Chronic Middle Ear Diseases: Classification, Etiology, Diagnosis, and Treatment

Chronic middle ear diseases comprise a group of long-standing or recurrent pathological conditions affecting the structures of the middle ear (the tympanic cavity, tympanic membrane, and auditory ossicles). They are characterized by persistent inflammation, presence of fluid (effusion), and structural changes involving the mucosa and osseous structures, frequently resulting in progressive hearing loss.

Chronic diseases of the middle ear include:

• Otitis media with effusion (serous, secretory otitis media) — a disorder characterized by the presence of effusion within the middle ear cavity in the absence of pain. Clinically, it is classified as acute (up to 3 weeks), subacute (3–8 weeks), and chronic (8–12 weeks). However, in practice, it is often difficult to determine the exact onset of the disease; therefore, only acute and chronic forms are generally distinguished;
• Adhesive otitis media — a middle ear disorder characterized by structural changes of the tympanic membrane and its retraction into the tympanic cavity;
• Otosclerosis — an osteodystrophy involving the osseous structures of the middle and inner ear;
• Tympanosclerosis — sclerotic changes affecting the tympanic membrane and the mucosa of the tympanic cavity.

Chronic otitis media with effusion

Etiology of Chronic Secretory Otitis Media

The causes of the disorder are similar to those of acute secretory otitis media (refer to the article «Acute Otitis Media: Classification, Etiology, Diagnosis and Treatment). The principal cause is obstruction of the pharyngeal opening of the Eustachian tube, which may be inflammatory or allergic in nature. Without adequate treatment of the acute secretory otitis media, particularly in the setting of recurrent upper respiratory tract infections, the pathological process becomes chronic.

Anatomy of Chronic Secretory Otitis Media

Against the background of existing effusion within the middle ear cavity, the fluid undergoes further transformation. Over a period of 12–24 months, it gets saturated with protein components, becoming thicker and more viscous, ultimately transforming into a mucoid secretion.

After 24 months, the mucosa undergoes regressive changes, including degeneration of the serous glands and a reduction in the number of goblet cells. Consequently, the fluid component is no longer produced in the same quantity, and mucociliary transport is restored. In some cases, without appropriate treatment, the mucoid material subsequently turns into fibrous bands, eventually resulting in adhesive processes within the middle ear cavity.

Clinical Presentation of Chronic Secretory Otitis Media

Typical symptoms include progressive hearing loss progressing to deafness, as well as tinnitus and a sensation of fullness in the affected ear.

Diagnosis of Chronic Secretory Otitis Media

Patients are evaluated according to the same algorithm used for acute secretory otitis media:

• Otoscopy — the tympanic membrane appears opaque, dull gray, and bulging in its inferior portion; the cone of light is distorted. A continuous level of whitish, opaque material is visible behind the tympanic membrane;
• Tympanometry — performed when middle ear effusion is suspected and serves as the cornerstone of diagnosis. If there is fluid present, the tympanogram corresponds to type B;
• Tuning fork tests — are performed to determine the type of hearing loss;
• Nasopharyngeal endoscopy — is recommended to identify the underlying cause of the disease;
• CT of the temporal bones and nasopharynx — indicated in complex or equivocal cases to clarify the diagnosis and assess the extent of disease.

Treatment of Chronic Secretory Otitis Media

As with acute secretory otitis media, treatment should initially be directed towards the underlying cause of the disease. Because the middle ear contents are highly viscous and have been present for a prolonged period, surgical treatment is recommended if conservative therapy is unsuccessful.

The objective of surgery is evacuation of the effusion and ventilation of the middle ear cavity. A paracentesis is performed with aspiration of the pathological contents. In some cases, a tympanostomy tube (ventilation tube) is inserted to maintain continuous middle ear ventilation and pressure equalization.

Adhesive Otitis Media

Etiology of Adhesive Otitis Media

This condition is a complication of slow-progressing chronic secretory otitis media and recurrent acute otitis media. Eustachian tube dysfunction is also characteristic of adhesive otitis media. Individuals with perennial allergic rhinitis and poorly developed mastoid air cells are particularly susceptible to this disease.

Anatomy of Adhesive Otitis Media

The process develops in the setting of persistent inflammation with effusion in the tympanic cavity. Over time, the pathological contents undergo a series of changes and become organized, with fibrin deposition in the form of adhesions that subsequently become denser and undergo sclerosis.

Scar bands form and fix the structures of the middle ear to one another, particularly:

• tympanic membrane;
• ossicular chain;
• Eustachian tube.

In some areas, the tympanic membrane becomes so severely retracted that retraction pockets develop, which may serve as a source for the formation of a retraction cholesteatoma. As a result, mobility of the sound-conducting chain is reduced, leading to conductive hearing loss.

Clinical Presentation of Adhesive Otitis Media

Patients report marked hearing loss that progressively worsens over time. Tinnitus and crackling sounds in the affected ear may also occur.

Diagnosis of Adhesive Otitis Media

• Otoscopy — the tympanic membrane is thinned and opaque, with scarring and calcifications; cone of light is not visualized. The tympanic membrane is retracted into the tympanic cavity.
• Tympanometry — reduced mobility of the tympanic membrane (type B).
• Audiometry— conductive hearing loss.
• Assessment of Eustachian tube patency — function is reduced.

Treatment of Adhesive Otitis Media

Treatment is aimed at restoring mobility of the tympanic membrane, reducing the amount of scar tissue, and restoring Eustachian tube function.

In the early stages, pneumatic massage of the tympanic membrane is performed, and the Eustachian tubes are insufflated. Proteolytic enzymes and glucocorticoids are administered intratympanically. Nasopharyngeal sanitation is performed, and adenoidectomy is carried out.

In cases of significant impairment or lack of response to conservative therapy, surgical treatment is performed. Scar tissue is excised, and mobility of the ossicles is restored. In advanced cases, tympanoplasty with ossicular prosthesis placement is performed. In cases of Eustachian tube dysfunction, a tympanostomy tube is placed in the tympanic membrane to prevent recurrence.

Otosclerosis

Etiology of Otosclerosis

The etiology of otosclerosis is unknown. The disease occurs more frequently in women aged 30–40 years and may manifest during hormonal changes, such as pregnancy or menopause. The disease has a genetic predisposition. It is believed that otosclerosis is linked to autoimmune processes as well as to the measles virus.

Anatomy of Otosclerosis

The disease is associated with abnormal remodeling of the bone tissue of the ear. The process is more commonly bilateral and may manifest asymmetrically, with changes predominating on one side.

Foci of otosclerosis may develop within the bony labyrinth or be located around the stapes. Healthy cochlear bone undergoes resorption and is replaced by new spongy tissue that is soft and highly vascularized and subsequently becomes sclerotic.

When the process extends to the region of the stapes footplate, pathological bone proliferation develops around the base of the stapes, fixing it to the oval window of the cochlea. Stapes ankylosis impairs sound conduction, resulting in conductive hearing loss.

The development of otosclerotic foci in the region of the scala of the labyrinth causes sensorineural hearing loss.

Clinical Presentation of Otosclerosis

Hearing loss, tinnitus, and a sensation of ear fullness are observed. Patients report difficulty understanding speech, which, however, improves in noisy environments. Symptoms progressively worsen as the disease advances.

Diagnosis of Otosclerosis

• Otoscopy — pathognomonic changes are typically absent. In some cases, thinning of the tympanic membrane is observed, as well as visualization of hyperemic mucosa in the region of the cochlear promontory (Schwartze sign), indicating an active phase of the process. A characteristic feature is a wide external auditory canal with a reduced amount of cerumen or its complete absence.
• Tuning fork tests — performed to determine the type of hearing loss, which may be conductive, sensorineural, or mixed.
• Pure-tone audiometry — performed to accurately determine the type and degree of hearing loss.
• CT of the temporal bones — performed to assess the extent of the process and the condition of the bony structures.

Treatment of Otosclerosis

Surgical treatment with stapedectomy is used to restore hearing. The goal of this procedure is to remove the otosclerotic foci and the affected stapes, followed by replacement with a titanium prosthesis.

Find more scientifically accurate content on our social media

Subscribe and don’t miss out the latest resources

Tympanosclerosis

Etiology of Tympanosclerosis

Tympanosclerosis develops in the setting of chronic suppurative or secretory otitis media, as well as following acute otitis media. A genetic predisposition to the development of tympanosclerosis has been established.

Anatomy of Tympanosclerosis

Sclerotic processes develop as a consequence of a prolonged inflammation in the tympanic cavity. As a result of degenerative and fibroplastic changes in the tympanic membrane and mucoperiosteum, tympanosclerotic (TSC) foci develop within the deep layers of the mucosa.

It is important to note that the mucoperiosteum (the mucous membrane of the middle ear), in addition to lining the bony walls of the tympanic cavity, also covers the ossicles.

Histologically, TSC lesions consist of scar tissue with foci of hyaline degeneration and deposits of calcium phosphate salts. Visually, they appear as dense white, sharply demarcated, “wax-like drops” within the mucosa.

TSC foci restrict the mobility of the tympanic membrane and ossicular chain, impairing sound conduction.

The preferred sites for TSC deposition are narrow, blind-ending areas with reduced aeration. These areas include the attic, the region of the malleus-incus joint, and the area surrounding the vestibular window.

Clinical Presentation of Tympanosclerosis

Patient’s main complaint is hearing loss. In addition, symptoms associated with the underlying disease may be present, including otorrhea, tinnitus, and ear pain.

Diagnosis of Tympanosclerosis

• Otoscopy — characteristic tympanosclerotic plaques may be identified on the tympanic membrane. However, typical changes may be absent in some cases.
• Pure-tone audiometry — demonstrates conductive hearing loss.
• CT of the temporal bones — allows identification of multiple irregular foci of ossification (induration) within the tympanic cavity or tympanic membrane.

Treatment of Tympanosclerosis

Only surgical treatment is used for this condition. Patients undergo tympanic cavity sanitation with tympanoplasty and ossiculoplasty. Complete removal of TSC foci is important to prevent recurrence.