Also known as chronic catarrhal or fibrous otitis media. Adhesions are mostly located in the posterior part of the middle ear, with the tympanic membrane thickening and adhering to the promontory. The ossicles may be partially or completely adhered around the oval window, with fibrous tissue embedding the stapes and the long process of the incus together on the oval window, which may be partially or completely sealed. Histological examination reveals dense fibrous tissue beneath the mucosal epithelium, which may contain calcification or new bone formation, though much less than tympanosclerosis, making pathological differentiation difficult. The ossicles may also be partially absorbed, leading to ossicular chain discontinuity. Ojala (1953) classified adhesive otitis media into the late stage [third stage]: (1) Acute eustachian tube inflammation: Eustachian tube obstruction leads to negative pressure in the tympanic cavity and fluid exudation. (2) Exudate organization: Adhesions form, with mucosal edema in the middle ear and mastoid air cells, and the exudate containing cholesterol crystals. The mastoid air cells become filled with connective tissue. (3) Mastoid air cell gas absorption: The bony structure of the air cells is absorbed. Early-stage eustachian tube edema and obstruction may resolve in the late stage [third stage], restoring patency. MacNaughtan (1956) suggested that treating acute otitis media solely with antibiotics while neglecting tympanic membrane drainage is the primary cause of middle ear adhesions. Buckingham (1969) proposed that eustachian tube dysfunction is the main contributing factor to the disease.

History of otitis media, bilateral hearing loss, tinnitus, but vertigo is rare. The tympanic membrane is rarely normal, often thickened, opaque, with an uneven surface and disappearance of the light cone. Mobility is limited, sometimes atrophic and thin, sometimes with calcified ecchymosis outside the scar, inward invasion adhesion, and occasionally adhesion to the promontory resembling a large perforation. Conductive deafness, sometimes mixed deafness, due to severe adhesion of the tympanic membrane, making acoustic impedance testing of little value. Mastoid X-rays show few mastoid air cells, opacity, and sometimes semicircular canal shadows.

bubble_chart Diagnosis

Otosclerosis has a family history, conductive deafness without a history of otitis media, normal tympanic membrane, an As-type compliance curve on tympanometry, normal mastoid on X-ray, and patent Eustachian tubes. This condition is difficult to distinguish from tympanosclerosis and is often diagnosed through exploratory tympanotomy.

bubble_chart Treatment Measures

The surgical outcome is poor; the Eustachian tube must be patent, otherwise the surgery will definitely fail.

An endaural incision is adopted, and tympanoplasty is performed as appropriate. Under the microscope, the tympanic membrane is carefully separated from the promontory without tearing. After separation, a thin silicone membrane or gelatin sponge is used as a spacer to prevent readhesion. Topical cortisone solution may be applied. Six months later, an intermediate stage [second stage] surgery is performed for ossiculoplasty, such as prosthesis replacement or ossicular grafting. Fenestration may also be attempted. In short, the therapeutic effect is uncertain.