TITLE: EXTERNAL AUDITORY
SOURCE: Department of Otolaryngology, UTMB: Grand Rounds Presentation
DATE: April 9, 1997
RESIDENT PHYSICIAN: Kyle Kennedy, M.D.
FACULTY PHYSICIAN: Jeffrey Vrabec, M.D.
SERIES EDITOR: Francis B. Quinn, Jr., M.D.
to Grand Rounds Index|
"This material was prepared by resident physicians in partial fulfillment of educational
requirements established for the Postgraduate Training Program of the UTMB Department
of Otolaryngology/Head and Neck Surgery and was not intended for clinical use
in its present form. It was prepared for the purpose of stimulating group discussion
in a conference setting. No warranties, either express or implied, are made with
respect to its accuracy, completeness, or timeliness. The material does not necessarily
reflect the current or past opinions of members of the UTMB faculty and should
not be used for purposes of diagnosis or treatment without consulting appropriate
literature sources and informed professional opinion."
Lesions of the external auditory canal (EAC) are disease entities
frequently encountered by the otolaryngologist. These disorders
range in complexity from the simple impaction of cerumen to neoplasia
of the temporal bone. The EAC is not simply a conduit for sound from
the environment to the tympanic membrane. A thorough understanding
of the basic aspects of EAC development, anatomy, and physiology are
requisite for the rational management of diseases affecting this
structure. A discussion of these topics will be followed by an
overview of the most frequently encountered EAC lesions with which
the practicing otolaryngologist should become familiar.
The EAC derives from the 1st branchial cleft or groove which lies
between the 1st (mandibular) and 2nd (hyoid) branchial arches. The
1st branchial cleft is derived from ectoderm and initially consists
of dorsal and ventral portions. During embryogenesis, the dorsal
portion persists to form the EAC while the ventral portion
disappears. Persistence of the ventral portion may later result in
the development of a 1st branchial cleft anomaly such as a cyst,
sinus, or fistula. The ectoderm of the medial 1st branchial cleft
begins to invaginate around the 4th week of embryonic development and
lies adjacent to the endoderm of the corresponding 1st pharyngeal
pouch. This pouch subsequently becomes the tympanic cavity. By the
5th week of embryonic development, mesoderm has grown between the
ectodermal and endodermal layers, and ultimately, the tympanic
membrane forms at this site. Invagination of the 1st branchial cleft
toward the tympanic cavity during the 8th week results in formation
of the primary external meatus, and this structure corresponds to the
future lateral third of the EAC. Thickening and extension of the 1st
cleft ectoderm medially during the 9th week forms a solid cord of
cells known as the meatal plate. The meatal plate remains solid
until the 21st week when the medial cells in the plate begin to
degenerate. Recanalization of the developing EAC thus occurs in a
medial to lateral direction and is complete by the 7th month.
Although the tympanic membrane, ossicles, and otic capsule have
reached adult size at birth, the EAC undergoes further developmental
changes from birth through approximately 9 years of age. At birth,
the tympanic membrane is oriented almost horizonatally, and, together
with squama of the temporal bone, form the roof of the EAC. The EAC
is almost straight. The tympanic ring is incompletely fused, and the
floor of the bony canal is only partially ossified, a portion of
which is composed of the lamina fibrosa. The tympanic ring is
completely fused by the age of 2, and the bony canal is completely
ossified by age 3 or 4. Incomplete ossification in the
anteroinferior canal may result in a persitent defect known as the
foramen of Huschke. By about age 9, the tympanic membrane is
oriented at approximately 45 degrees from the horizontal, and the EAC
has developed the characteristic S shape, as seen in the adult.
In the adult form, the EAC is an S-shaped structure approximately 2.5
cm in length. Due the oblique orientation of the tympanic membrane,
the posterosuperior canal wall is approximately 6 mm shorter than the
anteroinferior canal wall. The narrowest portion of the canal is the
isthmus located at the bony-cartilaginous junction. The lateral
portion of the EAC is oriented in a posterosuperior direction, and
the medial portion of the canal is oriented in an anteroinferior
direction. For this reason, pulling the auricle outward, upward, and
backward permits adequate visualization of the tympanic membrane in
The lateral one-third of the canal is composed of an incomplete tube
of elastic cartilage in its anterior, inferior, and a portion of its
posterior walls. The superior and the remainder of the posterior
wall are composed of a bridge of dense fibrous connective tissue
which is adherent to the squamous portion of the temporal bone and is
continuous with the periosteum of the bony canal medially. Two or
three vertically-oriented fissures of Santorini in the anteroinferior
aspect of the cartilaginous canal render it more flexible but also
permit the possible extension of infection from the EAC to the
parotid gland. The medial two-thirds of the EAC is composed of a
complete bony canal in the temporal bone extending laterally from the
tympanic membrane. The tympanic portion of the temporal bone
contributes the anterior and inferior aspects of the bony canal while
the squamous and mastoid portions of the temporal bone contribute the
superior and posterior aspects, respectively.
When examining the EAC, it is important to bear in mind the
anatomical relationship of the EAC to surrounding structures.
Medially, the anterior wall lies adjacent to the temporomandibular
joint, and laterally, it lies adjacent to the parotid gland. The
inferior wall also lies adjacent to the parotid. As previously
mentioned, defects in the EAC wall such as the fissures of Santorini
or the foramen of Huschke may allow pathologic processes originating
in the EAC to reach adjacent structures. The tympanic margin of the
temporal bone is a wedge-shaped portion of bone at the medial end of
the superior canal wall which separates the EAC from the epitympanum.
Laterally, the superior canal wall is separated from the middle
cranial fossa by a thicker bony plate. A thinner bony plate
separates the posterior canal wall from the mastoid air cells.
Keratinizing stratified squamous epithelium lines the EAC. The skin
of the bony canal is thin (approximately 0.2 mm in thickness) and
continuous with the epithelium of the lateral aspect of the tympanic
membrane. Epidermal rete ridges and skin adnexal structures are
absent in the skin of the medial canal as is a subcutaneous layer,
and the skin is adherent to the underlying periosteum of the bony
canal. The skin of the cartilaginous canal is approximately 0.5 to 1
mm thick and contains a well-developed dermis and subcutaneous layer.
Hair follicles are present as are numerous sebaceous and ceruminous
glands (modified apocrine glands). No eccrine sweat glands are
located in the EAC. Large, coarse terminal hairs and small, fine
vellus hairs can be seen and are mostly present in lateral third of
the cartilaginous canal. The glandular secretions combine to produce
cerumen, which is principally composed of lipids.
The blood supply of the medial EAC is provided by the deep auricular
artery, a branch of the internal maxillary artery. The deep
auricular artery enters the canal at the bony cartilaginous junction
and sends a group of vessels medially along the superior canal wall
toward the tympanum, and this comprises the vascular strip. The
lateral canal is supplied by the posterior auricular and superficial
temporal arteries. Venous drainage is via posterior auricular and
superficial temporal veins, which subsequently combine to form the
external jugular vein. Lymphatics typically follow the veins and
drain to parotid and postauricular lymph nodes as well as superficial
cervical nodes along the external jugular vein.
Innervation of the EAC is complex and overlapping. Cranial nerves V,
VII, IX, and X provide contributions. The auricle itself also
receives a portion of its sensory innervation from the cervical
plexus via the great auricular nerve. The auriculotemporal branch of
the mandibular division of CN V supplies the superior and anterior
aspects of the canal, as well as the anterior portion of the tympanic
membrane. The posterior and inferior aspects of the canal are
supplied by CN VII, IX, and X via the auricular branch of the vagus
(Arnold's nerve). Arnold’s nerve branches from the vagus in the
jugular foramen and then enters its own canaliculus within the
temporal bone. It receives contributions from CN VII and IX as it
traverses the temporal bone and then exits the bone via the
tympanomastoid suture or stylomastoid foramen. This complex
innervation mediates clinical phenomena such as referred otalgia from
other structures within the head and neck and the initiation of
coughing during manipulation of the ear canal.
As mentioned previously, the EAC does not merely serve as a simple
conduit for sound. Its physiology is more complex than would be
expected from its usual appearance, and the EAC has important
auditory and nonauditory functions. The structure of the canal and
the physical barriers it presents act to prevent excess moisture and
various foreign bodies from entering the medial EAC. This helps to
maintain the stability of medial EAC environment adjacent to the
tympanic membrane under a wide variety of climatic and other
In terms of its acoustic properties, the EAC has a unique structure
which results in the canal becoming a resonator for frequencies
between 3000 and 4000 Hertz. This augments the transmission of sound
from the environment to the middle and subsequently the inner ear.
Cerumen is primarily a lipid-containing material produced by the
ceruminous or modified apocrine glands of the lateral portion of the
EAC. Under normal circumstances, the cerumen which is produced in
the EAC is usually transported laterally along the canal wall in
conjunction with the normal epithelial migration and is subsequently
extruded. Mechanical disruption of this process, as with a Q-tip or
placement of a hearing aid, may result in formation of a cerumen
impaction. This condition is arguably one of the most common
disorders of the EAC and is treated with cerumenolytics or physical
removal of the inspissated cerumen. The hydrophobic properties of
cerumen render it an important physical barrier to moisture entering
the EAC, and components of cerumen such as lysozyme are thought to
provide antibacterial characteristics to cerumen.
Epithelial migration of the lining of the EAC is a well-known
phenomenon and is essential for the self-cleansing mechanism of this
structure. In most cases, the epicenter of this migratory process
appears to reside in the vicinity of the umbo of the tympanic
membrane. The epithelial migration takes place at a rate of
approximately 0.07mm/day and serves to cleanse the canal of debris,
foreign bodies, and bacteria.
The warm, dark, moist environment of the EAC is ideal for bacterial
growth. The composition of the normal flora of the canal tends to
remain relatively stable and acts as a deterrent to colonization of
the canal by pathologic organisms. Studies of culture results from
normal ears show a predominance of Staphylococcus epidermidis,
Corynebacterium species, and micrococci. A variety of less prominent
bacterial species such as Staphylococcus aureus and assorted Gram
negative bacilli may be found, along with the occasional presence of
a saprophytic fungus. Of note, Pseudomonas aeruginosa is not
typically cultured from normal ears, and its presence suggests
evidence of infection.
EAC Atresia and Stenosis
Congenital aural atresia or stenosis is reported to occur in
approximately 1 in 10,000 to 1 in 20,000 live births. As noted
previously, the external and middle ear structures are derived from
the 1st and 2nd branchial arches and 1st branchial cleft and
pharyngeal pouch. The EAC/tympanic cavity anomalies typically occur
together and microtia may be present. The membranous labyrinth is
derived from the ectodermal otocyst, and cochlear and vestibular
function are usually normal. The vestibular portion of the stapes
footplate derives from the otic capsule, and stapes mobility is
usually present despite deformity of the superstructure. The lateral
ossicles are typically deformed in conjunction with the EAC atresia
or stenosis. These auricular malformations may occur in isolation or
in conjunction with other recognizable craniofacial syndromes, and
when combined with one of these syndromes, a predictable mode of
inheritance is often present. Approximately one-third of the cases
demonstrate bilateral involvement.
For simplicity, these congenital aural malformations may be
classified into two broad categories, major and minor malformations.
This classification scheme is based on auricular and EAC/tympanic
cavity development. Major malformations are those involving absence
of the EAC and tympanic membrane, and EAC stenosis is sometimes
included in this category. The tympanic cavity is often reduced in
size with ossicular deformity. Microtia and abnormalities of the
facial nerve are common. Minor malformations primarily involve
middle ear abnormalities. The tympanic cavity may be normal in size,
but there is absence, deformity, or fixation of the ossicles. The
EAC and tympanic membrane are normal or only slightly reduced in
size, and the auricle itself is normal or only slightly deformed.
Again, facial nerve abnormalities are common.
Surgical correction of these abnormalities may be possible, albeit
quite challenging, depending upon evaluation of the individual
patient. Inadvertent facial nerve or labyrinthine injury during the
procedure are major concerns. The presence of EAC stenosis may
predispose to the formation of canal cholesteatoma.
First Branchial Cleft Anomalies
1st branchial cleft anomalies are rare and represent approximately 1%
of all branchial cleft anomalies. As mentioned previously, these
anomalies are thought to arise as a result of failure of the normal
obliteration of the ventral portion of the 1st branchial cleft. As
with other branchial cleft anomalies, a cyst, sinus, or fistula may
develop. Type I and Type II anomalies are usually described. The
Type I anomaly originates from ectoderm of the 1st branchial cleft
only and represents a duplication anomaly of the membranous EAC. The
usual location is posterior, medial, and inferior to the conchal
cartilage, and there may be an opening into the EAC itself. The Type
II anomaly consists of elements of both ectodermal origin from the
1st branchial cleft and mesodermal origin from the 1st and 2nd
branchial arches. These lesions are usually located in the
anterlateral neck anterior to the sternocleidomastoid muscle and
often have a tract coursing over the mandible and through the parotid
toward the bony-cartilaginous junction of the EAC. The relationship
of this tract with regard to the location of the facial nerve is
These lesions may go undiagnosed for long periods of time and often
come to clinical attention as a result of an infection, which
sometimes requires incision and drainage. Treatment consists of
careful, complete surgical excision with particular attention toward
preservation of the facial nerve.
Local trauma to the epithelial lining may occur as a result of a
variety of insults. There is no end to the types of objects that
patients will place into their ear canals in an attempt to alleviate
a sense of pruritus or remove a piece of real or imagined cerumen.
The ubiquitous Q-tip is not the least of these offenders.
Iatrogenically, overzealous or inappropriate attempts at cerumen
removal or other canal manipulation by the physician may achieve the
same result. Damage to the canal epithelium may lead to abrasion,
hematoma, or laceration. Indeed, perforation of the tympanic
membrane occurs all too frequently. Any disruption of the integrity
of the epithelial protective mechanisms predisposes to the
possibility of infection and otitis externa. Avoidance of
unnecessary canal manipulation of all types is the best treatment.
Any object small enough to fit into the meatal opening of the EAC is
a potential canal foreign body. This is a frequent problem in the
pediatric patient. Inanimate objects, as well as insects, may be
encountered. If the object is small enough to pass the isthmus into
the medial EAC, removal may require additional finesse. Otoscopic or
microscopic visualization and the appropriate instruments are
mandatory for removal of the foreign body. In the uncooperative and
many pediatric patients, sedation or general anesthesia may become
necessary for safe removal. After removal of the foreign body,
careful inspection of the EAC and tympanic membrane should be
performed to assess for any additional injury which needs to be
Temporal Bone Injury
Temporal bone injury with resultant trauma to the EAC may occur as a
result of blunt or penetrating forces. Blunt head trauma may result
in temporal bone fracture, classically described as longitudinal or
transverse based on the orientation of the fracture line in relation
to the long axis of the petrous pyramid. Approximately 80% of
temporal bone fractures are longitudinal and result from a blow to
the lateral aspect of the skull. These fractures usually extend
through the EAC and tympanic membrane into the middle ear then
lateral to the otic capsule and parallel to the course of the
eustachian tube. The fracture line is usually in the posterosuperior
aspect of EAC and may be visible at this site. Conductive hearing
loss predominates, and approximately 20% of the cases involve facial
nerve injury. Transverse temporal bone fractures are usually the
result of trauma to the frontal or occipital aspects of the skull.
EAC injury rarely occurs with this type of fracture. Sensorineural
hearing loss and vestibular symptoms are more common, and facial
nerve injury is seen in approximately 50% of the cases. In patients
suspected of having temporal bone fracture, careful examination of
the EAC may give important clues as to the character and extent of
the injury, and cranial nerve assessment is imperative. Management
is individualized based on the nature of the injuries discovered.
Penetrating temporal bone injuries such as those from stab or gunshot
wounds may be devastating to the auditory and vestibular apparatus,
and the incidence of associated neurovascular injury is substantial,
especially with gunshot wounds. Approximately 50% of gunshot wounds
to the temporal bone involve the EAC. Depending on the nature of the
injury, aggressive management may be necessary in order to prevent
adverse sequelae such as infection or canal stenosis. This may
include debridement, topical therapy with antibiotic and or steroid
preparations, and packing.
As the EAC is a skin-lined cul-de-sac, an extensive variety of
dermatologic disorders may affect this area. Since the majority of
dermatologic therapy is topical and the epithelium of the EAC is
somewhat less readily accessible, some of these lesions may be more
difficult to manage than their counterparts in other epidermal
Acne is the result of obstruction of hair follicles with the
subsequent accumulation of sebum and cellular debris. An open or
closed comedone is the consequence. Should the process become
progressive, extension outside the hair follicle may occur with local
inflammation and possible infection. Severe cases may become cystic
or nodular. The etiology is multifactorial and not fully understood.
The condition is common in adolescence and typically improves with
the passage of time. Topical therapy with preparations such as
benzoyl peroxide, retinoids, and/or antimicrobials is adequate in
most cases and control of infection and inflammation is important to
limit residual cutaneous effects.
Furuncles and Carbuncles
A furuncle is typically a localized infectious process which develops
within a hair follicle in the skin near the junction of the concha
and canal skin. The infection is usually by a Gram positive organism
such as Staphylococcus aureus. Several adjacent lesions may coalesce
to form a carbuncle. The lesions may be quite painful and may result
in EAC obstruction if large. Local care and topical or oral
antibiotic therapy is usually sufficient for therapy, but larger
lesions with sufficient purulent collections may require incision and
drainage if spontaneous drainage does not occur.
Atopic dermatitis is a chronic, generalized dermatitis which displays
intensely pruritic lesions in a patient with a strong personal and
family history of atopy. It may occur in conjunction with allergic
rhinitis or asthma, and the activity of the disease may wax and wane.
Exacerbations or flares may be caused by various allergens or
environmental stresses depending upon the patient. The mechanism by
which atopic dermatitis is not entirely clear but is thought to be
related to alterations in the activity of T helper lymphocytes. The
gross appearance of the lesions themselves is often nonspecific,
especially in the early stages. Erythematous patches with small
papules may be evident in involved areas of the skin with secondary
changes such as excoriations due to the intense pruritus. Spongiosis
or intercellular edema is often visible histologically in the
epidermis of early lesions. When chronic, lesions frequently display
lichenification and other evidence of cutaneous chronic inflammatory
changes. The lesions are also prone to bacterial superinfection with
organisms such as Staphylococcus aureus. Subsequent impetiginization
with formation of characteristic honey-colored crusts may then
follow. Dermatographism can often be demonstrated in these patients
in which mechanical stimulation of the skin produces a wheal and
flare reaction. Onset typically occurs early in life with lesions
present on the face and extensor surfaces. Later on, lesions often
arise on the flexural surfaces such as the antecubital or popliteal
fossae. Topical steroid preparations are the mainstay of therapy,
and antihistamines are an important adjunct to alleviate the
pruritus. Systemic steroids may become necessary to control severe
cases, and topical or oral antibiotics may be necessary where
infection is present.
Contact dermatitis is a localized cutaneous reaction which occurs in
response to contact with an inciting agent. Irritant or allergic
contact dermatitis are the two forms of this disease which may be
distinguished. Innumerable substances may act as irritants which may
result in a localized cutaneous inflammatory response if the degree
of exposure is adequate. These substances range from frankly noxious
stimuli such as acids or alkalis to less obvious items such as
grooming products. Allergic contact dermatitis requires exposure to
an actual initial exposure to an antigenic hapten followed by a
period in which an anamnestic response may be developed. Subsequent
exposure to the inciting agent then produces a magnified response.
Lesions are typicall erythematous, edematous, pruritic lesions which
may display vesiculation or exudate. The lesions cannot be
distinguished histologically from those of atopic dermatitis. The
external ear is a frequent site of involvement. Of note to
otolaryngologists is the fact materials used in the manufacture of
hearing aids and ear plugs are common offending substances, as is
neomycin, a frequent component of many otic preparations. A
sensitivity to neomycin should be suspected in any patient being
treated with one of these preparations for an otitis which is not
improving as anticipated. These patients may also be sensitive to
related antibiotics such as gentamicin. Identification and avoidance
of the offending substance is the treatment of choice.
Seborrheic dermatitis is a chronic inflammatory condition typically
affecting particularly oily areas of the skin. The scalp, face,
ears, or trunk may be involved. Mild cases may range from simple
dandruff to involvement of the periorbital areas about the eyebrows,
nasal alae, and periauricular area, as well as the EAC. Lesions may
be mildly erythematous and slightly raised with a greasy scale. They
may be pink or orange in color and demonstrate thickening of the
plaques and lichenification if chronic. Malassezia furfur, a
lipophilic yeast, is thought to play at least some role in the
development of this condition. Treatment consists of topical
steroids and keratolytics, as well as medicated shampoos for scalp
Psoriasis is a chronic, inflammatory condition affecting
approximately 2 to 5% of the U.S. population, and the external ear
is involved in about one-fifth of the cases. The etiology is unclear
and appears to be multifactorial. The lesions are typically raised,
scaly, and proliferative in nature. Circumscribed erythematous
papules may coalesce to form larger patches with thick scale which is
silver-white in color. Histologically, epithelial hyperplasia is
evident with hyperkeratosis and parakeratosis. Microabscesses are
often present and there is uniform elongation of rete ridges into an
edematous papillary dermis. A superficial perivascular lymphocytic
infiltrate can be seen in the dermis also. Removal of the plaque
often results in pinpoint bleeding known as Auspitz’s sign.
Koebner’s phenomenon describes the formation of lesions induced in
areas of involved skin by minor trauma. Topical therapy suffices in
most patients and consists of topical steroids and tar preparations.
Some patients require ultraviolet phototherapy or photochemotherapy
and systemic therapy with agents such as azulfidine, cyclosporine,
and methotrexate are reserved only for the most severe cases.
Herpes zoster is known to affect the EAC and usually does so in a
unilateral dermatomal distribution. The involvement typically begins
with pain or burning sensation and may be followed by a vesicular
eruption in several days. Adjacent vesicles may coalesce and rupture
to form crusts. The Ramsay Hunt syndrome or herpes zoster oticus
describes herpetic vesicular eruption in the EAC with concomitant
facial nerve involvement resulting in paresis or paralysis.
Treatment is with local care and antibiotics for any secondary
infection. Antivirals such as acyclovir are of benefit, particularly
if the diagnosis is established and therapy is instituted early in
the course of the illness. It has been noted that patients receiving
antiviral therapy experience a significantly more rapid clinical
improvement in the pain associated with this disorder.
Infectious Eczematoid Dermatitis
Eczematoid dermatitis may occur when infectious material from the
middle ear or EAC itself causes inflammation of the epithelium of the
EAC and periauricular skin. The otorrhea can lead to additional
infection and crust formation and requires thorough local care and
Primary (essential) pruritus occurs when a patient has a sense of
itching in the absence of any local or systemic illness which may
cause this symptom. It is important to eliminate the possibility of
these underlying causes (e.g. diabetes mellitus, hepatic or renal
disease, leukemia, lymphoma) to encourage the patient not to induce
local trauma to the canal by scratching. Topical steroid therapy may
Patients with psychiatric disorders which manifest as compulsive
behavior may produce neurotic excoriations by repeated scratching.
The skin of the EAC may become thickened and lichenified by chronic
inflammation. Topical steroids and local care may be of help, and it
may become necessary to treat an infection should it arise.
Other patients display delusions of parasitosis, in which they are
convinced that they have something crawling in their ears or on their
skin. They may complain of intense pruritus, and it is necessary to
rule out infestations or systemic illnesses which may cause this
symptom. Factitial dermatitis may result from a patient
intentionally producing local ear trauma in order to achieve some
secondary gain and should be suspected when no recognizable clinical
pattern to the lesions is apparent.
Bacterial Otitis Externa
Otitis externa is a term which represents a spectrum of inflammatory
changes in the EAC typically of an infectious etiology. The EAC,
with its normal protective and self-cleansing mechanisms intact, is
usually quite resistant to infectious processes. When a local insult
of any nature results in disruption of the integrity of the
epithelium, infectious organisms may gain access to the underlying
tissues and cause an inflammatory response of varying degrees.
The usual offending organisms involved in otitis externa are
Pseudomonas aeruginosa, Proteus mirabilis, Staphylococcus species,
Strepotococcus species, and various other Gram negative bacilli.
Mixed infections are not uncommon, and cultures from the canal are
usually not necessary in the typical case of otitis externa.
Patients may present with complaints of aural pain, itching,
fullness, or decreased hearing. Depending upon the time of initial
presentation, the physical examination may reveal different stages of
involvement, including pre-inflammatory, acute, and chronic stages.
In the pre-inflammatory stage, mild edema and erythema of the canal
are evident. The acute inflammatory stage may further be categorized
as mild, moderate, or severe. These represent a progressive increase
in the degree of edema, erythema, and exudate which are evident in
the canal. It may no longer be possible to visualize the tympanic
membrane. The more severe the involvement, the more likely that
infectious inflammatory changes may extend outside the confines of
the EAC to the adjacent tissues, thus leading to perichondritis,
chondritis, or cellulitis. Recalcitrant cases of otitis externa may
evolve into a chronic inflammatory stage which results in thickening
of the EAC epithelium with scaling and other changes. This
situation, if it persists, could lead to acquired stenosis of the
Effective medical management of otitis externa requires frequent
meticulous cleansing of the canal, appropriate topical or systemic
antibiotic coverage, alleviation of inflammation and pain, and steps
for prevention of future episodes. Aural toilet with thorough
removal of debris and exudate on a regular basis is mandatory.
Antibiotic coverage for Pseudomonas aeruginosa and Staphylococcus
species is necessary and Cortisporin otic suspension and gentamicin
are frequent choices of topical therapy. Oral antibiotic therapy
with penicillinase-resistant penicillins and the cephalosporins often
provide adequate coverage, and the oral fluoroquinolones have been a
valuable addition to the armamentarium. Intravenous antibiotics may
be required in more extensive infections. Topical steroid
preparations and aluminum sulfate-calcium acetate solutions are
beneficial in alleviating inflammation, edema, and crusting in the
EAC. Placement of a wick is often necessary in those instances in
which canal edema is extensive to provide stenting of the canal walls
and topical medications to penetrate the canal adequately. Surgery
therapy is rarely required but may be needed to correct sequelae of
chronic inflammation and prevent recurrence.
Otomycosis results from fungal infections of the EAC and is often
secondary to chronic infections of bacterial origin. Fungal otitis
externa comprises approximately 10% of the cases of otitis externa in
the U.S., and this percentage is even larger in warmer, more humid
areas. Aspergillus and Candida are the most common species.
Patients particularly complain of EAC pruritus, and physical
examination may reveal fungal debris in the canal which may be white,
black, or gray in appearance. Thorough cleansing of the canal is
important in treatment, and administration of topical antifungal
preparations may be necessary to alleviate the infection. Acidifying
agents and drying powders alter the microenvironment of the EAC and
make it inhospitable for fungal growth. Treatment of any other
underlying bacterial infection is important as well.
Bullous Otitis Externa
Bullous otitis externa involves the formation of vesicular or bullous
lesions of the bony canal. The of ten hemorrhagic lesions may
rupture with resultant secondary infection. Pseudomonas may be an
etiologic agent and appropriate topical therapy is indicated with
avoidance of unneccessary manipulation of the canal.
Granular Otitis Externa
Granular otitis externa demonstrates the formation of usually small
lesions of granulation tissue in the EAC. It may occur in the
setting of an untreated or partially treated otitis externa of some
cause and is treated by careful removal of visible granulations and
administration of appropriate topical antimicrobials. In the
diabetic, debilitated, or immunocompromised patient, it is imperative
that this condition be distinguished from necrotizing otitis externa.
Necrotizing (Malignant) Otitis Externa
Necrotizing otitis externa is a serious infection usually encountered
in elderly diabetic, immunocompromised, or otherwise debilitated
patients. Pseudomonas aeruginosa is the pathogen most often
involved. These patients present with persistent otalgia, persistent
otorrhea, granulation tissue in the EAC, and sometimes cranial nerve
involvement, particularly of cranial nerve VII. The granulation
tissue in the canal is characteristically present in the floor of the
canal at the bony-cartilaginous junction. Computed tomography is
study of choice to image the extent of these lesions and gallium and
technetium scanning may provide information in localizing the focus
of infection. The gallium scan will revert to normal with quiescence
of disease, whereas the changes evident on technetium scanning may
lag behind for many months. This disease may progress to frank
osteomyelitis of the skull base if left unchecked. Management must
be aggressive and meticulous with frequent, thorough debridement of
canal granulations and topical as well as systemic antibiotic
therapy. Oral or intravenous antibiotic therapy is based on severity
of infection, and anti-pseudomonal coverage is mandatory. However,
other pathogens may be involved, and therapy is modified based on
culture and sensitivity results. Medical management may suffice if
intervention is early in the course of disease, but more aggressive
surgical therapy may be indicated in recalcitrant cases or those
which are progressive.
Aural polyps are the result of hyperplastic inflammatory
proliferation of middle ear mucosa as a consequence of chronic otitis
media. The polyps may extend into the EAC via tympanic membrane
perforations and even completely obstruct the canal lumen in severe
cases. These are friable masses which, on histology, demonstrate
pseudostratified columnar epithelium often with squamous metaplasia.
The stroma is edematous, and acute and chronic inflammatory cell
infiltrates are evident. Management is by removal and treatment of
the underlying chronic ear disease.
An exostosis is a benign bony growth originating from periosteum,
usually in the bony medial EAC. They are often multiple and
demonstrate a characteristic concentric lamellar bony organization
without intervening vascular tissue. They are often asymptomatic and
are seen in surfers and others with chronic exposure to cold water.
These sessile lesions may become obstructive and lead to conductive
hearing loss, infection, or otalgia.
Osteomas are the most common bony neoplasm of the temporal bone and
are benign, usually pedunculated lesions often seen arising from the
anterior EAC wall at the bony cartilaginous junction. They consist
of fibrovascular tissues covered by a layer of disorganized bony
tissue and present the same symptoms as exostoses. Treatment is the
same for both and consists of complete excision with preservation of
as much of the normal EAC architecture as possible.
Fibrous dysplasia is a disorder of unclear pathogenesis in which
proliferating fibroosseus tissue replaces normal medullary bone. It
is classified as monostotic, polyostotic, and McCune-Albright
syndrome. McCune-Albright syndrome is characterized by polyostotic
involvement with skin pigmentation and endocrinopathies. These white
to red, rubbery, cystic masses are composed of a vascular stroma
surrounding irregularly woven bone. The monostotic form is the most
common, occuring in approximately 70% of the cases. Of these cases,
20 to 25% involve bones in the head and neck. Approximately
one-fifth of head and neck cases involve the temporal bone.
Cholesteatoma formation is the most common complication, and the
disease usually becomes quiescent after puberty. Therefore,
conservative management is most often indicated in the pediatric
Eosinophilic Granuloma (Histiocytosis X)
Histiocytosis X represents an idiopathic group disorders involving
histiocytic proliferation and eosinophilic infiltration in the skull
and other tissues throughout the body. Onset is often in childhood,
and on electron microscopy, the histiocytes demonstrate
characteristic cytoplasmic organelles known as Birbeck bodies.
Eosinophilic granuloma is the mildest, localized form of the disease.
Hand-Schuller-Christian syndrome is more chronic and involves
multiple organs. Letterer-Siwe syndrome entails aggressive,
multisystem involvement and has the worst prognosis. Only about 10%
of patients demonstrate the classic triad of osteolytic skull
lesions, exophthalmos, and diabete insipidus. Approximately 80% of
the cases of eosinophilic granuloma have head and neck involvement.
Temporal bone lesions are bilateral in about 30% of cases and lead to
pain and swelling with otorrhea, canal granulations and edema, and
bony erosions. Localized lesions may resolve spontaneously but
surgical excision with or without adjunctive radiotherapy or
chemotherapy may is often required, depending on localized or
Cholesteatoma and Keratosis Obturans
Canal cholesteatoma is an often cystic collection of squamous
epithelium usually seen in an older age group. Unilateral
involvement with pain, purulent otorrhea, bony erosion, and
periostitis are often present. Topical antibiotic therapy is
administered for supervening infection. Frequent, meticulous
debridement in the office setting is necessary to control the
lesions, and the majority of patients do not require surgical
intervention. Indications for surgery would include failure of
medical management with evidence of impending complication from
extension of the lesion into the middle ear or mastoid, including
conductive hearing loss or facial nerve paresis or paralysis.
Keratosis obturans, an accumulation of squamous debris in the EAC, is
often bilateral in a younger age group and causes pain, canal
hyperemia, and granulation with occasional hearing loss. Thorough
debridement on a regular basis is required to successfully manage
keratosis obturans. Chronic inflammation plays at least some role in
the propagation of these lesions, and it evident that the application
of topical steroid is beneficial in slowing this process.
Ceruminous Gland Tumors Ceruminous gland tumors of the EAC are
relatively uncommon neoplasms. They usually present as polypoid
masses with or without an antecedent history of otorrhea or
infection. The ceruminous adenoma demonstrates normal glandular
structures on histology with hyperproliferation of the myoepithelial
component. These lesions may become obstructive and lead to
complications. They are difficult to distinguish from their
malignant counterparts on clinical grounds, and biopsy is required.
When a mass lesion of the EAC is discovered, perhaps 80 to 90% of the
time it is benign. Unfortunately, when a malignant lesion does
present, it has often progressed to an advanced stage. Symptoms may
mimic those of chronic infection. Otalgia, otorrhea, an EAC mass,
and hearing loss are the most common presenting features. Increased
pain and evidence of bony erosion are indicators which are suspicious
for malignancy. Malignant neoplasms of the ear arise from the EAC in
approximately 20 to 30% of the cases. Furthermore, malignancies of
the temporal bone usually originate from the EAC. The lesions may
arise from the epithelium or its adnexa. Squamous cell carcinoma is
by far the most common histologic type encountered, comprising
approximately 80% of the cases. Glandular neoplasms such as
ceruminal adenocarcinoma occur as well. As already mentioned, these
difficult tumors are often insidious and quite advanced at the time
of diagnosis. The prognosis is usually poor, and the lesions are
very challenging to manage. Metastases are uncommon, and death is
usually the result of extension to vital contiguous structures.
Treatment is based on feasibility of resection with extent of
resection dependent upon extent of tumor involvement. The limits of
resection may include lateral, subtotal, or total temporal bone
resection. Adjuvant radiation therapy may also required, depending
on the extent of the lesion.
The external auditory canal is a more complex anatomic and
physiologic structure than is often initially appreciated. A
thorough understanding of its development, structure, and function is
necessary to rationally manage the wide variety disorders that the
otolaryngologist encounters in this area of the head and neck.
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