0 Bewertungen0% fanden dieses Dokument nützlich (0 Abstimmungen)
34 Ansichten12 Seiten
Middle ear infections, known as otitis media, are very common in young children and a leading cause of hearing loss in this age group. This document discusses the history, epidemiology, definitions, and etiology of two types of otitis media - acute otitis media and chronic otitis media with effusion. It explores the role of Eustachian tube dysfunction and inflammation in the development and pathogenesis of middle ear infections and effusions.
Middle ear infections, known as otitis media, are very common in young children and a leading cause of hearing loss in this age group. This document discusses the history, epidemiology, definitions, and etiology of two types of otitis media - acute otitis media and chronic otitis media with effusion. It explores the role of Eustachian tube dysfunction and inflammation in the development and pathogenesis of middle ear infections and effusions.
Middle ear infections, known as otitis media, are very common in young children and a leading cause of hearing loss in this age group. This document discusses the history, epidemiology, definitions, and etiology of two types of otitis media - acute otitis media and chronic otitis media with effusion. It explores the role of Eustachian tube dysfunction and inflammation in the development and pathogenesis of middle ear infections and effusions.
Infections of the middle ear space and their sequelae
have plagued mankind from the beginning of time.
First described by Hippocrates in 450 BC, this uni- versally observed process continues to present one of the most perplexing medical problems of infancy and childhood, while being the leading cause of hearing loss in this age group. It is estimated that 70% of children will have had one or more episodes of otitis media (OM) by their third birthday. 1 This disease process knows no age boundaries but occurs mainly in children from the newborn period through approximately age 7 years, when the inci- dence begins to decrease. It occurs equally in males and females. A racial prevalence exists, with a higher incidence occurring in specic groups such as Native Americans, Alaskan and Canadian Natives, and Aus- tralian aboriginal children. African American chil- dren appear to have less disease than do American white children, but this observation has yet to be adequately explained. Important epidemiologic factors include a higher incidence of OM in children attending day- care centers, a seasonal variation with more disease being present in the fall and winter versus the spring and summer, and a genetic predisposition to middle ear infection. Other epidemiologic factors include a lower incidence and duration of OM in breast-fed children and a higher incidence in chil- dren with altered host defenses. 2 Anatomic changes such as cleft palate and other craniofacial anomalies as well as congenital and acquired immune de- ciencies are also important factors. One of the ear- liest signs of acquired immune deciency syndrome (AIDS) in infants is recurring episodes of OM. This has been observed in more than 50% of neonates with AIDS. 3 DEFINITIONS Unfortunately, numerous terms have been used to describe the various inammatory conditions of the middle ear space (Table 91). This has resulted in both confusion and a lack of uniformity in report- ing. An attempt to standardize nomenclature was undertaken in the early 1980s and will be used throughout this chapter when discussing this disease process. 4 Otitis media represents an inammatory con- dition of the middle ear space, without reference to cause or pathogenesis. Middle ear effusion is the liquid resulting from OM. An effusion may be either serous (thin, watery), mucoid (viscid, thick), or purulent (pus). The process may be acute (0 to 3 weeks in duration), sub- acute (3 to 12 weeks in duration), or chronic (greater than 12 weeks in duration). Otitis media may occur with or without effu- sion. In those cases without effusion, inammation of the middle ear mucous membrane and tympanic membrane may be the only physical nding. Occa- 249 C HA P T E R 9 Otitis Media and Middle Ear Effusions Gerald B. Healy, MD, Kristina W. Rosbe, MD TABLE 91. Synonyms Used in the Past for Otitis Media Acute Otitis Media Otitis Media with Effusion Suppurative Serous Purulent Secretory Bacterial Mucoid Glue ear Middle ear effusion sionally, infection may involve only the tympanic membrane (myringitis), without involving the mucosa of the middle ear space. This chapter deals primarily with two disease processes: acute otitis media (AOM) and chronic oti- tis media with effusion (COME). Acute otitis media represents the rapid onset of an inammatory process of the middle ear space associated with one or more symptoms or local or systemic signs. These usually include otalgia, fever, irritability, anorexia, vomiting, diarrhea, or otorrhea. Physical examina- tion usually reveals a thickened, erythematous or bulging tympanic membrane with limited or no mobility to pneumatic otoscopy. Erythema of the tympanic membrane may be an inconsistent nding and may be absent in certain systemic illnesses such as immune deciency, when the patient cannot mount a sufcient inammatory response to present this more classic nding. The acute onset of fever, otalgia, and, on occasion, a purulent discharge is usu- ally evidence of AOM. Following such an episode, the patient may move into a subacute or even chronic phase in which uid is present in the middle ear space, although active infection may be absent. Chronic otitis media with effusion indicates the presence of asymptomatic middle ear uid, usu- ally resulting in conductive hearing loss. The tym- panic membrane may present numerous physical ndings including thickening, opacication, and impaired mobility. An air-uid level and/or bubbles may be observed through a translucent tympanic membrane. This entity is distinguished from AOM in that the signs and symptoms of acute infection are lacking (eg, otalgia, fever, otorrhea). ETIOLOGY Eustachian tube (ET) dysfunction is considered the major etiologic factor in the development of middle ear disease. Politzer rst proposed the ex vacuo the- ory of OM in 1867. 5 The theory postulates that chronic negative pressure, secondary to ET malfunc- tion, results in the development of a transudate into the middle ear space. Numerous experiments have been carried out by many authors to substantiate this theory. It is traditionally maintained that the effusion is sterile; therefore, therapy should be aimed chiey at relieving ET dysfunction. Most proponents of the theory have proposed that there are essentially two types of ET obstruction resulting in middle ear effusion: mechanical and functional. Mechanical obstruction may be either intrinsic or extrinsic. Intrinsic mechanical obstruction is usually caused by inammation of the mucous membrane of the ET or an allergic diathesis causing edema of the tubal mucosa. Extrinsic mechanical obstruction is caused by obstructing masses such as adenoid tissue or nasopharyngeal neoplasms. Some observers believe that infants and younger children may suffer from functional ET obstruction as a result of either decreased tubal stiff- ness or an inefcient active opening mechanism. Proponents believe that either form of obstruction results in inadequate ventilation of the middle ear with resulting negative middle ear pressure. This theory supports the development of a rational med- ical or surgical approach to alleviate the obstruction and thus overcome negative pressure. The ET has three functions (1): ventilation of the middle ear associated with equalization of air pressure in the middle ear with atmospheric pres- sure, (2) protection of the middle ear from sound and secretions, and (3) drainage of middle ear secre- tions into the nasopharynx with the assistance of the mucociliary system of the ET and middle ear mucous membrane. The second etiologic theory was rst suggested by Brieger in 1914 and proposes an inammatory origin to OM. 6 Since that time, several other authors have supported this theory. In 1958, Senturia reported a 41% incidence of positive bacterial cul- tures in 130 specimens taken from patients with a diagnosis of serous otitis media. 6 Other series have supported this nding. 7 Sades observation that the basic histopathologic mechanism in otitis media with effusion (OME) is an inammatory hypertro- phy of the middle ear mucous membrane and hyperplasia of its mucous glands also tends to sup- port an inammatory basis. 8 Protein analysis of middle ear effusions indi- cates a higher concentration of total protein, lactate dehydrogenase, malate dehydrogenase, and acid phosphatase than in serum. This nding has led to the speculation that this material represents an exu- date rather than a transudate, giving further evi- dence that this is an inammatory process. Some proponents of the inammatory theory feel, how- 250 Ballengers Otorhinolaryngology ever, that inammation occurs secondary to ET dys- function; thus, the inammatory response is not the primary etiologic factor. Numerous other factors may well contribute to the development of middle ear disease. These include allergy, ciliary dysfunction, nasal and/or sinus dis- ease, and immaturity of the immune system. In the last 10 years, the role of allergy in OME has been extensively investigated. 9,10 Otitis media in the pediatric population is felt to be associated with allergy in 5 to 80% of cases. Inhalant allergies are felt to play a greater role than food allergies. Most stud- ies have been unable to demonstrate, however, an increase in serum immunoglobulin E (IgE) in chil- dren with OME. 11 Allergic rhinitis, itself, is not felt to be the cause of OME. A viral or bacterial infection may prime the environment, which, in response, produces inam- matory mediators. These mediators begin the phys- iologic cycle, creating ET dysfunction, pressure gradients, and transudation of uid. 12 Middle ear mucosa is rarely the target organ. The nasopharynx is felt to be the major site of action with subsequent spread via the ET to the middle ear. Allergy is felt to affect ET function in several ways. Nasal obstruction can occur secondary to mast cell degranulation with increased vascular permeability, increased mucosal blood ow, and increased mucus production. Retrograde extension of inammatory mediators from the anterior nose to the nasophar- ynx as well as allergen contact with the nasopharynx can cause ET edema and obstruction with a second- ary increase in the pressure gradient through nitro- gen gas exchange and subsequent transudation of uid. 12 Animal models have demonstrated immune- mediated inammation as a contributing factor in the pathogenesis of OME. The role of immune com- plexes in experimental models has also been estab- lished. Normal middle ear mucosa is not felt to be immunocompetent tissue. During inammation, however, it is transformed into a secretory epithe- lium containing multiple goblet cells with inltra- tion of macrophages and lymphocytes. This immune response may result from circulating anti- bodies that enter the middle ear through increased vascular permeability. Otitis mediaprone children have been shown to have higher levels of IgG antibody and IgG-anti- gen immune complexes in their serum and middle ears versus a nonOM-prone cohort. Immunoglob- ulin may be the predominant immune mechanism in the middle ear. It is felt that bacteria may actually cause immunosuppression of cell-mediated immu- nity. Immunoglobulin A is thought to be a late defense mechanism and may actually prevent bacte- riolysis by IgG and complement, acting as a blocking antibody. Others have proposed an IgE-mediated hypersensitivity reaction to viral antigens. Immune tolerance is the concept that immu- nization through the oral or pulmonary route may modulate the middle ear immune response. Studies have shown that oral immunization after systemic sensitization actually increased immune-mediated OME. Vaccines are now becoming available, includ- ing the recently US Food and Drug Administration (FDA)-approved pneumococcal conjugate vaccine. 13 MICROBIOLOGY Numerous studies have documented the microbiol- ogy of OM. 14,15 Approximately 30% of middle ear effusions demonstrate known pathogens for OM. 16 Although the treatment of AOM is directed toward the elimination of the bacteria from the middle ear space, viruses may also play an important etiologic role in this disease process. 17 The most common bac- terial pathogens responsible for acute infection include Streptococcus pneumoniae and nontypable Haemophilis inuenzae. These two microorganisms account for approximately 60% of the cases associ- ated with bacterial infection. Group A Streptococcus, Branhamella catarrhalis, Staphylococcus aureus, and gram-negative enteric bacteria are less frequent causes of OM (Figure 91). Because of the difculty in obtaining viral cul- tures, fewer specic data are available regarding their occurrence in patients with OM. However, respira- tory syncytial virus accounts for a majority of the viral infections of the middle ear space. 17 Otitis media may accompany exanthematous viral infec- tions such as infectious mononucleosis and measles. Over the years, chronic effusions have been thought to be sterile. However, more recent studies have conrmed the presence of bacteria in middle ear uid, and studies show that the bacterial spec- trum closely resembles that found in AOM. 18 This Otitis Media and Middle Ear Effusions 251 information becomes increasingly important when consideration is given to the treatment of patients with both of these disease processes (Figure 92). DIAGNOSIS In most cases, a careful history and physical exami- nation will lead to the accurate diagnosis of OM. A careful history should elicit classic symptoms of OM. In the patient with the acute form of the dis- ease, otalgia, fever, irritability, vomiting, and diar- rhea may be present. Less frequently, otorrhea, vertigo, and facial paralysis may be associated with an acute infection of the middle ear space. In those patients in whom infection has spread into the mas- toid air cell system and beyond, swelling of the postauricular area may be present. In COME, hearing loss may be the only symp- tom. The most denitive part of the diagnosis is an appropriate physical examination to conrm the presence or absence of middle ear pathology. A complete examination of the head and neck should be undertaken rst to identify the possibility of any predisposing condition such as craniofacial anom- aly, nasal obstruction, palatal defect, or adenoid hypertrophy. In patients with unilateral OM, the nasopharynx should be visualized to rule out the possibility of neoplasm. Otoscopy represents the most critical part of the examination to establish the diagnosis of OM (Figure 93). Use of the pneumatic otoscope is essential. The existence of chronic middle ear effusion is most eas- ily conrmed when there is a denite air-uid level or when bubbles are clearly visible within the middle ear space (Figure 94). However, ndings commonly associated with OME include a severely retracted tympanic membrane with apparent foreshortening of the handle of the malleus and a reduction in tym- panic membrane mobility (Figure 95). Occasionally, the tympanic membrane may be dull or thickened and have an amber hue (Figure 96). In severe cases, middle ear uid may become purplish or blue, indi- cating hemorrhage within the tympanic cavity. The color of the tympanic membrane is important but is not conclusive in making a diagno- sis. An erythematous tympanic membrane alone 252 Ballengers Otorhinolaryngology FIGURE 92. Bacterial incidence in chronic otitis media with effusion. FIGURE 91. Bacterial incidence in acute otitis media with effu- sion. may not be indicative of a pathologic condition because the vasculature of the tympanic membrane may be engorged as a result of the patients crying or the presence of fever. Acute otitis media usually presents with a hyperemic tympanic membrane that is frequently bulging and has poor mobility (Figure 97). Occa- sionally, perforation may be present, and purulent otorrhea is clearly visible. The use of tympanometry has been popular- ized to conrm the ndings of pneumatic otoscopy. This modality provides an objective assessment of the mobility of the tympanic membrane as well as the ossicular chain. By measuring tympanic mem- brane impedance, one can accurately predict condi- tions of the middle ear space (see Chapter 5). The ultimate diagnostic test to conrm the presence of OM involves aspiration of middle ear contents. In acute situations, myringotomy or tym- panocentesis may be undertaken to confirm the diagnosis, obtain material for culture, and relieve pus under pressure in an effort to avoid further com- plications. This may be necessary in patients who are unusually ill or toxic secondary to OM or in patients with severe suppurative complications. It may also be necessary in those patients who are having an unsatisfactory response to antibiotic therapy, in toxic newborns, or in patients who are significantly immune decient. With the rise in bacteria resistant to initial antibiotic therapy, tympanocentesis has been exam- ined for its role in more specic antibiotic therapy. 19 Bluestone recommends tympanocentesis for several indications: (1) OM in patients with severe otalgia or toxic patients; (2) unsatisfactory response to antimi- crobial therapy; (3) onset of OM in a patient already receiving antibiotics; (4) OM associated with a con- rmed or potential suppurative complication; and (5) OM in a newborn, sick neonate, or immunosup- pressed patient. This procedure does have signicant risks including conductive and sensorineural hearing losses if not done properly. Otolaryngologists and pediatricians must be well trained in the technique to prevent these serious complications. The hearing loss associated with OM should be documented whenever possible, especially in patients in whom chronic effusion is present. Although the presence of a conductive hearing loss does not conrm the diagnosis of COME, its pres- ence does contribute to the conrmation of middle ear fluid. It is also important in documenting response to therapy. MANAGEMENT ACUTE OTITIS MEDIA Acute otitis media represents one point in a contin- uum of the disease process known as otitis media. The current standard of care strongly indicates that patients diagnosed as having an acute middle ear process should receive antimicrobial therapy for at least 10 to 14 days. In light of the fact that culture material is usually not readily available, therapy is begun on an empiric basis with treatment being aimed at the more common microorganisms found Otitis Media and Middle Ear Effusions 253 FIGURE 93. Normal right tympanic membrane at otoscopy. in the acute process. Some have recommended with- holding antimicrobial agents in certain cases. 20 How- ever, in light of the fact that suppurative compli- cations have markedly declined during the antibiotic era, antibiotic therapy is still strongly recommended in the acute process. 20 The standard initial treatment for AOM is amoxicillin, 40 mg/kg every 24 hours in three divided doses, or ampicillin, 50 to 100 mg/kg every 24 hours in four divided doses for 10 days. In chil- dren allergic to penicillin, a combination of erythro- mycin, 40 mg/kg every 24 hours, and sulsoxazole, 120 mg/kg every 24 hours in four divided doses, may be substituted. If -lactamase-producing H. inuen- zae or B. catarrhalis is suspected, either amoxicillin- clavulanate, 40 mg/kg every 24 hours in three divided doses, or trimethoprim-sulfamethoxazole, 8 mg/kg of trimethoprim and 40 mg/kg of sul- 254 Ballengers Otorhinolaryngology FIGURE 94. Otitis media with effusion. Note bubbles conrm- ing the presence of uid. FIGURE 95. Advanced otitis media with effusion with markedly retracted right tym- panic membrane, with an apparent foreshortened handle of the malleus and thick, mucoid effusion. famethoxazole every 24 hours, may be used in two divided doses. Cexime (Suprax, Lederle Laborato- ries, Wayne, NJ), 8 mg/kg in one dose, or cefprozil (Cefzil, Bristol-Myer-Squibb, Princeton, NJ), 15 mg/kg every 24 hours in two divided doses, may also be used effectively. A single intramuscular injection of ceftriaxone (Rocephin, Hoffman-Roche, Nutley, NJ), 50 to 100 mg/kg mixed with 1% lidocaine, not to exceed 1.5 mL, may be used in patients with vom- iting (Table 92). Newer treatment for -lactamase- producing microorganisms include high-dose amoxicillin at 80 mg/kg every 24 hours. 21 Dosages of appropriate antimicrobial agents for use in AOM are noted in Table 92. Most patients who are receiving antibiotic therapy for AOM have significant improvement within 48 hours. If the child has not improved or the condition has worsened, tympanocentesis for cul- ture and possibly myringotomy for drainage may be indicated. The patient may be re-examined some time during the course of therapy to ensure that the treatment has been effective. Most children will have an effusion present at the completion of a 10- to 14-day course of antibi- otic therapy. Such effusions may last up to 12 weeks before spontaneous clearance can be expected. 22 Additional therapy such as analgesics, anti- pyretics, and oral decongestants (antihistamines and sympathomimetic amines) may be useful. Oral decongestants may relieve nasal congestion, provid- ing some aeration of the ET. Their efcacy has not been proven, however. The patient may remain in a subacute phase of the disease process for several weeks. Repeated episodes of AOM plague many chil- dren, especially during the rst 3 to 4 years of life. Several issues should be considered and evaluated in the management of such patients. A search should be made for a concomitant source of infection in the upper respiratory tract such as chronic adenoiditis or chronic sinusitis. Mild immune immaturity, espe- cially in the IgG subclass group, may be responsible for this relentless process. Testing of immunoglobu- lins should be considered in relentless cases. Such patients may be divided into two groups, the first being children who clear their effusion between episodes, whereas the second is made up of patients who have a persistent effusion between Otitis Media and Middle Ear Effusions 255 TABLE 92. Daily Dosage for Common Antibiotic Agents in Acute Otitis Media Agent Dosage/24 hr Amoxicillin 40 mg/kg in 3 doses Ampicillin 50100 mg/kg in 4 doses Erythromycin- 40 mg/kg (E) and Sulsoxazole 120 mg/kg (S) in 4 doses Amoxicillin-clavulanate 40 mg/kg in 3 doses Trimethoprim- 8 mg (TMP) and 40 mg sulfamethoxazole (SMZ)/kg in 2 doses Cexime 8 mg/kg in 1 dose FIGURE 96. Chronic otitis media with effusion. episodes. In the latter group, chronic hearing loss becomes an additional major issue, especially as it impacts speech and language development. 1 Several options are available for those patients who clear their effusion between episodes. The rst option includes antibiotic therapy for each separate episode; a second option would be the use of antibi- otic prophylaxis on a prolonged basis, whereas the third would include myringotomy and ventilation tube insertion. The administration of pneumococcal vaccine also may be useful. Amoxicillin, or a suitable substitute in peni- cillin-allergic patients, may be given once daily at bedtime as prophylaxis. This form of therapy is usu- ally administered during the months in which OM has its highest prevalence. In children in whom the middle ear does not clear between acute episodes, ventilation tubes may be necessary to address the concomitant hearing loss associated with the process. Their use may also be necessary in those patients with antibiotic allergy or intolerance. CHRONIC OTITIS MEDIA WITH EFFUSION Medical Therapy Chronic otitis media with effu- sion may occur as a sequela to AOM or in patients who have had no documented recent episodes of acute suppurative disease. Numerous associated fac- tors must be considered; thus, a careful history should be taken for the possibility of underlying allergy, sinus disease, or nasopharyngeal obstruction, which may be secondary to hypertrophic adenoids or even neoplasm. Numerous methods of management have been advocated over the years for the persistent form of the disease. Antihistamine-sympath- omimetic amine preparations were used frequently to clear the effusion. However, controlled clinical trials have demonstrated a lack of efcacy. 23 The use of corticosteroids, either applied topically in the nose or given systematically, has been reported to be advantageous in clearing middle ear fluid. 24 Unfortunately, there is a paucity of data to demon- strate efficacy; therefore, their use cannot be strongly recommended at this time. The most effective medical therapy used to this point has been antibiotic administration. Numerous trials have concluded that some patients may respond to a 21- to 30-day course of full-dose antibi- otic therapy. 25 The demonstration of viable bacteria in the middle ear effusions of chronically diseased ears has led to this recommendation. In light of the similarity of the bacterial spectrum, the same antibiotics recommended for AOM may be used in this disease. This form of therapy is strongly rec- 256 Ballengers Otorhinolaryngology FIGURE 97. Acute otitis media showing an erythe- matous, bulging tympanic membrane. ommended in any child who has not received antibiotic treatment before consideration is given to myringotomy and ventilation tube insertion and/or adenoidectomy. Historically, there was debate as to whether OME should be treated with antibiotics since there exists a certain spontaneous resolution rate. Physi- cians in other countries have traditionally not treated OM with antibiotics as frequently as is done in the United States. Rosenfeld and Posts meta- analysis of studies of antibiotic therapy for OME found a statistically signicant efcacy for short- term resolution of OME. 16 Gates stated that approx- imately 40% of children with OME treated with antibiotics still have an effusion after 30 days, whereas 10% have a documented effusion 3 months after initial therapy. 26 Another factor that has not been studied well to date is what the impact of COME is on language development and learning in the child with conductive hearing loss secondary to COME and at what time point this decit becomes an unacceptable risk. The success of prophylactic antibiotic therapy for OME had also not been stud- ied in a systematic fashion. In children with concomitant disease of the upper respiratory tract such as chronic sinusitis or adenoiditis, consideration must be given to the simultaneous control of these diseases. In addition, systemic problems such as allergy or immunode- ciency must also be addressed if long-term reversal of the middle ear abnormality is to be achieved. With the emerging role of allergy in OME, the role of corticosteroid therapy has been re-examined. Investigators have demonstrated that a brief course of oral corticosteroids is efcacious for the short- term cure of OME. The proposed therapeutic mech- anisms include stabilization of phospholipids to prevent arachidonic acid formation and subsequent inammatory mediator formation, possible decrease in peritubal lymphoid tissue size, enhanced secretion of ET surfactant, and reduced middle ear uid vis- cosity by action on mucoproteins. 27 The risks of oral corticosteroid therapy in children remain a concern, however. Studies have demonstrated an increase in the development of AOM if corticosteroids are not prescribed with antibiotics, transient depression in adrenal function, and the potential for disseminated varicella infection and its complications. Because of these risks, Rosenfeld recommends a trial of antibi- otics and corticosteroids only if the next step would be tympanostomy tube placement. There have been no good randomized controlled trials to examine the risk-to-benet ratio. 27 Relapses have been demon- strated within several weeks after treatment. The effects of nasal corticosteroids or immunotherapy on OME have not been studied. Surgery The use of ventilation tubes with or with- out adenoidectomy has become the ultimate treat- ment of COME. This surgical intervention immediately corrects the conductive hearing loss associated with the middle ear process and dimin- ishes the patients tendency toward recurrent infec- tion. It should be strongly considered in the following situations: 1. Recurrent AOM a. Unresponsive to antibiotic therapy b. Signicant antibiotic allergy or intolerance 2. Negative middle ear pressure with impending cholesteatoma 3. Chronic effusion of the middle ear space with a duration of greater than 3 months a. Conductive hearing loss of greater than 15 dB b. Nasopharyngeal neoplasm for which treatment such as radiation therapy may be necessary Although some controversy exists over the use of ventilation tubes, they do provide a safe method for normalizing middle ear pressure and, in most cases, restoring hearing to normal. They are usu- ally associated with minimal morbidity, although tympanosclerosis or persistent perforation may be seen in a few instances. In most circumstances, it is difcult to determine whether these ndings are a result of the underlying middle ear pathology with middle ear atelectasis or secondary to the ventila- tion tube itself. Numerous types of tubes are avail- able for ventilation of the middle ear space, but, basically, they are all designed to provide equaliza- tion of pressure across the tympanic membrane (Figure 98). Some designs favor intubation of greater duration but also carry a slight risk of an increased incidence of persistent perforation upon extrusion. Depending on the age of the patient, tube insertion may be carried out under local or general anesthesia. It is usually advisable to allow spontaneous extrusion of the tubes to occur. Most tympanostomy tubes remain in the tympanic membrane for Otitis Media and Middle Ear Effusions 257 approximately 6 to 12 months, with some extruding earlier and some later. The most common complication of tube inser- tion is otorrhea. This may be secondary to either reux of nasopharyngeal secretions, especially dur- ing an upper respiratory infection, or as a result of pathogens entering the middle ear through the lumen of the ventilation tube. It is commonly believed that contaminated water that is allowed to enter the middle ear through the tympanostomy tube may result in AOM media with otorrhea. In these instances, the external ear canal should be carefully cleaned and a culture obtained from the middle ear by aspirating through the tympanostomy tube. After this has been accomplished, oral antibi- otics should be initiated as well as topical antibiotic therapy. The usual treatment includes the use of antibiotic agents commonly prescribed for other forms of AOM. To avoid this possible complication, water protection of the ears is usually advised when con- tamination may be a possibility. This may be accom- plished through the use of earplugs or cotton covered with petrolatum jelly, both of which can be inserted into the ear canal to provide adequate pro- tection. In summary, tympanostomy tubes can pro- vide a useful means of ventilating the middle ear space, controlling hearing loss secondary to middle ear effusion, and controlling recurrent infection. Adenoidectomy may be useful as an adjunct to myringotomy in the treatment of middle ear effu- sion. 28 Removal of adenoid tissue improves the ven- tilatory function of the ET, thus allowing for appropriate equalization of pressure. The adenoid has been felt to play a role in OM in two ways: when hypertrophic, by causing mechanical obstruction of the ET, and when small, as a bacterial reservoir. 29 The adenoid is thought to be an important site for pri- mary contact of inhaled microorganisms. Two stud- ies are frequently cited regarding the use of adenoidectomy in OME. Gates demonstrated greater long-term efcacy in the treatment of OM in chil- dren 4 to 6 years of age when adenoidectomy was added to tympanostomy tube placement or myringotomies even if this was the rst surgical intervention in a child. 26 Paradise et al, on the other hand, recommend adenoidectomy only if a child fails initial tympanostomy tube placement. 30 Studies have also shown that the recurrence rate of AOM may be reduced by adenoidectomy. 30 In addition, other confounding factors may warrant adenoidec- tomy such as evidence of chronic adenoiditis, nasal obstruction, or recurrent or chronic sinusitis sec- ondary to nasal obstruction. 258 Ballengers Otorhinolaryngology FIGURE 98. Ventilation tube in place in the right tympanic membrane. CONCLUSION The future solution to OM, acute or chronic, does not lie in current therapy regimens. Manipulation of the immune system to provide enhanced protec- tion will probably result in a signicant decrease in the incidence of this disease process. Vaccination may play a signicant role in this endeavor. Both nontypable H. inuenzae and S. pneumoniae are leading etiologic factors in the development of bac- terial OM and have polysaccharide capsules. Poly- saccharide vaccines lack immunogenicity in infants and children under 2 years. Based on the same premise as the successful H. inuenzae type b vac- cine, in which the capsular polysaccharide is conju- gated with a protein, a heptavalent pneumococcal conjugate vaccine, PCV7 (Prevanar, Wyeth-Lederle Vaccines), has become available. PCV7 and other pneumococcal vaccines may prove to be an impor- tant step in the prevention of AOM. This vaccine is recommended for universal use in children 23 months and younger. The American Academy of Pediatrics recommends that if immunization is ini- tiated in infants younger than 7 months, four doses of PCV7 be given concurrently with other recom- mended childhood immunizations at 2, 4, 7, and 12 to 15 months. If immunization is initiated in infants who are between 7 and 23 months of age, who have not received their prior doses of PCV7, fewer doses are recommended. Children with congenital immunodeficiency, chronic cardiac disease, and infection with human immunodeficiency virus, chronic pulmonary disease, and other serious chronic conditions are especially vulnerable to pneumoccocal infection. 31 Attempts are under way to develop conjugated vaccines against nontypable H. influenzae and B. catarralis, which also has a polysaccharide capsule. It is too early to determine the impact of vaccination on the incidence of AOM. Other factors such as the role of gastroesophageal reux or the role of such substances as surfactant have yet to be determined. Currently, OM represents a costly medical problem worldwide. In some cultures, its morbidity with associated hearing loss, learning difculties, and secondary central nervous system complications are almost unmeasurable. This signicant medical problem deserves more research attention than it receives so that signicant costs and morbidity asso- ciated with it can be reduced. Berman et al have developed a cost-effectiveness model for OME ther- apy. 32 Their recommendations include a trial of cor- ticosteroids and antibiotic therapy at the 6-week follow-up visit if no resolution, another course of antibiotics at the 9-week visit, and tympanostomy tube placement if no resolution at 12 weeks. With OM continuing to be one of the most common rea- sons for physician visits in children today, nding the safest, most efcacious, and cost-effective treat- ment remains an important goal. REFERENCES 1. Teele DW, Klein JO, Rosner B. Otitis media with effusion during the rst three years of life and the development of speech and language. Pediatrics 1984;74:2827. 2. Daly KA. Epidemiology of otitis media. Otolaryngol Clin North Am 1991;24:77586. 3. Ammann AJ, Shannon K. Recognition of acquired immune deciency syndrome (AIDS) in children. Pediatr Rev 1985;7:1017. 4. Senturia BH, Bluestone CD, Klein JO, et al. Report of the Ad Hoc Committee on Denition and Classi- cation of Otitis Media with Effusion. Ann Otol Rhi- nol Laryngol 1980;89:34. 5. Politzer A. Diagnose und Theraphaie der ansammI- ung seroeser Fluessigkeit in der Thrommelhoehle. Wien Med Wochenschr 1867;17:2447. 6. Senturia BH. Studies concerned with tubo-tympani- tis. Ann Otol Rhinol Laryngol 1958;67:44067. 7. Healy GB, Smith HG. Current concepts in the man- agement of otitis media with effusion. Am J Otol 1981;2:13844. 8. Sade J. The biopathology of secretory otitis media. Ann Otol Rhinol Laryngol 1970;81:5970. 9. Bernstein JM. Immunologic reactivity in the middle ear in otitis media with effusion. Otolaryngol Clin North Am 1991;24:84558. 10. Bernstein JM. The role of IgE-mediated hypersensi- tivity in the development of otitis media with effu- sion: a review. Otolaryngol Head Neck Surg 1993; 109:61120. 11. Bernstein JM, Doyle WJ. Role of IgE-mediated hypersensitivity in otitis media with effusion: patho- physiologic considerations. Ann Otol Rhinol Laryn- gol 1994;103:159. 12. Bernstein JM. Role of allergy in eustachian tube blockage and otitis media with effusion: a review. Otolaryngol Head Neck Surg 1996;114:5628. Otitis Media and Middle Ear Effusions 259 13. Lieu TA, Ray GT, Black SB, et al. Projected cost-effec- tiveness of pneumococcal conjugate vaccination of healthy infants and young children. JAMA 2000;283: 14608. 14. Bluestone CD, Klein JO. Microbiology in otitis media in infants and children. Philadelphia: WB Saunders; 1988. 15. Bluestone CD. Current therapy for otitis media and criteria for evaluation of new antimicrobial agents. Clin Infect Dis 1992;14 Suppl 2:S197203. 16. Rosenfeld RM, Post JC. Meta-analysis of antibiotics for the treatment of otitis media with effusion. Oto- laryngol Head Neck Surg 1992;106:37886. 17. Mein JO, Teele DW. Isolation of viruses and mycoplasmas from middle ear effusions: A review. Ann Otol Rhinol Laryngol 1976;85 Suppl 25:1404. 18. Healy GB, Teele DW. The microbiology of chronic middle ear effusions in young children. Laryngo- scope 1977;87:14728. 19. Bluestone CD. Role of surgery for otitis media in the era of resistant bacteria. Pediatr Infect Dis J 1998;17: 10908. 20. VanBuchem FL, Peters MF, Vant Hof MA. Acute oti- tis media: a new treatment strategy. Par Med J (Clin) Res 1985;290:10337. 21. Jacobs MR. Drug-resistant Streptococcus pneumo- niae: rational antibiotic choices. Am J Med 1999;106 Suppl 5A:19S25S. 22. Teele DW, Mein JO, Rosner BA. Epidemiology of oti- tis media in children. Ann Otol Rhinol Laryngol 1980;89:56. 23. Cantekin EI, Mendel EM, Bluestone CD, et al. Lack of efcacy of a decongestant-antihistamine combi- nation for otitis media with effusion (secretory otitis media) in children. N Engl J Med 1983; 308:297301. 24. Schwartz RH, Puglese J, Schwartz DM. Use of a short course of prednisone for treating middle ear effu- sion: a double-blind cross-over study. Ann Otol Rhi- nol Laryngol 1980;89 Suppl 68:296300. 25. Healy GB. Antimicrobial therapy of chronic otitis media with effusion. Int J Pediatr Otorhinolaryngol 1984;8:137. 26. Gates GA. Adenoidectomy for otitis media with effu- sion. Ann Otol Rhinol Laryngol 1994;103:548. 27. Rosenfeld RM. New concepts for steroid use in oti- tis media with effusion. Clin Pediatr 1992;31:61521. 28. Gates GA, Avery CS, Phihooa TJ, et al. Effectiveness of adenoidectomy and tympanostomy tubes in the treatment of chronic otitis media with effusion. N Engl J Med 1987;317:144488. 29. Honjo I, Takahashi H, Sudo M, et al. Pathophysio- logical and therapeutic considerations of otitis media with effusion from viewpoint of middle ear ventila- tion. Int J Pediatr Otorhinolaryngol 1998;43:10513. 30. Paradise JL, Bluestone CD, Rogers KD. Efcacy of adenoidectomy for recurrent otitis media: results from parallel random and non random trials. Pedi- atr Res 1987;21:28691. 31. Black S, Shinefield H, Fireman B, et al. Efficacy, safety, and immunogenicity of heptavalent pneumo- coccal conjugate vaccine in children. Northern Cali- fornia Kaiser Permanente Vaccine Study Center Group. Pediatr Infect Dis J 2000;19:18795. 32. Berman S, Roark R, Luckey D. Theoretical cost effec- tiveness of management options for children with persisting middle ear effusions. Pediatrics 1994;93: 35363. 260 Ballengers Otorhinolaryngology