Otitis externa includes infections and inflammation of the external
auditory canal and auricle. It is divided into acute diffuse and
Also known simply as otitis externa or swimmer’s
ear, this infection is characterized by pruritus, pain,
and tenderness of the external ear. Physical signs include erythema
and edema of the external auditory canal, which may spread to the
tragus and auricle. Other signs are clear or purulent otorrhea and
crusting of the external canal. As the disease progresses, the pain
may become intolerable and occur with mastication or any movement
of the periauricular skin. Increasing edema may eventually narrow
the canal lumen and can lead to hearing impairment. In severe cases,
infection may spread to the periauricular soft tissues and lymph
nodes, and there may be lateral protrusion of the auricle secondary
Predisposing factors for the development of otitis externa are
trauma to the skin of the external auditory canal and elevation of
the local pH. Factors include frequent contact with water from swimming
or bathing in hot tubs, pools, or freshwater lakes, and living in
a humid environment. Trauma is most commonly due to scratching or
by overzealous disimpaction of cerumen. Cerumen is an acidic mixture
of sebaceous and apocrine gland secretions and desquamated epithelial cells.
It forms a physical barrier that protects the skin of the external
auditory canal, whereas the acidic pH has antimicrobial properties.
The most common organisms are Pseudomonas aeruginosa, Enterobacteriaceae and Proteus species,
and Staphylococcus aureus, with P.
aeruginosa the commonest organism causing malignant
Otomycosis, or fungal otitis externa, is found in tropical climates
and in the immunocompromised or after previous long-term therapy
with antibiotics. Most cases are caused by Aspergillus or Candida.12
Noninfectious causes include contact dermatitis from topical
medications or resins in hearing aids, seborrhea, and psoriasis.
Although not generally an occupational disease, otitis externa resulting
from mite infestation has been reported in poultry workers.13
The treatment consists of analgesia, cleansing of the external auditory
canal, acidifying agents, topical antimicrobials, and, sometimes, steroids.
Cleansing may be done with gentle irrigation using hydrogen peroxide
and gentle suction.
Nonototoxic ototopical antibiotics are first-line therapy, particularly when
the integrity of the TM is unknown or in the presence of a known TM
perforation or tympanostomy tubes. The ototopical quinolones, ofloxacin and ciprofloxacin,
are effective and have antistaphylococcal and antipseudomonal activity.
In addition, topical ofloxacin has been approved by the U.S. Food
and Drug Administration for use in infants and children, and is
the only ototopical antibiotic approved by the Food and Drug Administration
for use with an open middle ear.14
Table 237-5 lists the components of many
otic preparations. Considerations to guide the choice of agent include
the risk of ototoxicity, cost, and compliance. Although there are
few established cases of ototoxicity, there is a theoretical risk
of both auditory and vestibular toxicity with the use of aminoglycosides,
polymyxin, and acetic acid preparations.3,4,14 Although
this risk appears to be negligible in the presence of an intact
TM, there is evidence of systemic absorption of topical aminoglycosides.15,16
Table 237-5 Some
Common Topical Otic Preparations
The burning associated with the acidic preparations may reduce
compliance. Patients unable to tolerate the low pH of otic preparations
may instead use the slightly more alkaline ophthalmic drops.
If cost is a factor and there are no known contraindications,
acetic acid drops may be used, as they are less expensive than the
quinolones. In this case, a suspension should be used and not a
solution; theoretically, this has less chance of middle ear penetration and resultant ototoxicity.
Instill the medication into the cleansed ear with the ear facing
up, with this position held for 3 minutes. If edema of the external
canal obstructs the lumen, insert a commercial wick or piece of
gauze into the canal and keep it moist with the otic drops.
Bacterial and fungal cultures may guide treatment of nonresponsive
cases. Oral antibiotics are reserved for febrile patients and those
with periauricular extension. Instruct patients with otitis externa
to avoid predisposing factors to eliminate recurrences. Strategies
include ear plugs while swimming or bathing (cotton wool impregnated
with petroleum jelly or commercial ear plugs), brief use of a hair
dryer to remove water from the ear canal, and avoiding cotton-tipped
applicators or other devices to remove cerumen.
Specific treatment of otomycosis consists of systemic antifungal
agents such as fluconazole (200 milligrams × 1
dose, then 100 milligrams daily for 3 to 5 more days).11 Aspergillus is
not sensitive to most oral antifungals with the exception of itraconazole.17 Topical
steroid drops may be used in the setting of seborrhea and psoriasis.
Instruct patients to follow up with their primary physician or
an otolaryngologist in 1 week to be evaluated for the more serious
disease of malignant otitis externa if the condition worsens at
any time or does not respond to treatment.
Malignant otitis externa is a potentially life-threatening infection
of the external auditory canal involving the pinna and soft tissues
with variable extension to the skull base. In >90% of cases,
it is caused by P. aeruginosa.11 When
infection is limited to the soft tissues and cartilage, it is called necrotizing
otitis externa. When there is involvement of the temporal
bone or skull base, it is called skull-base osteomyelitis.
Malignant otitis externa begins as a simple otitis externa that
then spreads to the deeper tissues of the external auditory canal and
infects cartilage, periosteum, soft tissue, and bone, with the normal anatomy
of the ear serving as the conduit for the spread of infection. The cartilaginous
floor of the external auditory canal has clefts (the fissures of
Santorini) through which the infection may spread to deeper structures.
Infection may spread to the mastoid air cells, sigmoid sinus, parotid
gland, and skull base, as well as to the seventh cranial nerve as
it exits the stylomastoid foramen and the ninth, 10th, and 11th
cranial nerves at the jugular foramen.
Diabetes and immunosuppression predispose to the onset of pseudomonal infection.
The cerumen of diabetic patients has a higher pH than that of normal
controls and represents an additional breakdown in local defense
mechanisms. Small blood vessel disease of diabetics may lead to cartilaginous
degeneration, further promoting the spread of infection.
An individual with persistent otitis externa despite 2 to 3 weeks
of topical antimicrobial therapy should be suspected of having malignant
otitis externa. The typical presentation is otalgia and edema of
the external auditory canal with or without otorrhea. Otalgia may
be out of proportion for routine otitis externa. Granulation tissue
may be evident on the floor of the external auditory canal.
Examine both ears, inspecting both pinnas from the anterior,
lateral, and posterior aspects. The infected ear will be erythematous,
edematous, and will be more prominent than the unaffected ear. Assess
nearby structures. Parotitis may be present, and trismus indicates
involvement of the masseter muscle or temporomandibular joint. Cranial
nerve involvement is a serious sign. The seventh cranial nerve is
usually the first nerve affected by cranial extension, and the presence
of dysfunction of the ninth, 10th, or 11th cranial nerve implies
even more extensive disease. Lateral or sigmoid sinus thrombosis
and meningitis are more serious possible complications. The next
step is radiographic confirmation and staging of the disease with CT
of the head.
Malignant otitis externa in children tends to be rapidly progressive,
so children may be ill appearing upon presentation with fever, leukocytosis, and
even bacteremia/sepsis. Also, the TM, middle ear, and facial
nerve are more likely to be involved in children than in adults.
Acquired immunodeficiency syndrome patients tend to be younger,
have etiologic organisms other than Pseudomonas,
and tend to have a worse prognosis than patients without acquired
Institute antibiotics in the ED using imipenem in children or an
aminoglycoside and antipseudomonal penicillin, or a cephalosporin or
quinolone in adults.11 Selected cases of early
infection may be managed as outpatients with oral quinolones. Mild
cases are likely to completely resolve with a single course of antibiotic
therapy, while more advanced stages may require IV antibiotics ±
Otitis media (OM) is primarily a disease of infancy
and childhood (see Chapter 114, Ear and Mastoid Disorders in Infants and Children, in the Pediatrics section).
Although adults may present with OM, its incidence and prevalence
peak in the preschool years and then decrease with increasing age.
There is little or no literature to suggest that the diagnosis or
management of OM in adults differs from that in children. The decrease
in incidence of OM from childhood through adolescence is thought
to be due to the changing anatomy of the eustachian tube. Between
infancy and adulthood, the eustachian tube angle and length both increase,
promoting drainage of the middle ear and offering a greater physical
barrier to the migration of bacteria from the nasopharynx into the
In one study, 70% of all OM cases had a viral etiology when
a causative organism could be cultured.18 The most
common bacterial pathogens recovered in acute OM were Streptococcus
pneumoniae (49%), Haemophilus
influenzae (29%), and Moraxella
catarrhalis (28%). The Haemophilus organism
grown most commonly is of the nontypable variety, so most children
are not really conferred any protection with the H. influenzae type
b vaccine that they now receive regularly. Most adults have never
received this vaccine so remain unprotected from all Haemophilus flu
strains. The predominant organisms involved in chronic OM are S.
aureus, P. aeruginosa, and anaerobic bacteria.19 The
heptavalent pneumococcal vaccine (PCV7) approved for use in the
U.S. provides protection against S. pneumoniae serotypes
responsible for what was a large proportion of bacterial isolates
that used to cause OM. Many of these pathogens were drug-resistant
isolates as well. However, it is not surprising that the widespread
use of PCV7 has caused a relative increase contribution of several
of the non-PCV7 serotypes. Many of which are also penicillin-nonsusceptible.20,21
The typical patient with OM presents with otalgia with or without
fever. Otorrhea and hearing loss are variably present, while tinnitus,
vertigo, and nystagmus are uncommon but possible findings. The TM may
be retracted or bulging. It may be red in color, indicating inflammation,
or it may be yellow or white, as a result of middle ear fluid. Pneumatic otoscopy
almost uniformly demonstrates impaired mobility. Always assess facial
nerve function because of its proximity to the middle ear.
There are no treatment guidelines specifically for adults. It
is becoming more popular if the patient is >2 years old and afebrile
without severe ear pain to consider analgesia only and wait for
48 hours to see if symptoms resolve on their own.22 Most
of these cases will be due to a viral etiology. High-dose amoxicillin
is effective against all three major pathogens, but approximately
30% of H. influenzae and up to 80% of M. catarrhalis have
developed β-lactamase, conferring some degree of
resistance to amoxicillin. With the advent of the pneumococcal vaccine, penicillin-resistant
pneumococci dropped from 15.4% to 6.7% in one study
done on the West Coast of the U.S.23
The preferred initial treatment is still amoxicillin. The dose
in adults (weighing >40 kg) is 500 to 875 milligrams every 12 hours,
or 250 to 500 milligrams every 8 hours, for 7 to 10 days. Alternative
agents include trimethoprim-sulfamethoxazole, azithromycin, or cefuroxime
(a second-generation cephalosporin). For otitis media unresponsive
to initial therapy after 72 hours, consider changing to cefuroxime
Provide pain control with acetaminophen or ibuprofen, or narcotics
for severe pain. Topical agents such as antipyrine/benzocaine
otic may also be given. Otitis media with effusion requires treatment
with the same antimicrobials, but for 3 weeks, and prednisone may
Adults with simple acute otitis media should receive follow-up
to assess treatment efficacy and to ensure that there is no anatomic
obstruction to the eustachian tube, as, for example, from occult
neoplasm. Any patient who presents with complications of OM or who
appears septic should have urgent consultation for diagnostic and
therapeutic tympanocentesis and possible admission for IV antibiotics.
Complications of OM are intratemporal and intracranial. Perforation
of the TM is a common intratemporal complication and most often
occurs in the pars tensa from the increased pressure of middle ear
secretions, with resultant otorrhea. Healing usually occurs in 1
week, although a chronic perforation may result. A temporary conductive
hearing loss may occur secondary to fluid in the middle ear. The
hearing loss should resolve as the fluid is resorbed. Acute serous
labyrinthitis may occur when bacterial toxins enter the inner ear
via the round window. Facial nerve paralysis is an uncommon complication
but requires emergent otolaryngology consultation.
Acute mastoiditis results from spread of infection from the middle
ear to the mastoid air cells by the aditus ad antrum. When this
opening becomes blocked, the mastoid cavity becomes a closed space,
and the mastoid air cells become inflamed and fill with fluid. Spread
through venous channels to the overlying periosteum is referred
to as acute mastoiditis with periostitis. In addition
to otalgia and fever, patients with mastoiditis will have postauricular
erythema, swelling, and tenderness, with protrusion of the auricle
and obliteration of the postauricular crease. Although the diagnosis
can usually be made based on the history and physical examination,
certain radiographic tests are indicated. Mastoid radiographs will
demonstrate mastoid clouding because of fluid accumulation, and
CT may delineate the extent of bony involvement. Mastoiditis requires
admission for IV antibiotics, tympanocentesis, and myringotomy.
Vancomycin or nafcillin is usually considered to be the first-line
initial empiric agent of choice (Sanford guide, 2008).24 Other
regimens include cefotaxime and ceftriaxone for acute mastoiditis
and imipenem or piperacillin/tazobactam in the chronic
setting. Incision and drainage of subperiosteal abscess or mastoidectomy
may ultimately be required.
Aural cholesteatoma are collections of epidermis and exfoliated
keratin within the middle ear or mastoid. As the cholesteatoma expands,
it may erode the ossicular chain, bony labyrinth, or facial nerve
canal. Cholesteatomas are often infected and their intracranial
extensions may be life threatening.
Intracranial complications of OM are more likely with chronic
than with acute OM and are, in general, decreasing with the widespread
use of antibiotics in the treatment of OM. However, suppurative
intracranial extension is a severe complication, and suggestive
signs and symptoms should be investigated appropriately. Meningitis
and brain abscess are the most common intracranial complication
of OM; the most prevalent causative organisms are S. pneumoniae and H. influenzae type
b, although the H. influenzae type b vaccine has
drastically reduced this complication. Extradural abscess and subdural
empyema are also potential complications.
Lateral sinus thrombosis is another ominous complication of acute
OM. It arises from extension of infection and inflammation in the
mastoid, with eventual inflammation of the adjacent lateral or sigmoid
sinus. Reactive thrombophlebitis with mural clot formation, intraluminal
empyema, or perforation of the venous wall may occur.
Headache is the most common symptom, with papilledema, sixth-nerve palsy,
and vertigo being less frequently present. Angiography with venous
phase and MRI are more sensitive than CT in diagnosing lateral sinus
thrombosis. The employed antibiotic regimen should cover Staphylococcus, Streptococcus,
and upper respiratory anaerobes, and have good penetration of the
blood–brain barrier. A combination of IV penicillin or
nafcillin, ceftriaxone, and metronidazole is one initial empiric regimen.25,26
Bullous myringitis is a painful condition of the ear characterized
by bulla formation on the TM and deep external auditory canal. The
blisters are believed to occur between the highly innervated outer
epithelium and the inner fibrous layer of the TM, explaining the
severe otalgia. The blisters may be blood filled, serous, or serosanguineous.
Reactive middle ear effusions may accumulate. Otorrhea as a result
of ruptured bullae is short lived. A reversible hearing loss is
commonly associated with the condition and may be conductive, sensorineural,
or mixed. Mycoplasma pneumoniae, Chlamydia
psittaci, and numerous viral pathogens have been implicated,
but the association is not clear.27 Treatment is
pain control, whereas antibiotics for uncomplicated bullous myringitis
is optional. Antibiotics can be given for concomitant otitis media.