Chronic OM, Mastoiditis, Petrositis Flashcards
Leading cause of childhood hearing loss
Persistent OM with effusion
Infectious complications of OM (3)
Acute and chronic mastoiditis, petrositis, intracranial infection
Noninfectious complications of OM (4)
TM perforation, Ossicular erosion, labyrinthine erosion, tympanosclerosis
Patients with history of chronic OME: Hereditary theory
Hypoaeration of the mastoid is more prone to OME
Patients with history of chronic OME: Environmental theory
Chronic OME resulrs in hypopneumatization of the mastoid
Pathophysiology of decreased size of mastoid air cells in OM
Chronic inflammation in early childhood leads to new bone formation within the middle ear and mastoid leading to decrease size of mastoid air cells
A) Atelectasis vs B) Adhesive OM: 1) Middle ear space, 2) TM status, 3)Mucosal surfaces
A1 partially or completely obliterated 2 not adherent to medial wall of middle ear 3 intact mucosa; B1 totally obliterated, adherent to medial wall of the middle ear, mucosal surfaces not present
Pathophysiology of atelectasis
Repeated bouts of AOM leads to weakness and thinning of the membrane, allowing atelectasis
Severe retraction of the TM can erode: (2)
Long process of incus, stapes superstructure
Sade and Berco 4 stages of TM retraction
1) retracted, 2) attached to incus, 3) middle ear atelectasis, 4) adhesive OM
Judicious use of these can potentially reverse middle ear atelectasis
Ventilating tubes
Cholesteatoma resemble these (why it is a misnomer)
Cholesterol crystals * Do not contain cholesterol
Otorrhea from infected cholesteatoma is often malodorous due to frequent infection of this kind of bacteria
Anaerobes
Complications of cholesteatoma (5)
Vertigo, hearing loss, labyrinthine fistula, FN paralysis, intracranial infection
Typical location of attic retraction cholesteatoma
Posterosuperior TM
Differential diagnosis for aural polyp in a chronically infected ear
Cholesteatoma
Origin of congenital cholesteatoma
Originates from areas of keratinizing epithelium within the middle ear cleft
Pathogenesis of acquired cholesteatoma (4)
Invagination of TM, Basal Cell Hyperplasia, Epithelial Migration, Squamous Metaplasia of Middle ear epithelium
How attic cholesteatomas form, pars flaccida retraction pockets deepen due to negative middle ear pressure, possibly repeated inflammation. Desquamated keratin cannot be cleared from the recess resulting in Cholesteatoma
Invagination Theory
Usual area of TM affected by retraction and why?
Pars flaccida, less fibrous, less resistant to displacement
Presence of these in the cholesteatoma matrix can lead to epithelial proliferation and invasion of the cholesteatoma
Bacterial biofilms
Epithelium invasion to the lamina propria by proliferating columns of epithelial cells due to alterations in basal lamina
Basal cell hyperplasia
Keratinizing squamous epithelium from surface of the TM invades or migrates into the middle ear from a perforation
Epithelial Invasion * Once in contact with a different epithelial surface, they stop migrating. Due to inflammatory damage to the innert mucosal lining of the TM, outer keratinizing epithelium migrates inward to create a cholesteatoma
Metaplastic transformation of simple squamous or cuboidal epithelium of middle ear into keratinizing epithelium, enlarging with accumulated debris and contact with TM, causing TM lysis with subsequent perforation
Squamous Metaplasia
Most common bacteria in cholesteatoma (3)
Pseudomonas, S. Aureus, Anaerobic cocci (Peptococcus, Peptostreptococcus)
Goals of cholesteatoma surgery (2)
Eradicate disease first, then reconstruct hearing mechanism of middle ear
Consideration and kind of ear surgery depends on (7)
Nature and extent of the diseade, complications, mastoid pneumatization, ET function, hearing status, patient reliability, skill and experience of surgeon
Simple perforation manifests as what type of hearing loss (frequency? type?)
Low frequency conductive
This depends on the free movement of gases from the eustachian tune into the mastoid air cells.
Aeration * Gases must travel around the ossicles in the epitympanum to get into the antrum
Edema and inflammation of mucosa between these 2 corridors can lead to chronic obstruction and infection of the attic leading to irreversible mucosal and bony changes in the antrum and mastoid
Between tendon of tensor tympani and stapes, between short process of incus and stapedial tendon
Aside from cholesteatoma, presence of this tissue can also lead to bony erosion
Granulation tissue
