonquinolone antibiotic plus a
steroid.[23]
Mild fungal infections can usually be treated with an acetic
acid solution, whereas more severe cases may have to be
treated with a topical antifungal agent, such as 1%
clotrimazole.
In the setting of chronic, noninfectious, therapy-resistant
OE, a prospective study by Caffier et al demonstrated that
daily use of 0.1% tacrolimus cream (administered via an ear
wick [see below] that was changed every second to third day)
resulted in high rates of resolution (46% through 1-2 years
of follow-up) after 9-12 days of therapy.[24] The study also
demonstrated longer periods of symptom-free intervals for
those who experienced a recurrence.

Ear wick

If the ear canal is severely swollen, an ear wick may be

inserted to facilitate the delivery of topical medications (see
the image below). The wick may be commercially prepared
from a hard sponge material that expands when wet (eg, the
Merocel ear wick or the Pope Oto-Wick), cut from a bigger
sponge by the physician, or made from narrow gauze (0.25-in.
packing works well).

Otitis externa with ear

wick in place. Note discharge from canal and swelling of canal.
After the placement of the wick in the ear canal (a process
that, unfortunately, causes brief but significant discomfort),
the topical antibiotic drops are placed on the external end of
the wick to be carried into the recesses of the ear canal.
This is done 2-4 times daily, depending on the recommended
dosing frequency for the medication. The wick may fall out as
the edema decreases. In any case, it should be removed after
2-3 days.
Analgesics
Pain control is essential to quality patient care. OE can be
quite painful, and patients frequently request analgesics.
These agents ensure patient comfort and may have sedating
properties.
Inexpensive,
simple
nonsteroidal
antiinflammatory drugs (NSAIDs) reduce inflammation and
irritation and can be paired with opiates to improve pain
symptoms Over-the-counter acetaminophen is appropriate
for most patients. In some cases, systemic analgesics are
helpful before ear cleaning or wick placement.
Oral and intravenous antibiotics
Most persons with OE do not require oral medications. Oral
antibiotics are generally reserved for patients with fever,
immunosuppression, diabetes, adenopathy, or an infection
extending outside the ear canal. They should be given to
individuals with cellulitis of the face or neck skin or to
persons in whom severe edema of the ear canal limits
penetration of topical agents.
IV antibiotics are used in individuals with necrotizing
(malignant) OE; they may also be appropriate for patients
with severe cellulitis or persons whose symptoms do not
respond to topical and oral antibiotics. A prolonged course of
IV antibiotics, lasting for up to 6 weeks, may be required. If
the patient is stable, IV antibiotics may be administered at
home. Begin treatment with antibiotics to cover
pseudomonads, and alter the regimen as necessary on the
basis of culture results.
Surgical Debridement and Drainage
Surgical debridement of the ear canal is usually reserved for
necrotizing OE or for complications of OE (eg, external canal
stenosis). It is often necessary in more severe cases of OE
or in cases where a significant amount of discharge is present
in the ear. An otolaryngologist usually performs debridement
using magnification and suction equipment. Debridement is
the mainstay of treatment for fungal infections.
Occasionally, an abscess forms in the ear canal; this usually
occurs in cases of OE caused by S aureus. Treatment of the
abscess is often accomplished by means of a simple incision
and drainage procedure that is usually performed by an
otolaryngologist using a needle or a small blade.

Activity
During treatment of OE and for 1-2 weeks after its
resolution, advise the patient to keep the ear canal dry.
During bathing or showering, advise the patient to place an
earplug or cotton ball lightly coated with petroleum jelly in
the ear canal to prevent water penetration.
Patients involved in aquatic activities may resume these
activities once the infection has been eradicated, generally
within 4-5 days. Aquatic athletes may return to the pool
earlier than 4-5 days; generally, after 2-3 days of refraining
from any water activity, they can return to their usual
activities. However, the head must be kept dry until the
infection has been eradicated.
The best way of keeping the ear dry, obviously, is to avoid
aquatic activities altogether, but the more common practice
is simply to limit such activities to those that do not expose
the ear to the water (eg, kicking while using a foam floatation
board to keep the head above water).
Prevention
Some patients experience multiple recurrences of OE and
thus benefit from the adoption of a preventive strategy. The
following recommendations related to ear hygiene may help
prevent recurrent OE:
Eliminate any self-inflicted trauma to the ear canal,
such as may occur with the use of cotton swabs or
the insertion of objects (eg, bobby pins) into the
EAC
Avoid frequent washing of the ears with soap; this
leaves an alkaline residue that neutralizes the acidic
pH of the EAC
Avoid swimming in polluted waters
Ensure that the ear canals are emptied of water
after swimming or bathing; the use of a blow dryer
on a low setting after swimming to dry the ear canal
has been suggested as a preventive measure, though
no studies have demonstrated this suggestion to be
effective
Instill prophylactic eardrops after each exposure to
water to assist in drying and acidifying the ear canal;
a combination of 70% isopropyl alcohol and acetic
acid in a 2:1 ratio may be used
Some have recommended wearing earplugs for swimming and
bathing. If worn, earplugs should be wiped with rubbing
alcohol after use. Others have argued that the use of
earplugs should be avoided, on the grounds that they may
cause trauma to the ear canal and thereby predispose to the
development of OE.
Consultations
For simple OE, consultation with an otorhinolaryngologist
generally is not necessary. However, such consultation is
appropriate if the patient has severe OE, is not responding to
treatment as expected, has a suppurative complication or a
perforated tympanic membrane, or is suspected of having
necrotizing (malignant) OE. Debridement of the ear canal is
often necessary for resolution of the infection.
Necrotizing OE necessitates consultation with an
otorhinolaryngologist, an infectious disease specialist, and, in
some instances, a neurosurgeon.

Long-Term Monitoring
Suctioning of the EAC on a weekly basis is required until
debris has been removed.
Patients must be monitored to ensure complete resolution of
OE. Even in mild cases, follow-up is important for evaluating
the response to treatment. In the view of some physicians, a
follow-up visit 1 week after starting treatment is usually
adequate; some prefer a shorter interval (eg, 2-3 days after
the initiation of therapy).
Medication Summary
Most cases of otitis externa (OE) are caused by superficial
bacterial infections and can be treated with over-thecounter analgesics and topical eardrops. Commonly used
topical eardrops are acetic acid drops, which change the pH
of the ear canal; antibacterial drops, which control bacterial
growth; and antifungal preparations. Oral or parenteral
antibiotics are reserved for severe cases. Otic antibiotic and
steroid combinations have shown to be highly successful in
treatment. The corticosteroid ingredient decreases
inflammation and can help to ease the pain. These eardrops
treat bacterial infection and reduce canal edema. The agents
commonly prescribed for treating otitis externa are
associated with cure rates between 87% and 97%.[19] In
severe cases, oral or intravenous (IV) antibiotic therapy and
narcotic analgesics may be required.
Antibiotics
Class Summary
Most cases of OE are caused by superficial bacterial
infections. Accordingly, most individuals with this condition
may be treated with topical antibiotic preparations. Some
preparations also contain a corticosteroid ingredient. The
small amount of steroid that is present in the solution can
help to ease the pain and edema associated with OE.
Hydrocortisone/neomycin/polymyxin
B
(Cortisporin,
Cortomycin)
Hydrocortisone/neomycin/polymyxin is an antibacterial and
anti-inflammatory agent for otic use, available as a solution
or a suspension. It is used to treat steroid-responsive
inflammatory conditions for which a corticosteroid is
indicated and in which bacterial infection or a risk of
bacterial infection exists.
View full drug information
Ofloxacin otic
Otic ofloxacin is a pyridine carboxylic acid derivative with
broad-spectrum effect that inhibits bacterial growth by
inhibiting DNA gyrase. It is available as a 0.3% (3 mg/mL)
solution.
View full drug information
Ciprofloxacin otic (Cetraxal)
Otic ciprofloxacin is a fluoroquinolone that inhibits bacterial
synthesis (and thus growth) by inhibiting DNA gyrase. It has
activity against pseudomonads, streptococci, methicillinresistant Staphylococcus aureus (MRSA), Staphylococcus
epidermidis, and most gram-negative organisms but has no
activity against anaerobes. It is available with or without

hydrocortisone. Cetraxal is an otic solution available as 14

single-use applicators containing 0.25 mL of 0.2% solution
each. Ciloxan is an ophthalmic solution that may be used for
OE.
Dexamethasone/tobramycin (TobraDex)
Tobramycin interferes with bacterial protein synthesis by
binding to 30S and 50S ribosomal subunits, thereby causing
defects in the bacterial cell membrane. Dexamethasone
decreases inflammation by suppressing migration of
polymorphonuclear leukocytes (PMNs) and reducing capillary
permeability. TobraDex is an ophthalmic solution that may be
used for OE.
View full drug information
Gentamicin ophthalmic (Garamycin, Gentak)
Gentamicin is an aminoglycoside antibiotic used for gramnegative bacterial coverage. It is available as an ophthalmic
solution that may be used for OE. This solution is a
compounded medication, with each 1 mL containing 3 mg of
gentamicin sulfate and 1 mg of betamethasone sodium
phosphate.
View full drug information
Ciprofloxacin and dexamethasone otic (Ciprodex)
Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA
synthesis (and thus growth) by inhibiting DNA gyrase and
topoisomerases, which are required for replication,
transcription, and translation of genetic material. It has
activity against pseudomonads, streptococci, MRSA, S
epidermidis, and most gram-negative organisms but not
against anaerobes. Dexamethasone decreases external
auditory canal (EAC) inflammation by suppressing migration
of PMNs and reducing capillary permeability; it also relieves
pain symptoms.
This otic suspension is indicated for use in OE, as well as for
use in otitis media in individuals with tympanostomy tubes.
View full drug information
Ciprofloxacin and hydrocortisone otic suspension (Cipro HC
Otic)
Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA
synthesis (and thus growth) by inhibiting DNA gyrase and
topoisomerases, which are required for replication,
transcription, and translation of genetic material. It has
activity against pseudomonads, streptococci, MRSA, S
epidermidis, and most gram-negative organisms but not
against anaerobes. Hydrocortisone decreases inflammation by
suppressing migration of PMNs and reducing capillary
permeability.
Otic, Other
Class Summary
Inflammation and accumulated debris allow the growth of
bacterial species. This growth is counteracted by the use of
mild acidifying medications, such as acetic acid solutions.
These agents are useful for fungal OE or for mild OE
believed to be of bacterial origin. They can also be useful for
prevention.

Acetic acid in aluminum acetate (Borofair)

Aluminum acetate has a drying effect. Acetic acid works well
in superficial bacterial infections of OE.
View full drug information
Hydrocortisone and acetic acid otic solution (VoSoL HC)
Acetic acid is antibacterial and antifungal; hydrocortisone is
anti-inflammatory, antiallergic, and antipruritic. The
combination of the 2 agents is inexpensive and works well in
treating superficial bacterial infections of OE.
Alcohol vinegar otic mix
A homemade mix of 50% rubbing alcohol, 25% white vinegar,
and 25% distilled water is as effective as pharmaceutical
acidifying agents and less expensive. It is very useful for
prevention and can be used as a flushing solution for fungal
infections.
Oral Antibiotics
Class Summary
Oral antibiotics are used to treat severe infection or
cellulitis. Fluoroquinolones are the drugs of choice by virtue
of their coverage of Pseudomonas species.
View full drug information
Ciprofloxacin (Cipro)
Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA
synthesis (and thus growth) by inhibiting DNA gyrase and
topoisomerases, which are required for replication,
transcription, and translation of genetic material. It has
activity against pseudomonads, streptococci, MRSA, S
epidermidis, and most gram-negative organisms but not
against anaerobes.
Analgesics
Class Summary
OE can be quite painful, and control of this pain is essential
to quality patient care. Analgesics ensure patient comfort
and may have sedating properties. Inexpensive, simple
nonsteroidal anti-inflammatory drugs (NSAIDs) reduce
inflammation and irritation and can be paired with opiates to
improve pain symptoms.
View full drug information
Acetaminophen (Tylenol, FeverAll, Aspirin-Free Anacin,
Tylenol Children)
Over-the-counter acetaminophen is appropriate for most
patients. It is the drug of choice for pain in patients who are
known to be hypersensitive to aspirin or NSAIDs, who have
upper GI gastrointestinal (GI) disease, or who are taking oral
anticoagulants.
View full drug information
Acetaminophen and codeine (Tylenol #3)
The combination of acetaminophen and codeine is indicated
for the treatment of mild to moderate pain.
Antifungals, Other
Class Summary

A small but significant percentage of OE cases are due to

Aspergillus species or other yeasts and fungi (otomycosis).
Some cases of fungal OE can be treated with acidifying
drops; topical antifungal agents are used to treat otomycosis
refractory to these drops. The mechanism of action of
topical antifungal agents usually involves inhibition of the
pathways (eg, enzymes, substrates, and transport) necessary
for sterol/cell membrane synthesis or those involved in
altering the permeability of the fungal cell membrane (eg,
polyenes).
View full drug information
Clotrimazole 1% otic solution (Lotrimin AF)
Otic clotrimazole solution is a compounded medication.
Clotrimazole is a broad-spectrum antifungal agent that
inhibits yeast growth by altering cell membrane permeability,
causing the death of fungal cells.
View full drug information
Nystatin powder (Nystop, Nyamic, Pedi-Dri)
Nystatin is a fungicidal and fungistatic antimicrobial obtained
from Streptomyces noursei; it is effective against various
yeasts and yeastlike fungi. It changes the permeability of
the fungal cell membrane after binding to cell membrane
sterols, causing the cellular contents to leak. Treatment
should continue until 48 hours after the disappearance of
symptoms. Topical application of nystatin reduces fungal
growth.