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Chronic suppurative otitis media (CSOM): Pathogenesis, clinical manifestations, and diagnosis

Authors
Jessica Levi, MD
Robert C O'Reilly, MD
Section Editor
Glenn C Isaacson, MD, FAAP
Deputy Editor
Carrie Armsby, MD, MPH

Disclosures: Jessica Levi, MD Nothing to disclose. Robert C O'Reilly, MD Nothing to


disclose. Glenn C Isaacson, MD, FAAP Nothing to disclose. Carrie Armsby, MD, MPH
Nothing to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements
for references to be provided to support the content. Appropriately referenced content is required
of all authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Apr 2015. | This topic last updated: Dec 03, 2013.

INTRODUCTION Chronic suppurative otitis media (CSOM) is the most common childhood
infectious disease worldwide and is the most common cause of hearing impairment in the
developing world, although it is infrequently seen in the developed world [1]. It is characterized
by drainage from the middle ear for at least two weeks and is associated with a tympanic
membrane (TM) perforation that is usually painless [2,3]. The otorrhea may be persistent or
intermittent. CSOM is usually preceded by an episode of acute infection.

The epidemiology, pathogenesis, clinical features, diagnosis, and management of CSOM are
reviewed here. Acute otitis media (AOM) and otitis media with effusion in children and acute
and chronic otitis media in adults are reviewed separately. (See "Acute otitis media in children:
Epidemiology, microbiology, clinical manifestations, and complications" and "Otitis media with
effusion (serous otitis media) in children: Clinical features and diagnosis" and "Acute otitis
media in adults (suppurative and serous)" and "Chronic otitis media, cholesteatoma, and
mastoiditis in adults".)

EPIDEMIOLOGY CSOM is uncommon in the developed world, with an prevalence of less


than 1 percent in the United States [3], for example, but is seen more frequently in the
developing world, with an prevalence ranging from 6 to 46 percent in other geographic areas and
populations [4-6]. One theory regarding the higher prevalence in developing countries is that the
cost of treatment is prohibitive. In a Nigerian study, the cost of CSOM treatment per patient per
year amounted to more than the national monthly minimum wage [7]. Public education and
awareness in developing countries are also an issue. In one study of 203 mothers of children with
CSOM living in two slums in Bangladesh, 65 percent were aware of the disease and sequelae,
but only 40 percent had knowledge about the treatment [8].

CSOM typically occurs in the young child. About 60 percent of children were affected by 6
months of age in a Nigerian study [9], 18 months of age in a study from the Solomon Islands
[10], and 24 months of age in an Ethiopian study [5]. The mean age of onset of CSOM was about
11 months in a prospective two-year study of 465 children aged zero to four years in an Inuit
population in Greenland [6]. In contrast, a South Indian study found that preschool children (age
2 to 5 years) were equally as likely as school-age children (age 6 to 10 years) to be affected by
the disease [4].

Most studies have found that males and females are equally affected, although some have found
a male predominance [10-12]. In one study, the "simple form" occurred in both sexes equally,
but the cholesteatomatous form was more common among males [13].

In nearly all studies, a unilateral preponderance is not seen. The reported frequency of bilateral
disease ranges from 27 to 55 percent [5,8].

Risk factors An increased incidence of CSOM is seen in children with a history of multiple
episodes of acute otitis media (AOM) [14,15], early otitis media (defined as otitis media
occurring in the first few months of life) [16], and chronic secretory otitis media [17]. Risk
factors for CSOM represent a combination of common risk factors for AOM as well as factors
associated with low socioeconomic status and inadequate healthcare [18]. These include:

Living in crowded conditions [14,15]

Living in a large family [6,14,15]

Daycare attendance [6,14,15]

Low parental education level [14,19]

Poor nutrition and lower levels of zinc, selenium, calcium, and vitamin A [5,10,20,21]

Passive smoke exposure [6]

History of tympanostomy tubes [14]

Frequent upper respiratory tract infections [6,10,14] and nasopharyngitis [5]

Infectious and chronic diseases, such as measles, human immunodeficiency virus (HIV)
infection, tuberculosis, diabetes, and cancer [5,10,22]

Other comorbid conditions, such as cleft lip/palate, Down syndrome, cri du chat syndrome,
choanal atresia, and microcephaly [12,14]
Unhygienic practices, such as bathing in contaminated ponds and rivers, unsterile ear piercing,
and cleaning ears with cotton buds [8,12]

While there are many environmental and social risk factors for CSOM, the rate of CSOM has not
changed in countries, such as Greenland, despite many changes in social conditions [6]. A
genetic predilection is also suspected to play a role. This is suggested by the increased risk of
CSOM seen in the Inuit of Alaska, Canada, and Greenland, Australian Aborigines, and certain
Native Americans (particularly the Apache and Navajo) [6,18].

Family history may also play a role in AOM and CSOM. A family history of otitis media
increased the risk of CSOM [15]. Maternal history of otorrhea [6] and CSOM [19] are risk
factors for development of CSOM in children.

PATHOGENESIS CSOM generally results from an acute ear infection that is not diagnosed
promptly or is inadequately treated. Infrequently it can result from chronic otitis media with
effusion. CSOM can occur in a patient with a previously intact tympanic membrane (TM) or a
TM with a preexisting perforation or tympanostomy tube. There are also reports of CSOM
following traumatic perforations [23]. Suppuration can also occur after tympanostomy tube
placement. (See "Tympanostomy tube otorrhea in children: Causes, prevention, and
management".)

Some have proposed that CSOM is, at least in part, the result of chronic Eustachian tube
dysfunction (ETD) and resulting histologic changes in the middle ear, coupled with a
nasopharyngeal reservoir of pathogens [3,24]. However, in one series, there was no correlation
between cultures from the external auditory canal (EAC) or middle ear and nasopharyngeal
cultures, indicating the nasopharynx does not serve as a reservoir for the bacteria causing CSOM
[25]. A suggested alternative is that the nasopharyngeal bacteria may contribute to the initial
acute otitis media (AOM) preceding CSOM, but bacteria from the EAC enter the middle ear
through the perforated TM as the infection becomes chronic, leading to a secondary infection
and chronic drainage [18]. Contaminated water may also play a role in the pathogenesis of
CSOM. Swimming or bathing in unclean water can lead to middle-ear contamination with
bacteria when a TM perforation exists [3,18].

Biofilms have also been implicated in the pathogenesis of CSOM. The role of biofilms in
patients with cholesteatoma is better defined, but there is some evidence that biofilms also play a
role in CSOM. In several small studies, biofilms were detected in 14 to 92 percent of patients
with CSOM [26-30]. Biofilms may account for some of the difficulty in treating CSOM, since
they are difficult to eradicate.

Organisms In studies from the 1980s, Pseudomonas and Proteus were the most common
microbial isolates in patients with CSOM [10,31]. However, the incidence of community-
acquired methicillin-resistant Staphylococcus aureus (MRSA) has increased over the years and is
now the most common isolate reported, followed by methicillin-sensitive S. aureus (MSSA) [32-
34]. In addition, increasing numbers of patients have anaerobic bacteria as part of the
microbiology in CSOM, with Peptostreptococcus, Fusobacterium, Prevotella, and
Porphyromonas being the most common anaerobic isolates [35]. Fungi are also identified in
cultures from patients with CSOM [36].

Bacteriology in patients with CSOM and cholesteatoma may be different. In one series of 119
children with CSOM, those with cholesteatoma were 30 times more likely to have mixed
infections compared with patients with noncholesteatomatous CSOM [37]. Among 368 patients
(adults and children) with CSOM, those with cholesteatoma were more likely to have S. aureus
than Pseudomonas, while those patients with no cholesteatoma had the reverse [38].

Role of immune system Interferon-gamma (IFN-gamma) has been shown to have


immunoregulatory properties in otitis media with effusion, and it may play a similar role in
CSOM. Middle-ear secretions were collected and examined in 358 children with CSOM [39].
The children were then treated and followed for nine months. IFN-gamma concentrations were
significantly lower in the 61 percent of children in whom CSOM resolved compared with the 39
percent of children who had persistent drainage (mean IFN-gamma concentration 27.2 versus
73.1 pg/mL, respectively). Levels of IFN-gamma also inversely correlated with concentrations of
immunoglobulin G (IgG), IgE, and IgA in the fluid.

Immunoglobulin levels were below normal in 3 of 69 (4.3 percent) of patients with CSOM in
one series, suggesting a defect in humoral immunity in a small subset of patients [40]. Additional
factors that may impact the ability to clear an infection include the high rate of biofilm formation
seen in patients with CSOM compared with chronic otitis media with effusion in one series [41]
and decreased ciliary beat frequency in the middle ear in another series [42].

Environmental allergies may be more common in patients with CSOM. Positive allergy testing to
perennial aeroallergens was seen in 16 of 20 (80 percent) patients with CSOM compared with 8
of 17 (47 percent) patients with AOM and 5 of 15 (33 percent) controls without otitis media [43].
IgE was elevated in the serum and middle-ear secretions of these patients, with an increased ratio
of middle ear to serum levels in patients with CSOM compared with those with AOM.

CLINICAL PRESENTATION The most common presenting complaint is hearing loss,


followed by ear discharge [5,12]. The definition of "chronic" in the entity of CSOM is somewhat
controversial, although the most common suggested cutoff for duration of suppuration is six
weeks (range, two weeks to three months) [3]. The otorrhea may be persistent or intermittent.
Patients do not typically complain of ear pain. Any report of fever, dizziness, or pain should alert
the clinician to consider complications of CSOM (see "Chronic suppurative otitis media (CSOM):
Prevention, treatment, prognosis, and complications", section on 'Complications'). Most patients
have had the disease for over six years before seeking medical care (range 0 to 20 years) [11,12].
One study found that 52.8 percent of their patients had ear discharge for more than a year. In
another series, 73 percent of patients had recurrent disease, while 27 percent had continuous
disease [5].

Hearing loss Hearing loss (threshold of hearing >25 dB) occurs in about 50 to 60 percent of
patients with CSOM [8,22,44]. It is moderate to severe in up to two-thirds of patients [5,13,44-
46], with an average hearing threshold of 40 dB in one series of 115 patients with CSOM [44].
Conductive hearing loss is more common than sensorineural hearing loss [44,47], and patients
appear to have greater hearing loss in the low frequencies [48] and increase bone conduction
thresholds in most series [49-51]. Hearing loss may occur in the contralateral ear despite lack of
evidence of bilateral disease [46]. Longer duration of otorrhea is associated with greater degree
of hearing loss [48], and lower socioeconomic status, but not age of onset or number of episodes,
is associated with an increased risk of hearing loss [47]. The site of the perforation corresponded
to degree of hearing loss, with posterior perforations having greater decibel level loss, probably
as a result of loss of protection of the round window membrane from impinging sound pressure
waves [48]. In many series, the hearing loss is strictly a result of middle-ear pathology in most
cases of CSOM and the inner ear is typically not affected [49,52,53]. However, others have
found that mixed hearing loss (conductive and sensorineural) is common [54].

Cholesteatoma Cholesteatoma (picture 1) should be considered when CSOM does not resolve
with maximal medical treatment. It occurs in 1 to 18 percent of all patients with CSOM
[4,8,13,55]. Cholesteatoma, in conjunction with CSOM, should be distinguished from isolated
cholesteatoma, which can have a similar presentation, but is a distinct entity. (See 'Differential
diagnosis' below and "Cholesteatoma in children".)

Physical exam findings A large central perforation of the tympanic membrane (TM) (picture 2
and picture 3) is the most common and perforation of the posterosuperior quadrant is the least
common [8,48]. Discharge can range from purulent to fetid to cheese-like, and can fill the ear
canal. There is typically not significant edema of the external auditory canal. There may be
granulation tissue present, but it should be distinguished from retraction-pocket cholesteatoma in
which the granulation tissue occupies the pars flaccida of the TM. Middle-ear mucosa, when it is
seen, can be polypoid or edematous and can appear pale, red, or may be normal.

DIAGNOSIS The diagnosis of CSOM is based upon consistent clinical findings (eg, hearing
loss, chronic ear discharge). Cultures are not required to make the diagnosis and are generally
reserved for unresponsive disease. They should be obtained through the perforation or
tympanostomy tube, since culture samples taken from the external auditory canal (EAC) may be
unreliable or misleading [56]. However, patients usually fail medical treatment for reasons other
than microorganism resistance. Thus, alternative or additional diagnoses should be considered
and a computed tomography (CT) scan of the temporal bones obtained to evaluate for
cholesteatoma or other processes when a patient is unresponsive to appropriate medical treatment.
(See 'Clinical presentation' above and 'Differential diagnosis' below.)

In one study, 110 patients with CSOM were randomized to culture-directed or broad-spectrum
antimicrobial therapy [57]. Culture-directed therapy for two weeks led to a dry ear in 95 percent
of cases, whereas broad spectrum antibiotics resulted in a dry ear in 74 percent. However, this
difference was not significant, suggesting that routine performance of cultures is not necessary.
In addition, there is poor correlation between cultures taken from the EAC, which is how they
are most often obtained, versus the middle ear. In one study, they correlated for Pseudomonas in
32 percent and anaerobes in 45 percent [25].

DIFFERENTIAL DIAGNOSIS The most common and important condition in the differential
diagnosis for CSOM is isolated cholesteatoma, particularly the acquired form, which can also
present with hearing loss and/or chronic otorrhea. It can be difficult to distinguish the two
entities, since cholesteatoma can also occur in conjunction with CSOM. Keratin debris seen on
exam, as opposed to just purulence, and prolonged duration of suppuration both are suggestive of
cholesteatoma. Symptoms such as dizziness or facial nerve weakness should also make one
consider cholesteatoma. A careful physical exam along with computed tomography (CT)
scanning of the temporal bones, which may reveal bone erosion or destruction, should identify
cholesteatoma in most cases. (See 'Cholesteatoma' above and "Cholesteatoma in children".)

The differential diagnosis also includes acute and chronic otitis media. The perforated tympanic
membrane (TM) is what distinguishes CSOM from both acute and otitis media with effusion, in
which the ear drum is intact. Acute otitis media (AOM) can lead to TM perforation in some cases
and may progress to CSOM. The duration of symptoms is the main differentiating factor
between these two conditions. (See 'Clinical presentation' above and "Acute otitis media in
children: Epidemiology, microbiology, clinical manifestations, and complications", section on
'Clinical manifestations' and "Acute otitis media in children: Epidemiology, microbiology,
clinical manifestations, and complications", section on 'TM perforation' and "Otitis media with
effusion (serous otitis media) in children: Clinical features and diagnosis", section on 'Clinical
features'.)

CSOM can also occur in the presence of tympanostomy tubes, which is discussed in greater
detail separately. (See "Tympanostomy tube otorrhea in children: Causes, prevention, and
management".)

Other conditions to consider include (see "Evaluation of otorrhea (ear discharge) in children" and
"Hearing impairment in children: Etiology"):

Foreign body, particularly in young children with chronic drainage (see "Evaluation of otorrhea
(ear discharge) in children", section on 'Foreign body').

Petrous apicitis (petrositis, infection of the petrous bone and air cells), which generally presents
with retro-orbital pain, cranial nerve six palsy, and ear drainage (see "Acute mastoiditis in
children: Clinical features and diagnosis", section on 'Pathogenesis' and "Acute mastoiditis in
children: Clinical features and diagnosis", section on 'Complications').

Tuberculosis of the temporal bone, particularly in underdeveloped areas or among at-risk


populations (eg, nursing home or prison contacts, poor healthcare), can present as painless
otorrhea. Testing for tuberculosis can help differentiate this from CSOM (see "Tuberculosis
disease in children" and "Skeletal tuberculosis").

Langerhans cell histiocytosis (see "Clinical manifestations, pathologic features, and diagnosis
of Langerhans cell histiocytosis" and "Evaluation of otorrhea (ear discharge) in children", section
on 'Granulation tissue'). A CT scan will help differentiate this entity from CSOM.

Malignancy (rare in pediatric populations) (see "Evaluation of otorrhea (ear discharge) in


children", section on 'Neoplasm'). These patients usually present with pain. A CT scan will help
differentiate this as well.
SUMMARY

Chronic suppurative otitis media (CSOM) is the most common childhood infectious disease
worldwide and is the most common cause of hearing impairment in the developing world,
although it is infrequently seen in the developed world. (See 'Introduction' above and
'Epidemiology' above.)

CSOM generally results from an acute ear infection that is not diagnosed promptly or is
inadequately treated. The acute otitis media (AOM) then progresses to tympanic membrane (TM)
perforation and subsequent contamination from dirty bathing water or possibly a nasopharyngeal
reservoir. (See 'Pathogenesis' above.)

CSOM is characterized by hearing loss and drainage from the middle ear for at least two weeks
that is associated with a TM perforation. The otorrhea can be recurrent or persistent. CSOM is
usually painless. (See 'Clinical presentation' above.)

The diagnosis of CSOM is based upon consistent clinical findings (eg, hearing loss, chronic ear
discharge). Cultures are not required to make the diagnosis and are generally reserved for
unresponsive disease. (See 'Diagnosis' above.)

The most common and important condition in the differential diagnosis for CSOM is isolated
cholesteatoma, which can also present with hearing loss and/or chronic otorrhea. It can be
difficult to distinguish the two entities, since cholesteatoma can also occur in conjunction with
CSOM. (See 'Differential diagnosis' above.)

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