International Journal of Pediatric Otorhinolaryngology 42 (1998) 207 223

Epidemiology and pathogenesis of chronic suppurative otitis media: implications for prevention and treatment1
Charles D. Bluestone *
Department of Pediatric Otolaryngology, Childrens Hospital of Pittsburgh, 3705 Fifth A6enue, Pittsburgh, PA 15213, USA Received 17 March 1997; received in revised form 8 August 1997; accepted 12 August 1997

Abstract Despite advances in public health and medical care, chronic suppurative otitis media is still prevalent around the world. It is most common in developing countries and in certain high risk populations in developed nations, as well as among children who have tympanostomy tubes inserted. Since this chronic infection is caused by persistent acute otorrhea, which in turn is usually secondary to acute otitis media, prevention should be directed toward prompt and appropriate treatment of the acute middle-ear infection. Repair of chronic perforations should prevent recurrence, since reinfection is due either to reux of pathogenic organisms from the nasopharynx into the middle ear, or water contamination from the external canal. Information from epidemiological studies, which show that populations can be categorized into highest, high, low and lowest prevalence, can be helpful in setting national priorities for prevention and treatment. 1998 Elsevier Science Ireland Ltd. Keywords: Chronic suppurative otitis media; Chronic otitis media; Pathogenesis; Epidemiology

* Tel.: + 1 412 6925902; fax: + 1 412 6926074. 1 Presented at the World Health Organization & CIBA Foundation Joint Workshop on Prevention of Hearing Impairment from Cronic Otitis Media, CIBA Foundation, London, 19 21 November 1996. 0165-5876/98/$19.00 1998 Elsevier Science Ireland Ltd. All rights reserved. PII S 0 1 6 5 - 5 8 7 6 ( 9 7 ) 0 0 1 4 7 - X

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Chronic suppurative otitis media (CSOM) remains one of the most common chronic infectious diseases of childhood in many developing countries, especially among the poor and in certain populations in developed nations, in many parts of the world. With the rising popularity of tympanostomy tubes for management of recurrent acute otitis media (AOM) and chronic otitis media with effusion (OME) in highly industrialized nations, CSOM can also become a potential problem for any child who has them inserted. Since this infection is associated with chronic hearing loss, which may affect development of speech, language, cognition and school performance and with the ever present potential danger of life-threatening suppurative complications, effective prevention and treatment is imperative. Before embarking on public health programs to prevent and treat CSOM in infants and children, the prevalence of this infection must be determined, populations at risk must be identied and an understanding of its etiology and pathogenesis is required.

1. Denitions Chronic suppurative otitis media is a stage of ear disease in which there is chronic infection of the middle ear-cleft, i.e. eustachian tube, middle ear and mastoid and in which a nonintact tympanic membrane (e.g. perforation or tympanostomy tube) and discharge (otorrhea) are present. This stage of ear infection has been called simply chronic otitis media, but this term can be confused with chronic OME, in which no perforation is present. Another potentially confusing issue is including chronic perforation, in the absence of middle-ear infection, as CSOM; more precisely it should only be termed a chronic perforation. A perforation may occur as a complication or sequela of otitis media (or following tympanostomy tube extrusion or removal, or as the result of trauma) and the patient never experiences an episode of otorrhea, or the initial episode of drainage does not become chronic [1]. Despite this strict denition, a review of the literature reveals that many reports that describe the epidemiology of CSOM include in this disease entity chronic perforation, with and without otorrhea. Also, some clinicians consider a chronic perforation associated with infection to be active, and when infection is absent, inactive [2]. Chronic otomastoiditis is another term used by clinicians, but this term is also synonymous with CSOM. Aural cholesteatoma may also be included under the disease entity CSOM, but cholesteatoma may or may not be associated with chronic infection.

2. Epidemiology

2.1. Chronic suppurati6e otitis media

Chronic suppurative otitis media is a major health problem in many populations around the world, affecting diverse racial and cultural groups living not only in

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temperate climates but in climate extremes ranging from the arctic circle to the equator. From a review of approximately 50 reports published during the past 30 years, there appears to be four groups of populations based upon the prevalence of the disease (Table 1). The populations in which the prevalence of CSOM (dened in the published reports as chronic perforation with and without suppuration, but not cholesteatoma) has been reported to be the highest are the: (1) Inuits of Alaska (30 46%) [3 5], Canada (7 31%) [612] and Greenland (712%) [1315]; (2) Australian Aborigines (12 33%) [1626] and (3) certain Native Americans, e.g. Apache and Navajo tribes; (4 8%) [2732]. Apparently these North American Indian tribes have higher rates than others [33]. One study from the Eastern Canadian Arctic compared the rates in Cree Indian school children with Inuit children living in the same area and found the rate in the Inuit to be 22%, but only 1% in the Cree [11]. Populations with moderately high rates are: (1) certain natives of the South Pacic islands, such as the Solomon Islands (46%) [34], N.Z. Maori (4%) [35,36], Malaysia (4%) [37] and Micronesia (4%) [3840] (in contrast to these high rates in
Table 1 Prevalence of suppurative otitis media Population Highest Inuits Alaska Canada Greenland Australian Aborigines Native Americans Apache, Navajo South Pacic Islands Solomon Islands N.Z. Maori Malaysia Micronesia Africa Sierra Leone Gambia Kenya Nigeria Tanzania Low Korea India Saudi Arabia US UK Denmark Finland Prevalence (%) References

30 46 7 31 7 12 12 33 4 8 4 6 4 4 4 6 4 4 4 2 3 2 2 1.4 B1 B1 B1 B1

[3 5] [6 13] [14 16] [17 25] [27 32] [34] [35,36] [37] [38 40] [41] [43] [44] [45,46] [47 49] [51] [52] [53] [54,55,57] [58,59] [60] [56]

High

Lowest

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some islands of the South Pacic, natives of Melanesia have an extremely low rate; less than 1% [41]); and (92) some African populations, such as Sierra Leone (6%) [42], Gambia (4%) [43], Kenya (4%) [44], Nigeria (4%) [45,46] and Tanzania (23%) [47 49]. Not all African native populations have these high rates. One study of South African rural blacks found a rate of less than 1% [50]. In Spain the rate of CSOM in one Gypsy population was 4%, whereas in the same region the rate was only 1% in Caucasians. Populations with relatively low rates of CSOM are Korea (2%) [51], India (2%) [52] and Saudi Arabia (1.4%) [53]. Studies from highly-industrialized nations have reported the lowest rates (none or less than 1%), such as the US [5456], Finland [57], the UK [58,59] and Denmark [60]. In one adult population in Great Britain, the rate has been reported to be 3.1% [2]. But, with the widespread use of tympanostomy tubes in these countries, CSOM occurs as a not uncommon complication in infants and children [61]. Risk factors that have been attributed to the high rates of CSOM in these populations are: lack of breastfeeding, overcrowding, poor hygiene, poor nutrition, passive smoking, high rates of nasopharyngeal colonization with potentially pathogenic bacteria and inadequate and unavailable health care [7,11,24,62].

2.2. Cholesteatoma
Acquired cholesteatoma is a relatively uncommon nding in populations that have a high rate of CSOM, such as Inuits, Native Americans and Australian Aborigines. One study of Greenland Inuits estimated the rate to be 6.6 per 100 000 children aged birth to 14 years [14]. In another study from Sierra Leone in which the rate of CSOM in 2015 children was 6.4%, only one child was found to have a cholesteatoma [42]. However, there is some anecdotal evidence that these populations may be experiencing an increase in the incidence of cholesteatoma with improvements in living conditions and health care. In the developed countries, in which the rates of CSOM (as a sequela of otitis media [OM]) are low, the rates of cholesteatoma are relatively high. In one study of Iowa children 10 19 years of age, the incidence was 9.2 per 100 000 [63].

3. Hearing and chronic suppurative otitis media Hearing has been assessed in children with OME. In a study of Pittsburgh infants and children who had documented OME, the average speech awareness threshold in 222 infants 7 24 months of age was 24.66 dB hearing level and in 540 older children aged 2 12 years the average air conduction threshold was 27dB [64]. There have only been a few studies of hearing in populations that have a high rate of CSOM, but the average hearing loss is usually worse than that reported when OME is present. One recent excellent study from Sierra Leone evaluated the hearing in children who had perforation with

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Fig. 1. Possible outcomes of acute otitis media. Chronic suppurative otitis media (CSOM) can develop: (1) following acute perforation and otorrhea; (2) following recurrent acute otorrhea in the presence of a chronic perforation; and; (3) less commonly, as a sequela of chronic otitis media with effusion (OME).

and without suppuration. Of the 37 ears that had dry perforations, 33 (89%) had a pure tone average of 26 dB or greater and of the 100 ears that had CSOM, 96 (96%) also had this degree of hearing loss [42].

4. Pathogenesis The etiology and pathogenesis of CSOM is multifactorial, in which one or more of the risk factors noted above are involved. But CSOM begins with an acute onset of OM, either AOM or OME. Thus, the factors that have been associated with AOM may be initially involved, such as infection (usually viral and bacterial); anatomic factors, such as eustachian tube dysfunction; host factors, such as young age; immature or impaired immunologic status; presence of upper respiratory allergy; familial predisposition; presence of older siblings in the household; male sex; race (e.g. native Americans, Australian Aborigines); method of feeding (bottle vs breast); and environmental (e.g. smoking in the household) and social factors [1]. Probably the most important factors related to the onset of OM in infants and young children are immaturity of the structure and function of the eustachian tube and immaturity of the immune system [65]. When infants and young children are exposed to upper respiratory tract infections, OM is a common complication. Fig. 1 shows the possible outcomes of an episode of AOM which may result in CSOM. Since OME, persistent middle-ear effusion (MEE) and chronic perforation

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of the tympanic membrane are included in these outcomes, our current concepts of the pathogenesis of these entities, as well as CSOM, will be reviewed.

4.1. Acute otitis media

The pathogenesis of AOM is likely to occur with the following pattern in most children: the patient has an antecedent event (usually an upper respiratory viral infection) that results in congestion of the respiratory mucosa of the upper respiratory tract, including the nasopharynx and eustachian tube; congestion of the mucosa in the eustachian tube results in obstruction of the tube; negative middleear pressure develops and, if prolonged, is followed by aspiration of potential pathogens (viruses and bacteria) from the nasopharynx into the middle ear. Since the eustachian tube is obstructed, clearance of the MEE, due to the infection, accumulates in the middle ear; microbial pathogens proliferate in the secretions, resulting in a suppurative and symptomatic otitis media. In a recent study conducted by Buchman and colleagues [66], this cascade of events was reproduced in 27 adult volunteers, in whom inuenza A was inoculated into the nose. All subjects developed a nasal infection, 16 (59%) subsequently developed high negative MEE and in one subject an acute otitis media was present; the middle-ear aspirate revealed the virus and Streptococcus pneumoniae. For children with recurrent episodes of AOM or OME, anatomic or physiologic abnormality of the eustachian tube appears to be an important, if not the most important, factor. The child with such an underlying abnormality of the eustachian tube may be subject to recurrent episodes of AOM. The pathogenesis of recurrent AOM in 50 otitis-prone children (dened as greater than 11 episodes of AOM) was studied in Sweden by Stenstrom and co-workers [67]. Employing a pressure chamber to test eustachian tube function, they found the otitis-prone children to have signicantly poorer active tubal function than 49 normal (control) children who had no history of AOM. This nding indicates that the pathogenesis of recurrent AOM is the result of functional (i.e. failure of the opening mechanism of the eustachian tube), as opposed to mechanical, obstruction of the eustachian tube. However, it is likely that infants and young children who have short, oppy eustachian tubes can reux or insufate (following closed-nose swallowing, blowing the nose, or crying) nasopharyngeal secretions into the middle ear during a viral upper respiratory tract infection. Another possible mechanism is progressive ascending infection from the nasopharynx into the mucosa of the eustachian tube.

4.2. Otitis media with effusion

The acute onset of OME, although relatively asymptomatic in children, most likely has a similar sequence of events as described above for AOM, since bacteria can be isolated from the MEE of patients with OME [68,69], but prolonged negative pressure within the middle ear can cause a sterile OME. Otitis media with effusion has been produced in the monkey animal model following excision of [70] and injection of botulinum toxin into [71,72] the tensor veli palatini muscle, which

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resulted in an opening failure of the eustachian tube, middle-ear underpressures and effusion. These experiments conrm the hydrops ex vacuo theory of the pathogenesis of MEE, which postulates that in the absence of eustachian tube opening, the gas exchange from the middle ear into the microcirculation of the mucous membrane causes a middle-ear under pressure, followed by transudation of effusion. Swarts and associates [73] were also able to produce MEE in the monkey shortly after inducing negative middle-ear pressure by ushing the middle ear with CO2. Because tubal opening is possible in a middle ear with an effusion, aspiration of nasopharyngeal secretions might occur, thus creating the clinical condition in which OME and recurrent acute bacterial OM occur together. In two studies by McBride and colleagues [74] and by Buchman and co-workers [75] that involved adult volunteers, nasal challenge with rhinovirus resulted in eustachian tube obstruction, negative middle-ear pressure and in two subjects, development of OME. The two individuals who had a OME had negative middleear pressure prior to the challenge. None of the subjects who had normal middleear pressure before the challenge developed an effusion, which would indicate that a viral infection will result in a OME if the patient has a pre-existing dysfunction of the eustachian tube [75]. Doyle and colleagues [76] also demonstrated that intranasal challenge of inuenza A virus in 33 healthy adult volunteers resulted in eustachian tube obstruction, negative middle-ear pressure and in ve of 21 infected subjects, development of MEE. Most likely, inuenza A virus is more virulent than rhinovirus. Periods of upper respiratory tract infection may then result in atelectasis of the middle ear (i.e. high negative middle-ear pressure), sterile OME, or acute bacterial OM

4.3. Persistent middle-ear effusion

The pathogenesis of persistent MEE after the initial stage of an acute viral/bacterial infection in the middle ear, or following transudation of effusion when high negative pressure is within the middle ear, is probably similar. There is stimulation of cytokines, such as interleukins 1, 2, 6 and 8, tumor necrosis factor and interferon-gamma from inammatory cells of the middle-ear mucous membrane [7783], followed by two pathways of inammation: (1) upregulation of submucosal receptors, primarily selectins and integrins that trap lymphocytes into the mucosa, which also produce cytokines and inammatory mediators; and (2) stimulation of inammatory mediators, such as leukotrienes, prostaglandins, thromboxane, prostacycline and platelet activating factor [8491], which in turn can promote uid leakage from the mucous membrane. At this stage, there is probably an increase in blood ow within the mucous membrane, due to engorgement of blood vessels and angioneogenesis, which then results in further negative pressure within the middle ear due to increase in perfusion of N2 into the microcirculation of the mucosa [92]. In addition, the effusion that is produced is trapped in the middle ear due to the anatomy of the system, i.e. a closed space in which there is a narrow outlet (the eustachian tube). Also, the mucociliary system and the pumping action of tubal opening and closing is most likely impaired; thus, persistent MEE.

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4.4. Chronic perforation

Chronic perforation of the tympanic membrane develops after an acute perforation is present. Tympanic membrane perforations that are acute (and not due to trauma) are usually secondary to AOM but may also occur during the course of chronic OME [26]. Since a spontaneous perforation commonly accompanies an episode of acute middle-ear infection that is untreated with an antimicrobial agent, but also occurs despite adequate treatment, it may be part of the natural history of the disease process rather than a complication. Because such a perforation allows purulent material to drain into the external canal and enhances drainage of pus down the eustachian tube, a perforation of the eardrum that adequately drains the middle ear may prevent further spread of infection within the temporal bone or, more importantly, into the intracranial cavity. Chronic perforation of the tympanic membrane usually occurs when an acute perforation fails to heal. If CSOM is present, the perforation may close spontaneously following appropriate treatment. The healing of a chronic perforation is probably being prevented by the presence of squamous epithelium at the edges of the perforation.

4.5. Chronic suppurati6e otitis media

When there is acute drainage through an intact tympanic membrane that persists for 2 weeks to 3 months or longer the infection is CSOM. (There is no consensus on the duration of otorrhea to be termed chronic.) Thus, acute otorrhea precedes CSOM; the acute otorrhea is caused more often by AOM, but may also occur in certain high-risk populations, such as the Australian Aborigine, when chronic OME is present [26]. Factors most likely related to the progression of acute otorrhea into the chronic stage have been noted above, but most likely the process, if extended, results in a chronic osteitis of the middle-ear cleft [93]. When a chronic perforation is present, in which there is no evidence of infection, reinfection probably occurs in one of two ways: (1) Bacteria from the nasopharynx can gain access to the middle ear due to reux, or insufation (during nose blowing, crying in the infant, or during closed-nose swallowing when nasal obstruction is present) of nasopharyngeal secretions, through the eustachian tube, since the middle-ear gas cushion is lost. In most instances, these bacteria are initially the same as those isolated when AOM occurs behind an intact tympanic membrane, such as S. pneumoniae and Haemophilus inuenzae and when acute otorrhea develops when tympanostomy tubes are in place [94]. Following the acute otorrhea, Pseudomonas aeruginosa, Staphylococcus aureus and other organisms from the external ear canal enter the middle ear through the non-intact tympanic membrane, which results in secondary infection and chronic otorrhea. (2) CSOM also occurs when the middle-ear cleft is contaminated by organisms (e.g. P. aeruginosa) that are present in water that enters through the non-intact eardrum during bathing and swimming. It is likely that eustachian tube dysfunction is involved in the process. In a study of eustachian tube function in the ears of Japanese children and adults who had

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chronic perforations, Iwano and colleagues [95] found impaired active opening function of the tube. They concluded the tube was functionally obstructed; however, organic (i.e. mechanical or anatomic) obstruction was also considered to be involved in the pathogenesis in adults.

4.6. Populations at high risk

As described above, there are certain populations that are at high risk of developing chronic perforation of the tympanic membrane with and without CSOM. What host factors contribute their high rate of disease? One important possible explanation is that these groups have eustachian tubes that make them more prone to middle-ear infection than others. Unfortunately, the evidence for this hypothesis is limited to only a few studies. Doyle [96] identied anatomical differences in the bony segment of the eustachian tube in studies of the bony craniofacial structures of Eskimo, American Indian, Caucasian and Negro individuals. Signicant differences among the racial groups were present in the length, width and angle of the tube in the groups, implicating an anatomical basis for racial predisposition to, or protection from, otitis media. In an important clinical study, Beery and coworkers [97] studied 25 White Mountain Apache Indians ranging in age from 3 to 36 years and found that their eustachian tubes were semipatulous (of low resistance) in comparison to those of a group of Caucasians. In this study, the function of the eustachian tube was assessed directly through chronic perforations of the eardrum, employing the ination-deation and forced-response tests. Ratnesar [98] calibrated the eustachian tube with ureteric catheters in Canadian Inuits and Caucasian individuals and found the tube to be larger in Inuits than in Caucasians. These studies would appear to indicate that these racial groups and the segment of the Caucasian population that has CSOM, have eustachian tubes that permit reux of nasopharyngeal secretions into the middle ear; reux AOM develops and the tympanic membrane perforates. In some individuals, the reux of nasopharyngeal secretions continues after the initial episode, whereas in others the process recurs with each upper respiratory tract infection, or following contamination during swimming. The perforation enhances the reux of the secretions from the nasopharynx, since the middle ear-mastoid gas cushion is abolished. Most likely individuals who have a perforation of the tympanic membrane rarely have a cholesteatoma in the posterosuperior quadrant of the pars tensa or in the pars accida; migration of epithelium through the perforation is possible, but not common. Since most cholesteatomas are the nal step in a sequence of events that begins with negative middle-ear pressure, progresses to atelectasis and then leads to a retraction pocket, the development of a cholesteatoma should be rare when a central perforation is present, since the middle-ear pressure is ambient. Therefore, even though children and adults who have CSOM have a morbid process, they appear to be protected from developing an attic or posterosuperior type of cholesteatoma. This may explain the low incidence of cholesteatoma in racial groups that have a high rate of chronic perforation.

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In addition to the possible common problem of racial differences in eustachian tube function in high-risk populations, there may be differences in colonization of the nasopharynx early in life. A prospective study of Australian Aboriginal neonates found that they have more rapid colonization of the nasopharynx than Caucasian neonates [24]. In a recently reported study of children in Greenland who had AOM (44% had acute otorrhea) revealed they had a massive nasopharyngeal load of potentially pathogenic bacteria [15]. The pathogens isolated in these two studies were similar to those isolated from middle-ear isolates in the developed countries [99]. Also, the disease that precedes the perforation may be different. In a study of Inuit children, Timmermans and Gerson [9] described a more indolent form of OM they termed chronic granulomatous OM. After one or more episodes of AOM (usually treated with antimicrobial agents), there was a sudden onset of otorrhea without pain or fever. The discharge may persist for years, interspersed with periods of variable length in which the ear is dry. A large central perforation of the tympanic membrane developed and granulomatous tissue lled the middle ear cavity. One study reported that environment plays a role in one high-risk population, but that genetic differences are probably more important in those who are at high risk. Spivey and Hirschorn [100] reported on the incidence of three illnesses common on the White Mountain Apache reservation-pneumonia, diarrhea and OM. Illness rates of reservation-born Apache children adopted into non-Apache homes off the reservation at an early age were compared with non-Apache siblings in the adoptive home and those of the reservation children. Adopted Apache children had more illness rates than their non-Apache siblings, but less pneumonia and diarrhea than Apache children on the reservation. Yet, rates of OM were similar to that of Apache children who remained on the reservation. This important study seems to indicate that Apache children are indeed more susceptible to these illnesses than non-Apache children and that environmental factors on the reservation increases their risk, but OM risk is relatively unaffected by these factors. As described above in the study of the same Native American population by Beery and colleagues [97], dysfunction of the eustachian tube may be involved in the pathogenesis. Another possible factor related to an increased susceptibility is that those populations at highest risk, such as Inuits, Australian Aborigines and Native Americans and those at high risk, such as natives of the Solomon Islands and Maoris of N.Z., are immunocompromised. Yet, there have been no reports of impairment of immunity in these racial groups. However, in our population at the Childrens Hospital of Pittsburgh, we frequently uncover a previously undiagnosed immaturity, or more rarely impairment in immunity in infants and young children who have frequently recurrent episodes of otorrhea following tympanostomy tube insertion. Also, atopy may be a factor in the pathogenesis of CSOM, but again there are no published reports that assessed this possibility in high-risk racial groups. However, one study from Finland reported higher serum IgE levels and nasal eosinophils and basophils in nasal secretions in patients with CSOM, than control subjects [101]. Hypothetically, the middle ear and mastoid could be a target

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organ, but also allergic secretions could reux through the Eustachian tube into the middle ear. Future research into the possible role of immunity and allergy in the pathogenesis of CSOM is warranted.

5. Implications for prevention and treatment From this review, it appears that there are special populations who are at highest risk of developing CSOM who live in diverse geographic regions in the world (Fig. 2), which would make climate an unlikely explanation for their disease. In these racial groups, it is likely that the pathogenesis of their disease is due to genetic differences in their eustachian tube function (or possibly a defect in immunity). The tube is most likely hyperpatent, which may be due to a semipatulous or patulous lumen, or the tube is too short, or both. (Histopathologic studies of temporal bones of young individuals who had cleft palate and those who had Down syndrome both of these conditions are at high risk for OMhad statistically shorter eustachian tubes than age-matched specimens from individuals without these disorders [102].) Nevertheless, environmental and behavioral factors are also important in these racial groups, as well as the availability of adequate health care. Thus, these other factors (i.e. other than abnormalities of the eustachian tube) would make other

Fig. 2. Areas of the world in which there are prevalence data available for chronic suppurative otitis media (CSOM) in children. Area in which the prevalence is highest, high, low and lowest are shown. It is apparent from the map that populations at highest and high risk are in areas of the world with diverse climates.

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populations also at risk. Since we cannot alter the structure and function of the eustachian tube in the populations at highest risk of CSOM, our efforts should be directed toward improvement in health care and living conditions in all populations that have a high prevalence of CSOM. In addition to improving the general public health of those at risk, such as sanitation, clean water, personal hygiene and nutrition, new mothers should be informed of the benets of breastfeeding and encouraged to refrain from smoking in the household. Since CSOM most commonly follows an attack of untreated AOM, efforts should be directed toward early diagnosis and treatment of acute ear infection with antimicrobial agents. For those who develop acute otorrhea despite timely treatment of AOM-some individuals in populations at highest risk, even after receiving antibiotics for AOM, will still develop perforation and aural discharge-appropriate and adequate management of their otorrhea is indicated to prevent CSOM. Children whose discharge resolves but the perforation becomes chronic should be informed about the hazards of water contamination; these perforations should be repaired, i.e. tympanoplasty. Similarly, if CSOM develops, tympanoplasty should be performed after resolution of the infection is achieved with ototopical antibiotics, aural toilet, oral antimicrobial agents [103] and if necessary, intravenous antimicrobial therapy [104]. The foregoing recommendations are also appropriate when tympanostomy tubes are in place, except that removing the tube (as opposed to tympanoplasty) may be required to prevent recurrent CSOM [1]. Since there is some concern in some developing countries, such as in Africa, that CSOM is the most important cause of hearing impairment, we should direct our efforts toward prevention of this common childhood infection.

References
[1] C.D. Bluestone, J.O. Klein, Otitis media, atelectasis and eustachian tube dysfunction, in: C.D. Bluestone, S.E. Stool, M.A. Kenna (Eds.), Pediatric Otolaryngology, WB Saunders, Philadelphia, 1996, pp. 388390. [2] G.G. Browning, D. Gatehouse, The prevalence of middle ear disease in the adult British population, Clin. Otolaryngol. 17 (1992) 317 321. [3] G.J. Kaplan, J.K. Fleshman, T.R. Bender, et al., Long-term effects of otitis media: a ten-year cohort study of Alaskan Eskimo children, Pediatrics 52 (1973) 577 585. [4] C.F. Tschopp, Chronic otitis media and cholesteatoma in Alaskan native children, in: B.F. McCabe, J. Sade, M. Abramson; (Eds.), Cholesteatoma: First International Conference, Aesculapius, Birmingham, 1977, pp. 290 292. [5] J.A. Brody, T. Overeld, R. McAlister, Draining ears and deafness among Alaskan Eskimos, Arch. Otolaryngol. 81 (1965) 2933. [6] D. Ling, R.H. McCoy, E.D. Levinson, The incidence of middle ear disease and its educational implications among Bafn Island Eskimo children, Can. J. Public Health 60 (1969) 385 390. [7] O. Schaefer, Otitis media and bottle-feeding: an epidemiological study of infant feeding habits and incidence of recurrent and chronic middle ear disease in Canadian Eskimos, Can. J. Public Health 62 (1971) 478489. [8] J.D. Baxter, D. Ling, Ear disease and hearing loss among the Eskimo population of the Bafn Zone, Can. J. Otolaryngol. 3 (1974) 110 122.

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