Dr. vikas

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 canals.

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

AtresiaAural 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 growthNo mastoid

growth

Normal Atresia

Atresia

Embryology

Mastoid growth affects the facial nerve position

Normal 120o

CurveAcute Curve in

Atresia

Atresia

12/11/201411

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

AtresiaModerate 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

Surgical Considerations

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

Surgical ConsiderationsTiming 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 Merocelwicks 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.

AETIOLOGYInflammation

- 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,)

Meatal surgery (removal of an osteoma)

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.

SurgeryFIBROUS 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.

Pathological conditions

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.

FurunculosisFuruncle of the external auditory canal.

Localized rather than generalized oedema of otitisexterna.

The affected ear is extremely painful, feels blocked and exudes a scanty serosanguinousdischarge.

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 furunculosisinclude 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. Aluminiumacetate 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 recolonizethe 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 myringitisshould 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.

MANAGEMENT OPTIONS

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

DIAGNOSISHistory

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 otitisexterna.

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 externaDEFINITION

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 neoplasticprocess

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

Pseudomonas aeruginosa is the most common pathogen

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 immunocompromisedstate, 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 externais 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 andfindings

Severe otalgiaConductive hearing lossYounger agesOccasionally bilateralAssociation with lung and sinus diseaseCan present with a plugged feeling

OtorrhoeaNormal hearingItchiness or painOlder populationsUsually unilateral

Pathology Keratin plug occluding canalTympanic membrane thickenedEar canal balloonedHyperaemia of canal skin sometimes with granulations

Keratin in random patternTympanic membrane normalLocalized osteitis/erosion of ear canal usuallyPosterioinferior Sequestration of bone

Treatment Removal of plugLocal treatments of granulationsBiopsyMay need continued cleanings

Surgically remove cholesteatoma and abnormal boneGraft with fasciaBiopsy

Differential diagnosis

Wax impaction with infectionNeoplastic disease

Necrotizing otitis externaBenign sequestrumNeoplastic 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 externaType 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 fibrovascularchannels

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

Multiple exostosis osteoma

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

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

•Consider the nature of the foreign body when choosing

management options

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

require surgical removal via

Herpes zoster oticusDEFINITION

Herpes zoster oticus is defined as a herpetic vesicular rash on the concha, external auditory canal or pinnawith a lower motor neurone palsy of the ipsilateralfacial 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

THANK YOU