Middle ear effusion represents one of the most common causes of conductive hearing loss. The amplification and transmission functions of the tympanic membrane and ossicles are impeded by fluid in the middle ear space. Some of the causes of middle ear effusions are listed in Table 6-2. Typical examination findings include a tympanic membrane that appears to be dull yellow or amber. An air-fluid level or bubbles may be seen behind the eardrum. With chronic, refractory effusions, extravasation of blood into the middle ear can give the eardrum a bluish color.

Treatment of otitis media with effusion depends on the cause. Eustachian tube dysfunction is most frequently an underlying factor and may be caused by immature tubal anatomy or eustachian tube obstruction in the nasopharynx. Factors that
may lead to eustachian tube dysfunction and middle ear effusion are allergic rhinitis, nasopharyngitis, adenoiditis, recurrent otitis, sinusitis, postsurgical nasopharyngeal scarring, cleft palate, or malignant tumor of the nasopharynx. Malignant nasopharyngeal tumor must always be ruled out in cases of recurrent unilateral otitis media in adults. Most cases of chronic middle ear effusion result from eustachian tube dysfunction without physical obstruction. Treatment usually involves antibiotic therapy and watchful waiting. Most patients improve without further treatment. If the effusion persists, the ventilatory function of the eustachian tube is replaced by insertion of a temporary or permanent tube (pressure-equalizing tube) in the tympanic membrane after the middle ear fluid is removed through an incision in the membrane (myringotomy).

Acute otitis media usually results from obstruction of the eustachian tube caused by an upper respiratory infection (Table 6-2). Impairment of middle ear ventilation results in fluid collection. Bacteria may spread directly from the nasopharynx to the middle ear and cause purulent otitis media. The hearing loss tends to improve if the infection is managed promptly and thoroughly.

Chronic otitis media is generally defined as otitis media present for a prolonged time and producing irreversible changes in histologic features and physiologic processes of the middle ear. It is a frequent cause of chronic conductive hearing loss, usually as a result of damage to the eardrum or ossicles (the sound conduction mechanism). When antimicrobial treatment is inadequate, surgical intervention is directed toward achieving the following three goals: (1) resection of diseased tissue; (2) restoration of a pneumatized system; and (3) correction of conductive hearing loss. Hearing restoration techniques are successful only if the first two goals are met.

Benign lesions are more common than malignant neoplasms in the middle ear; either may cause conductive hearing loss. Glomus tumors (paraganglioma) of the temporal bone are benign vascular tumors arising from the chemoreceptor cells close to the jugular bulb. Malignant tumors include squamous cell carcinoma, adenocarcinoma, and sarcoma.

Otosclerosis accounts for the greatest number of cases of conductive hearing loss among persons 5 to 50 years of age. It is a genetically inherited disease affecting approximately 9% of the white population and 1% of black populations studied worldwide. Women are twice as likely as men to be affected. Both ears are usually involved.

In otosclerosis, portions of the bony labyrinth (otic capsule) are reabsorbed and replaced with new, highly vascular, spongy bone, which tends to overgrow the normal bony labyrinth. Otosclerosis may cause progressive fixation of the stapes footplate in the oval window, producing a progressive conductive hearing loss. Most patients with otosclerosis experience unilateral or bilateral conductive hearing loss in early adulthood. Although the hearing loss from otosclerosis usually is conductive, the cochlea also may be affected, producing sensorineural hearing loss. Patients consequently may manifest conductive, sensorineural, or mixed patterns of hearing loss. The conductive component of otosclerosis can be corrected surgically in properly selected cases. Amplification (hearing aid) is also successful.

Sudden conductive hearing loss caused by disorders in the middle ear may occur with barotrauma, resulting in hemotympanum (hemorrhage into the middle ear), tympanic membrane perforation, or serous otitis media. These conditions are frequently accompanied by tinnitus and fullness in the ear. Trauma to the side of the head may result in acute disruption of the ossicular chain with or without perforation of the tympanic membrane or bleeding into the middle ear space and may be the cause of sudden conductive hearing loss. These types of hearing loss often are reversible, either with time or surgical intervention.

Congenital hearing loss is defined as that present at birth. Causes range from genetically inherited hearing loss to in utero exposure to viral or toxic insult to perinatal injury. Genetically inherited sensorineural hearing loss affects about half of all profoundly deaf children. Congenital deafness frequently is associated with anomalous development of other systems, and hearing loss may be the first symptom of such syndromes (Table 6-3). Most nonsyndromic hearing loss is assumed to have a genetic basis, inherited as a recessive phenotype.

Universal newborn hearing screening has been mandated in most states of the United States. This enables early identification of congenital hearing loss to allow early intervention. Previously, congenital hearing loss was commonly not diagnosed until speech/language consequences developed. All babies are now screened for hearing loss prior to discharge from the birth hospital. The absence of adequate auditory stimulation for a young
person may impair development and maturation of central auditory pathways.