Detailed Study Notes on Middle Ear Pathologies and Treatments

Eustachian tube Dysfunction

Inability of the Eustachian tube to perform its 3 primary functions: protect the middle ear from pathogens, ventilate the middle ear to regulate pressure, and help drain secretions from the middle ear

symptoms of ETD

otalgia, ear pressure, decreased hearing, tinnitus, disequilibrium and autophony

ETD prevalence

most common in children under 5, males, in Native Americans, and in patients with lower socioeconomic status.

ETD incidence

affects 70-90% of children by age 2, 1% of adults

ETD risk factors

young age, cleft palate, reflux, exposure to tobacco smoke or radiation, history of adenoidectomy

ETD site of lesion

nasal cavity or Eustachian tube itself due to inflammation, peritubal muscles

ETD etiology

Anatomical development: Eustachian tube is 13 mm long and positioned horizontally (10 degrees) in infants and young children. Fully developed adult Eustachian tube reaches 35 mm long and 45 degree angle.

ETD pathology

inflammation of the nasal cavity, middle ear or Eustachian tube leads to obstruction, upper respiratory infection, chronic sinusitis, allergic rhinitis, gastroesophageal reflux, nasal polyps, tabacco use.

Obstruction leads to negative pressure within the middle ear space= TM retraction

Obstruction of the eustachian tube

leads to negative pressure in the middle ear and the TM is retracted

Patulous Eustachian tube

can be caused by extensive weight loss, pregnancy, MS, depletion of peritubal soft tissue mass or change in tissue characteristics. It can’t close as effectively

ETD audiologic evaluation

otoscopy, tympanometry, comprehensive audiometry

ETD medical evaluation

case history, pneumatic otoscopy, rhinoscopy, examination of the nasopharynx (CT and MRI), and tuning fork

ETD audiologic management

typically none unless amplification is needed

Acute ETD

3 months or less

Chronic ETD

greater than 3 months

ETD medical management

oral steroids, intranasal steroid sprays, antihistamines, decongestants, allergy medication, myringotomy and PE tubes, balloon dilation

Otitis media

infection of the middle ear space secondary to eustachian tube dysfunction and inflammation

Otitis media symptoms

hearing loss, otalgia, aural fullness, fever and irritability

Otitis media incidence and prevalence

More common in young children and occurs less frequently in children over 1 year. Incidence of chronic OM with effusion is reported at 15-20%

PE tube prevalence

PE tube placement is the most common ambulatory surgery for children in the US. 670,000 tube insertions annually at an average cost of $2700 per procedure.

Otitis media risk factors

increased rates for children in daycare and pediatric patients in an ICU setting (because lying flat), down syndrome, cleft lip and palate, exposure to tobacco smoke, lower socioeconomic status, use of pacifiers, and family history

OM etiology and pathology

upper respiratory viral infection, ETD, bacterial colonization in the middle ear space that leads to infection.

Eustachian tube anatomy : OM

mucous flows from the middle ear through the Eustachian tube into the nasopharynx, The ET is shorter, wider, and more horizontal in infants and young children, supine position.

Otitis media with effusion

fluid without signs of infection

Acute otitis media

purulent effusion with systemic symptoms, reoccurring AOM if 3+ episodes within 6 months or 4+ episodes in a year.

Chronic otitis media

presence of serious effusion for 30+ days

Chronic suppurative otitis media

persistant inflammation and disease of the middle ear and mastoid cavity- “glue ear”

Otitis media site of lesion

Nasopharynx, eustachian tube dysfunction, middle ear, mastoid, tympanic membrane, EAC

Otitis media audiologic evaluation

otoscopy, tympanometry, comprehensive audiology

Otitis media medical evaluation

pneumatic otoscopy, head and neck exam

Otitis media medical management

Antibiotics, myringotomy and PE tube placement, adenoidectomy and monitoring

Otitis media complications if left untreated

speech/language delay, meningitis, labyrinthitis, petrositis, facial paralysis and mastoiditis

Otitis media complications if treated

blocked tube in 7-10% of ears, myringosclerosis, persistent TM perforation in 1-6% of ears with PE tubes, anesthesia

Tympanic membrane perforation

a hole or tear in the tympanic membrane which connects the external auditory canal to the middle ear space

Tympanic membrane perforation symptoms

otalgia, otorrhea, hearing loss, tinnitus, vertigo

Tympanic membrane perforation incidence and prevalence

incidence is not well established since many heal spontaneously, primarily seen in younger populations, more common in men

Tympanic membrane site of lesion

TM is composed of 3 layers: epidermal, fibrous, membranous

TM perforation audiologic evaluation

otoscopy, tympanometry, comprehensive audiometry, no swimming and no lyric HA

TM perforation medical evaluation

otoscopy, head and neck exam, tuning fork

TM perforation audiologic management

minimal, amplification if chronic, ear mold impressions for custom water protection

TM perforation medical management

observation, water precautions, tympanoplasty: graft placement

Cholesteatoma

a collection of keratin-producing squamous epithelial cells within the middle ear

acquired cholestatoma

collection of squamous epithelial cells that collect either adjacent to or through a comprised tympanic membrane

congenital cholesteatoma

presence of squamous cells within the middle ear with no history of TM perforation, otitis media or ETD

Cholesteatoma symptoms

hearing loss, otorrhea, otalgia, vertigo, facial nerve paralysis, meningitis

Cholesteatoma incidence and prevalence

congenital cholesteatomas occur at a rate of 0.12 per 100,000

acquired cholesteatomas in caucasians about 3 per 100,000 in children, 9.2 per 100,000 for all ages, predominantly in males, more prevalent in caucasian and African populations, more prevalent in less developed countries

Congenital Cholesteatoma Etiology and pathology

remnants of embryonic epithelial cell nests trapped in middle ear during development

Acquired Cholesteatoma Etiology and pathology: Primary

Chronic middle ear inflammation leads to weakening of the fibrous layer of the TM then leads to negative middle ear pressure that retracts weakened TM and debris becomes trapped in a retention pocket that causes further inflammation and granulation tissue develops

Acquired Cholesteatoma Etiology and pathology: Secondary

Epithelial migration through a TM perforation, changes in middle ear mucosa following recurrent infections of the middle ear space

Cholesteatoma etiology and pathology

cholesteatomas tend to expand, tunnel into the middle ear, and erode the bone via: mechanical pressure destruction, biochemical degradation from bacterial toxins of granulation tissue, or cellular absorption of bone

Bacteria in a cholesteatoma

pseudomonas aeriginosa, staphylococcus aureus, escherichia coli, streptococcus epidermidis

Congenital cholesteatoma site of lesion

in the anterior meso-tympanum or protympanum, petrous apex of the temporal bone, epidermoid cyst

Acquired cholesteatoma site of lesion

posterior epitympanic space or “Prussak’s Space”, can easily erode the malleus and short process of the incus, or the anterior aspect of the epitympanic space, can erode the handle of the malleus

Cholesteatoma audiologic evaluation

otoscopy, comprehensive audiometry, tympanometry

Cholesteatoma medical evaluation

case history, otoscopy, tuning fork, imaging

Cholesteatoma audiologic management

amplification, air or bone conduction devices

Cholesteatoma medical management: nonsurgical intervention

close clinical follow up, observation and cleaning of retraction pockets, water precautions, antibiotic drops, PE tube placement

Cholesteatoma medical management: surgical intervention

mastoidectomy: removal of disease process within the mastoid cells

tympanoplasty: cholesteatoma is removed from the middle ear and TM is repaired

Otosclerosis

bone-remodeling disease of the temporal bone that leads to fixation of the stapes footplate

Otosclerosis symptoms

conductive hearing loss, tinnitus, vertigo/dizziness

Otosclerosis incidence and prevalence

most common cause of conductive hearing loss in adults, more common in caucasian patients, more common in women, typically presents in patients 20s-40s

Otosclerosis site of lesion

fistula ante fenestrum, round window, cochlear otosclerosis- spiral ligament

Otosclerosis etiology and pathology

exact etiology is unknown, some theories are genetics, family history, sex, viral infections. Endochondral bone in otic capsule becomes highly vascularized and the bone is resorbed then immature bone develops and becomes spongiotic. Over time this bone becomes sclerotic. When this occurs at the oval window, the stapes footplate becomes fixed and the ossicular chain falls to conduct sound into the cochlea efficiently resulting in conductive hearing loss

otosclerosis audiologist evaluation

otoscopy, comprehensive audiology: low frequency conductive hearing loss with Carhart’s notch at 2000 Hz, word rec, acoustic reflexes (absent)

Otosclerosis medical evaluation

otoscopy: Schwartz’s sign: reddish blush on promontory of TM, tuning fork, imaging

Otosclerosis audiologic management

amplification, cochlear implants

otosclerosis medical management

Stapedectomy, stapedotomy

Stapedectomy

removing a portion of or the entire stapes footplate and replacing a prosthesis from the long process of the incus to a graft on the oval window

Stapedotomy

removal of the stapes superstructure, creating a hole in the fixed footplate, and placing a prosthesis from the incus to the stapedotomy site