CLASSIFICATION OF OTITIS MEDIA AND SURGICAL PRINCIPLES

OTITIS MEDIA: SURGICAL PRINCIPLES BASED ON PATHOGENESIS

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CLASSIFICATION OF OTITIS MEDIA AND SURGICAL PRINCIPLES Timothy T. K. Jung, MD, PhD, and Jonathan 8.Hanson, MD

Otitis media (OM) is the most common disease of childhood with the exception of viral upper respiratory infections (URIs).Among children in Boston studied from birth to 7 years of age, more than 90% had at least one episode of acute OM (AOM), and 75% had three or more episodes.75Investigators estimate that of the 120 million prescriptions written for oral antibiotics each year in the United States, more than 25% are for the treatment of patients with OM. Myringotomy with insertion of a tympanostomy tube is the most common surgical procedure performed in children for which general anesthesia is required. The societal impact of OM in the United States is significant. Stool and Field7] estimate that 15 million cases of AOM affect children in the United States each year. Estimates of direct and indirect costs attributed to the medical and surgical treatment of children with OM 5 years old and younger exceed $5 billion per year.*] Risk factors that contribute to OM have been the subject of great interest in seeking methods to prevent this major health problem. In a large Pittsburgh study of healthy low socioeconomic status and repeated exposure to many other children, at home or in day care, were the most important sociodemographic risk factors. The protective effect of breast-feeding and the detrimental effects of exposure to smoke were found to be significant in the first year. Certain disease states, such as cleft palate, immunodeficiency,ciliary dyskinesia, trisomy 21, and cystic fibrosis, were all associated with an increased risk for OM. This article reviews the pertinent literature, discusses the authors’ view on the pathogenesisand classification of OM in children and adults, and discusses therapy with an emphasis on surgical options appropriate at each stage.

From the Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, Loma Linda University School of Medicine, Loma Linda, California OTOLARYNGOLOGIC CLINICS OF NORTH AMERICA VOLUME 32 * NUMBER 3 JUNE 1999

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PATHOGENESIS OF OTITIS MEDIA Effective strategies in the treatment of patients with any disease process are borne out of an understanding of its pathogenesis. Multiple, interrelated factors contribute to the development of OM, including infection, dysfunction of the eustachian tube (ET),allergy, and barotrauma. Eventually, irreversible damage can occur as a result of the inflammatory conditions elicited by these factors.

Infection Acute OM often follows viral URI, and investigators have well established that the incidence of AOM is highest in winter months, when the incidence of viral URI is highest.66Examination of 1024 children with AOM in nine studies since 1982 showed evidence of viral presence in middle ear effusions (MEEs),with or without bacteria, in 19%.j2By promoting adherence of bacteria in the inflamed nasopharynx, and by destroying the normal mucociliary defense mechanismsof the ET and middle ear, a viral URI facilitates extension of pathogenic bacteria into the ET and middle ear cleft. The bacteriology of AOM is well established and varies little throughout the world. Data from the Pittsburgh Otitis Media Research Center70revealed that in 2807 ears with AOM, the predominant bacteria cultured from the MEEs were Streptococcus pneumoniae (35%),Haemophilus influenzae (23%),and Moraxella catarrhafis (14%).Group A streptococci and a-hemolytic streptococciwere each present in 3% of AOM effusions, and Staphylococcus aureus and Pseudomonas aeruginosa were each present in 1%."Other" bacteria, present in 39%of patients with AOM, included oral flora, enteric bacteria, yeast, and fungi. The incidence of p-lactamase-producing strains of H. influenzae and M . catarrhalis increased from 1981 to 1989, when 37% of H. influenzae and 88% of M . catarrhalis produced 0-lactamase. In ears with otitis media with effusion (OME), the distribution of bacteria is different than in ears with AOM, although the predominant bacteria remain the same: S. pneumoniae, 7%; H. infiuenzae, 15%;and M . catarrhalis, 10%. In patients with OME, "other" bacteria constituted 45%.Overall, 70% of ears with a chronic effusion were culture positive.70 The bacterial flora isolated in patients with chronic, suppurative OM is a polymicrobial mixture of aerobes and anaerobes. One study using strict anaerobic and both aerobic and techniques found aerobes only (39%),anaerobes only (ll%), anaerobic bacteria (50%) in 183 patients with chronic OM.15Each patient had an average of 3.2 species isolated: 1.6 aerobic, and 1.6 anaerobic. The predominant aerobe, P. aeruginosa, and the predominant anaerobe, Peptostreptococcus sp, were isolated in 37% and 40% of patients, respectively. Only one specimen had no growth. The notion that adenoid tissue contributes to OM mainly as a consequence of obstruction of the ET or nasal cavity was assumed for years, but recent literature concludes that the role of adenoid tissue in the pathogenesis of OM is primarily as a focus of i n f e c t i ~ n . ~ The ~ ,adenoid, ~ ~ , ~ ~ positioned in the posterior nasopharynx, serves as an area of contact between inhaled bacteria and lymphoid cells. Its proximity to the orifice of the ET, when combined with a mechanism for transport of mucus into the middle ear (e.g., nose blowing, closed-nose swallowing, sniffing, or a patulous ET), provides a logical link between bacterial or viral colonization of the adenoid and OM.

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Dysfunction of the Eustachian Tube Normal function of the ET is vital in maintaining a healthy middle ear. It allows exchange of gases between the middle ear and the nasopharynx when it opens during swallowing; it transports fluid from the middle ear to the nasopharynx using mucociliary flow; and, when closed, it prevents reflux of mucus and bacteria from the nasopharynx into the middle ear during changes in nasopharyngeal pressure. Failure of any of these functions constitutes dysfunction of the ET. Although it is a consistent finding in children with OME, the magnitude to which it is caused by OM or to which it contributes to the cause or persistence of disease, is difficult to ascertain. Dysfunction of the ET may be characterized as breakdown in dynamic function, passive function, or a combination of these. Bacterial, viral, and allergic nasotubal inflammation causes not only obstructive mucosal swelling but also destruction of normal mucociliary Nasopharyngeal tumors obstruct the orifice of the ET, and many patients with these also present with MEE.87Radiation for these tumors injures tubal cilia, which adds a passive dysfunction to the obstruct i ~ nDysfunction .~~ of the ET in patients with cleft palate is not purely mechanical because Bluestone et a17 and Takahashi et aP3 cite significant passive functional problems in the ET in these patients also. A patulous ET, a failure of tubal closing, may produce OME not only by promoting reflux of nasopharyngeal mucus and bacteria into the middle ear during sneezing or nose blowing but also by allowing repeated and persistent evacuations of the middle ear during habitual sniffling.83 Patients who have primary ciliary dyskinesia can be expected to have abnormal ciliary function of the ET and commonly have OME in addition to bronchiectasis and sinusitis.29 The role of surfactants in normal ET functioning was first suggested by Flisberg and c o l l e a g ~ e sThe . ~ ~presence or absence of surfactants, which reduce surface tension at an air-water interface, are believed to influence the opening pressure of the ET. Recent studies have demonstrated a measurable decrease in opening force by placing exogenous surfactant into the middle ear or ET.19,81 Allergy and Immunologic Factors Allergy has long been recognized as one of the causative factors of OME. Nasotubal mucosal congestion associated with inhalant allergy and obstruction of the ET was mentioned earlier. A significantassociation has been reported between food allergy and serous OM (SOM);Z and recurrent AOM is more prevalent among children suffering from immunodeficiency.84An experimental model of allergyinduced OME has been successfully produced in animals.67 Barotrauma Barotrauma caused by changes in barometric pressure that occur during diving, flying, or therapy using hyperbaric oxygen can produce OM even in the presence of a normal ET. During ascent, air in the middle ear passes through the ET as it expands. In rapid descent, air in the middle ear and ET is compressed, and the ET collapses when the difference in pressure between the environment and the middle ear space becomes too great. If unequalized, the resultant high negative pressure in the middle ear produces MEE with bleeding or transudation of serum.

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The presence of an artificial airwayl and a history of dysfunction of the ET before therapyI6 greatly increases the risk for hyperbaric oxygen-induced barotrauma and the development of SOM. Inflammatory Mediators Each of the causative factors just mentioned stimulates mucosa and inflammatory cells in the middle ear to release inflammatory mediators. Inflammatory mediators and enzymes identified in patients with MEEs include histamine, prostaglandins, leukotrienes, kinins, proteases, hydrolytic enzymes, platelet-activating factor, tumor necrosis factor, y-interferon, and nitric ~ ~ i d When e . pro~ duced, these inflammatory agents increase vascular permeability and secretory activity of the middle ear cavity, resulting in MEE. CLASSIFICATION AND TREATMENT OF OTITIS MEDIA Many terms are used to refer to the various stages of OM. Although each is widely used, agreement on the pathophysiologic implications of each term is not universal. Otitis media is a general term used to describe any inflammatory process involving the middle ear cleft. The stages of OM are subdivided and classified according to the nature of the effusion present: purulent otitis media (POM), SOM, and mucoid otitis media (MOM).55 Clinical 0bservation,5~studies in human temporal bone,%and animal studiesz8 have revealed that these various forms of OM are dynamically interrelated regarding their cause and pathogenesis and do not represent separate entities. Rather, they represent the same disease process as it progresses in continuum. For example, POM can lead to SOM, and either of these to MOM, and finally to chronic otitis media (COM) when pathologic conditions in the middle ear have become irreversible (Fig. 1). Patients with COM may exhibit perforations of the tympanic membrane or ossicular destruction with resultant hearing loss, and both are often

Resolution

COM

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G;1 /.ME\

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Sequetae

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Silent OM

Figure 1. Otitis media with effusion (OME) is classified according to the type of fluid in the middle ear cleft: purulent otitis media (POM), serous otitis media (SOM), or mucoid otitis media (MOM). One form of OME may overlap with another, or advance to another stage in the disease continuum. OME may resolve, or it may lead to sequelae, silent otitis media, or the irreversible pathology of chronic otitis media (COM). (Adapted from Paparella MM, Schachern P: New developments in treating otitis media. Ann Otol Rhino1 Laryngol Suppl 163:7,1994; with permission.)

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seen when cholesteatoma or granulation tissue is present. Chronic otorrhea through a perforated tympanic membrane is referred to as chronic suppurative OM and is usually associated with COM. OME denotes the presence of chroniceffusion in the middle ear cleft regardless of cause or type of effusion. Although OME includes POM in the stages following acute OM, OME implies a silent, subacute stage of OM without the acute symptoms of fever and severe otalgia. The term OME also encompasses SOM, MOM, secretory OM, and ”glue ear,” a popular term used in literature from the United Kingdom. Treatment directed toward any form of OM must be individualized for each patient. Certain factors considered in a clinical investigation may indeed alter the therapeutic plan. A complete assessment must include the magnitude of hearing loss, the presence of developmental delay or a behavioral disorder; the expectations of the caregiver; any structural changes evident in the tympanic membrane; and prognostic factors, such as low socioeconomic status, attendance in day care, bilaterality, or young age. Some information, such as disease burden and family dynamics, may only be accurately obtained through the primary care physician, with whom communication is vital. Purulent Otitis Media Purulent OM is characterized by purulent fluid bathing the middle ear. This type of fluid is found in patients with AOM and recurrent AOM. In the Greater Boston Otitis Media Study,” 498 children were followed up to 7 years of age, and 93% experienced at least one episode of AOM, and 74% had three or more episodes. Acute Otitis Media

Acute OM is an acute bacterial infection of the middle ear cleft characterized by a rapid onset of otalgia, fever, and (in young children) ear tugging, sleeplessness, and irritability. In the early stages of AOM, erythema and edema in mucosa of the middle ear correspond otoscopically with an erythematous tympanic membrane. As the infection progresses, purulent exudate accumulates in the middle ear, and the tympanic membrane visually appears opaque, full, or bulging. The membrane may rupture, allowing the purulent effusion to drain. The tympanic membrane has diminished mobility as evidenced by a flat tympanogram, and audiologically conductive hearing loss is present as long as a significant MEE remains. Antimicrobial therapy is the first line of treatment in uncomplicated cases and is initially directed toward the most common pathogens. Amoxicillin has been the empiric drug of choice for treating patients with AOM because it is active against S. pneumoniae and most strains of H. influenzae, but in many areas the incidence of (3-lactamase-producing organisms in patients with AOM is increasing, and the efficacy of amoxicillin as the best initial therapy in these locations is being quest i ~ n e d . ~In ’ , ~patients ~ allergic to penicillin, erythromycin-sulfisoxazole or trimethoprim-sulfamethoxazole is an appropriate alternati~e.’~ Reevaluation within 24 hours is warranted for any signs of progression; otherwise, symptoms should improve significantly within 48 to 72 hours after appropriate therapy is begun. Failure to improve should prompt discontinuation of the initial agent, and a second-line drug resistant to p-lactamase (e.g., amoxicillin-clavulanate or cefaclor) should be ~ h o s e nThe . ~ duration of antibiotic therapy is an issue debated and not yet resolved but is generally 7 to 10 days. Following antibiotic therapy for AOM,

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resolution of the MEE takes a variable amount of time. In the Boston study, 70% of children had OME at the end of 2 weeks, 40% at 1-month follow-up, 20% at 2month follow-up, and 10% at 3-month follow-up after treatment.4z Surgical intervention in the setting of AOM is necessary when specific knowledge of the causative organism requires tympanocentesis.Tympanocentesis is performed by inserting an 18-gauge spinal needle attached to a I-mL syringe into the anteroinferior quadrant of the tympanic membrane. Anesthesia is not necessary. Fluid is aspirated and sent for culture and sensitivity. According to Bluestone and Klein,6 indications for tympanocentesis in AOM include severe otalgia, severe illness, or a toxic appearance; unsatisfactory response to antimicrobialtherapy; onset of AOM in a child who is receiving appropriate and adequate antimicrobial therapy; AOM associated with confirmed or potential suppurative complications; and AOM in a neonate or immunologically deficient patient. A diagnostic tool, tympanocentesis may, by temporarily decompressing the middle ear space, significantly alleviate pain but alone offers no therapeutic Myringotomy has a limited role in the treatment of patients with uncomplicated AOM. Like tympanocentesis, it is effective in providing symptomatic relief but alone offers no advantage in resolving the infection nor in clearing the MEE over treatment with amoxi~illin.~~ In cases complicated by paralysis of the facial nerve, meningitis, or other intracranial extension, however, myringotomy should be performed without delay to drain the middle ear space and to obtain material for culture.20 Surgical therapy is required in many of the intratemporal and intracranial complications that are associated with AOM. In general, the principles governing operative intervention in this setting are removal of infected bone, adequate drainage of the suppurative focus in bony or soft tissue, preservation of function, and prevention of additional morbidity or permanent sequelae. A detailed discussion of specific surgical options for each complication is beyond the scope of this article. Recurrent Acute Otitis Media

Howie et a132termed children who had six or more bouts of AOM before the age of 6 years as otifis prone. Klein4I defined three bouts of AOM in 6 months or four episodes in 12 months as having recurrent AOM. Marchant and C01lison~~ labeled those with three or more episodes of AOM in 18 months as otitis prone. Klein’s criteria offer a commonly used guideline when additional treatment is considered for children with frequent AOM. A recent report found an increasing incidence of recurrent AOM in the United States that seems closely related to an increase in the use of child care and a higher prevalence of allergic conditions in children.44When a child is diagnosed with recurrent AOM, prevention is indicated. Predisposing factors, such as a positive family history, submucous cleft palate, child care in a large group setting, allergy, ciliary dyskinesia, chronic sinusitis, immunologic deficiencies, or nasopharyngeal tumor should be identified. After these factors have been considered, several methods of prophylaxis may be used. Chemoprophylaxis has been found to prevent AOM,6°,78 and it has become a routine aspect of managing patients with recurrent AOM in the primary care setting. A popular regimen uses amoxicillin (20 mg/kg in one dose at bedtime) or sulfisoxazole (50 mg/kg once per day) during the winter and spring months. Concern over this practice is building with the increasing incidence of resistant bacterial strains. A recent study in Denver found no protective effect of once-daily or twice-daily amoxicillin over placebo and discouraged amoxicillin prophylaxis altogether.62Paradise57argued against chemoprophylaxis in most cases and encouraged earlier referral for tympanostomy tubes. If patients are being managed

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with antibiotic prophylaxis, they must be examined every 1 or 2 months. If OME develops or recurrent AOM persists in these patients while on prophylactic antibiotic therapy, myringotomy with insertion of tympanostomy tubes should be considered. Considerable evidence suggests that AOM may be prevented by systemic immunization against middle ear bacterial and viral pathogensz6For patients with recurrent AOM, vaccination should be considered. Myringotomy with insertion of ventilation tubes was found by Gebhart,25in a prospective randomized study, to be more effective in preventing AOM than observation without prophylaxis. Casselbrant and others9found that tympanostomy tubes were no better than amoxicillin in preventing new episodes of AOM but that patients with tubes had significantly shorter episodes. A patent tympanostomy tube provides a fair substitute for a dysfunctional ET by both aerating and draining the middle ear through the tympanic membrane. Although not without some risk and expense, the insertion of tubes improves health in the middle ear in most patients, and the frequency of recurrent infection decreases. Adenoidectomy has been recommended for the prevention of recurrent AOM. In a prospective randomized trial with follow-up at 1 and 2 years, subjects with adenoidectomy suffered 28% fewer episodes of AOM after 1 year and 35% fewer episodes after 2 years of follow-up than control subjects at first-year and secondyear Adenoidectomy is invasive, however, and is not advised initially for the prevention of recurrent AOM. It is usually recommended only after antibiotic prophylaxis or myringotomy with insertion of tubes has been used. A clinical situation easing the decision for adenoidectomy is a child who has recurrent AOM in addition to frequent acute pharyngotonsillitis or chronic obstructive adenotonsillitis. Tonsillectomy has not been shown to decrease the frequency of AOM.

Serous Otitis Media A serous effusion in the middle ear is a clear, watery transudate that occupies the middle ear cleft. It may be present in the continuum of types of fluid associated with OME, regardless of their cause. Patients with SOM may complain of fullness or hearing loss, but it is often asymptomatic.Otoscopy reveals an amber or strawcolored tympanic membrane with normal contour. Air bubbles or an air-fluid level seen through the tympanic membrane is often seen in older children or in adults whose SOM is nearing resolution, and it indicates a favorable prognosis. Pneumatic otoscopy or tympanometry likely reveals impaired mobility of the tympanic membrane, and audiometry may demonstrate a mild conductive hearing loss. Although serous effusion may be present in any process causing OME, discussion in this section is limited to the management of patients with SOM associated with barotrauma and radiation therapy for nasopharyngeal carcinoma. Hyperbaric oxygen therapy involves the inhalation of 100% oxygen at a pressure of more than 1 atm. In a study of 33 adult patients who underwent hyperbaric oxygen therapy, SOM developed in 100%of 12 patients with a prior history of ET dysfunction and in 52% of patients overa11.I6Decongestants are often used adjunctively, but their efficacy in preventing barotrauma and SOM is unproved. Myringotomy with placement of tympanostomy tubes allows ventilation of the middle ear, relieving or preventing painful barotrauma and SOM in patients with dysfunction of the ET. Indications for myringotomy with placement of tubes are inability to autoinflate (i.e., ventilator dependence, tracheostomy, laryngectomy, or coma) and persistent pain or hernotympanum after beginning therapy despite

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decongestant use.4The presence of SOM without pain or evidence of barotrauma carries little morbidity and may be observed and treated with tympanostomy tubes only if the effusion is persistent and symptomatic 3 months after therapy ends. Serous OM is a well-recognized complication of nasopharyngeal carcinoma and was present in 38% of patients at presentation and in 46% of patients after radiation therapy in a study of 175 patients with the disease.74Irradiation of the nasopharynx causes both inflammation of the middle ear and dysfunction of the ET. Treatment of the ensuing SOM can be a perplexing problem. Myringotomy with insertion of ventilation tubes not long ago was considered appropriate therapy.80Tympanostomy tubes help to ventilate the middle ear and provide some relief of the conductive hearing loss, but long-term follow-up has found significantly more otorrhea and complications in the middle ear and a significantly greater deterioration of air conduction in tube-ventilated ears compared with ears after repeated myringotomies without tubes.%Tang and others74advise avoiding myringotomy altogether, with or without insertion of tubes, citing increased middle ear complications in operated ears. Mucoid Otitis Media

Mucoid OM implies both an intact tympanic membrane and the presence of any chronic MEE more tenacious than the thin, watery fluid of SOM. The effusion is often cloudy and thick or semisolid in character. Most children with a persistent effusion after treatment for AOM develop MOM. In approximately 20%of children in whom OME develops, it persists beyond 2 monthsloand may last for years.49 MOM represents the most advanced disease state in the spectrum of OME before the irreversible damage of COM occurs. A prospective study of 1679 healthy childred9revealed that 9.1%had developed MOM at some time by age 12 years, with more than two thirds of those cases occurring in the first 3 years. In addition, in children with MOM, 83% less than 3 years old had recurrent AOM in the year prior, but only 33%of 3- to 12-year-oldshad recurrent AOM in the previous year. This confirms previous findings that in many children, especially older ones, OME develops without any clinical evidence of antecedent AOM. A different etiopathogenic process has been proposed for patients with MOM of silent onset, and most believe that secretion of fluid from abnormal middle ear mucosa is responsible, hence the synonym for MOM: secretory OM. This may occur as a result of subclinical antigenic stimulation from bacterial products or from live microorganisms known to be present in the effusions of patients with OME.70 Otitis media with effusion is often asymptomatic, but hearing loss may be manifested in children as inattentive behavior, delayed speech, or a failed hearing screening at school. Adults may complain of fullness in the ear and decreased hearing acuity. By the time of the examination, the tympanic membrane in patients with MOM has an amber color, is thick and opaque, has mild to moderate retraction, and has increased capillary vascularity on the surface. A dark blue tympanic membrane is associated with longstanding MOM combined with cholesterol granuloma.” Impaired tympanic membrane mobility, detected by pneumatic otoscopy or tympanometry, and conductive hearing loss are valuable diagnostic signs of OME. Predisposing factors, such as palatal cleft, ciliary dyskinesia, chronic sinusitis, or a nasopharyngeal mass, must be considered before treatment is begun. Medical therapy for patients with OME has been directed toward its causes, such as infection, inflammation, allergy, and dysfunction of the ET. Antibiotic therapy has demonstrated a higher clearance rate of MEEs compared with the use of

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a p l a c e b 0 , 3 ~ but * ~ ~although .~~ the antibiotics were found to be effective, the magnitude of that efficacy is This justifies a trial of antimicrobial therapy followed by observation for clearance in asymptomatic patients without significant hearing loss. In experimental OM, a corticosteroid-antibiotic combination was more effective than antibiotic alone in the resolution of MEE.36An oral corticosteroid, in combination with an antibiotic, was found to provide a 6-month resolution of OME in 25% of patients treated.65Despite this, studies of oral corticosteroids so far have failed to demonstrate a consistent beneficial effect that would justify their routine use in patients with OME. A recent study found that a topical nasal steroid in combination with an oral antibiotic may be useful in treating patients with OME,n and further research in this area is sure to follow. The use of decongestants and antihistamines has been shown to be ineffective in the treatment of patients with OME/ but these should be used for concurrent sinonasal disease, if present. Finally, techniques for inflation of the middle ear using catheterization or autoinflation of the ET have not proven effective in relieving negative pressure in the middle ear; in fact, inflation may worsen therefore, inflation is not recommended." Surgical intervention should be considered when observation and medical therapy fail to demonstrate timely resolution of the effusion. Persistence of OME causes hearing loss that, in children, may result in behavioral disorders or impaired speech, language, and reading skills. The bacteria, bacterial products, enzymes, and inflammatory mediators present in the unresolved MEE contribute to progression of local disease and eventually to irreversible changes associated with COM. If MEE persists for 3 months, surgical therapy is indicated, and options include tympanostomy tube placement, adenoidectomy, or adenoidectomy plus myringotomy or tubes. Myringotomy alone proved no better than observation,46 and tonsillectomy was found to be ineffective in altering the course of OME,5O thus, neither alone is recommended for the treatment of patients with OME. Unresponsive disease may require exploratory tympanotomy with or without mastoidectomy. First suggested in the late nineteenth century, myringotomy with insertion of a ventilation tube became popular only after its reintroduction by Armstrong in 1954.' Placement of tubes is effective in clearing MEE, and in restoring hearing. Mandel and others&found that subjects with tympanostomy tubes had more disease-free time and better hearing than did children with myringotomy alone or control subjects observed without surgery. Gates and othersz4found fewer episodes of effusions, more effusion-freetime, less medical and surgical retreatments, and less time with abnormal hearing in patients with OME treated with tympanostomy tubes. Placement may occur in the office setting for older children or adults, but the majority are inserted in children under general inhalational anesthesia on an outpatient basis. A complete discussion on types of tympanostomy tubes, placement techniques, management of complications, and other indications for their use is found elsewhere in this issue. Adenoidectomy has been shown to be effective in the management of patients with OME. found that clearance rates of MEE after 12 months were significantly higher in patients with adenoidectomy than in the control group. Paradise and others58found a significant reduction in time with effusion. Gates and othersz2 found that patients treated with adenoidectomy experienced less time with effusion and fewer repeated surgeries in the 2 years that followed compared with patients not treated with adenoidectomy. The latter two studies found that the beneficial effect of adenoidectomy is unrelated to the size of adenoids. The most common risk associated with adenoidectomy is postoperative bleeding, reported by Helmus and others31 in only 4 of 1000 cases (0.4%). All

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episodes of bleeding occurred within the first 6 hours. Transient velopharyngeal incompetence following adenoidectomy is not uncommon but it may persist if the adenoids were removed in a child with an unrecognized submucous cleft palate and may require a second procedure to ameliorate. Nasopharyngeal stenosis is rare but may occur as a result of overzealous electrocautery or curettage. In deciding which children would benefit from adenoidectomy, clinicians must take into consideration the potential benefits versus the costs and potential risks. When weighing these factors, the threshold for performing adenoidectomy is often crossed for clinicians when a patient has recurrence of OME after placement of one or more tympanostomy tubes in the past. Gates and othersz3recommend that adenoidectomy be considered in the initial surgical treatment of patients with OME, noting that the potential avoidance of repeated placement of tympanostomy tubes may justify the greater initial expense of adenoidectomy. This is certainly reasonable in children with concurrent obstructive sleep apnea or recurrent adenotonsillitis, but treatment must be individualized and must account for factors unique to each patient. In some children and adults with OME, despite reasonable medical and surgical intervention, disease may remain in the middle ear, manifesting as continued effusion or conductive hearing loss. The tympanic membrane inherently offers a limited view of the pertinent anatomy, so failure of the therapy outlined earlier must raise a question concerning the origin of the persistent disease. In these situations, exploration is advocated, and exploratory tympanotomy with or without mastoidectomy may be required. Silent OM and masked mastoiditis are well d e ~ c r i b e d , 2and ~ , ~inspection ~ may reveal osteitis, thick mucoid fluid, cholesterol granuloma, or granulomatous polypoid mucosa. If not already present, a tympanostomy tube should be placed. Although mastoidectomy and exploration of the middle ear are rarely necessary for patients with OME, they are essential tools in the diagnostic and treatment armamentarium. A high index of suspicion must be maintained for silent disease in the middle ear and mastoid.

Chronic Otitis Media Chronic OM is the most advanced disease state in the spectrum of OM, and by definition it is associated with some form of irreversibly pathologic condition in the middle ear. Of 144 temporal bones in patients with COM, da Costa et all3 reported that 97% had granulation tissue, 92% had ossicular changes, 24% had tympanosclerosis, 20% had tympanic membrane perforation, 14%had cholesterol granuloma, and 10%had cholesteatoma. Obliteration of the middle ear space may be seen as a result of severe tympanic membrane retraction, which occurs in both middle ear atelectasis (in which middle ear mucosa is preserved) and in adhesive OM, in which loss of mucosa results in the adherence of the tympanic membrane to the promontory and the ossicles. The diagnosis of COM can usually be made by history, otoscopy,microscopic ear examination, and appropriate audiometric assessment. Most patients have a past history of frequent AOM, intermittent foul-smelling otorrhea, hearing loss, or a combination of these. Less often, presenting complaints include tinnitus, vertigo, or otalgia. Otoscopic findings may reveal tympanic membrane perforation with or without otorrhea, tympanosclerosis, polypoid middle ear mucosa, or severe tympanic membrane retraction with or without cholesteatoma. Perforation of the tympanic membrane can occur with a normal middle ear (e.g., trauma or extrusion of tympanostomy tubes), so perforation is neither diagnostic of COM nor required to make the diagnosis. For example, a normal tympanic membrane

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may belie underlying pathologic conditions in the middle ear in patients with silent OM, a concept introduced by Paparella et aP6;suspicion for this is essential in making the diagnosis. The use of otoendoscopesin the office via a laser-assisted tympanostomy may successfullyidentify middle ear disease in patients with silent OM." Tuning fork examination and audiologic evaluation may reveal a mixed or conductive hearing loss. A fistula test may be positive if a labyrinthine fistula is present as a result of bony destruction. The use of radiographic imaging in patients with COM is not standardized and can include routine mastoid roentgenograms. CT produces high-definition images of bone and soft tissue, and although MR imaging provides superior definition of soft tissues, bony anatomy is poorly resolved in MR imaging; therefore, compared with MR imaging, CT is the study of choice in patients with uncomplicated COM.43How often preoperative CT is performed in clinical practice varies from highly selective (used only when complications are suspected) to universal (when all ears with COM are imaged). The practice of most surgeons lies in a category somewhere between these two extremes. The clinician should assess the extent to which the information gained with preoperative imaging becomes sufficiently clinically significant to justify its cost should be assessed by the individual clinician. Medical treatment is limited to the control of active otorrhea, which can initially be treated with frequent suction cleaning and topical antibiotics, as a powder or suspension, with or without hydrocortisone. The topical antimicrobial is selected empirically to eradicate the most commonly isolated aerobic pathogens, P. aeruginosa and 5'. a u ~ e u s but , ~ ~cultures in unresponsive cases may prompt an adjustment. Irrigation with 2% acetic acid solution, often made with one part white vinegar to one part distilled water or 70% alcohol, may also be effective. In uncomplicated cases, systemic antibiotics are reserved for intractable otorrhea with a culture-specificpathogen. In adults, an oral fluoroquinolone(e.g., ciprofloxacin) may be helpful, but in children, because no oral agent effective against P. aeruginosa is yet approved in the United States, intravenous antibiotics are often necessary. Fortunately, several investigators have reported that in chronic suppurative OM without cholesteatoma, aggressive treatment with intravenous antimicrobialsyields long-term success in 75% of patient^.'^,^^,^^ The primary goals of surgical management of patients with COM are to identify and remove infected, irreversibly diseased tissue, aerate the middle ear and mastoid, close the middle ear, reconstruct the hearing mechanism, and prevent the morbidity of future sequelae or complications. Procedures used in achieving these goals include exploratory tympanotomy, myringoplasty, tympanoplasty, ossiculoplasty, and tympanomastoidectomy, which include the open-cavity, closedcavity, and intact-bridge modifications. The adjunctive use of otoendoscopes to identify disease intraoperatively has increased the surgical options and advanced the frontiers of minimally invasive surgery for COM." Any surgical approach should be flexible and individualized, using adaptable techniques appropriate for the pathologic conditions encountered.

SUMMARY Otitis media is an important disease of children and adults and is caused by multiple interrelated factors, including infection, ET dysfunction, allergy, and barotrauma. These factors stimulate middle ear mucosa and inflammatory cells to release inflammatory mediators, which, in turn, increase vascular permeability and secretory activity, resulting in MEEs. The stages of OM may not only overlap

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and interchange between POM, SOM, and MOM b u t also may progress from any stage i n a continuum toward COM without timely intervention. The treatment of patients w i t h OM varies according t o t h e type and stage of disease. The primary treatment of patients with A O M is systemic antibiotics, adding tympanocentesis when bacterial identification is required. For patients with recurrent AOM, appropriate therapy includes chemoprophylaxis, vaccination, myringotomy with insertion of tympanostomy tubes, or adenoidectomy. Tympanostomy tubes prevent and relieve barotrauma in patients receiving hyperbaric oxygen therapy. Current evidence suggests that repeated myringotomies or observation are preferable t o the placement of tympanostomy tubes, for treating t h e SOM that follows radiation therapy. For patients w i t h OME, antibiotic therapy is the only nonsurgical treatment modality shown t o be effective. Following a course of antibiotics, if the MEE persists beyond 3 months, surgical options include placem e n t of tympanostomy tubes, adenoidectomy, or adenoidectomy plus myringotomy or tubes. The primary treatment modality for patients w i t h COM is surgery, which is necessary t o eradicate disease and reconstruct t h e hearing mechanism.

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