CHAPTER 10 ROLE IN CERTAIN COMPLICATIONS AND SEQUELAE OF MIDDLE-EAR DISEASE Chronic draining ears are prevented by effective treatment of acute draining ears. The chapter includes • The ET system as it directly relates to pathogenesis and management of the following diseases/disorders: • Perforation of the tympanic membrane with and without otitis media • Chronic suppurative otitis media • Atelectasis and retraction pocket of the tympanic membrane • Acquired cholesteatoma • Cholesterol granuloma • Surgical method to permanently close the ET when related to intractable otorrhea in the presence of a radical mastoidectomy. • Recommended surgical techniques to repair a perforation of the tympanic membrane (myringoplasty and tympanoplasty) when ET dysfunction is still problematic, such as in children. The complications and sequelae of otitis media and related diseases and disorders are either extracranial (intratemporal) or intracranial. The extracranial complications and sequelae are mastoiditis, labyrinthitis, facial paralysis, apical petrositis, perforation of the tympanic membrane, chronic suppurative otitis media, atelectasis of the tympanic membrane–middle ear, retraction pocket of the tympanic membrane, cholesteatoma, tympanosclerosis, adhesive otitis media, ossicular chain disarticulation and fixation, and cholesterol granuloma.1 The intracranial suppurative complications of otitis media are meningitis, subdural empyema, cerebritis, extradural and brain abscess, lateral sinus thrombosis, and otitic hydrocephalus.2 The functions and dysfunctions of the ET system can have a direct or an indirect role in the pathogenesis and management of these conditions. Direct and Indirect Roles of the ET System Of these complications and sequelae, dysfunction of the ET system has a direct role in pathogenesis and management, such as perforation of the tympanic membrane, chronic suppurative otitis media, atelectasis, retraction pocket, cholesteatoma, and cholesterol granuloma, but for the remaining extracranial and intracranial complications and sequelae, the tube has an indirect role. The initial disease may have been caused by dysfunction of the tubal system, but the status of the function of the system has little or no role in the pathogenesis of the other complications or sequelae. Nevertheless, the function of the tubal system can have an important role in management decisions of these other complications and sequelae, even though the tubal system did not actually cause them. For example, despite the lack of involvement of the tubal system in causing fixation or dysarticulation of the ossicular chain, the status of the system should be considered when deciding whether to perform an ossiculoplasty in a young child who is a potential candidate but whose known poor ET function has required tympanostomy tube placement. Delaying the procedure until tubal function improves would be a prudent decision. The progression of a middle-ear infection into a suppurative extracranial complication, (mastoiditis, labyrinthitis, facial paralysis, or apical petrositis), anatomic (inflammatory) obstruction of the middle-ear end of the system notwithstanding, is not directly caused by dysfunction of the tubal system; however, when treating these complications, the status of the function of the ET is important. If there is known chronic ET dysfunction, placement of a tympanostomy tube for treatment of the otitis media and prevention of future attacks is indicated. Related to intracranial suppurative complications, tubal function does not have a primary role in the progression of the middle-ear and mastoid infection into the intracranial cavity, but surgical management of the middle ear and mastoid is influenced by the status of the ET system, such as decisions related to performing a closed tympanomastoidectomy and tympanoplasty (with or without tympanostomy tube placement) versus a modified or radical mastoidectomy. For the secondary or indirect role that the function of the tubal system has in these management decisions, the reader is referred to our other publications.1–5 Perforation of the Tympanic Membrane Perforation of the tympanic membrane that is a complication of otitis media can be either acute or chronic. Otitis media may or may not be present, and when present, otorrhea may or may not be evident. In this chapter, I discuss only the role of the tube in the pathogenesis of acute and chronic perforations and its role in management. I have covered the other aspects of perforations in other texts.1,5 A perforation may also occur following spontaneous extrusion of a tympanostomy tube or following its removal, which are both discussed in Chapter 9, “Role in Management of Middle-Ear Disease.” Acute Perforation Role of the ET System in Pathogenesis A perforation of the tympanic membrane is not a frequent complication in most patients who develop an episode of acute otitis media, especially when appropriate and prompt antibiotic treatment is administered. Why some children seem to suffer a perforated eardrum with each episode of acute otitis media whereas others do not could be related to differences in the pathophysiology of the tubal system (too open, too short), the virulence of the pathogen, or the immunologic status of the host. It is common for a perforation to occur in high-risk populations, such as Australian Aborigines or certain Native Americans, presumably owing to the presence of a tube that is too open. In a study of White River Apache Native Americans, Beery and colleagues tested the function of the tube through chronic perforations in children and adults and reported that they had patulous or semipatulous ETs.6 An ET with low resistance would permit a larger bolus of bacteria-laden purulent material from the nasopharynx to enter (by reflux, aspiration, or insufflation) the middle ear, resulting in perforation and otorrhea, causing a more fulminating infection than would occur if the tube had either normal or high resistance. The outcomes of acute otitis media related to the development of a perforation are shown in Figure 10–1. The most common outcome after an uncomplicated attack of otitis media is spontaneous resolution of the middle-ear infection, but in about 10%, a persistent middle-ear effusion will become chronic (otitis media with effusion) after 3 months. In some patients, an acute perforation can occur after which the otorrhea can resolve and the perforation heal, but in other individuals, there is resolution of the otitis media and the perforation remains open and become chronic. In still other patients, the acute otitis media with perforation and otorrhea does not resolve and the perforation does not heal, resulting in progression to chronic suppurative otitis media (see Chronic Suppurative Otitis Media). Role of the ET System in Management For patients who are prone to recurrent acute otitis media and who frequently perforate their tympanic membrane, preventive measures should be instituted. Those who develop frequent perforations should receive treatment promptly, the current debate related to treat or not to treat selected patients with antibiotics notwithstanding. When a perforation occurs during an episode of acute otitis media, systemic antibiotics and ototopical agents are recommended. The tympanic membrane will frequently heal after the suppurative process in the middle-ear ends. The defect usually closes within a week after onset of infection. When persistent discharge lasts longer than the initial 10-day course of antibiotic treatment, the child requires more intensive evaluation and aggressive management. In addition to obtaining a culture of the purulent material from the middle ear and adjusting antimicrobial agents, frequent cleaning of the canal, followed by instillation of ototopical drops, may also be required. The middle-ear infection can progress into the chronic stage. But, as concluded in my discussion of chronic suppurative otitis media subsequently, the most effective method to prevent chronic middle-ear infection, when an acute perforation is present, is to effectively treat the acute infection, which prevents the progression to chronic disease: chronic disease must begin with an acute stage. In addition to certain high-risk populations who frequently develop a perforation during an attack of acute otitis media (Apaches), other individuals who are not members of a known high-risk group can also develop recurrent perforations, probably owing to one or more of the underlying risk factors cited earlier, which include an abnormal ET system. Pathophysiology of the anterior (pharyngeal) end of the system should be thoroughly evaluated for pathology that might promote nasopharyngeal secretions to enter the middle ear through the tube, such as hypertrophied adenoids or nasal allergy (the Toynbee phenomenon), causing insufflation of secretions into the middle-ear cleft. Chronic Perforation As shown in the flow diagram (Figure 10–2), an acute perforation may fail to heal and become chronic. Otitis media may or may not be present and when present can be acute, recurrent acute, or chronic (chronic suppurative otitis media). Role of the ET System in Pathogenesis Certain racial groups have a higher incidence of chronic perforations than others, such as Native Americans,8,9 Alaskan Natives,9 and the Aboriginal population of Australia.10 It is likely that these high-risk populations have a pathophysiology (i.e., the tube is too open) similar to that reported by Beery and colleagues in the White River Apaches in the southwest United States.8 Also, it is well known that in some parts of Africa, certain native populations frequently develop a chronic perforation. But other individuals, not belonging to these special populations, may also be at risk of developing a chronic perforation. Even though the perforation provides ventilation and drainage functions for the middle ear, a chronic perforation is susceptible to acute and chronic otitis media with otorrhea. Figure 10–2 demonstrates that nasopharyngeal secretions can enter the middle ear from the nasopharynx. In addition to the obvious possibility of contamination of the middle ear owing to water in the external auditory canal when a nonintact tympanic membrane is present, a perforated eardrum impairs the protective function of the tubal system at the middle-ear end. The physiologic protective function of the ET system is too open. The middle ear and mastoid gas cells no longer have a gas cushion to prevent nasopharyngeal secretions from entering the ear, which can then result in reflux otitis media (see Chapter 5, “Pathophysiology”). The infection can progress into chronic suppurative otitis media. Repair of the eardrum defect in these cases should be considered to restore the physiologic middle-ear gas cushion (see the following section). Role of the ET System in Management When an acute episode of otitis media occurs, appropriate medical treatment is indicated. Usually, ototopical antibiotic therapy will be sufficient, but systemic antimicrobial agents may be needed if the otitis media or the underlying upper respiratory tract infection is severe. When recurrent infections are a problem, a search for underlying pathology at either end of the tubal system should be considered. At the pharyngeal end, adenoids, allergy, and tumor should be of concern, and at the middle-ear end of the system, the possibility of cholesteatoma should be entertained. When recurrent otitis media occurs when there is a chronic perforation, repair of the tympanic membrane should be considered. Repair of the Tympanic Membrane In general, the outcomes of myringoplasty and tympanoplasty are more favorable in adults than in children; infants and children younger than 7 years have less favorable outcomes after attempts to repair the eardrum defect than do older children and adults. Most likely, the reasons for the less favorable surgical outcomes in children are related to the uncertain status of the function of the tube in this age group, which is attributable to developmental anatomic differences (see Chapter 3, “Anatomy”) and to differences in the function of the tube (see Chapter 4, “Physiology”). Important decision-making factors when chronic perforation is present and repair is contemplated11: • The age of the child • The duration of the perforation • Unilateral versus bilateral perforations • The status of the contralateral ear when that tympanic membrane is intact • ET function • The presence or absence of recurrent or chronic otorrhea (and the frequency, severity, and duration of otorrhea) • The presence or absence of cholesteatoma • The season of the year Related to ET tube function, the following are guidelines for repair of a chronic perforation: 1. For those 6 years of age or older, the presence of a unilateral perforation when the contralateral tympanic membrane is intact and the middle ear has been free of disease for 1 year or longer. In children, this practice is helpful because a watchful waiting period of four seasons permits observation for not only the fall, winter, and spring respiratory tract seasons but summer as well because allergic rhinitis may be involved in the pathogenesis of their middle-ear disease (I call this “Vivaldi’s law,” in honor of the composer of “The Four Seasons”). Because the two ears are connected to the same child, and in children tubal function is usually similar bilaterally, one can assume that when following a child for four seasons or longer while observing the contralateral ear with an intact tympanic membrane, tubal function should be adequate to withstand repair of the tympanic membrane. Some surgeons believe that otoscopic and tympanometric assessment of the contralateral ear, if the tympanic membrane is intact, is helpful in predicting the success of tympanoplasty. However, the study by Manning and colleagues did not support this practice.12 In a review of 209 tympanoplasties in 183 children, Kessler and colleagues found that the presence of otitis media in the contralateral ear was significantly associated with postoperative reperforation.13 Contrary to those surgeons who would refrain from repairing a unilateral perforation when recurrent otitis media with otorrhea is a problem, I do not consider recurrent drainage a contraindication. In fact, recurrent otorrhea would make repair of the tympanic membrane a compelling indication because the perforated eardrum may be permitting reflux or insufflation of secretions from the nasopharynx to enter the middle ear. As depicted in Figure 10–3, the flask model illustrates the loss of the gas cushion in the body of the flask when there is a hole in it. In the human, a nonintact tympanic membrane is an ET system that is too open at its distal, middle-ear end (the system’s protective function is impaired). Also, the protective function of the system is lost when a perforated eardrum is present because contamination from the canal (water) can result in a middle-ear infection. Thus, closure of the defect would prevent contamination of the middle ear from the canal and potentially prevent reflux of nasopharyngeal secretions (see Chapter 4). But when the otitis media with otorrhea becomes chronic, treatment of the chronic suppurative otitis media should precede repair (see below). The presence of a middle ear and mastoid that has persistent infection can usually lead to an unfavorable outcome following repair, such as postoperative failure of the graft. 2. The presence of bilateral perforations in patients whose ET system is now considered within normal limits as a result of growth and development or when a nonsurgical (allergy control and treatment) or surgical (adenoidectomy, repair of a cleft palate) management has improved the tubal system’s function. Because these patients have bilateral perforations, a contralateral ear with an intact tympanic membrane is not available to observe for at least 1 year. A test of tubal function may be helpful in these cases, especially children. VALUE OF ET FUNCTION IN PREDICTING OUTCOME Performing ET function tests prior to recommending repair of a chronic perforation may be beneficial in determining the outcome of the surgery. Holmquist studied tubal function in adults before and after tympanoplasty and reported that the operation had a high rate of success in patients with good function (those who could equilibrate applied negative pressure) but that in patients without good tube function, surgery frequently failed to close the perforation.14 Miller and Bilodeau and Siedentop reported similar findings,15,16 but Ekvall, Lee, and Schuknecht; Andreasson and Harris; Cohn and colleagues; and Virtanen and colleagues found no correlation between the results of the inflation–deflation tests and the success or failure of tympanoplasty.17–21 Kumazawa and colleagues reported that they consider preoperative evaluation using ET function tests to be helpful in prognosis.22 Most of these studies failed to define the criteria for “success,” and the postoperative follow-up period was too short. At our center, we assessed ET function in children before tympanoplasty and found that of 51 ears of 45 children, 8 ears could equilibrate an applied negative pressure (−200 mm H2O) to some degree, and in 7 of these ears, the graft healed, no middle-ear effusion occurred, and no other perforation developed during a follow-up period between 1 and 2 years. However, as was found in studies in adults, failure to equilibrate an applied negative pressure did not predict failure of the tympanoplasty.23 In another similar study, we reported that good tubal function was shown to be predictive of a favorable outcome, but poor tubal function was not helpful in predicting failure. In this study, an additional test of ET function was performed in conjunction with the inflation–deflation test that was used in the first study, the forced-response test. With the use of the forced-response test, there was a significant association between outcome and preoperative tube function, as determined by combining active and passive function parameters. In addition, these investigators reported that other factors, such as graft placement (medial or lateral), contralateral middle-ear status, and the age of the child, were not associated with outcome.12 Testing procedures are described in Chapter 8, “Diagnosis and Tests of Function”). In my opinion, and from the outcome of these studies, it is evident that if the patient has good tubal function, regardless of age, the success of tympanoplasty is likely to be favorable, but if poor function is present, these tests will not help the clinician in deciding to operate. Nevertheless, the value of testing a patient’s tubal function lies in the possibility of determining from the test results whether a young child is a candidate for tympanoplasty. On the basis of other findings alone, one might decide to withhold surgery until the child is older. These tests are also of value in the diagnosis of severe or total anatomic (mechanical) obstruction. The patient should be examined for the possible presence of a nasopharyngeal tumor. If none is found, the cause of obstruction could be mucosal swelling of the middle-ear end of the tube, which may respond to a medical treatment, such as ototopical medication. If the obstruction persists despite medical treatment and if a repair of the perforation is to be performed, an exploration of the middle ear and bony (protympanic) portion of the ET should be part of the examination (tympanoplasty, not myringoplasty). It is possible that an occult cholesteatoma will be found to be the cause of the obstruction. SURGICAL METHOD RELATED TO ET FUNCTION If a chronic perforation of the tympanic membrane is to be surgically repaired, a method should be chosen that would have the most successful outcome. I have provided a detailed discussion and description of the surgical methods I use to repair a perforated tympanic membrane elsewhere,11 but, in general, I preferred performing a tympanoplasty using a laterally placed fascia graft, as opposed to a medial graft, when the perforation is relatively large. Outcomes of watching the contralateral, intact tympanic membrane for at least four seasons and preoperative tubal function testing notwithstanding, patients who have a perforation secondary to otitis media have or have had dysfunction of the tubal system. Therefore, I prefer to place the graft laterally so that if postoperative middle-ear negative pressure occurs, for example, during an upper respiratory tract infection, a lateral graft will be pulled (“sucked”) onto the remnant of the tympanic membrane as opposed to being pulled off the eardrum and into the middle ear when a medial graft is used. The lateral graft technique is particularly useful in children whose tubal function is almost always questionable, especially in high-risk populations, such as those who have a cleft palate or Down syndrome. When a tympanoplasty must be performed and the function of the ET is most likely poor, such as middle ear (and mastoid) surgery for cholesteatoma, a tympanostomy tube should be inserted. Chronic Suppurative Otitis Media An understanding of the role of the ET system in the pathogenesis of chronic suppurative otitis media (without cholesteatoma) is vitally important in management. In this section, I direct my discussion only to the role that the tubal system plays in these two aspects of this stage of middle-ear infection. For other issues, such as medical treatment and recommended surgical procedures, the reader is referred to our other texts.1,5,11 Role of the ET System in Epidemiology In a review of the epidemiology of chronic suppurative otitis media, several conclusions can be drawn related to the possible role that tube tubal function plays in certain populations.24 First, this chronic infectious disease is a major health problem. Table 10–1 is a list of some of the available studies conducted in various countries and populations around the world. As can be seen from Table 10–1, I have separated them into four groups of populations based on the prevalence of the disease. Figure 10–4 shows that chronic suppurative otitis media affects diverse racial and cultural groups living not only in temperate climates but also in climate extremes ranging from the Arctic Circle to the equator (see Chapter 2, “Epidemiology”). It is also apparent that the highest-risk groups live in disparate geographic areas with varying climates, which implies an underlying pathogenesis common to these special populations. Some investigators have reported that the risk factors attributed to the high rates of chronic suppurative otitis media in these populations are a lack of breast-feeding, overcrowding, poor hygiene, poor nutrition, passive smoking, high rates of nasopharyngeal colonization with potentially pathogenic bacteria, and inadequate and unavailable health care.9,25–27 But, as I discuss later, in my opinion, the underlying status of the function of the tubal system must be considered to be an extremely important risk factor. Prevalence Group* Population Prevalence, % Highest Alaska Inuits 30–46 Canada Inuits 7–31 Greenland Inuits 7–12 Australian Aborigines 12–25 Apache, Navajo 4–8 High Solomon Islands 4–6 New Zealand Maori 4 Malaysia 4 Micronesia 4 Sierra Leone 6 Gambia 4 Kenya 4 Nigeria 4 Tanzania 2–3 Low Korea 2 India 2 Saudi Arabia 1.4 Lowest United States < 1 Finland < 1 United Kingdom < 1 Adapted from Bluestone CD.24 *Prevalence is separated into ranking of prevalence from highest to lowest from a search of the available literature. Role of the ET System in Pathogenesis The etiology and pathogenesis of chronic suppurative otitis media are multifactorial, in which one or more of the risk factors noted earlier are involved. But chronic suppurative otitis media begins with an episode of acute otitis media. Thus, the factors that have been associated with acute otitis media may be initially involved, such as upper respiratory tract infection; anatomic and functional factors, such as ET dysfunction; host factors, such as young age; immature or impaired immunologic status; the presence of upper respiratory allergy; familial predisposition; the presence of older siblings in the household; male sex; race; method of feeding (bottle vs breast); and environmental (smoking in the household) and social factors. Probably the most important factors related to the onset of acute otitis media in infants and young children are immaturity of the structure and function of the ET and immaturity of the immune system.28 An attack of acute otitis media, in which the tympanic membrane ruptures with otorrhea, usually precedes chronic suppurative otitis media, but in Australian Aborigines, chronic otitis media with effusion is initially present,29 which is uncommon. Factors most likely related to the progression of acute otitis media into the chronic stage have been noted earlier, but most likely the process, if long-standing, results in a chronic osteitis of the middle-ear cleft.30 Figure 10–5 shows the sequence of events after the onset of an episode of acute otitis media, when the tympanic membrane is intact, that leads to chronic suppurative otitis media. Because a spontaneous perforation commonly accompanies an episode of acute otitis media that is untreated with an antimicrobial agent and, less commonly, despite adequate treatment, it may be part of the natural history of the disease process rather than a complication. Figure 10–5 also shows the sequence of events following the onset of an attack of acute middle-ear infection when the tympanic membrane has a chronic perforation. The presence of a tympanostomy tube would have a similar pattern, which is discussed in Chapter 9. As shown in Figure 10–6, when the tympanic membrane is intact and an upper respiratory tract infection occurs, the infected nasopharyngeal secretions are either aspirated, insufflated, or refluxed though the tube into the middle ear. The bacterial organisms are the three most common: Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. If a perforation complicates the course and otorrhea ensues, bacteria from the ear canal (Pseudomonas, Staphylococcus aureus) can secondarily enter the middle ear through the perforated tympanic membrane (a secondary bacterial infection). If resolution of the otitis media and healing of the perforation fail to occur, chronic suppurative otitis media can follow. It is important to note that chronic disease is always initiated by acute disease. When a tympanic membrane has a chronic perforation (or a tympanostomy tube is present) and there is no evidence of otitis media, reinfection of the middle ear and mastoid can occur in one of two sequences of events: 1. Figure 10–7 shows that during the course of an upper respiratory tract infection, infected nasopharyngeal secretions can enter the middle ear owing to the secretions being refluxed or insufflated (crying in the infant, nose blowing, or swallowing when there is nasal obstruction present—the Toynbee phenomenon31) through the ET since the middle-ear gas cushion is lost. In most instances, these bacteria are initially the same as those isolated when acute otitis media occurs behind an intact tympanic membrane, such as S. pneumoniae and H. influenzae.32 Following the acute otorrhea, Pseudomonas aeruginosa, Staph. aureus, and other organisms from the external ear canal enter the middle ear through the nonintact tympanic membrane, which results in a secondary infection, acute otorrhea, and chronic suppurative otitis media. Table 10–2 is a list of the bacteria isolated from Pittsburgh children’s ears that had chronic suppurative otitis media, the most common of which are not those that are isolated from ears that have acute otitis media and otorrhea.33 Pseudomonas is the most common bacterial organism isolated from chronic suppurative otitis media around the world, which implies a similar sequence of events involved in the disease around the globe. Bacteria Isolated Number of Isolates* (N = 118) Pseudomonas aeruginosa 56 Staphylococcus aureus 18 Diphtheroids 8 Streptococcus pneumoniae 7 Haemophilus influenzae (nontypable) 6 Bacteroides sp 3 Candida albicans 2 Candida parapsilosis 2 Enterococcus 2 Acinetobacter 2 Staphylococcus epidermidis 1 Morganella morgagni 1 Providentia stuartii 1 Klebsiella sp 1 Proteus sp 1 Serratia marcescens 1 Moraxella 1 Pseudomonas cepacia 1 Providencia rettgeri 1 Pseudomonas maltophilia 1 Achromobacter xylosoxidans 1 Eikenella 1 Adapted from Kenna MA et al.33 *Number exceeds 80 due to more than one organism isolated in 38 ears. 2. Because the protective function of the ET system at the middle-ear end (the nonintact tympanic membrane) is lost, chronic suppurative otitis media also can occur when the middle ear is contaminated by organisms (e.g., P. aeruginosa) present in water that enters the eardrum defect during bathing in a hot tub and swimming, especially in rivers. As shown in Table 10–1, certain populations are at high risk of developing chronic suppurative otitis media. Populations at highest risk are those who live in diverse geographic regions in the world, which would make climate an unlikely explanation for their disease. In these racial groups, it is more likely that the pathogenesis of their disease is due to genetic differences in their ET function. The tube is most likely hyperpatent, which may be due to a semipatulous or patulous lumen, a tube that is too short, or both. Histopathologic studies of temporal bones of young individuals who had cleft palate and those who had Down syndrome—both conditions are at high risk of otitis media—had statistically shorter ET than age-matched specimens from individuals without these disorders.34 We examined the possibility that the ET varies in certain racial groups. Indeed, in his PhD thesis, Doyle identified anatomic differences in the osseous segment of the ET in the bony craniofacial structures of Alaskan Inuit, American Indian, Caucasian, and Negro crania.35 He concluded that these differences may be related to known variations in prevalence rates: Inuits and Native Americans have a greater prevalence of otitis media than Negroes and Caucasians; the characteristic disease of the Inuit and Native Americans is chronic suppurative otitis media. Related to the Native American population, in a clinical study by Beery and colleagues, White Mountain Apache Indians were found to have tubes that were semipatulous (of low resistance) compared with those of a group of Caucasians.7 Similar findings have been reported by other groups, such as Canadian Inuits. Ratnesar calibrated the ET with ureteric catheters in Canadian Inuits and Caucasian individuals and found the tube to be larger in Inuits than in Caucasians.36 Environment is also important, but genetic differences are probably more important in those who are at high risk. One of the most impressive studies that assessed this hypothesis was the one that involved adopted Apache children who had more episodes of acute otitis media than did their non-Apache siblings and an illness rate similar to that of Apache children who remained on the reservation.37 Also, in a study from Greenland of 591 children who were ages 3, 4, 5, and 8 years, 9% had chronic perforation, with and without chronic suppurative otitis media, which was statistically most common in children who had both parents who were native Greenlanders.38 More than likely, ET dysfunction is involved in the process even in individuals who are not members of high-risk populations or who have an obvious craniofacial abnormality. In a study of ET function in the ears of Japanese children and adults who had chronic perforations, Iwano and colleagues found impaired active opening function of the tube.39 They concluded that the tube was functionally obstructed; however, organic (mechanical or anatomic) obstruction was also considered to be involved in the pathogenesis in adults. Role of the ET System in Management Understanding the role of the tubal system in the pathogenesis of chronic suppurative disease is not so important in treating the disease but is essential in prevention of recurrence. Treatment is initially medical and directed toward eliminating the infection from the middle-ear cleft. Because the bacteria most frequently cultured are gram negative, antimicrobial agents should be selected to be effective against these organisms. Experts now recommend the use of ototopical agents as first-line treatment as opposed to systemic antimicrobial drugs. Failure of aggressive medical treatment to cure the infection should signal the need to determine if there is an underlying pathology somewhere in the ET system, such as cholesteatoma in the middle ear–mastoid infection or tumor in the nose, nasopharynx, or paranasal sinuses. If this search fails to reveal a potential source for failure to eradicate the chronic infection, intravenous antimicrobial therapy should be attempted, and if this option fails, surgery, such as a tympanomastoidectomy, is usually indicated.33 A detailed discussion of medical treatment is in Bluestone and colleagues.1 However, when the middle ear and mastoid infection is cured by medical treatment and the tympanic membrane remains open, preventive measures should be instituted to prevent recurrence. Prevention of recurrence is related to the role of the tubal system in the pathogenesis of this chronic infection. Prevention of Recurrence If the infection can be eliminated using the methods previously described and the tympanic membrane remains open (persistent perforation or tympanostomy tube), prevention of recurrence can be achieved by the following options. The choice of these options will depend on the age of the child and the status of the function of the ET.