Diagnosis and

Management of External
and middle ear pathology
By Dr Gutu Daba
External ear pathology
 Otitis Externa
• Bacterial infection of external auditory canal
• Categorized by time course
• Acute
• Subacute
• Chronic
Acute Otitis Externa (AOE)
• “swimmer’s ear”
• Preinflammatory stage
• Acute inflammatory stage
• Mild
• Moderate
• Severe
AOE: Preinflammatory Stage
• Edema of stratum corneum and plugging of apopilosebaceous unit

• Symptoms: pruritus and sense of fullness

• Signs: mild edema

• Starts the itch/scratch cycle

AOE: Mild to Moderate Stage
• Progressive infection
• Symptoms
• Pain
• Increased pruritus

• Signs
• Erythema
• Increasing edema
• Canal debris, discharge
AOE: Severe Stage
• Severe pain, worse with ear
movement

• Signs
• Lumen obliteration
• Purulent otorrhea

• Involvement of periauricular soft

tissue
AOE: Treatment
• Most common pathogens: P. aeruginosa and S. aureus

• Four principles
• Frequent canal cleaning
• Topical antibiotics
• Pain control
• Instructions for prevention ( avoid water use)
 Chronic Otitis Externa (COE)
• Chronic inflammatory process

• Persistent symptoms (> 3 months)

• Bacterial, fungal, dermatological etiologies

COE: Symptoms
• Unrelenting pruritus
• Mild discomfort
• Dryness of canal skin
COE: Signs
• Asteatosis
• Dry, flaky skin
• Hypertrophied skin
• Mucopurulent otorrhea
(occasional)
COE: Treatment
• Similar to that of AOE
• Topical antibiotics, frequent cleanings
• Topical Steroids
• Surgical intervention
• Failure of medical treatment
• Goal is to enlarge and resurface the EAC
 Furunculosis
• Acute localized infection
• Lateral 1/3 of posterosuperior canal
• Obstructed apopilosebaceous unit
• Pathogen: S. aureus
Furunculosis: Symptoms
• Localized pain
• Pruritus
• Hearing loss (if lesion occludes canal)
Furunculosis: Signs
• Edema
• Erythema
• Tenderness
• Occasional fluctuance
Furunculosis: Treatment
• Local heat
• Analgesics
• Oral anti-staphylococcal antibiotics
• Incision and drainage reserved for localized abscess
• IV antibiotics for soft tissue extension
 Otomycosis
• Fungal infection of EAC skin
• Primary or secondary
• Most common organisms: Aspergillus and Candida
Otomycosis: Symptoms
• Often indistinguishable from bacterial OE
• Pruritus deep within the ear
• Dull pain
• Hearing loss (obstructive)
• Tinnitus
Otomycosis: Signs
• Canal erythema
• Mild edema
• White, gray or black fungal
debris
Otomycosis: Treatment
• Thorough cleaning and drying of canal
• Topical antifungals
• Acidifying drops
Bullous Myringitis
• Etiology: similar to AOM
• Confined to tympanic membrane
• Primarily involves younger children
Bullous Myringitis: Symptoms
• Sudden onset of severe pain
• No fever
• No hearing impairment
• Bloody otorrhea (significant) if rupture
Bullous Myringitis: Signs
• Inflammation limited to TM &
nearby canal
• Multiple reddened, inflamed
blebs
• Hemorrhagic vesicles
Bullous Myringitis: Treatment
• Management
• Analgesics only: if no middle ear fluid or SNHL

• Antibiotics: if middle ear fluid , SNHL or age <2yrs

Necrotizing External Otitis(NEO)
• Potentially lethal infection of EAC and surrounding structures

• Typically seen in diabetics and immunocompromised patients

• Pseudomonas aeruginosa is the usual culprit

• Extension of infection from the EAC into the temporal bone or skull
base resulting in severe, progressive osteomyelitis
NEO: Symptoms
• Poorly controlled diabetic with h/o OE
• Deep-seated aural pain
• Chronic otorrhea
• Aural fullness
NEO: Signs
• Inflammation and granulation at
bony cartilage jun.
• Purulent secretions
• Occluded canal and obscured
TM
• Cranial nerve involvement
NEO: Imaging
• Plain films
• Computerized tomography – most used
• Technetium-99 – reveals osteomyelitis
• Gallium scan – useful for evaluating Rx
• Magnetic Resonance Imaging
NEO: Diagnosis
• Clinical findings
• Laboratory evidence: ESR
• Imaging
• Physician’s suspicion
NEO: Treatment
• Antibiotic treatment for at least 6 weeks with serial gallium
scans monthly
• Two anti-Pseudomonas antibiotics
• Gentamicin/ Tobramycin+ Ticarcillin/Piperacillin

• Alternative antibiotics
• Mezlocillin or azlocillin, ceftazidime, imipenem, aztreonam, amikacin,
norfloxacin, and ciprofloxacin

• Local canal debridement until healed

• Pain control
• Use of topical agents:acidic, antibiotic or antibiotic steroid com
otic drops

• Aggressive diabetic control

• Surgical debridement for refractory cases
NEO: Mortality
• Death rate essentially unchanged despite newer antibiotics (37% to
23%)

• Higher with multiple cranial neuropathies (60%)

• Recurrence not uncommon (9% to 27%)

• May recur up to 12 months after treatment
Perichondritis/Chondritis
• Infection of perichondrium/cartilage
• Result of trauma to auricle
• May be spontaneous (overt diabetes)

• Symptoms
• Pain over auricle and deep in canal
• Pruritus
Perichondritis: Signs
• Tender auricle
• Induration
• Edema
• Advanced cases
• Crusting & weeping
• Involvement of soft tissues
Perichondritis: Treatment
• Mild: debridement, topical & oral antibiotic
• Advanced: hospitalization, IV antibiotics
• Chronic: surgical intervention with excision of necrotic tissue and skin
coverage
Relapsing Polychondritis
• Episodic and progressive inflammation of cartilages

• Autoimmune etiology?

• External ear, larynx, trachea, bronchi, and nose may be involved

• Involvement of larynx and trachea causes increasing respiratory

obstruction
Relapsing Polychondritis
• Fever, pain
• Swelling, erythema
• Anemia, elevated ESR
• Treat with oral corticosteroids
Herpes Zoster Oticus
• J. Ramsay Hunt described in 1907
• Viral infection caused by varicella zoster

• Infection along one or more cranial nerve dermatomes (shingles)

• Ramsey Hunt syndrome: herpes zoster of the pinna with otalgia and
facial paralysis
Herpes Zoster Oticus: Symptoms
• Early: burning pain in one ear,
headache, malaise and fever
• Late (3 to 7 days): vesicles, facial
paralysis
Herpes Zoster Oticus: Treatment
• Management
• Prednisone 1 mg/kg/day in divided doses for 7 days.
• A gradual taper over the next week is optional

• Valacyclovir 1gm TID for 7 days or

• Famciclovir 750 mg TID for 7days
• Corneal protection
Erysipelas
• Acute superficial cellulitis
• Group A, beta hemolytic
streptococci

• Skin: bright red; well-demarcated,

advancing margin

• Rapid treatment with oral or IV

antibiotics if insufficient response
Non inflammatory diseases and injuries
Deformities and malformations
Prominent ears
Extostosis
Osteoma
Preauricular sinus, pits, cyct, fistula, skin tags
Cerumen and cerumen impaction
 Produced by the cerumineous and sebaseous glands

 Forms a protective film, fattyacids, lysozymes, acidic milleu

 Self cleaning of the ear canal

 Cerumen impaction results from a disturbance of the normal self cleaning

mechanism or excessive secretion

 Sebum, exfoliative debris and contaminants

 Aging –drying of skin and narrow canal
• Sx : pressure sensation, HL, tinnitus, vertigo

• Dx: yellowish brown or dark material, soft or hard on otoscopy

• DDx: cholesteatoma, foreign bodies, tumors, dried blood

• Rx: instrumental removal(hooks or currete) or aural irrigation

Technique
• Hard cerumen can be softened by pretreatment with H2O2, glycerine
drops, olive oil, or detergents

• Bacteriologically pure water at 37 oc, syringe with blunt cannula

• Water jet directed posterosuperiorly

• Followed by otoscopy and hearing test

• CIs : positive otologic hx, single hearing ear affected, restless

uncooperative patient, foreign bodies(Vegtable)
Foreign bodies in the Ear Canal
• Present in both children and adults
• Common objects include erasers, pills, batteries, beads, peas & beans and insects

• Clinical Findings: present with pain, pruritus, conductive hearing loss, and bleeding.

• A persistent foreign body may lead to infection and the formation of granulation
tissue

• Batteries, may cause liquefaction necrosis, low-voltage injury, or pressure necrosis

of the EAC skin or tympanic membrane.
Treatment
• Removal should be done in an atraumatic
manner
• Direct visualization using the operating microscope

• Proper instrumentation (eg, right angle pick, curet,

forceps, and suction)

• Minimizing patient movement

• GA in children's
• Irrigation may help dislodge smaller objects

• 2% lidocaine may be used for the removal of insects

both to achieve topical anesthesia and also to kill the
insect.
Haematoma auris
• is a collection of blood between the auricular cartilage and perichondrium

• Etiology
• Trauma or spontaneous rupture of blood vessels

• while subcutaneous haematomas resorb without consequence,

• Subperichondrial serosanguinous fluid stimulates the proliferation of
mesenchymal cells in the overlying perichondrium, with these chondroblasts
forming new cartilage in seven to ten days which results in 'cauliflower ear'
'wrestler's' ear
• This occurs almost exclusively on the anterior
surface of the auricle where the skin is tightly
adherent to the underlying perichondrium
• so that shearing forces applied to the ear separate
the perichondrium from the cartilage
• Management
• Aspiration
• I & D (organized hematoma w/c occur after 10days)

• In order to prevent recollection

• The use of moulded pressure bandages or splints
• A drain left in the incision site

• A posterior incision, with excision of a disc of cartilage and placement of a suction

drain

• Through-and-through 'mattress' or 'quilting' sutures to apply compression

 Tumors of the external ear
• Basal cell ca: more common on the pinna
• SCC: more common in the EAC
Middle ear Pathology
 OTITIS MEDIA (OM)

• OM refers to an inflammatory process within the middle ear

cleft

• Classified ( acute or chronic >3month)

• The ET appears to be central to the pathogenesis of all forms

of OM
The normal physiologic functions of the ET are to:
• maintain the gaseous pressure within the middle ear cleft at a level
that approximates atmospheric pressure

• prevent reflux of the contents of the nasopharynx into the middle

ear

• clear secretions from the middle ear by both mucociliary transport

and a "pump action" of the eustachian tube.
• ET-dysfunction can be due to
• Anatomic obstruction
• Inflammation of ET mucosa (most common cause)
• Extrinsic compression by tumor or large adenoids

• Functional obstruction
• Failure of the normal muscular mechanism of
eustachian tube opening, as seen in cleft palate
• Insufficient stiffness of the cartilaginous portion of
the ET, often seen in infants and young children
• Other causes of impaired ET function
• More acute angle of the ET seen in children, compared with adults

• Down syndrome: abnormally patent or short ET

• Ciliary dysfunction: Viral infection, bacterial toxins, or inherited abnormalities

of ciliary structure, can predispose to OM
Classification of Otitis Media

Acute Otitis Media

• Suppurative
• Nonsuppurative
• Recurrent
Chronic Otitis Media
• Suppurative
Tubotympanic
Cholesteatoma
• Nonsuppurative
Otitis media with effusion
 Acute Otitis Media

• AOM is one of the most common infectious diseases seen in

children, with its peak incidence in the first 2 years of life

• Most of the population will suffer at least one episode of

AOM at some point in their childhood.

• Recurrent AOM is defined as >=3 episodes of acute

suppurative OM in a 6-month period, or >=4 episodes in a
12-month period, with complete resolution of symptoms and
signs between the episodes.
 Factors Relevant to the Epidemiology of Otitis Media

Environmental Factors
• Day-care attendance
• Not being breast-fed
• Exposure to tobacco smoke
• Seasonal variation in respiratory infections

Host Factors
• Genetics
• Immunodeficiency
• Birth defects
Cleft palate
Down syndrome
 Pathogenesis
• Abnormal function of the ET is the cornerstone of the pathogenesis of
OM
• In most cases of AOM, an antecedent viral URTI leads to edema and
congestion of respiratory mucosa of the ET and middle ear

• ET-obstruction & dysfunction

• Increase in -ve middle-ear pressure, causing an influx of bacteria and viruses
from the nasopharynx when the ET opens

• The bacteria and viruses in the middle ear then elicit an inflammatory
response

• Inflammation of the middle ear mucosa results in an effusion

• This effusion provides a favorable medium for proliferation of bacterial
pathogens
• Many studies, using tympanocentesis, have identified the most
commonly responsible organisms
• Streptococcus pneumoniae (30- 50%)
• Haemophilus influenzae non-typable(25–30%)
• Moraxella catarrhalis (10–20%)
• group A streptococci (1- 5%)

• Less frequently identified pathogens include

• Staphylococcus aureus
• G-ve organisms such as Pseudomonas aeruginosa, Escherichia coli, Klebsiella
species
Symptoms and Signs
• Before the onset of symptoms of AOM, the patient frequently has
symptoms of an URTI

• Older children usually complain of earache, whereas infants

become irritable and pull at the affected ear.

• A high fever is often present and may be associated with systemic

symptoms of infection, such as anorexia, vomiting, and diarrhea.

• Otoscopy classically shows a thickened hyperemic tympanic

membrane, which is immobile on pneumatic otoscopy

• Tympanic membrane perforation with otorrhea

 Differential Diagnosis
• Chronic suppurative otitis media (CSOM)

• Otitis externa

• Referred otalgia

• Meningitis
 Treatment
Nonsurgical Measures
Watchful Waiting
• >=2-year-old children with non-severe illness (mild otalgia and fever < 39
°C)
• not recommended for children < 2 years old if AOM is certain

Antibiotic Therapy
• Amoxicillin (80 mg/kg/d given in three divided doses for 10 days)
remains the first-line therapy
• In resistant cases, amoxicillin should be given in combination with
clavulanate

Adjunctive Therapy
• analgesics and antipyretics.
• decongestants
Surgical Measures
• Myringotomy

Prognosis
• The vast majority of uncomplicated episodes of AOM resolves without any adverse
outcome.

• If this effusion persists for more than 3 months, then a diagnosis of OME should be made.

• Of patients who develop a perforation of the tympanic membrane with otorrhea, a small
proportion go on to develop CSOM because of the failure of the tympanic membrane to
heal.
Prevention
• Prophylactic antibiotics:
• recommended for recurrent AOM
• once-daily oral amoxicillin at 20 mg/kg/d

• A pneumococcal vaccine for age< 2 years and >2

years who are at a high risk of recurrent AOM

• Tympanostomy tubes
• Adenoidectomy
Acute mastoiditis with subperiosteal abcess

Causes:
• Inadequate treatment of AOM,
• when the pathogens are very virulent
• when the patient has low resistance.

• It can also occur after an acute exacerbation of an

otitis media with cholesteatoma.

• The suppurative process spreads from the middle

ear to the mastoid and with faulty drainage causes
bone necrosis of the mastoid cells.
Signs and symptoms:
• increasing fever and illness
• increasing pain, especially over the mastoid area

• tender, fluctuating swelling and redness over the mastoid area causing the pinna to
protrude

• profuse discharge from a perforation of the ear drum or a bulging ear drum without
discharge

• often swelling or sagging of the posterior-superior part of the ear canal near the ear
drum
Treatment:
• Ceftriaxone and metronidazole IV
•I&D
• Mastoidectomy
OTITIS MEDIA WITH EFFUSION (OME)

Causes:
• blockage of the ET by an URTI (rhinitis, sinusitis),
allergic rhinitis, adenoid hypertrophy,
epipharyngeal tumour.

• OME mostly occurs in children below seven, but

also in HIV-positive adults with
lymphadenopathy and re-growth of the
adenoid.
Signs and symptoms:
• CHL
• feeling of ear pressure,
blocked ear
• sometimes ear-ache
• tinnitus
• retracted ear drum with
middle ear effusion,
sometimes with air
bubbles and a visible
fluid level (hair line)
Treatment:
• Treat URTI
• Most resolve spontaneously after some months

• Refer the patient, if the middle ears don’t clear up and the hearing
impairment persists after 3 months.
• adenoidectomy with grommet insertion
Chronic Suppurative Otitis Media
(Tubotympanic)
General Considerations
• is defined as a persistent or intermittent infected
discharge through a nonintact tympanic membrane
(ie, perforation or tympanostomy tube).

• Chronic perforation of the tympanic membrane can

occur without suppuration and is often referred to as
"inactive" CSOM.

• particularly prevalent in developing countries and is

more common in lower socioeconomic groups in the
developed world.
Pathogenesis
• Persistent of TM perforation in AOM
• association between OME and chronic
perforation

• After the extrusion of ventilation tubes

• Traumatic perforations

• The most commonly isolated bacteria responsible

for CSOM are P aeruginosa, S aureus, and the
Proteus species.
• Two main mechanisms by which a chronic perforation can lead to
continuous or repeated middle ear infections:

(1) Bacteria can contaminate the middle ear cleft directly from the
external ear because the protective physical barrier of the tympanic
membrane is lost.

(2) The intact tympanic membrane normally results in a middle ear

"gas cushion," which helps to prevent the reflux of nasopharyngeal
secretions into the middle ear via the eustachian tube.
Symptoms and Signs
• Otorrhea, hearing loss.
• polyp or granulation tissue formation

• Pain is not a usual feature of CSOM and its presence

should alert the physician to the possibility of a more
invasive pathology.
• Edematous middle ear mucosa

Special Tests
• A swab of the discharge for culture and sensitivity

• An audiologic evaluation
• CT scan; cholesteatoma, intracranial extension
Differential Diagnosis
• Cholesteatoma
• Chronic granulomatous conditions such as
Wegener granulomatosis, mycobacterial
infection, histiocytosis X, and sarcoidosis

• Pain is not usually a prominent feature of CSOM,

and its presence should raise the possibility of
necrotizing otitis externa (particularly in the
immunocompromised, eg, AIDS patients or
elderly diabetics) or a malignant neoplasm of the
eternal canal or middle ear.
Nonsurgical Measures

Aural Toilet: mopping, suctioning

Topical Antibiotics
• Topical antibiotics are more effective than
systemic antibiotics in the treatment of CSOM
• Topical antipseudomonal flouroquinolones

Systemic Antibiotics
• Systemic antibiotics tend to have a poor
penetration of the middle ear and are therefore
less effective than topical antibiotics.
Surgical Measures
• Tympanoplasty

• Tympanomastoid Surgery
• If refractory to medical treatment
• Cholesteatoma

• The aims of this procedure

• To aerate the middle ear and mastoid
• Remove chronically inflamed tissue
• Repair the tympanic defect
• Reconstruct the ossicular chain
Complications of OM
• Intratemporal complications include
• Mastoiditis
• Petrositis
• Labyrinthitis
• Facial nerve paralysis

• Intracranial complications include

• Extradural abscess
• Brain abscess
• Subdural abscess
• Sigmoid sinus Thrombophlebitis,
• Otic hydrocephalus
• Meningitis.
Impending signs of complications
• Persistence of infection for greater than 2 weeks

• Recurrence of symptoms within 2 weeks

• acute exacerbation of a chronic infection

• fetid discharge during treatment, and infection with H. influenza, type B or

anaerobes.

• fever associated with a chronic perforation,

• Pinna that is displaced inferolaterally and/or edema of the
posterosuperior canal wall skin

• Retro-orbital pain on side of the infected ear(petrositis), vertigo and

nystagmus in a patient with an infected ear(labryrinthitis)

• facial paralysis on the side of an infected ear

• headache or lethargy, papilledema, meningismus, or focal neurological

signs or seizures.
Cholesteatoma
• Named by Johannes Mueller in 1838
• Erroneous belief that one of the primary components of the tumor was fat
• “a pearly tumor of fat…among sheets of polyhedral cells”

• More appropriate name has been suggested to be keratoma to

describe tumor composition
Cholesteatoma
• Expanding lesion of the temporal bone composed of
• Cystic content: desquamated keratin center
• Matrix: keratinizing stratified squamous epithelium
• Perimatrix: granulation tissue that secretes multiple
proteolytic enzymes capable of bone destruction

 May develop anywhere within pneumatized portions

of the temporal bone
Most frequent
locations:
Middle ear space
Mastoid
Cholesteatoma
Classification
• Congenital
• Acquired
• Primary
• Secondary

Cholesteatoma Formation
 Multiple theories proposed regarding etiology
behind tumor formation
 Proposed mechanisms remain theories
Congenital Cholesteatoma
• Pathogenesis theories
• Failure of involution of ectodermal epithelial thickening that is present during
fetal development in proximity to geniculate ganglion

• Metaplasia of the middle ear mucosa

Congenital Cholesteatoma
Anterosuperior > Posterosuperior
quadrant quadrant
Primary Acquired Cholesteatomas
• Ultimately form due to underlying Eustachian tube dysfunction that
causes retraction of pars flaccida

• Results in poor aeration of epitympanic space which draws pars flaccida

medially on top of malleus neck, forming retraction pocket

• Normal migratory pattern of the tympanic membrane epithelium altered by

retraction pocket

• Enhances potential accumulation of keratin

Patient Evaluation
• Hearing evaluation to assess for conductive hearing loss
• Pure tone audiometry with air and bone conduction
• Speech reception thresholds
• Word recognition

• 512Hz tuning fork exam

• Always correlate with audiometry results

• Tympanometry
• May suggest decreased compliance or TM perforation
Patient Evaluation
• Preoperative imaging with computed tomographies (CTs) of temporal
bones (2mm -section without contrast in axial and coronal planes)

• Allows for evaluation of anatomy

• May reveal evidence of the extent of the disease
• Screen for asymptomatic complications
Patient Evaluation
• Preoperative counseling is an absolute necessity prior to surgery

• Primary objective of surgery is a safe dry ear which is accomplished

by:
• Treating all supervening complications
• Removing diseased bone, mucosa, granulation polyps, and cholesteatoma
• Preserving as much normal anatomy as possible

• Improvement of hearing is a secondary goal

Patient Evaluation
• Possible adverse outcomes must be discussed
• Facial paralysis
• Vertigo
• Further hearing loss
• Tinnitus

• Patient should understand that long-term follow-up will be necessary

and that they may need additional surgeries
Preventative Management
• Tympanostomy tube for early retraction pockets

• Surgical exploration for retraction persistence

Surgical Management
Mastoidectomy

• Canal-wall-down procedures (CWD)

• Canal-wall-up procedure (CWU)

Atticotomy
Cholesteatoma Sequelae
• Infection
• Otorrhea
• Bone destruction
• Hearing loss
• Facial nerve paresis or paralysis
• Labyrinthine fistula
• Intracranial complications

Complications are caused by expansion and infection

 Otosclerosis
• Primary metabolic bone disease of the otic capsule and
ossicles

• Results in fixation of the ossicles and conductive

hearing loss

• May have sensorineural component if the cochlea is

involved

• Genetically mediated
• Autosomal dominant with incomplete penetrance (40%) and
variable expressivity
Epidemiology
• Clinical otosclerosis – 2:1 (W:M)
• Possible progression during pregnancy (10%-17%)
• Bilaterality more common (89% vs. 65%)
• Age:15-45 most common age range of presentation
Pathophysiology

• Osseous dyscrasia
• Resorption and formation of new bone
• Limited to the temporal bone and ossicles
• Inciting event unknown
• Hereditary, endocrine, metabolic, infectious, vascular, autoimmune, hormonal
Pathology
• Two phases of disease
• Active (otospongiosis phase)
• Osteocytes, histiocytes, osteoblasts
• Active resorption of bone
• Dilation of vessels
• Schwartze’s sign

• Mature (sclerotic phase)

• Deposition of new bone (sclerotic and less dense than normal bone)
Pathology
• The most common type involves the stapes footplate
• Fissula ante fenestram: anterior to OW (anterior focus), the most common
site

• OW niche (obliterative OS): progressive involvement, completely obliterate

the OW niche

• Circumferential OS: around the margin of the foot plate

• RW (30%); complete closure is uncommon
Clinical presentation
• Slowly progressive hearing loss over a period of years
• CHL: primary presentation (maximum of 50 - 60 dB)
• SNHL
• MHL

• Patients may describe hearing speech more easily in noisy situations

• The CHL improves the signal to noise ratio by subduing background noise
(paracusis of Willis)

• Tinnitus is present in 75% of patients

• Dizziness occurs in up to 30%
• Otoscope finding
• Normal TM
• Schwartze sign

• Tuning fork examination should confirm a CHL

• The amount of air-bone gap required to flip the forks are about
• 10 -15 dB for the 256 Hz tuning fork
• 20 - 25 dB for the 512 Hz tuning fork
Differential Diagnosis
• Ossicular discontinuity
• Congenital stapes fixation
• Malleus head fixation
• Paget’s disease
• Osteogenesis imperfecta
• Superior semicircular canal dehiscence
Management Options
• Medical: Sodium Fluoride, biphosphonates

• Amplification

• Surgery: Stapedectomy vs. partial stapedectomy vs. stapedotomy

• Combinations