Abnormal eustachian tube function appears to be the most important factor in the pathogenesis of OME, particularly in children without a history of recent acute otitis. Noninfectious OME is believed to be a sequela of persistently high negative middle ear pressure resulting from functional or mechanical eustachian tube obstruction (4). Functional eustachian tube obstruction is defined as persistent eustachian tube collapse due to increased tubal compliance, an inactive opening mechanism, or both. Such functional eustachian tube obstruction most probably accounts for the agedependent predisposition of infants and young children to OME (5); it has been attributed to anatomic differences in the length, width, and angle of the eustachian tube (6). Similar anatomic-physiologic mechanisms also account for racial and familial differences in predisposition to OME (7). This correlation of anatomic abnormality, physiologic eustachian tube dysfunction, and increased predisposition to OME is most clearly demonstrated by the cleft palate population (8,9). Similarly, children with Down syndrome and other congenital craniofacial anomalies are high-risk groups for the development of OME (10).

Mechanical eustachian tube obstruction can be of an intrinsic or extrinsic nature. Intrinsic mechanical obstruction is typically attributed to tubal inflammation and secondary edema. Potential inflammatory provocateurs include infectious upper respiratory tract viruses (11), inhalant allergens in atopic individuals (12), household cigarette smoke exposure (13), and radiation therapy (14). Extrinsic mechanical obstruction has most often been attributed to adenoid hypertrophy. Less commonly, congenital nasopharyngeal cysts, juvenile angiofibroma, or nasopharyngeal malignancies in the adolescent and adult populations may play a similar obstructive role.

The exact role of enlarged adenoid tissue in the pathogenesis of OME most probably entails several mechanisms in addition to physical blockage of the nasopharyngeal end of the eustachian tube (15, 16, 17). A large adenoid or equivalent mass may obstruct the posterior choanae, contributing directly to increased nasopharyngeal pressure during swallowing and indirectly to nasopharyngeal-middle ear reflux. Adenoidal lymphoid tissue may also serve as a bacterial reservoir from which middle ear reinfection can occur (18).

Systemic factors may also predispose certain individuals toward the development or persistence of OME. Immunosuppression/immunodeficiency (19) and the immotile cilia syndromes (20) are two examples.

Otitis media with effusion has also been called silent otitis because of its common asymptomatic presentation. This is particularly true in infants and young children (21). The
absence of fever and constitutional symptoms in such cases often delays the diagnosis, and the effusions tend to be truly chronic in duration.

Children with chronic OME are often brought to the attention of their primary care physicians due to suspected hearing loss, often in association with speech delay. Older children may complain of ear pain or fullness; younger children may manifest this symptom by ear tugging. Occasionally children with OME present with balance difficulties.

An earlier diagnosis of OME in a subacute phase is often made in children following a recent AOM episode. Up to 40% of children have persistent middle ear effusion 4 weeks following a bout of AOM, and this middle ear fluid persists in 20% and 10% of children at 2 and 3 months’ status after diagnosis, respectively (22). Such persistent, postinfectious OME is particularly likely to occur in children under 6 years of age (23).

Children with chronic OME are also more prone to develop recurrent AOM than children whose middle ears are free of effusion (24). This interrelationship of AOM and OME accounts for the common presentation in young children of both recurrent and persistent middle ear disease.

The physical diagnosis of OME is made by otoscopic inspection of tympanic membrane translucency, color, position, and mobility. The pathognomonic appearance of trapped air within the effusion appearing as bubbles or an air-fluid level is only occasionally seen. More often, decreased translucency of the tympanic membrane results in a relative inability to visualize commonly seen middle ear landmarks such as the incudostapedial joint, promontory, and round window niche.

The color of the eardrum is variable. Both serous and mucoid effusions may impart an amber hue. Purulent effusions may appear white with associated increased vascularity of the pars tensa. Effusions of a mixed character with a nondescript dull gray tympanic membrane appearance are common.

Although any tympanic membrane position is possible, mild retraction of the eardrum indicative of negative middle ear pressure, as well as effusion, is often observed. The short process of the malleus appears more prominent and the manubrium foreshortened in such circumstances.

The presence of effusion with or without associated high negative pressure can significantly impede the movement of the eardrum in response to pneumatic otoscopy. The normal inward movement of the tympanic membrane with slight external canal positive pressure and outward movement with negative pressure is dampened or eliminated in characteristic fashion depending on both the contents and pressure of the middle ear (25). In experienced hands pneumatic otoscopy is both a sensitive and specific diagnostic tool (26).

Diagnostic accuracy can be further enhanced by the use of acoustic impedance measurements, particularly tympanometry. Measurements made with the electroacoustic impedance bridge provide an objective assessment of middle ear pressure and tympanic membrane compliance, and tympanometric tracings can be used to predict the presence or absence of middle ear effusion with a considerable degree of certainty (27). The accuracy of the diagnosis of OME is highest when pneumatic otoscopic and tympanometric findings are used in combination; sensitivity is 97% and specificity is 90% under such circumstances (28).

Acoustic reflectometry is an additional technique that shows promise as a means of detecting OME, particularly as a screening device in unskilled hands (29). The acoustic otoscope is a handheld instrument that contains both an 80-dB sound source and a microphone that measures both transmitted and reflected sound. The operating principle is that a sound wave within the external ear canal will be reflected from an intact tympanic membrane; the more sound reflected, the greater the likelihood of an effusion being present.

Finally, the documentation or confirmation of a mild conductive hearing loss may be the initial clue indicating the presence of otherwise asymptomatic OME in children. However, for reasons to be discussed, the assessment of hearing alone is not an accurate screening method for identifying the presence of middle ear effusion.

Hearing loss is the most common complication and sequela of OME. The loss is typically conductive and mild. Children ages 2 to 12 years with OME demonstrate mean three-frequency pure-tone averages and speech reception thresholds of 24.5- and 22.7-dB hearing level (HL), respectively; comparative mean bone-conduction scores average 3-dB HL (30). Less of an effect on hearing sensitivity is noted at 2,000 Hz in comparison to a slightly greater impairment in the 500- to 1,000-Hz lower frequency range.

The effect of OME on infant hearing levels is less easily discernible due to the limitations of sound-field behavioral audiometry. Testing for the better ear, average speech awareness threshold in infants ages 6 to 24 months with OME have been ascertained at 24.6-dB HL (31). More recent studies have utilized auditory brainstem response (ABR) testing to provide ear-specific data in this age group. Mild to moderately elevated ABR thresholds in the presence of middle ear effusion are documented (32).

The hearing loss associated with OME does fluctuate. The composite data from several studies indicate that, within the speech frequency range, approximately 90% of patients with OME exhibit a conductive hearing loss between 16- and 40-dB HL; however, at any one time, 49% of patients with OME would pass a hearing evaluation utilizing a 20-dB hearing threshold (33). This fluctuating nature of the hearing loss associated with OME is the reason the assessment of hearing is not an absolutely accurate screening method for this disorder.

The potential effect of the fluctuating mild to moderate hearing loss associated with OME on linguistic and intellectual development remains controversial. Three comprehensive
reviews of previously published studies show an association between OME in infancy and early childhood and later language delays and decreased learning skills (34, 35, 36). Clear documentation that the OME is the sole reason for the retarded development in such cases, however, is lacking. It is postulated that in young children the hearing impairment of OME, even when fluctuating and mild, has an adverse effect because it occurs during a critical period of language acquisition. This handicapping effect may be further augmented by disruption of normal parent-child interactions by the otitis disease process, and it may be particularly disabling in children with other educational impediments such as visual impairment, mental retardation, learning disorders, and neurosensory hearing losses.

The majority of the intratemporal and intracranial complications of otitis media occur secondary to AOM and chronic suppurative otitis media (Chapter 18); such complications are infrequently associated with OME. Exceptions to this rule include tympanosclerosis and tympanic membrane atelectasis with or without cholesteatoma formation.

Tympanosclerosis, more appropriately termed myringosclerosis when limited to the tympanic membrane, is characterized by the formation of white plaques in the eardrum or nodular deposits in the submucosa of the middle ear. Such plaques and nodules represent calcified hyalinized debris believed to be the end product of a chronic inflammatory or traumatic process (37). Although found more commonly in children who have had tubes, tympanosclerosis is reported in 10% to 20% of patients with bilateral OME in the nonintubated ear (38,39).

Displacement of the eardrum from its normal position toward the promontory is termed retraction or atelectasis. Several authors attribute such drum displacement to an inflammatory process occurring in underventilated ears, the atelectatic ear being viewed as representative of a more severe manifestation of eustachian tube dysfunction following OME (40,41). When thickening of the mucous membrane of the middle ear occurs in association with tympanic membrane atelectasis, the term adhesive otitis media is often applied. Such a proliferation of fibrous tissue may fix the ossicles, resulting in a conductive hearing loss. Osteitis with ossicular erosion, particularly of the long process of the incus, may also occur. In the presence of severe localized tympanic membrane atelectasis, a retraction pocket or even perforation may develop. Such retraction pockets, particularly in the posterosuperior quadrant, may be associated with both ossicular erosion and cholesteatoma formation.

Chronic OME in infancy and early childhood is additionally believed to result in reduced mastoid pneumatization, the functional significance of which, other than its association with tympanic membrane atelectasis, is uncertain (42).

Neurosensory hearing loss is a rare complication of otitis media, being more associated with labyrinthitis or possibly AOM than OME. The sudden development or progression of sensorineural hearing loss in a child with OME should raise suspicion of a congenital perilymphatic fistula (43).

Danish cohort studies have demonstrated a tremendous variability in the clinical course of untreated OME. Whereas 60% of children have one or more OME episodes that clear spontaneously within 1 to 3 months’ duration, 30% have much longer lasting episodes of 3 to 9 months’ duration, and 10% have extremely prolonged episodes persisting for 1 or more years (44). Otitis media with effusion, in the majority of children, appears to be a benign disease that will disappear, even without treatment, over a short period. A significant proportion of children, however, develop one or more episodes of chronic OME with the potential complications and sequelae thereof. These children and their adult counterparts with chronic OME are the principal patient groups for whom medical and surgical management become necessary.

Several nonsurgical options exist for the treatment of OME. One or more of these methods may be appropriate in the initial management of the child or adult with OME prior to embarking on surgical intervention.

Inflation of the middle ear has been purported to have a beneficial effect in the treatment of OME since the days of Politzer. Theoretically, air insufflated into the middle ear displaces middle ear effusion; repetitive insufflation should enhance middle ear drainage. Multiple methods of middle ear inflation by autoinflation or politzerization have been reported in the literature with variable results (45,46). The most recently described method of autoinflation, based on a modified Valsalva technique, utilizes an anesthesia mask attached to a flow meter allowing for quantitative control (47). These authors also report a new method of documenting eustachian tube opening during autoinflation using a combination of tympanometry and frequency spectrum analysis of ear canal sounds called sonotubometry. When these new techniques were applied in a randomized control study to 41 children with chronic OME unresponsive to antibiotic therapy, no therapeutic efficacy of sustained middle ear autoinflation was demonstrable.

The most common drug treatment of OME in children and adults had been the oral administration of systemic decongestant-antihistamine medications. A 1982 survey of American Academy of Otolaryngology members revealed that 91% of otolaryngologists considered such oral medications efficacious in the treatment of OME (48). A subsequent, double-blind, randomized, clinical trial was published in 1983 in which a 4-week course of an antihistamine-decongestant combination was compared with placebo in 553 children ages 7 months through 12 years with chronic OME (49). The study failed to show any beneficial drug effect. The rate of clearance of middle ear effusion, both unilateral and bilateral, was identical in both treatment groups.
A similarly designed study published in 1987 demonstrated the addition of an antihistamine-decongestant combination to amoxicillin or placebo to provide no additional advantage in OME resolution in the 518 children so compared (50).

Mucolytic agents such as guaifenesin and bromhexine have recently been investigated in animal studies and in limited observation trials in adults with OME (51,52). Although theoretically promising, no clinical role has yet been established for these agents.

Both systemic and topical corticosteroids have been suggested for use in the treatment of OME; clinical trials to date have only been performed with the former. The conclusions of the better designed of these studies assessing the efficacy of short-term systemic steroid use in treating OME have been conflicting. Schwartz et al. (53), using a double-blind, crossover study, reported 70% of children had cleared their middle ear effusions after a 1-week course of prednisone plus sulfonamide, compared with only 5% of those treated with sulfonamide alone. Although criticized due to the short duration of documented effusion in their study of children prior to treatment, the difference in clearance rates between the steroid and placebo groups is impressive. Macknin and Jones (54) found no difference between the use of dexamethasone or placebo in clearing middle ear effusions in children with well-documented chronic OME. However, their overall rate of effusion resolution was a very low 6%. Subtherapeutic steroid dosages and the absence of an antibiotic treatment baseline are criticisms of this study. Lambert (55), in prospective, double-blind, crossover fashion, assessed 60 children with chronic OME documented by combined pneumatoscopy and tympanometry. Concomitant amoxicillin was administered to both steroid and placebo groups. Prednisone plus amoxicillin proved no more effective than amoxicillin alone in resolving chronic OME. Overall, 60% of patients cleared their effusions. The results of the study actually supported a beneficial effect of antibiotic as opposed to steroid therapy.

Otitis media with effusion had been assumed to be sterile until microbiologic studies in the late 1970s revealed that approximately 50% of middle ear aspirates from children with chronic effusions demonstrated bacteria (56). Up to one fourth of the effusions demonstrated bacteria (56). Up to one fourth of the effusions grew pathogenic organisms, including Haemophilus influenzae, Branhamella catarrhalis, Streptococcus pneumoniae, Staphylococcus aureus, and Streptococcus pyogenes, in order of frequency. Later studies revealed beta-lactamase production to be common among the H. influenzae, B. catarrhalis, and S. aureus isolates (57). These microbiologic findings indicate that OME, despite its absence of acute signs and symptoms, may represent a low-grade infection in a substantial proportion of patients.

A trial of antibiotic therapy is highly desirable in previously untreated patients with OME. The antibiotics chosen and duration of therapy recommended are the same as those used in children with AOM. A number of small, nonblinded studies have reported trimethoprimsulfamethoxazole and erythromycin to be efficacious in the treatment of OME (58, 59, 60). Mandel et al. (50) showed in a randomized, double-blind, placebo-controlled study that a 14-day course of amoxicillin resulted in a significantly higher effusion-free rate at 2 and 4 weeks in the drug-treated group. However, a 50% recurrence rate was found when children who were effusion-free at 4 weeks were followed up for an additional 3 months. Thomsen et al. (61) demonstrated a more impressive resolution of middle ear effusion at 4 weeks following 1 month of amoxicillin-clavulanate potassium therapy (61%) compared with placebo (30%). The tympanometric-documented improvement in their antibiotic-treated children also persisted for a longer period, up to 8 months’ status after treatment.

Antibiotic therapy, perhaps with a beta-lactamaseresistant antibiotic, appears to be a worthwhile consideration in the initial management of OME. Even when successful, posttherapeutic surveillance is recommended due to a high anticipated rate of otitis recurrence.

Final mention under medical management must include those 25% to 30% of allergic children and adults who demonstrate serous OME as part of their overall upper respiratory tract presentation. In addition to the pharmacologic agents already mentioned, their total management often requires environmental controls, hyposensitization treatments, and dietary manipulation in some patients (62).

Patients who have persistent OME unresponsive to medical management, especially if present for at least 3 months, are reasonable candidates for surgical intervention. This is particularly true in patients with bilateral OME and associated hearing loss or patients with unilateral OME and secondary nonaudiologic middle ear complications.

The ideal otologic treatment of uncomplicated serous otitis media should achieve removal of the effusion, correct secondary hearing loss, and prevent recurrence through the provision of middle ear ventilation. Myringotomy with aspiration temporarily achieves the first two of these three goals. Myringotomy with aspiration is a reasonable initial treatment in adults and children who do not require general anesthesia for the procedure to be performed and who do not appear to have an underlying systemic condition that would suggest the need for sustained middle ear ventilation. In children of the age where the need for general anesthesia precludes the performance of repeated middle ear aspirations or in patients of any age with suspected chronic OME predisposition, the placement of tympanostomy tubes at the time of initial myringotomy is favored.

Four studies have compared the efficacy of myringotomy with aspiration alone versus myringotomy accompanied by tube placement in the absence of adenoidectomy or adenotonsillectomy surgery (38,63, 64, 65). All four studies found a significant difference in the length of the effusion-free period and in the duration of improved hearing favoring the intubated as opposed to nonintubated ears. Gates et al. (64), in particular, documented a 170-day difference in the average effusion-free interval in the tympanostomy tube versus myringotomy group. This difference was primarily accounted for by the average duration of tube function, which approximated 154 days.

Neel et al. (66) have hypothesized that the creation and maintenance of ambient pressure in the middle ear by way of ventilation tubes allows mucosal recovery and aeration of the middle ear-mastoid air cell system. The children in the Gates et al. study (64) are continuing to be followed from the time of tympanic membrane closure after tube extrusion in order to assess whether the prolonged middle ear ventilation afforded by the tubes does yield any long-term benefits.