Otitis Externa

Source
1. Current Diagnosis & Treatment – Otolaryngology 4th edition, 2020
2. Cummings Otolaryngology 7th ed, 2020
3. Bailey’s Head and Neck Surgery Otolaryngology, 5th Edition, 2014
4. Ballenger’s Otorhinolaryngology 18th edition, 2016
5. KJ Lee Essentials of Otolaryngology 11th edition, 2016

I. General Considerations
A. Definition
Otitis externa is an inflammatory and infectious process of the EAC.[1]
Otitis extema is a spectrum of infection of the EAC.[3]
B. Etiology
Pseudomonas aeruginosa and Staphylococcus aureus are the most commonly isolated
organisms. Less commonly isolated organisms include Proteus species, Staphylococcus
epidermidis, diphtheroids, and Escherichia coli. Fungal otitis extema is discussed in the
next section and accounts for roughly 10% of cases.[1]
C. Microbiology
Bacterial infections account for more than 90% of cases of AOE, with fungal
infections accounting for the rest.14 P. aeruginosa, S. epidermidis, and S. aureus represent
the first, second, and third most common bacterial isolates from AOE, respectively.6
Aspergillus and Candida are the most commonly recovered fungal isolates but represent
less than 2% of cases of AOE.6 Although rare as the primary cause of AOE, fungal OE
more commonly follows antibiotic treatment for a bacterial AOE.15 There is overlap in the
organisms responsible for AOE and COE. Pseudomonas and Staphylococcal species are
often identified in COE; however, gram-negative isolates such as Escherichia coli and
Enterococcus can be present. Similarly, fungal organisms are more likely to be a source of
COE.[2]
D. Bacteriology
The usual pathogens responsible for AOE are Pseudomonas aeruginosa, Proteus
mirabilis, staphylococci, streptococci, and various gram-negative bacilli. For the mild or
uncomplicated infection, culture of the canal is ordinarily not taken, because it will usually
demonstrate a mixed pattern of growth. For recalcitrant infections, culture may identify a
predominant organism and assist in the choice ofantibiotic therapy.[3]
II. Classification
The appearance of the canal varies according to the time cowse of infection: acute, subacute, or
chronic.[3]
A. Acute
1. Definition
Acute otitis extema (AOE) is a bacterial infection of the canal caused by a break in
the normal skin/cerumen protective barrier in the milieu of elevated humidity and
temperature.[3]
Acute otitis externa (AOE), also known as “swimmer’s ear” or “tropical ear,”
involves the rapid onset (<48 hours) of signs and symptoms of ear canal inflammation.
[2] Acute otitis externa is an acute, usually bacterial, infection of the skin of the
external auditory canal (Figure 14-5).[4]
2. Distribution
It is generally unilateral and associated with exposure of the ear canal to water or local
trauma.[2]

3. Epidemiology
This diagnosis accounts for approximately 2.4 million health care visits per year in
the United States and is more common in the summer months. The age group with the
highest incidence of AOE includes 5- to 10-year-olds. However, over half of such cases
are seen in adults over 20 years of age, and there appears to be a decline in incidence
among those over 50 years of age.[2]

4. Predisposing and Risk Factors

Factors that may predispose to AOE include a congenitally narrow canal or a canal
narrowed by exostoses; skin conditions including eczema, seborrhea, or psoriasis;
trauma from ear plugs or hearing aids; or attempts at wax removal.[2] Medical
comorbidities can have a dramatic impact on the course of OE. Conditions such as
immunocompromised states, including diabetes and HIV, can predispose to malignant
OE and should be evaluated carefully. Any history of radiotherapy and the status of the
tympanic membrane should also be considered.[2]

5. Pathogenesis
Although. commonly called “swimmer's ear;." AOE may be caused by anything
that results in the removal of the protective lipid :film from the canal, allowing bacteria
to enter the apopilosebaceous unit. It usually begins with itching in the canal and is
commonly caused by instrumenting the canal with a cotton swab or fingernail This
temporarily relieves itching but allows proliferation ofbacteria in locally macerated
skin and sets up an itch-scratch cycle. The warm, dark, moist setting of the canal is now
a perfect medium for rapid bacterial growth. Later, pain ensues as the swollen soft
tissues of the canal distract the periosteal lining of the bony canal. As the disease
progresses, purulent discharge begins, and the auricle and periauricular soft tissues may
become involved.[3]

6. Signs and Symptoms

 The presenting symptom for bacterial AOE is often moderate to severe otalgia
worsened with manipulation of the pinna. Symptoms are often present from several
days to a week. Early AOE may include pruritus and erythema with a scant clear
discharge. As the infection progresses, the pain and edema become worse and the
discharge becomes seropurulent. The edema of the canal skin combined with otorrhea
and debris in the canal may lead to a feeling of fullness and a conductive hearing loss.
[2]
Signs of AOE include erythema and circumferential edema of the EAC, otorrhea, and
lymphadenopathy of the preauricular or cervical lymph nodes. There is tenderness with
manipulation of the pinna in AOE, which must be differentiated from tenderness of the
mastoid tip in acute mastoiditis. A Weber test should localize to the side of the
infection if the canal is obstructed, and Rinne testing may show bone conduction
greater than air conduction. A complete neurologic examination should be conducted to
ensure that there is no evidence of extension to the facial nerve, vestibular organs, or
other cranial nerves.[2]
Viral acute OE is rare. Offending organisms include varicella, measles, and
herpesvirus. Herpes zoster can affect the ear canal without (herpes zoster oticus [HZO])
or with facial paralysis (Ramsay Hunt syndrome) and may also be associated with
sensorineural hearing loss or vertigo.[2]
In its later stages, it presents with severe pain in the affected ear and will frequently
be associated with drainage and decreased hearing, but early infection may cause only
itching and fullness. The clinician will usually elicit tenderness on manipulation of the
pinna and observe erythema and swelling of the ear canal skin. Often, the skin of the
bony external canal will be spared. Often the swelling of the canal skin prevents full
evaluation of the eardrum, making it uncertain whether the eardrum is intact and the
infection involves the middle ear. The infection may also cause excessive skin
desquamation, resulting in the accumulation of a large amount of keratin debris in the
canal.[4]

7. Natural History
The natural history of untreated AOE is one of increasing pain. swelling, and
disdwge from the canal. The infection may spread to the adjacent periauricular soft
tissues, face, and neck. In an immunocompromised patient, whatbegan as an isolated
superficial infection ofthe apopilosebaceous unit of the EA.C may progress to
perichondritis, chondritis, cellulitis, and erysipelas. Rich lymphatic and hematogenous
drainage pathways favor the spread of infection to local and regional sites in the head
and neck. Pew patients progress to such an advanced stage before seeking medical
attention.[3]

8. Management
The initial therapy should include a thorough cleaning of the canal. Not only can
the debris prevent an adequate examination, but the debris in the canal will harbor
microorganisms and prevent adequate penetration of drops. The importance of this
often-overlooked step cannot be overstated as it is a frequent cause of therapy failures.
After cleaning, the treatment usually involves the use of topical treatments in drop
form. In situations where canal swelling prevents adequate penetration of the drops, a
sponge wick can be used. Placed dry and compressed in the canal, the wick will swell
in response to the instilled drops. A wick provides two important actions: first, it draws
the antibiotic down into the canal to the site of infection; second, it puts pressure on the
walls of the canal to decrease the swelling. A wick, like any other packing, can also
turn into a nidus for infection, so should be removed or changed after a few days.[4]
Debridement of the EAC is an important adjuvant to medical therapy. This clears
the canal of debris and purulent drainage, allowing better penetration of the topical
agents. If the tympanic membrane cannot be visualized, a wick may have to be placed.
The wick can be a strand of cotton, a Merocel sponge, or antibioticimpregnated
gauze.18 This mechanically stents the skin of the canal open and allows topical agents
to pass to the more proximal portions of the canal. It may also mechanically limit
edema of the canal.[2]
The first line of treatment for AOE is largely preventive. Occlusive earplugs
should be used for swimming, and proper fitting of hearing aids helps to minimize the
trauma associated with their insertion and removal. Drying of the EAC should be
encouraged; however, cotton-tipped applicators or similar devices should not be used,
as they are likely to cause local trauma and exacerbate any inflammation that is already
present.[2]
Topical therapy is the treatment of choice for AOE, as oral antibiotics have been
shown not to be effective.16 Although several studies have been performed analyzing
the resistance patterns of bacterial isolates from AOE patients, the antibiotic levels
achieved by local administration far exceed the tested resistance concentrations. The
amount of antibiotic delivered locally is orders of magnitude greater than that achieved
by systemic administration.6 An ideal preparation would have broad-spectrum
antibiotic coverage, an acidic vehicle, no potential for ototoxicity, no allergic potential,
no precipitate in the canal, low cost, and a steroid to reduce inflammation. There is
currently no medication that has all of these properties. Commonly used topical
antibiotics includefluoroquinolones or an aminoglycoside combined with a second
antibiotic for pseudomonal coverage. There is no single antibiotic regimen that has
been shown to be superior to others.16 There are concerns with the use of an ototoxic
medication such as an aminoglycoside in the canal of a patient with a possibly
compromised tympanic membrane, and contact hypersensitivity to neomycin has been
shown to be common.17 The addition of a corticosteroid to the topical antibiotics
improves symptoms, as does acetic acid. Acetic acid (50% diluted) irrigation in the
absence of antibiotics maybe effective in early AOE. Over-the-counter solutions
containing rubbing alcohol and vinegar may also be useful; however, there is no
conclusive evidence of the efficacy of nonantibiotic topical therapy.[2]
Otic Antibiotic Preparations. The general treatment of acute external otitis is
with the use of antibiotic otic drops. Over the years, many preparations have been
commercially available (Table 14-1).[4]
 In ancient times, ear infections were treated by the instillation of vinegar into the
ear. The acetic acid lowers the pH of the ear canal and suppresses the growth of the
usual AOE pathogens of pseudomonas and staphylococcus. It will also suppress the
growth of most fungi as well. A number of commerciallyavailabe otic preparations are
acids and are meant to work in this way, eg, Domeboro (boric acid) and Acetasol
(acetic acid).[4]
For many years, the preferred otic drop preparation was a combination drop
containing neomycin, polymyxin-B and hydrocortisone. Sold under a number of brand
names most notably “Cortisporin,” this otic drop was usually sold in two forms: a
mineral-oil based liquid and an aqueous suspension. The mineral oil based drop had
excellent penetration in small canals and those filled with debris, but could be quite
painful if the drop entered the middle ear through an unknown perforation or tube. The
aqueous suspension was better tolerated in open ears, but had a strong tendency to
leave a white, filmy debris, the suspended solid crystals of hydrocortisone, which is
insoluable in water. This filmy debris would often be mistaken for a fungal overgrowth,
and the patient would be placed on an additional antibiotic.[4]
This dual antibiotic and a corticosteroid preparation have enjoyed a long history
of success in the treatment of AOE. The neomycin, an aminoglycoside, had high
activity against staphylococcus species and moderate activity against pseudomonas.
The polymyxin B had strong activity against pseudomonas as well as staphylococcus.
The hydrocortisone would lessen the inflammation, opening the ear and relieving the
pain. The neomycin and polymyxin-B, however, both have a long-known toxicity to the
 inner ear when used systemically. This raised some concern about their extensive use in
ears, often in situations where there is perforation or a ventilating tube. No cases of
certain eardrop-related ototoxicity have ever been documented, and chronic infection
itself is a risk to hearing, so it is difficult to make a case that these preparations are
dangerous, especially considering their decades of popular use.[4]
Otic drops containing quinolone solutions were brought to the market in the
1990s. These contained either ofloxacin (Floxin Otic) or ciprofloxacin (CiproHC Otic
or CiproDex, both also contain a corticosteroid). These drops offered an antibiotic with
known effectiveness against the common microorganisms encountered in AOE with no
known risk of ototoxicity. Heavily marketed, these drops soon became the most
frequent treatment used in acute otitis externa. Unfortunately, a steady increase in
quiniolone resistance has been seen in both staphylococcus and pseudomonas
microorganisms. In some areas, less than half of all cultures of pseudomonas
aeruginosa will be sensitive to quiniolones. In addition, these drops often lack other
characteristics, such as a lower pH, that suppresses the growth of other microorganism,
such as fungus.[4]
To address the issue of the appropriate treatment of otitis externa, a committee of
the American Academy of Otolaryngology- Head and Neck Surgery developed
evidence-based treatment guidelines for this disorder.16 Although antibiotic drops were
shown to give significantly higher symptomatic and bacteriologic cure rates, no
difference could be demonstrated between the various preparations.[4]
When to Use Systemic Antibiotics. Most acute otitis externa can adequately be
treated with debridement and otic antibiotic preparations. In some situations, systemic
antibiotics should be added. If the patient is diabetic or otherwise immunosuppressed,
systemic treatment will be a barrier to deeper and more life-threatening spread of the
infection. In cases where the swelling of the canal has become so profound that a wick
has had to be placed, systemic antibiotics will ensure adequate penetration.[4]
B. Subacute and Chronic
In patients in whom the disease does not resolve after treatment, a subacute or chronic
form may occur. This condition may be likened to eczema and is a spectrum of disease
ranging from mild drying and scaling of the canal skin to complete obliteration of the canal
by chronically infected hypertrophic skin.[3]
1. Chronic Otitis Externa
a. Definition
Chronic otitis externa (COE) represents a state of prolonged
inflammation of the EAC, although the causes of this inflammation are
incompletely understood and likely varied.[2]
b. Mechanisms
Several proposed mechanisms include the following:
 Exposure: Allergic OE may result from an allergic reaction to topical agents,
most commonly neomycin. A contact dermatitis can result from contact
with various agents, including hair
sprays, shampoos, ear buds, and hearing aid molds. Allergic reactions of the
EAC associated with fungal infections elsewhere in the body have also been
described.[2]
 Systemic: Amyloidosis, sarcoidosis, Wegener granulomatosis, Sjogren
disease, psoriasis, lichen planus, or systemic dermatitides such as seborrhea
 can involve the ear canal. The chronic inflammatory reaction typically
results in hyperkeratosis and lichenification of the ear canal skin.[2]
 Chronic infection: Granular OE is thought to result from chronic infection of
the ear canal by bacteria, fungi, or both. The ear canal skin and tympanic
membrane manifest granulation and excoriation.[2]
 Local factors: including moisture or elevated pH.[2]

c. Distribution and Epidemiology

COE is bilateral in over half of patients and affects 3% to 5% of the population.[2]

d. Prognosis
It often has a prolonged and variable course and is associated with poor
quality-of-life measures.1 Although the majority of cases are indolent, some
patients will develop fibrosis of the TM and medial canal skin. This will result in a
blind-ending ear canal in a process known as postinflammatory medial canal
fibrosis.[2]

e. Natural History
The natural history of chronic otitis extema is far less dramatic than its acute
counterpart. The chronic scaling and itching in the canal predispose to
manipulation of the canal, excoriation. and repeated episodes of AOE. With time,
the canal skin may become lichenified, and ultimately the canal may become
completely obliterated.[3]

f. Signs and Symptoms

COE is characterized by pruritus, usually mild discomfort, and aural fullness.
The clinical findings have been defined as a secretory, or wet type, and a dry, or
squamous type.13 The ear canal is often mildly to moderately erythematous, with
scant clear discharge (Fig. 138.1). The course can wax and wane, however, and
periodic aggressive treatment may be necessary.[2]
In the case of fungal OE, pruritus is often more severe and there is commonly
clear drainage. There may be “cotton-like” debris filling the EAC, which may
cause complete obstruction of the canal. Hyphae are commonly noted on the
superficial layer of the debris.10 Candidal infections commonly appear as
previously described, whereas Aspergillus infections often have a moist white
plug dotted with black debris (“wet newspaper”); this may induce a more
aggressive infection involving the epithelial and subcutaneous tissues (Fig. 138.2).
[2]
g. Treatment
Treatment of COE is focused on reducing the inflammation of the canal,
removing any inciting factors, and evaluating for any systemic conditions that may
contribute to inflammation. Dry ear precautions should be emphasized and the use
of cotton-tipped applicators should be abandoned. In the office, meticulous
cleaning of the EAC under binocular microscopy to remove any debris or discharge
is necessary both to obtain a complete examination and to remove material
obstructing the canal. Long-term use of topical antibiotic drops may be necessary
to address a potential underlying bacterial organism.[2]
In the case of fungal infection, removal of the superficial dead skin layer is
also recommended, followed by application of a topical antifungal preparation.10
Acidification of the EAC is effective in fungal OE, and topical treatment will cure
most cases; however, recurrence rates are high. Clotrimazole 1% solution
(Lotrimin) is available over the counter and provides broad-spectrum antifungal
activity. Cresylate otic and ketoconazole ointment are effective as well.19 An
alternative treatment is to paint the canal and tympanic membrane with dyes that
 possess antifungal properties (e.g., gentian violet). Tolnaftate (Tinactin) solution
can be used safely in the presence of a tympanic membrane perforation.20,21
Finally, persistent Aspergillus infections associated with considerable canal edema
or infections failing to respond to topical treatment may require the administration
of oral itraconazole. The senior author has found that virtually all cases of fungal
OE can be quickly resolved by debridement of the canal and then filling the canal
with a combination cream—clotrimazole and betamethasone (Lotrisone). The
cream is loaded into a 3-mL syringe and passed through an angiocath into the ear
canal.[2]
In cases where infection has been ruled out, topical steroid application serves
as the mainstay of treatment. In patients with severe disease or with acute
breakthroughs, oral steroids may be necessary. Other topical agents such as
tacrolimus have also been described13 but are not widely used.[2]
The acidity of the EAC has been shown to correlate with COE and with the
severity of disease.9 This finding supports the common use of acidifying agents,
such as a one-to-one mixture of white vinegar and rubbing alcohol, in this disease.
Commercial products are also available. Other agents that attempt to change the
environment of the EAC include topical alcohol preparations to attempt to remove
moisture.[2]
Contact or allergic dermatitis should be treated by eliminating the offending
agent, debridement, and the administration of a topical corticosteroid solution.22
Chronic granular OE can be difficult to treat. This is most frequently seen in
individuals who are dependent on their hearing aids. Minimizing or alternating
hearing aid use is crucial to the success of the treatment regimen.
Culture of the ear for bacteria and fungi may provide evidence of the causative
organisms. Repeated debridement, cauterization of the granulations, and filling of
the canal with topical antibiotic or antifungal creams can be effective. Topical
gentian violet may also be effective at drying the ear canal and eliminating the
chronic infection. Surgical therapy may be required for cases resistant to medical
management and office-based procedures.[2]
In patients with long-standing inflammation of the ear canal that does not
respond to traditional treatments using ototopical agents, we have found that filling
the ear canal with a mixture of equal parts of bacitracin and polymyxin ointment,
clotrimazole cream 1%, and betamethasone 0.05% can be highly effective. This
mixture of an antibiotic, antifungal, and steroid is inexpensive and
is easily instilled using a syringe and an 18-gauge angiocatheter tip. The ointment
can be debrided after 1 week and reapplied as needed.[2]
As with many chronic or recurrent infections, there is emerging evidence of
the role of biofilms in OE, and novel treatment strategies have been proposed to
dissolve or remove these biofilms.23 However, these treatments remain
experimental.[2]
h. Chronic Bacterial Otitis Externa
1) Etiology
 Associated with chronic skin conditions such as seborrhea dermatitis
and atopic dermatitis
 Chronic inflammation within the dermis and surrounding the apocrine
glands resulting in increased depth of rete pegs
  • Loss of normal sebaceous glands
2) Signs and Symptoms
 Thickened skin of the cartilaginous canal
 Keratosis—adherent skin debris
 Lichenification
 Pruritus
 Lack of otalgia
 Canal obliteration in late stage disease
3) Diagnosis
 Biopsy, especially if granulation is present
4) Pathogens
• Gram-negative species, especially Proteus
5) Treatment
 Frequent debridement
 Treatment of underlying skin condition
 Topical antibiotics
 Topical steroids
 Canaloplasty with split thickness skin graft for obliterative cases.[5]
III. Pathogenesis
In the preinflammatory stage, the ear is exposed to predisposing factors, including heat.
humidity, maceration, the absence of cerumen, and an alkaline pH. Loss of acidity has been
shown to be proportionate to the degree of infection. This can cause edema of the stratum
comeum and occlusion of the apopilosebaceous units. In the inflammatory stage, bacterial
overgrowth ensues, with progressive edema and intensified pain. Incomplete resolution or
persistent inflammation for more than 3 months refers to the chronic inflammatory stage.[1]

IV. Clinical Findings

Symptoms of otitis externa may vary, depending on the stage and extent of disease. The
clinical diagnosis is suggested by the presence of otalgia, otorrhea, aural fullness, pruritus,
tenderness to palpation, and varying degrees of occlusion of the EAC. The patient may also
present with hearing loss due to occlusion of the EAC by edema and debris. There may also be
pain on distraction of the pinna, EAC erythema, edema, otorrhea, crusting, and, in more
advanced disease, lymphadenopathy of the periauricular and anterior cervical lymph nodes.
Skin changes of cellulitis may be present in more severe infections. In the chronic stage, the
skin of the EAC may be thickened and there may be scant, clear discharge. The presentation
can sometimes be confused with acute otitis media with tympanic membrane perforation or
furunculosis (which isusually limited to 1 part of the EAC).[1]

V. Staging
The clinical course of external otitis may be divided into the following stages:
preinflammatory; acute inflammatory, which can be mild, moderate, or severe; and chronic
inflammatory. Typically, the preinflammatory stage begins when the stratum corneum becomes
edematous due to the removal of the protective lipid layer and acid mantle from the canal,
resulting in plugging of the apopilosebaceous unit. As obstruction continues, a sense of fullness
and itching begins. The disruption of the epithelial layer allows invasion of bacteria that either
reside in the canal or are introduced on foreign objects inserted into the canal, such as a cotton
swab or a dirty fingernail. This produces the acute inflammatory stage, which is accompanied
by pain and tenderness of the auricle. In the earliest stage, the skin of the EAC shows mild
erythema and minimal edema (Fig. 146.3). A small amount of dear or slightly cloudy secretion
may be seen in the canal. As pain and itching increase, the patient progresses to the moderate
stage, in which the canal shows more edema and a thicker more profuse exudate (Fig. 146.4).
Further progression of the inflammation in the absence of treatment produces the severe
inflammatory stage. characterized by increased pain and obliteration of the lumen of the canal.
A profuse, purulent exudate and edema of the canal skin may obscure the TM. In addition,
small white papules are often visible on the surface of the canal skin. P. aeruginosa or another
gram-negative bacillus can almost always be cultured at this stage. In the severe stage, the
physician often sees evidence of extension of infection beyond the canal to involve the adjacent
soft tissues and cervical lymph nodes (Fig. 146.5).[3]
 In the chronic inflammatory stage, the patient experiences less pain but more profound
itching. The skin of the external canal is thickened, and superficial flaking may be seen (Fig.
146.6). The auricle and concha often show secondary changes such as eczematization,
lichenification, and superficial ulceration. This condition is likened to eczema and may range
from mild drying and thickening of the canal to complete obliteration of the external canal by
chronically infected, hypertrophic skin (Table 146.1).[3]
VI. Complications
Complication of acute and chronic OE are described in Table 138.1.[2]
VII. Diagnosis and Investigations
A. History
The history and functional inquiry should include information regarding the length of
time. the number of occurrences, the nature and severity ofpain, antecedent otologic
disease, previous auricular instrumentation or trauma (especially the use of cotton-tipped
applicators), and any predisposing factors such as diabetes or radiotherapy or any condition
causing immunosuppression. Any previous otologic or head and neck surgery is noted.[3]
Pain, fullness, itching, and hearing loss are the four major symptoms of external
otitis, although not every patient has each symptom (4). Throughout the examination, the
examiner should remember the innervation of the EAC and recall that pain from other areas
of the upper aerodigestive tract may be referred to the ear.[3]
A thorough history should include the timing, duration, and severity of symptoms.
Exposure to swimming-pool water and aural toilethabits are an essential part of the history.
Periods of improvement or worsening of symptoms should be described, as well as
previous treatments. Systemic diseases—such as allergies, autoimmune disorders,
immunosuppression, HIV, diabetes, or skin or hair conditions—may elucidate an
underlying cause. Additionally, topical treatments used in and around the ears should be
evaluated.[2]

B. Physical Examination
On initial inspection, look at the ear itself and then at its relation to the head. Is it red,
swollen, or protruding? Is there obvious discharge? Are the auricle and periauricular tissues
normal in appearance or lichenified, with a heaping up of the normal epidermal
architecture? Is there erythema or cellulitis spreading to the periauricular tissues, face, and
neck? A gentle tug upward and backward will usually confirm the clinical suspicion.
Although not an infallible rule, the patient with AOE usually will not tolerate this
maneuver; patients with acute otitis mediaoften will.[3]
To make the correct diagnosis of infections of the external canal and to follow the
clinical response to treatment. Clean the canal thoroughly and examine it under good
illumination. A handheld otoscope will often suffice for a quick examination, but all
instrumentation of the ear is best done under the microscope with the patient lying supine in
the chair in anticipation of a possible vasovagal response mediated by Arnold nerve. a
branch of cranial nerve X.[3]
Although topical and local anesthesia may be tried before cleansing, they are usually
of little effect in hyperemic macerated tissue and no substitute for reassurance and patience.
Using graduated specula will often ease the patient into a complete examination. The canal
may be cleaned with suction, a cerumen loop, or alligator forceps. Gentleness and
thoroughness in cleaning the ear are very important.[3]
 Physical examination should include a complete examination of the auricle and of the
EAC under binocular microscopy in addition to a complete physical examination to
evaluate for signs of systemic diseases. Removal of debris from the canal will allow for
examination of the tympanic membrane and may serve a therapeutic function as well by
removing obstruction of the canal and agents contributing to the inflammation.[2]

C. Laboratory and Imaging Evaluation

Culture of the ear canal should be taken for bacteria and fungus, especially for
persistent infections. In cases of presumed OE that are resistant to treatment, biopsies
should be taken to exclude malignancy. Generally radiologic examination should be
reserved for cases where spread beyond the EAC is suspected.[2]

VIII. Differential Diagnosis

The differential diagnosis of conditions that are similar to external otitis is large and
includes necrotizing otitis externa. bullous external otitis, granular external otitis,
perichondritis, chondritis, relapsing polychondritis, furunculosis, and aubunculosis, as well as
many dermatoses, such as psoriasis and seborrheic dermatitis. All have features in common
with acute and chronic external otitis, yet have enough dissimilarities to be considered distinct
clinical entities.[3]
Carcinoma involving the FAC may present as infection and in its earliest stages is often
mistaken for infection and treated inappropriately. The most common malignant neoplasm of
the external ear is squamous cell carcinoma. although other primary carcinomas, such as basal
cell carcinoma,. malignant melanoma,. ceruminous adenoma or adenocarcinoma. and adenoid
cystic and metastatic carcinomas to the temporal bone with extension to the EAC such as
breast, prostatic, small (oat) cell, and renal cell carcinomas, have been described. The
occurrence of pain in an old previously stable mastoid cavity is the hallmark of carcinoma and
must be excluded by biopsy and other investigations.[3]

IX. Treatment
a. In General
Treatment for otitis externa involves meticulous debridement of the EAC with
binocular microscopy. Analgesia can be achieved with nonsteroidal anti-
inflammatory drugs (NSAIDs), opioids, or topical steroid preparations. A culture
maybe helpful for infections that are refractory to treatment. After cleansing is
complete, otic drop preparations that are antiseptic, acidifying, or antibiotic (or any
combination of these) should be used. These have been shown to be equally
effective in the management of uncomplicated otitis externa in a recent Cochrane
review at 1 week, with acidifying agents less effective beyond that point. If the
degree of stenosis of the canal is severe, a wick must be placed to stent open the
EAC and permit delivery of drops to the medial portion of the canal.[1]
Available antiseptic preparations include acetic and boric acids, ichthammol,
phenol, aluminum acetate, gentian violet, thymol, thimerosal (Merthiolate),
Cresylate, and alcohol. Available antibiotic preparations include ofloxacin,
ciprofloxacin, colistin, polyrnyxin B, neomycin, chloramphenicol, gentamicin, and
tobramycin. Polymyxin B and neomycin preparations are often used in combination
for the treatment of S aureus and P aeruginosa infections. Ofloxacin and
 ciprofloxacin have an excellent spectrum of coverage for pathogens encountered in
otitis externa. Preparations with steroids help reduce edema and otalgia. Lastly,
systemic antibiotics are reserved for infections that spread beyond the EAC. For
chronic otitis externa, a canalplasty may be indicated for thickened skin causing
chronic canal obstruction. First-line therapy also includes prevention, and patients
must be instructed to avoid EAC manipulation and water exposure ifthey have a
history of recurrent otitis externa (Figure 49-6).[1]

b. Medical Treatment
The four fundamental principles in the treatment of external otitis in all stages are
frequent and thorough cleaning, judicious use of appropriate antibiotics, treatment of
associated inflammation and pain, and recommendations regan::ling the prevention offuture
infections. In any stage of infection, thorough cleaning is a priority. Meticulous
debridement of exfoliated debris, purulence, and cerumen will do as much if not more than
simply placing the patient on ear drops. In the preinflammatory stage, a complete cleaning
maybe all that is required. In the absence of purulence, a brief course of an acidifying drop
such as aluminum sulfate-calcium sulfate (Domeboro) is efficacious in discouraging
bacterial or fungal growth.[3]

1. Acute Stage
Treatment of the acute inflammatory stage varies with the extent of disease.
In the mildest form, cleaning as above is indicated. An antibiotic otic drop is
recommended to cover what is probably a Pseudomonas infection. At this stage
edema of the EAC should not be severe, and the patient should be able to instill
drops into the ear by tilting the head to the side or by lying down with the
involved ear upright[3]
2. Moderate Stage
In the moderate stage of inflammation, edema ofthe canal may interfere with
the instillation ofdrops. The physician should then insert a wick into the canal and
instill drops on it. Often the canal may accommodate two oreventhree wick. As
the wick expands, it presses the soft tissues and periosteum toward the
nondistracted positioni this alone may relieve pain. All instrumentation of the ear
is best done under the microscope. The wick is removed by the physician at the
time of reexamination. If the edema has not been significantly reduced, repacking
is indicated. Antibiotic drops should be continued for at least 2 to 3 days after the
cessation of pain. itching, and drainage so that complete eradication of infection
may be ensured.[3]
In the moderate stage, an oral analgesic is often prescribed because pain can
be pronounced. Caution the patient to avoid manipulation of the canal. Swimmers
should be taught to towel dry the concha and lateral canal, to shake water out of
the canal, or to instill an acidifying drop after swimming. If the infection has not
spread beyond the boundaries of the external canal, the use of oral antibiotics will
be oflittle if any value. A final office visit is important to ensure that the infection
has completely resolved and the canal is back to its normal state.[3]

3. Severe Stage
In the severe stage, infection usually extends beyond the limits of the canal.
In addition to the cleaning, packing, and use of antibiotic drops as discussed
previously, attend to any soft tissue involvement by using an oral antibiotic with
broad-spectrum coverage. Successive generations of the cephalosporins widen
gram-negative coverage at the expense of gram-positive coverage.[3]
In addition to anti-Pseudomonas ear drops, common choices of oral
antibiotics are one of the antipseudomonal fluoroquinolones such as ciprofloxadn
or levofloxacin, antistaphylococcal penicillins, or cephalosporins. The
fluoroquinolone antibiotics are effective against Pseudomonas species. In
children under 12 years old, one should check with the pediatrician prior to
starting oral fluoroquinolones.[3]
Warm soaks (normal saline or a mild aluminum sulfate-calcium acetate
solution) are also useful in the treatment of the crusting and edema involving the
auricle and surrounding skin. Culture of the canal for aerobic bacteria and/or
fungi is indicated only for the severe stage or for patients who have previously
been treated without resolution. Treatment is generally continued for 10 to 14
days if there is a good response. In rare patients who do not respond to this
regimen. hospitalization. vigorous daily local care, repeat culturing, and
intravenous antibiotics are indicated.[3]

4. Chronic Stage
The chronic stage of external otitis is manifested by marked thickening of the
skin of the FAC due to long-standing infection. Examination reveals flakes of dry
scaly skin in the canal. Although removal of debris is recommended, this may be
difficult due to the narrowing of the lumen of the canal. Repeated cleaning and
instillation of antibiotics and steroids are indicated. Triamcinolone acetonide
0.25% cream or ointment (Kenalog), fluocinolone 0.01% oil (DermOtic), or
 dexamethasone sodium phosphate 0.1% ophthalmic drops (Decadron, Pred Forte
1%) may be used.[3]
In all cases of acute or chronic external otitis, instruct the patient to avoid
future infections by not instrumenting the ear. Foreign objects such as Q-tips
often excoriate the canal skin and push debris further into the canal rather than
remove it Patients who have repeated infections despite adhering to these
measures are best advised to use an acidifying drop composed ofequal measures
of vinegar and water, or ethyl alcohol and water, when exposed to high humidity.
One should suspect otomycosis if all other reasonable measures have failed and
should treat with drying agents, especially powders. Custom-made ear molds are
useful for these patients.[3]

5. Recalcitrant Otitis Externa

The physician will be able to judge very quickly which patients are
responding. Prolonged antibiotic drops may suppress the normal flora of the
external canal from returning and lead to a fungal superinfection. This should be
suspected, especially if a grayish matted discharge is found in the ear, even if
telltale hyphae are absent. A culture may have already been taken, and the result
should help to direct treatment. Again, the ear must be thoroughly and
meticulously cleaned, and if a fungus has been cultured such as Candida, this
should be treated appropriately with drying agents such as powders and an
antifungal drop or even systemically with an oral antifungal medication such as
fluconazole. If no progress is made in the office, the rare patient may have to be
admitted as an inpatient. Examine the ear under a microscope and carefully clean
it frequently. Look for subtle signs of chronic middle ear disease-granulation
tissue or the opening of a tiny perforation. The latter may be obscured by a
swollen TM, giving a "fishmouth· appearance to the perforation. A ·sewer cap"
of crust on the drum may reveal a cholesteatoma underneath. Examine every part
of the auricle carefully. Look for signs of underlying chondritis or perichondritis,
especially diffuse crusting or exudative weeping. Culture the ear (for aerobes,
anaerobes, and fungi). Examine the periauricular tissues carefully to look for
signs ofspreading infection. Computed tomography of the temporal bones may
give additional information. Look for opacification of the mastoid and signs of
bony erosion.[3]
Place the patient on daily aural drops, preferably one covering P. aeruginosa,
and intravenous antibiotics with gram-positive and gram-negative coverage. One
may wish to try intravenous ciprofloxacin to start. In very rare cases, a
cephalosporin together with an aminoglycoside is a logical combination if
monotherapy does not improve the ear. Therapy should be tapered according to
culture and sensitivities. Severely swollen ears may calm down with steroids.[3]
Many recalcitrant infections occur because of noncompliance or chronic
instrumentation of the canal skin. The patient should be counseled to amend bad
habits. The rare patient will need to be admitted for intravenous antibiotics and
daily aural toilet (Tables 146.2 and 146.3).[3]
c. Surgical Management of Hypertrophic Chronic Otitis Externa
When such local measures are insufficient to eradicate infection and reestablish the
lumen of the canal, it is necessary to remove the involved canal skin and any adjacent
involved cutaneous or cartilaginous tissue. This is very rarely required and may be
performed through the canal but is better done through a postauricular incision, which
allows visualization of the involved tissues. A generous amount of conchal cartilage is
removed to effect a wide meatoplasty. The bony canal is enlarged with a drill. Take care to
protect the facial nerve in its vertical segment; the use of an intraoperative facial nerve
monitor facilitates this. The canal is resurfaced with a split-thickness (8:1,000 inch) skin
graft that is temporarily held in place with stents or packing.[3]
It is the experience of many otolaryngologists that even the most recalcitrant infection
can be managed if the four basic principles-thorough cleaning, antibiotic treatment,. pain
control, and instruction of the patient-are meticulously followed. There is no substitute for
thorough and repeated local care (Table 146.4).[3]