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INTRODUCTION — Chronic suppurative otitis media (CSOM) is one of the most common childhood infectious disease worldwide and is a common cause of hearing impairment in resource-limited settings, although it is infrequently seen in resource-rich settings . It is characterized by chronic drainage from the middle ear associated with tympanic membrane (TM) perforation (picture 1) [2,3]. CSOM is usually preceded by an episode of acute otitis media (AOM).
The epidemiology, pathogenesis, clinical features, diagnosis, and management of CSOM are reviewed here. The prevention, treatment, and complications of CSOM are discussed in detail separately. CSOM in the setting of tympanostomy tubes is also reviewed separately. (See "Chronic suppurative otitis media (CSOM): Prevention, treatment, and complications" and "Tympanostomy tube otorrhea in children: Causes, prevention, and management".)
AOM, otitis media with effusion, and cholesteatoma in children, and acute and chronic otitis media in adults are reviewed separately:
TERMINOLOGY — It is important to distinguish CSOM from other chronic conditions affecting the middle ear:
●Chronic suppurative otitis media (CSOM) – CSOM is chronic inflammation of the middle ear associated with tympanic membrane (TM) perforation and chronic discharge (otorrhea) . The definition of "chronic" in the entity of CSOM varies somewhat. The World Health Organization defines CSOM as otorrhea lasting at least two weeks [1,4]; however, "chronic" is more commonly defined as symptoms persisting for >6 weeks. (See 'Ear discharge' below.)
●Tympanostomy tube otorrhea (TTO) – TTO is defined as active drainage through an existing tympanostomy tube and is primarily caused by bacterial infection. TTO can have early onset (within two weeks of tube placement) or late onset (>2 weeks after tube placement). TTO is reviewed in greater detail separately. (See "Tympanostomy tube otorrhea in children: Causes, prevention, and management".)
●Chronic otitis media with effusion (OME) – OME (also called serous otitis media) is defined as middle-ear effusion without acute signs of infection. Like CSOM, OME often occurs after acute otitis media (AOM) and is associated with conductive hearing loss; however, in OME the TM is not perforated and therefore otorrhea does not typically occur. OME is reviewed in greater detail separately. (See "Otitis media with effusion (serous otitis media) in children: Clinical features and diagnosis" and "Otitis media with effusion (serous otitis media) in children: Management".)
Prevalence — It is estimated that there are 31 million new cases of CSOM per year worldwide, with nearly one-quarter occurring in children <5 years old . CSOM is uncommon in resource-rich settings, with a prevalence of <1 percent in the United States . It occurs more frequently in resource-limited settings, with prevalences ranging from 6 to 46 percent depending on the geographic area and population studied [6-8]. One study of CSOM in a resource-limited setting found that the prevalence declined from 9 percent in the early 1990s to 5 percent in the early 2010s .
One theory regarding the higher prevalence in resource-limited settings is that the cost of treatment is prohibitive . Lack of public awareness about CSOM and delays in seeking care are also likely important contributors [11-13].
CSOM typically occurs in children under the age of two years [7,14,15]; however, high rates have also been reported in older children and adults [6,9]. In a prospective study that followed young children in Greenland (a region with a high rate of CSOM), the mean age of onset of CSOM was 11 months . In another prospective study carried out in Ethiopia, the mean age at presentation was 5.9 years; however, otorrhea had started before the age of two years in nearly 70 percent of patients .
Studies have varied regarding the relative frequencies among males and females [12,15-17]. Some studies have reported that males are more likely to develop the cholesteatomatous form of CSOM and are more likely to have persistent disease [18,19].
The reported frequency of bilateral disease ranges from 27 to 55 percent [7,11].
Risk factors — The risk of CSOM is increased among children with one or more of the following:
●A history of multiple episodes of acute otitis media (AOM) [20,21]
●Early otitis media (ie, occurring in the first few months of life) 
●Chronic secretory otitis media 
Additional risk factors for CSOM represent a combination of common risk factors for AOM as well as factors associated with low socioeconomic status and inadequate health care . These include:
●Living in crowded conditions [20,21]
●Living in a large family [8,20,21]
●Daycare attendance [8,20,21]
●Low parental education level [19,20]
●Passive smoke exposure 
●History of tympanostomy tubes 
●Infectious and chronic diseases, such as measles, human immunodeficiency virus infection, tuberculosis, diabetes, and cancer [7,15,27]
●Other comorbid conditions, such as cleft lip/palate, Down syndrome, cri du chat syndrome, choanal atresia, and microcephaly [12,20]
●Unhygienic practices, such as bathing in contaminated ponds and rivers, unsterile ear piercing, and cleaning ears with cotton buds [11,12]
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) [8,24].
●Tubotympanic type – In tubotympanic CSOM, the disease is confined to the pars tensa with central perforation. The risk of bone erosion and other serious complications (eg, intracranial infection) is low.
●Atticoantral type – In atticoantral CSOM, the disease involves the pars flaccida or posterosuperior marginal quadrant. Cholesteatoma is commonly present and intra- and extracranial complications may occur.
Tympanostomy tube otorrhea (TTO) is sometimes included as a third classification. TTO is reviewed separately. (See "Tympanostomy tube otorrhea in children: Causes, prevention, and management".)
Progression from AOM to CSOM — CSOM is likely a multifactorial disease resulting from interactions between bacterial, environmental, and host factors. CSOM generally results from acute otitis media (AOM) that is not diagnosed promptly or is inadequately treated. Infrequently it can result from chronic otitis media with effusion (OME). CSOM can occur in a patient with a previously intact tympanic membrane (TM) or a TM with a pre-existing perforation or tympanostomy tube. There are also reports of CSOM following traumatic perforations . (See "Acute otitis media in children: Epidemiology, microbiology, clinical manifestations, and complications", section on 'Complications and sequelae' and "Tympanostomy tube otorrhea in children: Causes, prevention, and management".)
Eustachian tube dysfunction (ETD) coupled with a nasopharyngeal reservoir of pathogens may play a role in the progression from AOM to CSOM [1,3,30]. In one study, ETD was observed twice as frequently in ears affected by CSOM compared with ears of control subjects . However, another study found no difference in the paratubal structures themselves in patients with CSOM compared with healthy controls . In another series, there was no correlation between cultures from the external auditory canal (EAC) or middle ear and nasopharyngeal cultures, indicating the nasopharynx may not serve as a reservoir for the bacteria causing CSOM .
An alternative theory is that the nasopharyngeal bacteria may contribute to the initial 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 .
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 in the setting of TM perforation [3,24]. However, swimming in chlorinated swimming pools does not appear to increase the risk of chronic ear drainage .
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 [35-41]. Biofilms may account for some of the difficulty in treating CSOM, since they are difficult to eradicate.
Other factors that may lead to the progression from AOM to CSOM include overproduction of mucin, decreased ciliary motion in the middle ear, and upregulation of proinflammatory cytokines [42,43]. (See 'Role of immune system' below.)
Role of immune system — Environmental allergies and abnormalities in humoral immunity and inflammatory cytokines are suspected to play a role in CSOM:
●Environmental allergies – 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 . Immunoglobulin E (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.
Among an adult population with CSOM, allergic rhinitis was more common among the patients with CSOM compared with controls (62.5 versus 37.5 percent, p = 0.02). The prevalence of allergic rhinitis (diagnosed by positive skin prick test) was also significantly higher among affected patients than controls (24.6 and 13.8 percent, respectively) .
●Humoral immunity – 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 .
●Inflammatory cytokines – Interferon-gamma (IFN-gamma) has been shown to have immunoregulatory properties in OME, and it may play a similar role in CSOM. Middle-ear secretions were collected and examined in 358 children with CSOM . 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 immunoglobulin A (IgA) in the fluid.
Another study found that proinflammatory cytokines were upregulated in patients with CSOM, which may indicate that differences in host response plays a role in why some children do not recover well from an episode of AOM and go on to develop CSOM .
MICROBIOLOGY — Studies regarding the relative frequencies of different pathogens vary somewhat depending on the geographic area and population studied. Commonly isolated bacteria include Staphylococcus aureus (methicillin-resistant [MRSA] and methicillin-sensitive [MSSA]), Pseudomonas, Proteus, coagulase-negative staphylococci, Enterococcus, and anaerobes (including with Peptostreptococcus, Fusobacterium, Prevotella, and Porphyromonas) [15,49-55]. Polymicrobial growth is common .
In patients with bilateral CSOM, the bacteria can be different in each ear . Bacteria isolated from swabs of middle ear discharge may differ from samples obtained more invasively. In a study of 244 patients with CSOM who underwent tympanomastoidectomy, bacterial growth in intraoperative mastoid granulation tissue cultures differed from preoperative middle ear discharge culture in 22 percent of cases .
Fungi are also identified in cultures from patients with CSOM, with Aspergillus being the most common [54,57]. The presence of fungi may be due to treatment with antibiotic drops and may not represent the original infectious organisms. Occasionally, tuberculosis is seen.
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 . Among 368 patients (adults and children) with CSOM, those with cholesteatoma were more likely to have S. aureus than Pseudomonas, while patients without cholesteatoma had the reverse .
In a 13-year study (culminating in 2013) involving mostly adult patients, there was little change in the bacteriology of CSOM; however, resistance patterns did change somewhat with increased resistance to quinolones and aminoglycosides among Pseudomonas isolates .
Ear discharge — CSOM is characterized by chronic purulent middle ear discharge. The definition of "chronic" in the entity of CSOM varies somewhat; the most common suggested cutoff for duration of suppuration is six weeks (range, two weeks to three months) .
The otorrhea may be persistent or intermittent. In one study, 73 percent of patients had intermittent drainage, while the remaining 27 percent had continuous otorrhea . Most patients have had ear drainage for >1 year (range 0 to 20 years) before seeking medical advice [12,16].
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, and complications", section on 'Complications').
Hearing loss — Hearing loss (threshold of hearing >25 decibels [dB]) occurs in approximately 50 to 60 percent of patients with CSOM [11,27,60]; however, estimates of the prevalence may vary substantially depending on the definition used .
Hearing loss is moderate to severe in up to two-thirds of affected patients [7,18,60,62,63]. In one series of 115 patients with CSOM, the average hearing threshold was 40 dB . Conductive hearing loss is more common than sensorineural hearing loss (SNHL), but both may occur [1,60,64-68].
Longer duration of otorrhea is associated with greater degree of hearing loss . Lower socioeconomic status is associated with a greater risk of hearing loss, but age of onset and number of episodes do not appear to be risk factors . The site of the perforation corresponded to degree of hearing loss, with posterior perforations having greater dB level loss, probably as a result of loss of protection of the round window membrane from impinging sound pressure waves . Hearing loss may occur in the contralateral ear despite lack of evidence of bilateral disease .
The hearing loss in CSOM usually results from middle-ear pathology and the inner ear is typically not affected; however, mixed hearing loss (conductive and sensorineural) can occur [66,69-71]. SNHL is thought to result from chemical inflammatory mediators produced from the chronic infection passing through the round window, causing the loss of hair cells in the cochlea . Ototoxicity of ototopical drops may also play a role .
Cholesteatoma — Cholesteatoma (picture 2) should be considered when CSOM does not resolve with maximal medical treatment. It occurs in 1 to 18 percent of all patients with CSOM [6,11,18,73]. 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 — Physical examination in patients with CSOM typically reveals tympanic membrane (TM) perforation and purulent middle ear drainage. Most commonly, a large central TM perforation is present (picture 1 and picture 3); perforation of the posterosuperior quadrant is the less common [11,65]. Discharge can range from purulent to fetid to cheese-like, and can fill the ear canal. There is typically minimal to no edema of the external auditory canal. There may be granulation tissue, 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 tympanic membrane perforation, since cultures taken from the external auditory canal may be unreliable or misleading . However, patients usually fail medical treatment for reasons other than microorganism resistance. Thus, alternative or additional diagnoses should be considered and a computed tomography 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.)
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. A perforated tympanic membrane (TM) 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 health care), 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.
●Chronic suppurative otitis media (CSOM) is the most common childhood infectious disease worldwide and is the most common cause of hearing impairment in resource-limited settings, although it is infrequently seen in resource-rich settings. (See 'Introduction' above and 'Epidemiology' above.)
●CSOM generally results from an acute otitis media (AOM) that is not diagnosed promptly or is inadequately treated. The AOM then progresses to tympanic membrane (TM) perforation and subsequent contamination from the external auditory canal (EAC) and/or nasopharyngeal reservoir. (See 'Pathogenesis' above.)
●Commonly isolated bacteria in CSOM include Staphylococcus aureus (methicillin-resistant [MRSA] and methicillin-sensitive [MSSA]), Pseudomonas, Proteus, coagulase-negative staphylococci, Enterococcus, and anaerobes (including with Peptostreptococcus, Fusobacterium, Prevotella, and Porphyromonas). Polymicrobial growth is common. (See 'Microbiology' above.)
●CSOM is characterized by purulent middle ear discharge that is chronic (typically >6 weeks) and hearing loss associated with a TM perforation. The otorrhea can be recurrent or persistent. CSOM is usually painless. (See 'Clinical presentation' above.)
●Physical examination in patients with CSOM typically reveals a large central TM perforation and purulent middle ear drainage (picture 1 and picture 3). There is usually minimal to no edema of the EAC. (See 'Physical exam findings' above.)
●The diagnosis of CSOM is based upon consistent clinical findings (eg, hearing loss, chronic otorrhea). 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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