eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Middle Ear & Mastoid

Middle Ear, Otitis Media With Effusion

Author: Richard D Thrasher III, MD, Private Practice, McKinney, Texas
Coauthor(s): Gregory C Allen, MD, Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Contributor Information and Disclosures

Updated: Nov 19, 2007

Introduction

Background

Otitis media with effusion (OME) is characterized by a nonpurulent effusion of the middle ear that may be either mucoid or serous. Symptoms usually involve hearing loss or aural fullness but typically do not involve pain or fever. In children, hearing loss is generally mild and is often detected only with an audiogram. Serous otitis media is a specific type of OME caused by transudate formation as a result of a rapid decrease in middle ear pressure relative to the atmospheric pressure. The fluid in this case is watery and clear.

Understanding the difference between OME and other forms of middle ear infections is important. Otitis media is a generic term defined as an inflammation of the middle ear without reference to a specific etiology or pathogenesis. Because all pneumatized spaces of the temporal bone are contiguous, inflammation of the middle ear may involve inflammation in the other 3 spaces: the mastoid, perilabyrinthine air cells, and the petrous apex. The term otitis media is often used to describe any of a continuum of related diseases: acute otitis media (AOM), recurrent acute otitis media (RAOM), OME, and chronic otitis media with effusion (COME).

AOM is a viral or bacterial infection of the middle ear that causes a rapid onset of signs and symptoms such as pain, fever, irritability, anorexia, and vomiting. Significant inflammation is present on physical examination, both on the tympanic membrane and in the middle ear effusion (MEE) in the form of purulence.

For further information, please also see the eMedicine articles Middle Ear, Inflammatory Diseases; Complications of Otitis Media; Middle Ear, Acute Otitis Media, Medical Treatment; and Middle Ear, Acute Otitis Media, Surgical Treatment

Pathophysiology

OME can occur during the resolution of AOM once the acute inflammation has resolved. Among children who have had an episode of AOM, as many as 45% have persistent effusion after 1 month, but this number decreases to 10% after 3 months.

Two main theories of the cause of AOM exist. The classic explanation proposes that eustachian tube dysfunction is the necessary precursor. The eustachian tube has been traditionally described to provide 3 main functions: equilibration of pressure between the middle and external ears, clearance of secretions, and protection of the middle ear. Its dysfunction can be caused by any number of circumstances from anatomic blockage to inflammation secondary to allergies, upper respiratory tract infection (URTI), or trauma.

If eustachian tube dysfunction is persistent, a negative pressure develops within the middle ear from the absorption and/or diffusion of nitrogen and oxygen into the middle ear mucosal cells. If present for long enough and with appropriate magnitude, the negative pressure elicits a transudate from the mucosa, leading to the eventual accumulation of a serous, essentially sterile effusion. Because the eustachian tube is dysfunctional, the effusion becomes a sessile medium ideal for the proliferation of bacteria and resultant AOM. This classic model is somewhat incorrect, since multiple studies have revealed that the same pathogenic bacteria are present in OME as in AOM.

The newer models describe the primary event as inflammation of the middle ear mucosa caused by a reaction to bacteria already present in the middle ear. Indeed, Bluestone and others have shown (using radiographic evidence) that reflux up the eustachian tube is demonstrable in children prone to otitis media. Furthermore, in 2007, Crapko et al demonstrated the presence of pepsin in the middle ear space of 60% of children with OME.¹ This reflux certainly may also occur in otherwise healthy individuals. The inflammatory mediators released as a result of bacterial antigenic challenge induce the up-regulation of mucin genes. The production of a mucin-rich effusion then provides an ample medium for the proliferation of bacteria and resultant AOM.

Yilmaz et al published a study in 2004 that documented significant changes in oxidative stress in patients with OME.² They demonstrated a significantly improved but not normalized level of oxidants following the placement of ventilation tubes. However, the role of antioxidants in the treatment of OME has yet to be fully investigated.

Regardless of the cause of AOM, eustachian tube dysfunction is nearly universal in OME. As further evidence, ligation of the eustachian tube in animals invariably leads to the formation of a persistent MEE. Once the acute inflammation and bacterial infection have resolved, a failure of the middle ear clearance mechanism allows MEE to persist. Many factors have been implicated in the failure of the clearance mechanism, including ciliary dysfunction; mucosal edema; hyperviscosity of the effusion; and, possibly, an unfavorable pressure gradient.

OME does not necessarily follow AOM. Theories to explain the development of MEE in this case include the secretion of fluid from inflamed middle ear mucosa. This theory proposes that the middle ear mucosa is sensitized by previous exposure to bacteria, and continued antigenic challenge from occasional reflux induces the production of the effusion. Again, multiple studies have revealed that the same flora of bacteria is present in OME as in AOM; these findings indicate that this effusion is not sterile, as was once believed.

OME is ubiquitous in children who have a cleft palate. The cause is simply the lack of proper insertion of the tensor veli palatini muscle in the soft palate. The muscle is, therefore, unable to open the eustachian tube on swallowing or wide mouth opening. A functional obstruction of the tube results.

Frequency

United States

Middle ear infections are the most common medical problem in infants and children of preschool age, and they are the most frequent primary diagnoses in children younger than 15 years who are examined at physicians' offices.

Clinical guidelines from a joint commission of specialties document that screening surveys of healthy children between infancy and 5 years show a 15-40% point prevalence in MEE. Furthermore, among children examined at regular intervals for a year, 50-60% of child care attendees and 25% of school-aged children were found to have a MEE at some point during the examination period, with peak incidence during the winter months.

Between 84% and 93% of all children experience at least 1 episode of AOM. Furthermore, approximately 80% of children have had an episode of OME when younger than 10 years. At any given time, 5% of children aged 2-4 years have hearing loss due to MEE that lasts 3 months or longer. The prevalence of OME is highest in those aged 2 years or younger, and it sharply declines in children older than 6 years.

In 1989, a 7-year study of otitis media conducted in the greater Boston area revealed the frequency of AOM. In children younger than 1 year, 62% had at least 1 episode of AOM, and 17% had 3 or more episodes. In children younger than 3 years, 83% had at least 1 episode of AOM, and 46% had 3 or more episodes.

In 1990, 12.8 million episodes of otitis media occurred in children younger than 5 years. Of children younger than 2 years, 17% had recurrent disease. Since at least 30% and as many as 45% of children with AOM had OME after 30 days, and 10% had OME after 90 days, at least 3.84 million episodes of OME occurred that year; 1.28 million episodes persisted at least 3 months.

Mortality/Morbidity

OME is the leading cause of hearing loss in children. It is associated with delayed language development in children younger than 10 years. The loss is usually conductive, with an average air conduction threshold of 27.5 dB, but OME has also been associated with sensorineural hearing loss. Both prostaglandins and leukotrienes have been found in high concentrations in MEE, and their ability to cross the round window membrane has been demonstrated. Chronic exposure to these metabolites of arachidonic acid may cause a temporary and sometimes permanent sensorineural hearing loss.

Race

The prevalence of OME is higher in Native Americans, particularly Navajo and Eskimo peoples, than in other races. The reason for the higher frequency in these populations has been attributed to a number of factors, but no findings have confirmed the most likely etiologies. No difference in prevalence rates between white and black populations exists.

Sex

No statistically significant difference exists between the sexes in terms of incidence or prevalence, although some findings suggest that males may have a slightly higher frequency.

Age

As mentioned above, the highest incidence of OME occurs in children younger than 2 years, and incidence decreases dramatically in those older than 6 years. The reasons for this age predilection are discussed in Causes.

Clinical

History

Otitis media with effusion (OME) nearly always follows AOM as it resolves. However, MEE can be present without preceding AOM, as in the case of serous otitis media after barotrauma.

• Neither the affected children nor their parents describe reports referable to a MEE in 40-50% of documented cases of OME. The most common report involving children comes from parents who are concerned with signs consistent with decreased hearing. Parents may notice that the television volume is too loud and that the child sits close to the television, does not respond when called (new onset), and often asks "what?" However, these signs are not consistent and do not reliably indicate potential MEE.
• Adults with OME report aural fullness and/or pressure, an ear being plugged, or decreased hearing. Reports of pain are rare.
• Associated findings during history taking may include a recent URTI, a recent plane trip or scuba diving trip, or current environmental allergies.

Physical

• Otoscopic findings of inflammation in AOM may include decreased mobility of the tympanic membrane (which has a bulging contour) that is manifested by difficulty in assessing the ossicular landmarks, yellowness and/or redness with hypervascularity, purulent MEE, and, occasionally, bullae. This appearance clearly contrasts with that of OME.
• Findings that suggest the presence of OME include observable air-fluid levels (which may be vertically oriented), serous middle ear fluid, and a translucent membrane with diminished mobility.
• Extensive inflammation and purulent MEE should not be evident.
• OME can also be associated with negative pressure in the middle ear. Negative pressure is suggested by the prominence of the lateral process, a more horizontal orientation of the malleus, and movement only with negative pneumatoscopy.
• Occasionally, tonsillar hypertrophy can accompany findings of OME. More commonly, adenoid hypertrophy is present, especially in patients with prolonged or recurrent OME.
• Additional findings may include turbinate bogginess, postnasal drip, rhinorrhea, and watery and/or erythematous eyes consistent with a concurrent URTI or environmental allergies.

Causes

The same flora found in AOM can be isolated in OME. With OME, the inflammatory process has clearly resolved, and the volume of bacteria has decreased. However, because of the similarity of AOM and OME, reviewing the pathogenic organisms in AOM is worthwhile.

• The most common bacteria in AOM, in order of frequency, are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. These pathogens are also the most frequent organisms associated with sinusitis and pneumonia. Together, these pathogens account for 85% of acute ear infections.
  • S pneumoniae is found in 35% of cases, and the prevalence does not seem to vary with age. The serotypes most commonly isolated, in order of frequency, are 19, 23, 6, 14, and 3.
  • H influenzae is found in 20% of cases. Of these cases, 25-45% involve beta-lactamase production, with a clear trend of increasing resistance.
  • M catarrhalis is found in 4-13% of cases of AOM, with a great frequency in winter and autumn. Of these cases, 70-100% involve beta-lactamase production.
  • Additional bacterial pathogens include Streptococcus pyogenes, Staphylococcus aureus, gram-negative enteric bacteria, and anaerobes. When an effusion is present for longer than 3 months, Pseudomonas species predominate.
  • In 30% of examined tympanocentesis specimens, microorganisms are not found. In a meta-analysis of results from 10 studies of tympanocentesis in AOM from the early 1990s, 29 (4.4%) of 663 patients had a virus that could be isolated. In other recent studies, viruses have been isolated in conjunction with bacteria in 15-20% of cases of AOM. Respiratory syncytial virus and influenza virus were the most frequent. The relation between viral and bacterial infection is controversial. Because viruses have been identified as the sole infective agents in only 4-6% of middle ear aspirates obtained from children with AOM, viruses may promote bacterial superinfection by impairing eustachian tube function.
• The only difference with the pathogens in OME compared with AOM is that the frequency of S pneumoniae is not as high, and H influenzae and M catarrhalis are moderately more common.
• Besides the actual pathogens, environmental factors have been shown in numerous epidemiologic studies to be strongly associated with increased prevalence of OME. These factors include bottle feeding, feeding while supine, having a sibling with OM, attending daycare, having allergies to common environmental entities, having a lower socioeconomic status, living in a home in which people smoke, and having a parental history of OME.
• Age is clearly another predisposing factor in the development of OME. In infants, the eustachian tube has a nearly horizontal orientation (relative to the ground) and develops the 45° angle (as in adults) after several years. In addition, the size and shape of the eustachian tube at birth, unlike those in adults, are unfavorable for ventilation of the middle ear. Multiple studies of children in Denmark revealed that by the time children were aged 1 year, tympanograms were either type B (flat) or type C (negative pressure) in 24% of their ears. Improvement occurred in the spring and summer, while worsening was more common in the winter. Type B tympanograms peaked in children aged 2-4 years, and, as expected with the prevalence of OME, decreased in children older than 6 years.
• Disruptions in the normal opening of the eustachian tube orifice in the nasopharynx are also associated with an increased prevalence of OME. These commonly occur in patients who have a cleft palate and in children with Down syndrome and other disorders affecting the palate. In addition, the decreased mucociliary clearance and higher viscosity of mucus in cystic fibrosis have been hypothesized to account for a higher prevalence of OME in patients with these conditions.
• In adults, recognizing unilateral OME is crucial. This entity must be considered a nasopharyngeal mass until definitively proven otherwise.

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