External auditory canal anatomy pathologies & management

External Auditory Canal
 The supporting framework of the canal wall is
cartilage in the lateral one-third and bone in the medial
two-thirds.
 Length of the canal is approximately 2.4 cm
 The lateral cartilaginous portion is about 8 mm long
and is continuous with the auricular cartilage.
 The two or three variably present perforations in the
anterior aspect of the cartilaginous canal are the
fissures of Santorini.
 The isthmus is the narrowest portion of the EAC, lies
just medial to the junction of the bony and

 Cartilaginous part is directed upwards, backwards &
medially while bony part is directed downwards, forwards
& medially.
 The canal is straightened by gently moving the auricle
upwards and backwards to counteract the direction of the
cartilaginous portion.
 In the neonate, there is no bony external meatus as the
tympanic bone is not yet developed.
 The tympanic membrane is more horizontally placed so
that the auricle must be gently drawn downwards and

 The medial border of the meatal cartilage is attached to
the rim of the bony canal by fibrous bands.
 The bony canal wall, about 1.6 mm long, is narrower than
the cartilaginous portion and itself becomes smaller
closer to the tympanic membrane.
 The medial end of the bony canal is marked by a groove,
the tympanic sulcus, which is absent superiorly. Although
the tympanic bone makes up the greater part of the
canal, and also carries the sulcus, the squamous bone
forms the roof.
 The tympanomastoid suture is a complex suture line
between the anterior wall of the mastoid process and the
tympanic bone.

 The external canal is lined with skin.
 Body skin normally grows directly from the basal
layers towards the surface where it is shed into the
surroundings.
 If this pattern of growth were to occur in the external
ear canal then the canal would soon become filled
with desquamated skin.
 Instead of maturation taking place directly towards
the surface, there is outward, oblique growth of the
epidermis of the canal skin and pars flaccida so that
the surface layers effectively migrate towards the
external opening of the canal.

Atresia
 Atresia is the absence of or closure of a passage of the body.
 This includes both congenital and acquired lesions.
 TOS defines acquired atresia of the external ear as 'intraluminal
sequelae of either intraluminal or extraluminal processes of varying
aetiology, resulting in a blind sac in the external acoustic meatus'.
Epidemiology
 1 in 10,000 to 15,000 births
 Up to 50% of the time associated with some craniofacial syndrome
 Unilateral : Bilateral, about 3:1
 30% are bilateral
 Atresia : Microtia, 7:1
 Slightly more common on the right
 Male : Female, 2:1

Atresia
Aural atresia associated with craniofacial
syndromes
 Treacher Collins (Mandibulofacial Dysostosis)
 Nager Syndrome (Acrofacial Dysostosis)
 Cruzoun’s Craniofacial Dysostosis
 Goldenhar’s Syndrome
 Hemifacial Microsomia

Atresia
Embryology – 7th Month
 Canalization complete
 Mastoid separation from mandible
Normal posterior-inferior
growth
No mastoid
growth
Normal Atresia

Atresia
Embryology
 Mastoid growth affects the facial nerve position
Normal 120o
Curve
Acute Curve in
Atresia

Classification of Deformities
After Colman-3 types
 Minor Aplasia-incomplete recanalization
 Moderate Aplasia- the tympanic bone has
developed but has failed to recanalize
 Severe Aplasia-complete absence of the external
canal

Atresia
Severe Aplasia- Complete Atresia, no tympanic
bone

Atresia
Moderate Aplasia
 The most common, solid mass of compact bone
that has failed to recanalize

Atresia
Minor Aplasia-partial recanalization
 Middle space constricted, often with severe ossicular
abnormalities

Radiological Evaluation
 High resolution CT in coronal and axial planes
 Axial to delineate malleus, incus and I-S joint and
round window
 Coronal to delineate stapes, oval window and
vestibule
 3-D CT of little help

Atresia Surgery
 First attempt to surgically correct aural atresia
was by Thomson in 1843
 Shambaugh, 1967, recommended unilateral
surgery only if the cochlear reserve allowed
hearing to improve by 25dB
 Jahrsdoerfer, 1978, first large series using the
anterior approach

Surgical Considerations
 Most consider repair in bilateral atresia
 Many are reluctant to operate on unilateral cases
 Not simply the hearing loss
 Expectations of hearing recovery
 Lifetime care of mastoid cavity
 Potential risks to facial nerve and labyrinth
 55-65% achieve 25 dB speech-hearing level

 Most surgeons choose the anterior approach to
avoid the mastoid cavity
 40% of patients with unilateral atresia are not
surgical candidates such as those with severe
aplasia as in Treacher Collins syndrome
 Bilateral atresia- best ear by CT done as child
approaches school age

Timing of surgery
 Usually performed after age 6 or 7 years
 This allows for microtia repair to be done first
 Canal cholesteatoma in the stenotic ear usually
develops in canals less than 2mm in diameter. If
ear unfavorable, canalplasty alone is offered

Surgical Technique
 Minor aplasia- canal widening and middle ear
ossicular work with tympanoplasty
 Moderate Aplasia
 Mastoid or posterior approach
 Anterior approach

Surgical Technique
Anterior Approach
 Middle ear approached through the atretic bone
with a limited mastoid opening

Surgical Technique
 The posterior wall of the
glenoid fossa becomes the
anterior wall of the new ear
canal
 The epitympanum is the first
part of the middle ear
encountered
 Fused ossicles identified

Surgical Technique
 Atretic bone removed at times with a curette
 Globular mass separated from the stapes to
avoid cochlear trauma
 Course of facial nerve determined
 Ossiculoplasty performed
 Tympanic membrane grafted
 Meatoplasty
 Split thickness skin graft (.006-.008 inches) lines
the canal

Surgical Technique
 The Meatoplasty must be aligned with the newly
created bony canal

Surgical Technique
 3cm X 5cm split thickness
skin graft
 The graft is positioned in the
canal and sewn to the
meatal margin
 Graft stabilized with Merocel
wicks and hydrated with ear
drops

MASTOID APPROACH
 This employs a more posterior route to the middle ear
cleft using the dura of the middle cranial fossa, the
sigmoid sinus and sino dural angles as landmarks to
the antrum with subsequent identification of the lateral
semicircular canal (LSCC), atretic plate and the facial
nerve.
 The atretic plate is removed in a similar fashion, trying
to centre the cavity on the stapes.
 The aim is to create a stable, small, cavity lined with
squamous epithelium.

Hearing Results
 Post-op hearing level of 30 dB or better In 50-
75% of patients with moderate or severe aplasia
 20 dB or better in 15-20%
 Bellucci 20 dB in 50% @ 2 years
 Schuknect similar results at 1.3 years
 De La Cruz 56 patients 53% @ 20 dB at 6 mo.
 Lambert early 60% @25 dB, 46% >1 yr.

Alternatives to Surgery
 Bone anchored hearing aid (BAHA)

Surgical Complications
 Persistent or recurrent conductive hearing loss
 Lateralization of graft
 Scar tissue
 SNHL
 VIIth Nerve injury
 30 % revision rate
 Re-stenosis
 Graft migration
 Inadequate hearing
 Chronic cavity infection

Acquired atresia of the
external ear

 Atresias may be
solid or
membranous.
 Solid atresia consists
of a continuous block
of either fibrous or
fibrous & bony
material which is
continuous with the
structure of the
tympanic membrane
and is of variable
extent.
Solid atresia, obliterating the medial aspect
of
the bony external ear canal.
Extensive funnel-shaped solid atresia.

 Membranous atresia is
typified by fibrous tissue
that has a covering of
ear canal skin on both
sides, thus separating
the ear canal into a
medial and lateral
segment.
 The medial part
inevitably collects
keratin from
desquamation of the
skin; this may become
an erosive process and
thus be defined as an
external auditory canal
cholesteatoma.
Membranous atresia in lateral external
auditory meatus.

Diagnosis
 The clinical diagnosis of acquired atresia is
supported by the use of computed tomography
(CT) scanning
 It particularly helps in the differentiation of solid
and membranous atresia.
 Solid atresia is a safe form of ear disease.
 Membranous atresia will inevitably produce
associated cholesteatoma and therefore erosion
of local structure.
 Surgical outcome is superior to solid atresia.

AETIOLOGY
Inflammation
- otitis externa;
- psoriasis, eczema and other dermatological
conditions;
- active chronic otitis media;
- Trauma
- burns, (thermal, chemical, electrical or post-irradiation)
Surgery –
 any operation involving a meatal approach
(tympanoplasty, etc,)

Pathogenesis
SOLID ATRESIA
 In cases associated with otitis externa or media the key
development is of granular medial otitis externa with granulations of
the tympanic membrane that persist for many months in spite of
treatment.
 The granulations become fibrotic and the eardrum thickens as the
medial meatal mass is re-epitheliazed.
 principle complaint is of conductive hearing loss.
MEMBRANOUS ATRESIA
 This originates in the lateral meatus as a web formation, which is
precipitated by a circular irritation from inflammation, trauma or
burns and ulceration of the skin around the entire circumference of
the external ear canal.
 The web-like stenosis forms after fibrosis and re-epitheliazation as
with solid atresias.
 Associated with medial cholesteatoma, which can potentially
produce local erosion and complications.

MANAGEMENT OPTIONS
Medical
 During the wet phase, the medial granulations can
be removed by aspiration and cauterization with
silver nitrate or trichloroacetic acid, and the ear
packed with ribbon gauze or a wick.
 This local treatment may result in a change to the
dry phase and prevent further progression of the
atresia.
 The conductive hearing impairment (if bilateral) may
be managed by hearing aid.

Surgery
FIBROUS ATRESIA
 The principle of surgery in fibrous atresia
is to remove the fibrous tissue by
elevating it from the ear canal bone, the
fibrous annulus and lamina propria of the
tympanic membrane.
 A circumferential incision is made lateral
to the blunt face of the atretic plate and a
plane of dissection developed between
the bone of the ear canal and the canal
skin, followed by the atretic plate and,
finally, lateral to the fibrous annulus and
lamina propria of the tympanic membrane.
 The epithelial defect is repaired by a fine
split skin graft which can be laid in single
or multiple pieces.
 A silastic disc or tube may be inserted to
stabilize the epithelial surface. Finally, the
ear canal is packed with ribbon gauze
soaked in antiseptic.

MEMBRANOUS ATRESIA
 Similar to fibrous atresia, membranous atresia can
be approached transcanal using an ear speculum.
 If the fibrous lesion is very thick a retroauricular
approach may be superior, allowing preservation of
the lateral and medial epithelial coverings to aid
repair of the ear canal skin.
 The whole lesion is excised with sacrifice of the
minimum of surrounding epithelium.
 Silastic sheets are overlaid, holding the lateral and
medial skin edges against the bone of the ear canal.

Furunculosis
 Localized form of otitis externa resulting from infection
of a single hair follicle.
 Hair follicles are only present in the lateral
(cartilaginous) segment of the external auditory canal.
 Furunculosis is, therefore, confined to the lateral
canal.
 Bacterial invasion of a single hair follicle results
initially in a well-circumscribed deep skin infection.
 As the infection progresses a pustule forms and this
progresses to local abscess formation, often with
considerable associated cellulitis and oedema.

Furunculosis
Furuncle of the external auditory canal.
Localized rather than generalized oedema of otitis
externa.
 The affected ear is
extremely painful, feels
blocked and exudes a
scanty serosanguinous
discharge.
 The pinna and tragus
are tender on palpation.
 Otoscopic examination
usually establishes the
diagnosis

 Characteristically, the oedema and inflammation
is restricted to the lateral segment of the canal,
with relative sparing of the medial canal and an
unaffected tympanic membrane.
 If the infection is advanced, the abscess may be
seen to be pointing into the canal or have
discharged already.
 If the oedema and secondary cellulitis spreads to
the post -auricular crease, the condition may be
mistaken for acute mastoiditis.

AETIOLOGY AND EPIDEMIOLOGY
 Staphylococcus aureus is the most common
organism causing furunculosis.
 Leukocidal toxins of S. aureus trigger lysis of
phagocytic cells and may have an important role in
cutaneous infection.
 Local risk factors include heat, humidity, trauma,
maceration.
 Recurrent furunculosis presents as repeated
episodes of infection at multiple sites.
 Conditions associated with recurrent furunculosis
include hypogammaglobulinaemia, diabetes mellitus
and dysphagocytosis.

OUTCOMES
 If untreated, the infection usually progresses to a
localized abscess which then discharges into the
external ear canal.
 With adequate drainage the infection will resolve
spontaneously.
 The infection can also spread towards the deeper
tissues, where it may cause a diffuse soft tissue
infection spreading to the pinna, post-auricular skin
and parotid gland.
 Repeated infection can cause permanent scarring
and fibrosis of the external canal with subsequent
meatal stenosis.

MANAGEMENT
 Furunculosis of the external canal is exquisitely
painful and appropriate analgesics should be
offered to all patients.
 Treatment choices include:
 oral or systemic antistaphylococcal antibiotics
(penicillinase-resistant penicillin, macrolide,
cephalosporin, clindamycin or quinolone);
 topical treatment (antibiotics, astringents,
hygroscopic dehydrating agents);
 incision and drainage.

MANAGEMENT OPTIONS
 Oral antibiotic treatment is recommended in the early
stages of the disease.
 Severe spreading soft tissue infection should be treated
with intravenous antibiotic therapy.
 Abscess formation is an indication for drainage.
 After the abscess has discharged, surgically or
spontaneously, topical treatment is preferable.
 Topical antibiotics are prescribed.
 Insertion of a wick into the ear canal facilitates treatment
in the presence of severe canal oedema and narrowing.

 Glycerol and ichthammol solution has a specific
antistaphylococcal action and is hygroscopic, thus
causing dehydration of the canal tissue. Aluminium
acetate solution is an astringent as well as a
hygroscopic agent.
 Options include:
 eradication therapy with nasal mupirocin;
 eradication therapy with oral flucloxacillin for 14 days;
 bacterial interference therapy:
 Deliberately implanting a nonpathogenic strain of S.
aureus(strain S02A is the most popular) to recolonize
the nares and skin.

BuIlous myringitis
 Bullous myringitis (myringitis bullosa
haemorrhagica) is the finding of vesicles in the
superficial layer of the tympanic membrane.
PATHOLOLOGY
 The vesicles occur between the outer epithelium
and the lamina propria of the tympanic
membrane.

AETIOLOGY
 Cultures from aspirates of the vesicles and middle ear
fluid are similar to that in acute otitis media.
 An infection by influenza virus or by Mycoplasma
pneumoniae has been suggested as the aetiological
agent but no evidence for this, other than circumstantial,
has been presented.
 Bullous myringitis occurs in all age groups but children,
adolescents and young adults are more frequently
affected

SYMPTOMS
 Sudden onset of severe, usually unilateral, often
throbbing pain in the ear is the most common
presentation?
 The symptoms usually set in during or following
an upper respiratory tract infection.
 A blood stained discharge can be present for a
couple of hours.
 Hearing impairment (conductive and/or
sensorineural) is common in the affected ear.

SIGNS
 Otoscopy reveals blood-filled, serous or
serosanginous blisters involving the tympanic
membrane and sometimes the medial aspect of the
ear canal.
 A serosanginous secretion can be seen if the blisters
rupture.
 The tympanic membrane is intact.
 In young children with bullous myringitis, middle ear
fluid was present in the majority (97 percent) but is
an uncommon finding in other age groups.
 The site of the sensorineural hearing loss is the
cochlea; however, the‘ pathogenic base is not
understood.

DIAGNOSIS
 The clinical entity, bullous
myringitis is based on
physical examination.
Vesicles in the superficial
layer of the tympanic
membrane are present.
 The main differential
diagnoses are acute otitis
media or herpes zoster
oticus.
Bullae on the tympanic membrane

Investigations
 Inspection of the ear using a microscope is essential for
diagnosis. Pneumatic otoscopy and tympanometry help
determine whether the middle ear contains fluid.
 Pure-tone audiogram including bone conduction
thresholds is essential for detection of sensorineural
hearing impairment.
 A serologic sample for herpes zoster is of value in cases
with sensorineural hearing loss and may be of help in the
differential diagnosis.

MANAGEMENT OPTIONS
 In cases without middle ear affection and without
sensorineural hearing loss, only analgesics are recommended.
 When the middle ear is affected, antibiotics can be used as in
the treatment of acute otitis media.
 In children less than two years of age, acute bullous myringitis
should be treated as acute otitis media.
 Antibiotics have also been recommended in cases with
sensorineural hearing impairment.
Effect of management
 Spontaneous resolution of the blisters and middle ear effusion.
 Complete recovery of the sensorineural impairment within
three months occurred in between 60 and 100 percent of
affected patients treated with amoxicillin.

Granular myringitis
DEFINITION
 Characterized by granulation tissue on the lateral
aspect of the tympanic membrane with possible
involvement of the external ear canal
 Some authors have suggested there are two
distinct entities:
 Myringitis externa granulosa- has granulations on
the lateral surface of the drum and the medial part
of the ear canal skin.
 Granular myringitis- only involves the eardrum.

PATHOLOGY
 Microscopic examination shows oedematous
granulation tissue with capillaries and diffuse
infiltration of chronic inflammatory cells.
 Large areas of the granulation tissue have no
covering epithelium.
 It has been suggested that a non-specific injury
involving the lamina propria of the tympanic
membrane suppresses epithelialization which leads to
the development of granulation tissue.

AETIOLOGY
 The incidence of granular myringitis is not related to sex,
age, systemic disease or season,
 High-ambient temperature, swimming, lack of hygiene,
local irritants and foreign bodies have all been suggested
as causative factors.
 bacterial and sometimes fungal infection is present in the
affected ear.
 Granular myringitis is also occasionally seen as a
postoperative complication of tympanic membrane
grafting.
 An incidence of up to 5 percent has been reported and the
use of tympanic homo grafts seems to result in a higher
incidence (8 percent).

SYMPTOMS
 The dominant symptom is a foul-smelling
discharge from the affected ear.
 There is usually little or no pain.
 Some individuals have a sensation of fullness or
irritation in the ear.
 The hearing is either not at all or only slightly
impaired.
 Associated tinnitus is uncommon.
 Some patients can be asymptomatic

SIGNS
 Purulent secretion is seen in the affected ear.
 The tympanic membrane is covered with secretions that
sometimes crust.
 After aural toilet the granulation tissue is revealed.
 There seems to be a localized and a diffuse form of
granular myringitis.
 The localized form is most common, in that small areas
of the drum are affected or one or more polyps are
present.
 Most commonly, the granulations are situated
posterosuperior on the eardrum and may affect the
adjacent canal wall.
 A slightly raised carpet of granulations, which covers the
tympanic membrane, is seen in the diffuse form.
 Perforation of the tympanic membrane is not present

Right granular myringitis. (a)
There is pus in the canal but the
pars tensa appears intact.
However, there is granulation
tissue arising from it posteriorly
extending on to the adjacent
canal wall. The intactness of the
pars tensa can be confirmed by
pneumatic otoscopy or
tympanometry.
(b) The ear is active, there being
pus in the canal and granulation

DIAGNOSIS
 In granular myringitis a discharge from the ear is present.
 Inflammation and granulation tissue are seen on the
lateral aspect of the tympanic membrane with possible
involvement of the external ear canal.
 Differential diagnoses are-
 chronic (suppurative) otitis media
 diffuse external otitis.
 Most cases can readily be differentiated by the normal
movement of the tympanic membrane on pneumatic
otoscopy and no signs of an inflammatory reaction in the
lateral ear canal.
 The lack of a conductive hearing impairment and a
normal computed tomography (CT) scan excludes
chronic otitis media.

Investigations
 Inspection of the ear using a microscope is essential for diagnosis
and treatment.
 Pneumatic otoscopy and tympanometry -to confirm that the middle
ear is normal and no perforation is present.
 Pure-tone audiometry - to exclude a conductive hearing impairment
due to chronic otitis media.
 Culture for bacteria as well as for fungi is important in detecting the
pathogens if conservative treatment with ear drops fails.
 Gram-negative bacteria (Pseudomonas aeruginosa, Proteus species
and Staphylococcus aureus) and Candida albicans are most
commonly Cultured.
 The bacterial culture does not differ from specimens found in
external otitis and chronic otitis media.
 HRCT scan can help exclude chronic otitis media.
 biopsy for histological examination should be carried out to exclude
carcinoma. If the granulations do not resolve with treatment,

OUTCOMES, NATURAL HISTORY AND
COMPLICATIONS
 Granular myringitis has a chronic course and
granulations may continue to grow slowly for years;
however, healing may happen spontaneously.
 The inflammation in the epithelial layer and lamina
propria of the tympanic membrane sometimes leads
to replacement with proliferating granulation tissue,
fibrosis and an atresia forming from the medial part
of the ear canal.
 When the fibrosis and atresia has extended laterally,
the atresia ceases to grow.

Benign necrotizing otitis
externa
 Idiopathic necrosis of a localized area of bone of the
tympanic ring, with secondary inflammation of the
overlying soft tissue and skin. There are a number of
synonyms for the condition:
 benign necrotizing otitis externa;
 benign necrotizing osteitis of the external auditorymeatus
canal;
 benign osteonecrosis of the external auditory meatus;
 aseptic necrosis of the external auditory meatus;
 idiopathic tympanic bone necrosis;
 necrosis and sequestration of the tympanic bone;
 necrosis and sequestration of the tympanic part of the
temporal bone;
 focal or circumscribed osteonecrosis of the external auditory

PATHOLOGY
 The pathology is nonspecific.
 The characteristic necrotic sequestrum of bone appears to
involve the superficial cortical layer primarily or
exclusively.
 Histology of the bone reveals dead lamellar bone with
inflammatory cells filling the marrow spaces.
 Usually there are very limited and mild inflammatory
changes of the adjacent skin and soft tissue
(subcutaneous tissue) of the external auditory meatus.
 Apart from the normal skin flora a wide range of bacteria
may be cultured, with Staphylococcus aureus being the
most frequent isolate.

AETIOLOGY
 The cause of this condition is unknown.
 Suggested etiologies include-
 vascular insufficiency because of its relatively poor
blood supply
 The micro angiopathy of diabetes
 Small arterial emboli have been suggested.
 Repeated local trauma is a popular theory, for
example ear bud abuse, picking of the ear or the
use of hearing aids.
 Aassociation with respiratory tract inflammatory
conditions

DIAGNOSIS
History
 The symptoms are characteristic of mild local
inflammation with perhaps pruritis, otorrhea or
otalgia.
 Exclude underlying conditions such as
previous radiotherapy, diabetes mellitus or
systemic disease with depression of the
immune system.
 There should also not be persistent deep
boring otalgia, suggestive of malignant otitis
externa.
Examination
 The condition is diagnosed clinically by the
characteristic positive findings of a small area
of deficient skin and soft tissue in the external
auditory meatus revealing a segment of
necrotic superficial bone.
 The condition is usually unilateral.

 Clinical examination should exclude the
characteristic granuloma and evidence of deep
osteitis of the temporal bone, such as cranial nerve
palsies, found in malignant otitis externa.
 There should be no evidence of an exophytic
tumour and no obstructive collection of keratin
debris expanding the canal as found in keratosis
obturans.
 The bony necrosis is usually limited

Diffrential diagnosis
 (a) Normal external auditory
canal.
 (b) Benign necrotizing otitis
externa. There is deficient
area of skin, and bony
sequestrum.
 (c) Canal cholesteatoma. A
sac of canal skin invades
bone.
 (d) Keratosis obturans. The
bony canal is 'ballooned' out.
 Of these, the condition most
similar to benign necrotizing
otitis externa is canal
cholesteatoma, the only real
difference being the
absence of a lining of

Investigations
 These are seldom indicated.
 If gross infection is present a pus swab may be taken. Should
Pseudomonas be cultured, the diagnosis should be queried in
favour of malignant otitis externa,
 Computed tomography may be indicated in order to identify the
extent of bone necrosis.
 If prominent inflammatory or granulation tissue coexists,
chronic 'granulomatous' conditions including syphilis and
tuberculosis should be excluded.
 Exophytic lesions in the ear canal may require brush cytology
and biopsy to exclude neoplastic conditions.
 Audiometry should be normal unless debris in the external
canal causes a mild conductive hearing impairment.

OUTCOMES. INCLUDING NATURAL
HISTORY
AND COMPLICATIONS
 Separation of the sequestrum, followed by epithial
growth to cover the bony defect, as encouraged by
conservative management, is the most likely
outcome.
 Canal cholesteatoma might be a consequence of
benign necrotizing otitis externa.
 Once there is an area of necrotic bone, squamous
epithelium might grow from the ulcer margins, under
the sequestrum, in an attempt to demarcate the
sequestrum.

MANAGEMENT OPTIONS
 Traditional conservative management consists of
removing the bony sequestrum once it separates
spontaneously with local toilet and local treatment to
control any infection.
 An oral antibiotic may be used.
 A more aggressive surgical approach has been
advocated, with early surgical removal of them
sequestrum down to healthy bone.
 Adjunctive hyperbaric oxygen may be considered
when there is progression despite intensive local
and systemic treatment and when there is necrosis
beyond the tympanic plate.

Malignant otitis externa
DEFINITION
 Malignant otitis externa is an aggressive and potentially life-threatening
infection of the soft tissues of the external ear and
surrounding structures, quickly spreading to involve the
periostium and bone of the skull base.
NOMENCLATURE
 Also called 'skull base osteomyelitis' and 'necrotizing external
otitis'
 It has been suggested that
 necrotizing external otitis should be used for aggressive soft
tissue infection in the absence of bony involvement
 skull base osteomyelitis be used for the condition once bone
infection is confirmed.
 Malignant otitis externa is a misnomer as it is not a neoplastic
process

STAGING
Stage
1 Clinical evidence of malignant otitis externa with infection of soft tissues
beyond the external auditory canal, but negative Tc-99 bone scan
2 Soft tissue infection beyond external auditory canal with positive Tc-99
bone scan
3 As above, but with cranial nerve paralysis
3a Single
3b Multiple
4 Meningitis, empyema, sinus thrombosis or brain abscess

PATHOLOGY
 Malignant otitis externa is the end -stage of a severe
infection thatoriginates from the external auditory canal
and progresses through cellulitis, chondritis, periostitis,
osteitis and finally osteomyelitis.
 Infection is thought to spread out of the cartilaginous
external auditory canal through the fissures of Santorini,
congenital defects in the floor of the external auditory
canal.
 Malignant otitis externa mainly affects the Haversian
system of compact bone and involvement of the
pneumatized portion of the temporal bone is a late
finding.
 The otic capsule is usually spared

Predisposing factors
 Elderly diabetic (both type I and type II) patients
 impaired host response to Pseudomonas
 microangiopathy in diabetic tissues, exacerbated by the vasculitic
properties of Pseudomonas.
 The cerumen in diabetic patients is also of a higher pH than that of
normal controls, which may reduce the bactericidal properties of their
cerumen.
 Non-diabetics accounted for almost a third of one large series.
 Children more commonly have a facial nerve palsy and involvement
of the middle ear.
 Other causes of immunocompromise, especially conditions that affect
cell-mediated immunity (e.g. AIDS), can also predispose to malignant
otitis externa

DIAGNOSIS
 Malignant otitis externa is a clinical
diagnosis made on the basis of pain,
exudate, granulations and oedema of the
external auditory canal , often supported by
a positive bone scan and/or the presence
of microabscesses at surgery.
 The combination of pain, granulations,
otorrhea and resistance to local therapy for
at least eight to ten days are highly
sensitive for making a diagnosis of
malignant otitis externa.
 Diabetes or other immunocompromised
state, Pseudomonas aeruginosa onculture,
a positive bone scan and cranial nerve
palsy are confirmatory factors that enhance
the specificity of the diagnosis.
 The erythrocyte sedimentation rate (ESR)
and C-reactive protein (CRP) levels are
nonspecific measures of inflammation that
are significantly raised in untreated cases.
 The ESR is often over 100 mm/hour.
Malignant otitis externa with granulations
of the floor of the right external auditory
canal

RADIOLOGY
 Technetium (Tc-99m) radio nuclide bone scans will detect bony involvement
even before high-resolution computed tomography (CT) scans can
demonstrate bone destruction.
 As the isotope is absorbed by osteoclasts and osteoblasts that continue
remodelling after the infection has resolved, the scan may remain positive for
up to nine months.
 As such, Tc-99m is only useful for detecting initial bony involvement.
 Gallium (Ga-67) is absorbed by leukocytes and is a more sensitive monitor of
infection.
 The scan quickly returns to normal after the infection has resolved and as
such, is a good measure to ascertain when to terminate treatment.
 In recent years, magnetic resonance imaging (MRI) has added much to the
management of this infection.
 Increased signal in the soft tissues beneath the skull base as a result of
inflammation does much to establish the extent of the disease. In addition, it

MANAGEMENT OPTIONS
Aural toilet
 Local toilet to the external auditory canal is essential to control the
granulations and improve local pain control.
 The use of topical antibiotics is controversial.
 They are likely to alter the microbiological flora of the external auditory
canal and prevent adequate culture and sensitivities at a future date
Systemic antibiotics
 The treatment of choice for the management of malignant otitis externa
is systemic anti-Pseudomonas antibiotics.
 The drug often needs to be given for at least six weeks and in advanced
cases, several months.
 These are often given initially, with transition to oral antibiotics once the
CRP and ESR start to fall.
Hyperbaric oxygen

MANAGEMENT OPTIONS
Surgery
 There is now widespread agreement that surgical
intervention for malignant otitis externa should be
reserved for a few selected cases and no longer has
the goal of removing all the infected tissue.
 Surgery for the removal of sequestra, collections of
pus and debridement of necrotized and granulating
tissues can be beneficial,but should only be used if
the patient is deteriorating clinically and if definable
surgical goals can be easily achieved.

Keratosis obturans and primary auditory
canal
cholesteatoma
 Keratotis obturans is the
accumulation of a large
plug of desquaminated
keratin in the external
auditory meatus, while
primary auditory canal
cholseteatoma is the
invasion of squamous
tissue from the ear into a
localized area of bony
erosion.
The keratoma has been removed from the
right ear with keratosis obturans and
shows expansion of the bony canal just
lateral to the tympanic membrane

Comparison of keratosis obturans and primary auditory canal cholesteatoma.
keratosis obturans primary auditory canal
cholesteatoma
Aetiology Abnormal epithelial migration. Abnormal bone leading to
migration of epithelium into this
bone
Clinical symptoms
and
findings
Severe otalgia
Conductive hearing loss
Younger ages
Occasionally bilateral
Association with lung and sinus disease
Can present with a plugged feeling
Otorrhoea
Normal hearing
Itchiness or pain
Older populations
Usually unilateral
Pathology Keratin plug occluding canal
Tympanic membrane thickened
Ear canal ballooned
Hyperaemia of canal skin sometimes with
granulations
Keratin in random pattern
Tympanic membrane normal
Localized osteitis/erosion of ear
canal usually
Posterioinferior Sequestration of
bone
Treatment Removal of plug
Local treatments of granulations
Biopsy
May need continued cleanings
Surgically remove cholesteatoma
and abnormal bone
Graft with fascia
Biopsy
Differential
diagnosis
Wax impaction with infection
Neoplastic disease
Necrotizing otitis externa
Benign sequestrum
Neoplastic disease

Otitis externa
 Otitis externa is a generalized condition of the skin of the external
auditory canal that is characterized by general oedema and
erythema associated with itchy discomfort and usually an ear
discharge.
Predisposing factors for otitis externa Type Factor
Anatomical Narrow external auditory meatus
Obstruction of normal meatus
DermatologicaI Eczema, sebhorrhoeic dermatitis
Allergic Atopy, nonatopic allergy, exposure to
topical medications
Physiological Humid environment,
immunocompromisation
Traumatic Skin maceration (bathing), ear probing,
laceration, radiotherapy
Microbiological Active chronic otitis media, exposure to
P. Aeruginosa (50-65%) or fungi

PATHOLOGY
 pre-inflammatory stage-protective lipid/acid
balance (normal pH 4-5) of the ear is lost
 acute inflammatory stage-progressively thickening
exudate, further oedema, obliteration of the lumen
and increasing pain.
 chronic inflammatory-thickening of the external
canal skin and fibrous canal stenosis

DIAGNOSIS
clinical diagnosis based on
the following symptoms
and signs: pain, itch,
oedema and erythema of
the external auditory
canal with purulent
otorrhoea and debris in
the meatus
Debris and inflammation in the left external
auditory meatus.
After removal of debris, the swollen
oedematous canal skin of otitis externa can be seen

MANAGEMENT OPTIONS
 Aural toilet-most effective single treatment for otitis
externa
 Topical medication-
 Steroid-antibiotic medication in the form of drops or
sprays
 Glycerol and ichthammol (90:10 percent) aural wick
(dehydrating and antiinflammatory properties and antibacterial activity)
 Systemic antibiotics
Prevention of recurrence-
 avoidance of water penetration into the ear (Cotton wool with
petroleum jelly)

Otomycosis
 Otomycosis accounts for approximately 10
percent of all cases.
 More common in hot, humid climates
 Often secondary to prolonged treatment with
topical antibiotics.
 Diabetes and immunocompromised states also
predispose to the condition.

Otomycosis with Aspergillus niger.
•Aspergillus accounts for 80-90
percent of cases
•Candida being responsible for the
remaining 10-20 percent.
CLINICAL FINDINGS
•The most common finding is black,
grey, green, yellow or white discharge
with debris that is often said to
resemble wet newspaper.
•Sometimes debris is seen with visible
fungal hyphae

MANAGEMENT
 Treatment is aural toilet and removal of the debris
and topical antifungal drops,
 In cases of resistant otomycosis, it is essential to
exclude fungal infection elsewhere, including
athelete's foot.
 The 'foot and ear’ dermatophytid reaction can occur
from a fungal infection in a remote location.
 Immunotherapy with dermatophyte Trichophyton ,
Oidiomycetes and Epidermophyton (TOE) extracts
and dust mite, is the treatment of choice.

Exostoses and Osteoma
 External auditory exostoses and osteomas are
benign clinical entities characterized by
hyperplastic growth of bone in the osseous EAC.
 Both types of lesions are most commonly noted
incidentally in asymptomatic patients.
 However,as EAC obstruction worsens, symptoms
of chronic debris trapping, recurrent otitis externa,
and hearing loss develop.

Exostoses Osteomas
 Bilateral & multiple
 Non-neoplastic bony
outgrowth
 Broadly based protrusions
originating from the
anterior and posterior
canal walls
 Lacks fibrovascular
channels
 EAC obstruction seen.
 Associated with cold
water exposure
 More often unilateral,
 Benign slow growing
tumor
 Pedunculated growth
located at suture lines
 Fibrovascular channels
are present
 lesser degrees of EAC
obstruction.
 Etiology is unknown

DIAGNOSIS
 characteristic otoscopic appearances of multiple and
usually bilateral sessile, hemispherical, bony
swellings arising deep in the external auditory canal,
adjacent to the tympanic membrane.
 In the presence of a tight stenosis of the deep ear
canal, a high resolution computed tomography (CT)
scan will help differentiate large exostoses from other
causes of stenosis, such as chronic otitis externa.
 A scan will also demonstrate complications, such as a
canal cholesteatoma, developing medial to the
exostoses.

MANAGEMENT
 Treatment is usually unnecessary in small
exostoses,
 but advice to avoid further cold water exposure
may be appropriate
 Management of exostoses and osteomas
consists of periodic cerumen disimpaction and
débridement and treatment of infection as
necessary.
 In cases refractory to medical treatment, a
meatoplasty operation may be necessary.

Foreign bodies in the ear
•Consider the nature of the foreign body when choosing
management options
Type of foreign body Method of removal
Living insects First kill with oil
Irregular/graspable objects Remove with crocodile forceps
organic/vegetabIe Do not syringe
Button batteries Do not syringe
Round, hard, smooth,
non-graspable
Syringe/remove with wax hook/removal
under anaesthetic

 Inexpert or ill-advised
attempts at removal may
cause serious
complications such as canal
lacerations, tympanic
membrane perforations and
ossicular fractures or
dislocations.
 Firmly impacted foreign
bodies medial to the
isthmus may warrant
removal in theatre and may

Herpes zoster oticus
DEFINITION
 Herpes zoster oticus is defined as a herpetic vesicular
rash on the concha, external auditory canal or pinna
with a lower motor neurone palsy of the ipsilateral
facial nerve
PATHOLOGY
 The disease is a reactivated varicella zoster infection
from dormant viral particles resident in the geniculate
ganglion of the facial nerve and the spiral and
vestibular ganglia of the VIIIth nerve.
Diagnosis is clinical
 hearing loss, tinnitus and/or vertigo

MANAGEMENT
 Improved outcomes obtained if commenced on
acyclovir and prednisolone within three days of the
onset of symptoms.
Haemorrhagic vesicle in the right external
auditory canal in herpes zoster oticus

External auditory canal anatomy pathologies & management

More Related Content

What's hot

Viewers also liked

Similar to External auditory canal anatomy pathologies & management

More from Vikas Jorwal

Recently uploaded

External auditory canal anatomy pathologies & management