Infections of the Ear

and Mastoid
Infections of the ear and associated structures can
involve both the middle and the external ear,
including the skin, cartilage, periosteum, ear canal,
and tympanic and mastoid cavities.

Both viruses and bacteria are known causes of

these infections, some of which result in significant
morbidity if not treated appropriately.
 Infections of the
External Ear Structures
Infections involving the structures of the external ear
are often difficult to differentiate from noninfectious
inflammatory conditions with similar clinical
manifestations.

Clinicians should consider inflammatory disorders

as possible causes of external ear irritation,
particularly in the absence of local or regional
adenopathy.
Aside from the more salient causes of inflammation,
such as trauma, insect bite, and overexposure to
sunlight or extreme cold, the differential diagnosis
should include less common conditions such as
autoimmune disorders (e.g., lupus or relapsing
polychondritis) and vasculitides (e.g., granulomatosis
with polyangiitis [Wegener's]).
1. Auricular Cellulitis
Auricular cellulitis is an infection of the skin
overlying the external ear and typically follows minor
local trauma.

It presents as the typical signs and symptoms of

cellulitis, with tenderness, erythema, swelling, and
warmth of the external ear (particularly the lobule)
but without apparent involvement of the ear canal
or inner structures.
Treatment consists of warm compresses and oral
antibiotics such as Dicloxacillin that are active
against typical skin and soft tissue pathogens
(specifically, S. aureus and Streptococci).

IV antibiotics such as a first-generation

cephalosporin (e.g., Cefazolin) or a penicillinase-
resistant penicillin (e.g., Nafcillin) occasionally are
needed for more severe cases, with consideration
of MRSA if either risk factors or failure of therapy
point to this organism.
2. Perichondritis
 Perichondritis, an infection of the perichondrium of
the auricular cartilage, typically follows local trauma
(e.g., ear piercing, burns, or lacerations).

 Occasionally, when the infection spreads down to the

cartilage of the pinna itself, patients may develop
chondritis.
The infection may closely resemble auricular
cellulitis, with erythema, swelling, and extreme
tenderness of the pinna, although the lobule is less
often involved in perichondritis.

The most common pathogens are P. aeruginosa

and S. aureus, although other gram-negative and
gram-positive organisms occasionally are involved.

Treatment consists of systemic antibiotics active

against both P. aeruginosa and S. aureus.
An antipseudomonal penicillin (e.g., Piperacillin) or a
combination of a penicillinase-resistant penicillin and
an antipseudomonal quinolone (e.g., nafcillin plus
ciprofloxacin) is typically used.

Incision and drainage may be helpful for culture

and for resolution of infection, which often takes
weeks.

When perichondritis fails to respond to adequate

antimicrobial therapy, clinicians should consider a
noninfectious inflammatory etiology such as
Relapsing Polychondritis.
3. Otitis Externa
 The term otitis externa refers to a collection of
diseases involving primarily the auditory meatus.

 Otitis externa usually results from a combination of

heat and retained moisture, with desquamation and
maceration of the epithelium of the outer ear canal.
The disease exists in several forms: Localized,
Diffuse, Chronic, and Invasive.

All forms are predominantly bacterial in origin,

with P. aeruginosa and S. aureus the most
common pathogens.

Acute Localized Otitis Externa (Furunculosis) can

develop in the outer third of the ear canal, where
skin overlies cartilage and hair follicles are
numerous.
As in furunculosis elsewhere on the body, S. aureus
is the usual pathogen, and treatment typically
consists of an oral antistaphylococcal penicillin (e.g.,
Dicloxacillin), with incision and drainage in cases of
abscess formation.
Acute Diffuse Otitis Externa is also known as
Swimmer's Ear, although it can develop in patients
who have not recently been swimming.

Heat, humidity, and the loss of protective cerumen

lead to excessive moisture and elevation of the pH
in the ear canal, which in turn lead to skin
maceration and irritation.

Infection may then occur; the predominant pathogen

is P. aeruginosa, although other gram-negative and
gram-positive organisms—and rarely yeasts—have
been recovered from patients with this condition.
The illness often starts with itching and progresses to
severe pain, which usually is elicited by manipulation
of the pinna or tragus.

The onset of pain generally is accompanied by the

development of an erythematous, swollen ear
canal, often with scant white, clumpy discharge.

Treatment consists of cleansing the canal to

remove debris and enhance the activity of topical
therapeutic agents—usually hypertonic saline or
mixtures of alcohol and acetic acid.
Inflammation also can be decreased by adding
Glucocorticoids to the treatment regimen or by using
Burow's solution (aluminum acetate in water).
Antibiotics are most effective when given
topically.

Otic mixtures provide adequate pathogen

coverage; these preparations usually combine
Neomycin with Polymyxin, with or without
Glucocorticoids.

Systemic antimicrobial agents typically are

reserved for severe disease or infections in
immunocompromised hosts.
Chronic Otitis Externa is caused primarily by
repeated local irritation, most commonly arising from
persistent drainage from a chronic middle-ear
infection.

Other causes of repeated irritation, such as

insertion of cotton swabs or other foreign objects
into the ear canal, can lead to this condition, as
can rare chronic infections such as syphilis,
tuberculosis, and leprosy.
Chronic otitis externa typically presents as
erythematous, scaling dermatitis in which the
predominant symptom is pruritus rather than pain;
This condition must be differentiated from several
others that produce a similar clinical picture, such
as Atopic Dermatitis, Seborrheic Dermatitis,
Psoriasis, and Dermatomycosis.
Therapy consists of identifying and treating or
removing the offending process, although successful
resolution is frequently difficult.
Invasive Otitis Externa, also known as Malignant
or Necrotizing otitis externa, is an aggressive and
potentially life-threatening disease that occurs
predominantly in Elderly Diabetic Patients and other
immunocompromised persons.

The disease begins in the external canal as a soft

tissue infection that progresses slowly over weeks
to months and often is difficult to distinguish from
a severe case of chronic otitis externa because of
the presence of purulent otorrhea and an
erythematous swollen ear and external canal.
Severe, deep-seated otalgia, frequently out of
proportion to findings on examination, is often noted
and can help differentiate invasive from chronic otitis
externa.

The characteristic finding on examination is

granulation tissue in the posteroinferior wall of the
external canal, near the junction of bone and
cartilage.
If left unchecked, the infection can migrate to the
base of the skull (resulting in skull-base
osteomyelitis) and onto the meninges and brain,
with a high-associated mortality rate.

Cranial nerve involvement is seen occasionally,

with the Facial Nerve usually affected first and
most often.
Thrombosis of the sigmoid sinus can occur if the
infection extends to that area.

CT, which can reveal osseous erosion of the

temporal bone and skull base, can be used to help
determine the extent of disease, as can gallium
and technetium-99 scintigraphy studies.

P. aeruginosa is by far the most common pathogen,

although S. aureus, S. epidermidis, Aspergillus,
Actinomyces, and some gram-negative bacteria have
also been associated with this disease.
In all cases, the external ear canal should be
cleansed and a biopsy specimen of the granulation
tissue within the canal (or of deeper tissues)
obtained for culture of the offending organism.

IV antibiotic therapy should be given for a

prolonged course (6–8 weeks) and directed
specifically toward the recovered pathogen.

For P. aeruginosa, the regimen typically includes

an anti pseudomonal penicillin or cephalosporin
(e.g., Piperacillin or Ceftazidime) with an
aminoglycoside.
A fluoroquinolone antibiotic is frequently used in
place of the aminoglycoside and can even be
administered orally because of the excellent
bioavailability of this drug class.

In addition, antibiotic drops containing an agent

active against Pseudomonas (e.g., ciprofloxacin)
usually are prescribed and are combined with
glucocorticoids to reduce inflammation.
Cases of invasive Pseudomonas otitis externa
recognized in the early stages sometimes can be
treated with oral and otic fluoroquinolones alone,
albeit with close follow-up.

Extensive surgical debridement, once an important

component of the treatment approach, is now
rarely indicated.
In necrotizing otitis externa, recurrence is
documented up to 20% of the time.

Aggressive glycemic control in diabetics is

important not only for effective treatment but also
for prevention of recurrence.

The role of hyperbaric oxygen has not been clearly

established.
Infections of Middle-Ear
Structures
Otitis Media is an inflammatory condition of the
middle ear that results from dysfunction of the
eustachian tube in association with a number of
illnesses, including URIs and chronic rhinosinusitis.

The inflammatory response to these conditions leads

to the development of a sterile transudate within the
middle ear and mastoid cavities.

Infection may occur if bacteria or viruses from the

nasopharynx contaminate this fluid, producing an
acute (or sometimes chronic) illness.
Acute Otitis Media
Acute otitis media results when pathogens from the
nasopharynx are introduced into the inflammatory
fluid collected in the middle ear (e.g., by nose
blowing during a URI).

The proliferation of these pathogens in this space

leads to the development of the typical signs and
symptoms of acute middle-ear infection.

The diagnosis of acute otitis media requires the

demonstration of fluid in the middle ear [with
tympanic membrane (TM) immobility] and the
accompanying signs or symptoms of local or
systemic illness (Table 31-2).
Etiology
 Acute otitis media typically follows a viral URI.

 The causative viruses (most commonly RSV,

influenza virus, rhinovirus, and enterovirus) can
themselves cause subsequent acute otitis media;
more often, they predispose the patient to bacterial
otitis media.
Studies using tympanocentesis have consistently
found S. pneumoniae to be the most important
bacterial cause, isolated in up to 35% of cases.

H. influenzae (nontypable strains) and M.

catarrhalis are also common bacterial causes of
acute otitis media, and concern is increasing about
community strains of MRSA as an emerging
etiologic agent.

Viruses, such as those mentioned above, have been

recovered either alone or with bacteria in 17–40% of
cases.
Clinical Manifestations
 Fluid in the middle ear is typically demonstrated
or confirmed with pneumatic otoscopy.

 In the absence of fluid, the tympanic membrane

moves visibly with the application of positive and
negative pressure, but this movement is dampened
when fluid is present.

 With bacterial infection, the tympanic membrane can also

be erythematous, bulging, or retracted and occasionally can
perforate spontaneously.
The signs and symptoms accompanying infection
can be local or systemic, including otalgia, otorrhea,
diminished hearing, fever, and irritability.

Erythema of the tympanic membrane is often

evident but is nonspecific as it frequently is seen
in association with inflammation of the upper
respiratory mucosa (e.g., during examination of
young children).

Other signs and symptoms that are occasionally

reported include vertigo, nystagmus, and tinnitus.
Treatment: Acute Otitis Media
 There has been considerable debate on the
usefulness of antibiotics for the treatment of acute
otitis media.

 A higher proportion of treated than untreated

patients are free of illness 3–5 days after diagnosis.

 The difficulty of predicting which patients will benefit

from antibiotic therapy has led to different
approaches.
In the Netherlands, for instance, physicians
typically manage acute otitis media with initial
observation, administering anti-inflammatory
agents for aggressive pain management and
reserving antibiotics for high-risk patients, patients
with complicated disease, or patients whose
condition does not improve after 48–72 h.
 In contrast, many experts in the United States
continue to recommend antibiotic therapy for
children <6 months old in light of the higher
frequency of secondary complications in this
young and functionally immunocompromised
population.

However, observation without antimicrobial therapy

is now the recommended option in the United States
for acute otitis media in children >2 years of age and
for mild to moderate disease without middle-ear
effusion in children 6 months to 2 years of age.
Treatment is typically indicated

1. For patients <6 months old;

2. For children 6 months to 2 years old who have
middle-ear effusion and signs/symptoms of
middle-ear inflammation;
3. For all patients >2 years old who have bilateral
disease, tympanic membrane perforation,
immunocompromise, or emesis; and
4. For any patient who has severe symptoms,
including a fever >39°C or moderate to severe
otalgia (Table 31-2).
Because most studies of the etiologic agents of
acute otitis media consistently document similar
pathogen profiles, therapy is generally empirical
except in those few cases in which tympanocentesis
is warranted—e.g., cases in newborns, cases
refractory to therapy, and cases in patients who are
severely ill or immunodeficient.
Despite resistance to penicillin and amoxicillin in
roughly one-quarter of S. pneumoniae isolates, one-
third of H. influenzae isolates, and nearly all M.
catarrhalis isolates, outcome studies continue to find
that amoxicillin is as successful as any other agent,
and it remains the drug of first choice in
recommendations from multiple sources (Table 31-2).

Therapy for uncomplicated acute otitis media

typically is administered for 5–7 days to patients 6
years old; longer courses (e.g., 10 days) should be
reserved for children <6 years old and patients
with severe disease, in whom short-course therapy
may be inadequate.
A switch in regimen is recommended if there is no
clinical improvement by the third day of therapy in
light of the possibility of infection with a B-
lactamase-producing strain of H. influenzae or M.
catarrhalis or with a strain of penicillin-resistant S.
pneumoniae.

Decongestants and antihistamines are

frequently used as adjunctive agents to reduce
congestion and relieve obstruction of the
eustachian tube, but clinical trials have yielded no
significant evidence of benefit with either class of
agents.
Recurrent Acute Otitis
Media
Recurrent acute otitis media (more than three
episodes within 6 months or four episodes within 12
months) generally is due to relapse or reinfection,
although data indicate that the majority of early
recurrences are new infections.

In general, the same pathogens responsible for

acute otitis media cause recurrent disease; even
so, the recommended treatment consists of
antibiotics active against B-lactamase-producing
organisms.
Antibiotic prophylaxis [e.g., with trimethoprim-
sulfamethoxazole (TMP-SMX) or amoxicillin] can
reduce recurrences in patients with recurrent acute
otitis media by an average of one episode per year,
But this benefit is small compared with the cost of
the drug and the high likelihood of colonization
with antibiotic-resistant pathogens.
Other approaches, including Placement of
Tympanostomy Tubes, Adenoidectomy, and
Tonsillectomy plus adenoidectomy, are of
questionable overall value in light of the relatively
small benefit compared with the potential for
complications.
Serous Otitis Media
In serous otitis media (otitis media with effusion),
fluid is present in the middle ear for an extended
period in the absence of signs and symptoms of
infection.

In general, acute effusions are self-limited; most

resolve in 2–4 wks.

In some cases, however (in particular after an

episode of acute otitis media), effusions can persist
for months.

These chronic effusions are often associated with

significant hearing loss in the affected ear.
In younger children, persistent effusions and
decreased hearing can be associated with
impairment of language acquisition skills.

The great majority of cases of otitis media with

effusion resolve spontaneously within 3 months
without antibiotic therapy.
Antibiotic therapy or myringotomy with insertion
of tympanostomy tubes typically is reserved for
patients in whom bilateral effusion
1. Has persisted for at least 3 months and
2. Is associated with significant bilateral hearing
loss.

With this conservative approach and the application

of strict diagnostic criteria for acute otitis media and
otitis media with effusion, it is estimated that 6–8
million courses of antibiotics could be avoided each
year in the United States.