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, Children’s 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 reflux 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; Epidemiol-
ogy

* 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
208 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223

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 suppura-
tive 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 identified and an understanding of its etiology and pathogenesis is required.

1. Definitions

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 definition, 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
 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223 209

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 (defined
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%) [6–12] and Greenland (7–12%) [13–15]; (2)
Australian Aborigines (12 – 33%) [16–26] and (3) certain Native Americans, e.g.
Apache and Navajo tribes; (4 – 8%) [27–32]. 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
Pacific islands, such as the Solomon Islands (4–6%) [34], N.Z. Maori (4%) [35,36],
Malaysia (4%) [37] and Micronesia (4%) [38–40] (in contrast to these high rates in

Table 1
Prevalence of suppurative otitis media

Population Prevalence (%) References

Highest Inuits
Alaska 30 – 46 [3 – 5]
Canada 7 – 31 [6 – 13]
Greenland 7 – 12 [14 – 16]
Australian Aborigines 12 – 33 [17 – 25]
Native Americans
Apache, Navajo 4–8 [27 – 32]
High South Pacific Islands
Solomon Islands 4–6 [34]
N.Z. Maori 4 [35,36]
Malaysia 4 [37]
Micronesia 4 [38 – 40]
Africa
Sierra Leone 6 [41]
Gambia 4 [43]
Kenya 4 [44]
Nigeria 4 [45,46]
Tanzania 2–3 [47 – 49]
Low Korea 2 [51]
India 2 [52]
Saudi Arabia 1.4 [53]
Lowest US B1 [54,55,57]
UK B1 [58,59]
Denmark B1 [60]
Finland B1 [56]
210 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223

some islands of the South Pacific, 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
(2–3%) [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 [54–56], 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 nutri-
tion, 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 finding 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 inci-
dence 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
 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223 211

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
212 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223

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 middle-
ear 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 con-
ducted by Buchman and colleagues [66], this cascade of events was reproduced in
27 adult volunteers, in whom influenza 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 (defined 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 significantly poorer active tubal function than 49 normal (control) children
who had no history of AOM. This finding 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, floppy
eustachian tubes can reflux or insufflate (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 as-
cending 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
 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223 213

resulted in an opening failure of the eustachian tube, middle-ear underpressures and

effusion. These experiments confirm the ‘hydrops ex vacuo’ theory of the pathogen-
esis 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 mem-
brane 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 flushing 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 middle-
ear pressure prior to the challenge. None of the subjects who had normal middle-
ear 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 influenza A virus in 33 healthy adult volunteers resulted in
eustachian tube obstruction, negative middle-ear pressure and in five of 21 infected
subjects, development of MEE. Most likely, influenza 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/bacte-
rial 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 inflammatory cells of the middle-ear mucous membrane
[77– 83], followed by two pathways of inflammation: (1) upregulation of submu-
cosal receptors, primarily selectins and integrins that trap lymphocytes into the
mucosa, which also produce cytokines and inflammatory mediators; and (2) stimu-
lation of inflammatory mediators, such as leukotrienes, prostaglandins, thrombox-
ane, prostacycline and platelet activating factor [84–91], which in turn can promote
fluid leakage from the mucous membrane. At this stage, there is probably an
increase in blood flow 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.
214 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223

4.4. Chronic perforation

Chronic perforation of the tympanic membrane develops after an acute perfora-

tion 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 reflux, or insufflation (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 influenzae 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
 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223 215

chronic perforations, Iwano and colleagues [95] found impaired active opening
function of the tube. They concluded the tube was functionally obstructed; how-
ever, ‘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] identified 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. Significant 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 inflation-deflation 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
reflux of nasopharyngeal secretions into the middle ear; reflux AOM develops and
the tympanic membrane perforates. In some individuals, the reflux of nasopharyn-
geal 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 reflux 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 flaccida; migration of epithelium through the perforation is possible, but not
common. Since most cholesteatomas are the final 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.
216 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223

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 filled 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 reserva-
tion 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 patho-
genesis.
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
Children’s 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
 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223 217

organ, but also allergic secretions could reflux 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 OM—had 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.
218 C.D. Bluestone / Int. J. Pediatr. Otorhinolaryngol. 42 (1998) 207–223

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 benefits 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,
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