INTRODUCTION — Acute otitis media (AOM) is defined by moderate to severe bulging (picture 1 and picture 2) of the tympanic membrane or new onset of otorrhea not due to acute otitis externa accompanied by acute signs of illness and signs or symptoms of middle ear inflammation [1]. (See "Acute otitis media in children: Clinical manifestations and diagnosis", section on 'Diagnosis'.)
The risk factors, microbiology, clinical features, and complications of AOM will be reviewed here. Related topics are presented separately:
● Acute otitis media in children: Clinical manifestations and diagnosis
● Acute otitis media in children: Treatment
● Acute otitis media in children: Prevention of recurrence
● Otitis media with effusion (serous otitis media) in children: Clinical features and diagnosis
● Otitis media with effusion (serous otitis media) in children: Management
● External otitis: Pathogenesis, clinical features, and diagnosis
● Acute otitis media in adults
EPIDEMIOLOGY — AOM is a leading cause of acute care visits and the most common reason for administration of antibiotics in children [2-4].
AOM is slightly more common in males than females [5-7]. It occurs at all ages but is most prevalent between 6 and 24 months of age, after which it begins to decline [8]. AOM is infrequent in school-age children, and adolescents. Children who have their first episode of AOM before age six months (ie, "early-onset AOM") are at increased risk for recurrent AOM [5,6,8]. Children who have few or no episodes of AOM before age three years are unlikely to have subsequent recurrent AOM. (See "Acute otitis media in children: Prevention of recurrence", section on 'Factors influencing choice'.)
The incidence of AOM in children in the United States decreased following universal immunization of infants with the 7-valent pneumococcal conjugate vaccine (PCV7) in 2000 and further declined after PCV7 was replaced with the 13-valent pneumococcal conjugate vaccine (PCV13) in 2010 [3,9-13]. In a prospective longitudinal cohort of 615 children <4 years from the post-PCV era (2006 to 2016), the cumulative incidence of ≥1 episode of AOM (confirmed by two validated otoscopists) was 23 percent at ≤1 year, 42 percent at ≤2 years, and 60 percent at ≤4 years [6]. In the classic study from the pre-PCV era (1989), the cumulative incidence of ≥1 episode of AOM was 62 percent at ≤1 year and 83 percent at ≤3 years [5]. A shift to more stringent diagnostic criteria for AOM between the pre-PCV7 and post-PCV13 eras also may have contributed to the decline in incidence [1,14].
The incidence of AOM in children also declined in other countries after introduction of pneumococcal conjugate vaccines to the routine immunization schedule [15-19]. Social distancing and other measures to prevent the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) at the onset of the coronavirus 2019 (COVID-19) pandemic resulted in the decrease of all respiratory tract infections, including AOM [20-22].
RISK AND PROTECTIVE FACTORS
●Risk factors – A number of risk factors for AOM have been established, the most of important of which is age.
•Age – The age-specific attack rate for AOM peaks between 6 and 12 months of age [6]. After that, the incidence declines with age, although there is a small increase between five to six years (the time of school entry). AOM is infrequent in school-age children and adolescents. (See "Acute otitis media in adults", section on 'Epidemiology of acute otitis media'.)
The prevalence of AOM in early life is probably related to multiple factors, including immature anatomy (eg, in infants, the Eustachian tube is shorter, more floppy, and more horizontally positioned than in adults, permitting nasal secretions to enter the middle ear more easily), physiology, genetic predisposition, and immunologic naiveté; other contributing factors have yet to be defined [23,24].
•Family history – Family history of AOM is a risk factor for AOM, particularly among children who have siblings [6]. In a prospective study of 615 children in the post-PCV era, the risk of AOM was increased in children with siblings and a family history of recurrent AOM (ie, >3 episodes of AOM or tympanostomy tube insertion for persistent/recurrent middle ear fluid in a sibling or either parent; odds ratio [OR] 3.7, 95% CI 2.5-5.8) [6].
The role of genetic factors in the development of AOM is suggested by a two-year prospective study of same-sex twins and triplets [25]. The estimate of discordance for an episode of AOM was greater among dizygotic than monozygotic twins (0.49 versus 0.04 percent).
Potential pathogenetic mechanisms for the heritability of AOM include anatomic, physiologic, and/or immunologic features. Polymorphisms in proinflammatory cytokine genes and genes involved in innate and adaptive immunity that increase susceptibility to otitis media and recurrent AOM have been identified [26-30].
•Day care – The transmission of bacterial and viral pathogens is common in day care centers. In observational studies from the post-PCV era, day care attendance was associated with an increased risk of AOM, with ORs ranging from 2.8 to 5.0 [6,31,32].
•Tobacco smoke and air pollution – Exposure to tobacco smoke increases the risk of AOM. In pooled analysis of three studies (1784 children), the risk ratio (RR) of AOM was 1.66 (95% CI 1.33-2.06) among children whose parents/caregivers smoked [33]. In another pooled analysis, the OR for recurrent AOM was 1.48 (95% CI 1.08-2.04) if either parent smoked [34]. The mechanism for this association is not entirely clear but may be related to increased nasopharyngeal and oropharyngeal carriage of otopathogens with exposure to smoke [35,36]. (See "Secondhand smoke exposure: Effects in children", section on 'Middle ear disease'.)
Ambient air pollution also has been associated with increased risk of AOM in observational studies, but the findings are inconsistent for many pollutants [37].
•Pacifier use – In observational studies from the pre-PCV era, pacifier use was been associated with increased risk of AOM [33,38]. In pooled analysis of two studies (4110 children), children who used a pacifier had a slightly higher incidence of AOM than children who did not (RR 1.24, 95% CI 1.06-1.46) [33].
•Race and ethnicity – Native American children, Alaskan and Canadian Inuit children, and indigenous Australian and Greenlander children have a higher incidence of severe and recurrent AOM than do White children [39,40]. In some indigenous Australian populations, 40 percent of the children may have chronic perforation of the tympanic membrane by 18 months of age [41]. In a prospective study, severe otitis media was also more likely to be reported in Bedouin than in Jewish children in Israel; severe otitis media was attributed to crowded living conditions and nasopharyngeal colonization earlier in life among Bedouin children; genetic differences were not investigated [42].
•Limited resources – Lack of access to medical care and local environmental factors lead to severe suppurative episodes of otitis media in children living in resource-limited settings [43]. Additional risk factors for chronic suppurative otitis media are discussed separately. (See "Chronic suppurative otitis media (CSOM): Clinical features and diagnosis", section on 'Epidemiology'.)
•Other risk factors – Other important risk factors in the development of single and recurrent episodes of AOM include [44]:
-Season (increased incidence during the fall and winter months, presumably due to respiratory virus activity)
-Altered host defenses and underlying disease (eg, human immunodeficiency virus [HIV], cleft palate, Down syndrome, allergic rhinitis)
●Protective factors
•Breastfeeding – Breastfeeding protects against AOM during the first two years of life [6,31,45-47]. Exclusive breastfeeding for at least six months is associated with the greatest protection, but any breastfeeding compared with no breastfeeding also appears to be beneficial. Limited breastfeeding or not having been breastfed is associated with an increased risk of AOM.
In meta-analysis of five observational studies (including>17,700 patients), exclusive breastfeeding from birth to age six months was associated with decreased risk of AOM before age two years (OR 0.57, 95% CI 0.44-0.75) [47]. In meta-analysis of five observational studies (including >19,600 patients), any breastfeeding was associated with decreased risk of AOM before age two years compared with no breastfeeding (OR 0.67, 95% CI 0.56-0.80). Although most of the studies included in these meta-analyses were from the pre-PCV era, studies from the post-PCV era also support the protective effect of breastfeeding.
Breastfeeding diminishes colonization of the nasopharynx by bacterial otopathogens (eg, Streptococcus pneumoniae, nontypeable Haemophilus influenzae) [33,46,48]. Additional reasons for the lower incidence of AOM among breastfed infants are uncertain but may be related to immunologic or nonimmune protective factors in breast milk, the facial musculature associated with breastfeeding, or the position maintained during feeding from the breast contrasted with bottle feeding [49,50]. (See "Infant benefits of breastfeeding", section on 'Biologically active components of human milk'.)
•Xylitol – Although daily administration of oral xylitol reduces the risk of AOM, the beneficial effect requires administration three to five times per day, which limits its practicability. The use of xylitol to prevent AOM in children is discussed separately. (See "Acute otitis media in children: Prevention of recurrence", section on 'Xylitol'.)
PATHOGENESIS — The middle ear is a narrow chamber that is part of an aerated system that includes the nares, the Eustachian tube, and the mastoid air cells (figure 1). The system is lined with respiratory mucosa; events affecting one area are usually reflected in similar changes throughout the system. Extension of the suppurative process to adjacent structures may lead to complications such as mastoiditis, labyrinthitis, petrositis, meningitis, and lateral sinus thrombosis. (See 'Complications and sequelae' below.)
The pathogenesis of AOM in at-risk children generally involves the following sequence of events [51-54]:
●The patient has an antecedent event (usually a viral upper respiratory tract infection) while colonized with an otopathogen(s) [45]. Some evidence suggests that co-colonization with bacterial otopathogens may be sufficient to trigger the cascade of events in the absence of viral respiratory infection [53,55,56].
●The event results in inflammatory edema of the respiratory mucosa of the nose, nasopharynx, and Eustachian tube.
●Inflammatory edema obstructs the narrowest portion of the Eustachian tube (the isthmus).
●Obstruction of the isthmus causes poor ventilation and negative middle ear pressure. This leads to the accumulation of secretions produced by the middle ear mucosa.
●Viruses and bacteria that colonize the upper respiratory tract enter the middle ear via aspiration, reflux, or insufflation.
●Microbial growth in the middle ear secretions often progresses to suppuration with clinical signs of AOM (bulging tympanic membrane [TM], middle ear fluid, erythematous TM).
●The middle ear effusion may persist for weeks to months following sterilization of the middle ear infection. (See "Acute otitis media in children: Treatment", section on 'Clinical course without antibiotics'.)
MICROBIOLOGY — The microbiology of AOM has been documented by cultures, viral studies, and molecular studies of middle ear effusion obtained by needle aspiration [57-59]. When a variety of microbiologic methods are used, bacterial and/or viral respiratory tract pathogens can be isolated from most middle ear aspirates from children with AOM [59-61]. In one series of 79 children with AOM and new onset otorrhea through a tympanostomy tube, bacteria (with or without viruses) were detected in 92 percent, viruses (with or without bacteria) in 70 percent, and both bacteria and viruses in 66 percent [60].
Bacterial pathogens — S. pneumoniae, nontypeable H. influenzae (NTHi), and Moraxella catarrhalis are the most common bacteria isolated from middle ear fluid in children with AOM [2,6,12,61-64].
Effect of infant immunization — Universal infant immunization with pneumococcal conjugate vaccines (PCVs) has affected the microbiology of AOM in children by altering the relative importance of the bacterial pathogens most frequently isolated from the middle ear fluid (ie, S. pneumoniae, H. influenzae, M. catarrhalis) as well as the most frequently isolated serotypes of S. pneumoniae. These changes affect the choice of antimicrobial therapy when treatment is indicated. (See "Acute otitis media in children: Treatment", section on 'Initial antibiotic therapy'.)
●Pre-heptavalent PCV (PCV7) – Before the introduction of PCV7 (table 1), PCV7 serotypes accounted for 60 to 70 percent of AOM isolates in the 6- to 59-month age group [65].
●Post-PCV7 – In the years immediately following introduction of PCV7, prospective studies in community-based pediatric practices noted declines in the proportion of S. pneumoniae isolates from middle ear fluid (from approximately 45 to 30 percent) and increases in the proportion of NTHi isolates (from approximately 40 to 55 percent) [2,62,66].
Although the proportion of NTHi isolates from the middle ear fluid increased, studies of the incidence of NTHi AOM were inconsistent, with some suggesting an increase while others suggested declines in NTHi AOM in early episodes but increased incidence in recurrent disease [2,64,66-69].
Following the introduction of PCV7, most pneumococcal isolates recovered from the middle ear of children with AOM and the nasopharynx of asymptomatic children were non-PCV7 serotypes [64,66,70-72]. Multidrug-resistant serotype 19A was reported as a cause of recalcitrant AOM [70,72,73] and coalescent mastoiditis [74]. Serotype 19A is included in the 13-valent PCV (PCV13), which replaced PCV7 in 2010 in the United States, and in the 15-valent PCV (PCV15), which became an alternative to PCV13 for children in the United States in 2022 [75]. Serotype 19A is not included in PCV10, which is used in many countries outside the United States.
●Post-PCV13 – With the introduction of PCV13 in 2010, the proportion of S. pneumoniae isolates continues to be lower than reported in the pre-PCV7 era and the proportions of M. catarrhalis and NTHi remain increased [6].
Following the introduction of the PCV13, studies of tympanocentesis-confirmed AOM in children in the United States and Israel demonstrated declines in overall episodes of AOM and in episodes of AOM due to PCV13 serotypes [12,76-78].
Although the study from Israel found no increase in AOM due to non-PCV13 pneumococcal serotypes or NTHi [78], in a prospective study of children with tympanocentesis-confirmed AOM in Rochester, New York, H. influenzae was the most commonly isolated pathogen and the majority of S. pneumoniae isolates were non-PCV13 serotypes [77]. Among the S. pneumoniae isolates, only 9 percent were PCV13 serotypes; 8 percent were serotype 22F or 33F, the two additional serotypes contained in PCV15, which was licensed for use in children ≥6 weeks of age in 2022 [75,77]. Similarly, in a study from Italy, non-PCV13 serotypes were isolated from the majority of children with pneumococcal AOM with spontaneous perforation [79], although it is unclear if this represents an increase in disease due to non-PCV13 serotypes or only a reduction in disease due to PCV13 serotypes.
Surveillance after licensure of PCV13 has also documented a decline in the prevalence of nasopharyngeal colonization with PCV13 serotypes, including 19A, in children with AOM [80-83].
●Post-PCV10 – The 10-valent pneumococcal conjugate vaccine (PCV10) includes the NTHi protein D as one of the conjugate proteins. PCV10 became available in 2010, although it is not licensed in the United States.
Introduction of PCV10 has been associated with decreased episodes of pneumococcal AOM and vaccine serotype AOM. In randomized clinical trials and in post-marketing, the efficacy of PCV10 against the first episode of clinical AOM in children younger than 24 months was 24 percent (95% CI 9-37 percent); the efficacy against moderate clinical AOM was 18 percent, (95% CI -6 to 26 percent) and the efficacy against severe clinical AOM was 33 percent (95% CI -21 to 62 percent) [18]. A statistically significant decrease in episodes of NTHi AOM has not been reproducibly demonstrated.
Streptococcus pneumoniae — S. pneumoniae is estimated to account for approximately 15 to 25 percent of bacterial isolates from the middle ear fluid of young children with AOM [6,78,84,85].
The proportion of pneumococcal isolates resistant to penicillin varies worldwide, but resistance is more likely in children with recurrent and/or persistent AOM and in those recently exposed to antimicrobial agents [51,64]. Studies of antimicrobial susceptibility among nasopharyngeal and middle ear isolates of S. pneumoniae identified increasing resistance to penicillin, amoxicillin, and third-generation cephalosporins among nonvaccine serotypes in 2013 to 2016 compared with 2010 to 2012 [76]. Despite increases in mean inhibitory concentration for amoxicillin, most isolates of S. pneumoniae remain susceptible, using pharmacodynamic breakpoints for high doses (90 mg/kg per day).
S. pneumoniae frequently causes first or early otitis media episodes, although H. influenzae and M. catarrhalis may cause early disease as well [7,86-88]. S. pneumoniae is isolated with equal frequency in bilateral and unilateral AOM [89,90].
S. pneumoniae is associated with greater clinical severity than other otopathogens, as reflected by higher fever, more intense otalgia, and the potential for complications such as bacteremia and mastoiditis [91]. It is also associated with a greater inflammatory response with elevated peripheral blood and middle ear fluid white blood cell counts compared with other pathogens [86].
Haemophilus influenzae — H. influenzae is estimated to account for approximately 50 to 60 percent of bacterial isolates from the middle ear fluid of young children with AOM [6,78,84,85].
Most H. influenzae isolates from the middle ear are NTHi [7,92]. In some settings, NTHi has become the most common bacteria isolated from children with AOM [93,94].
The patterns of H. influenzae resistance vary geographically, reflecting the dominant antimicrobial agent used in treatment of AOM. Approximately one-third to one-half of strains of H. influenzae recovered from middle ear fluids from children in the United States produce beta-lactamase [51,63,95]. In other parts of the world, resistance to ampicillin and cephalosporins may be associated with mutations in the penicillin binding proteins (beta-lactamase negative, ampicillin-resistance) [72,96-98]. (See "Epidemiology, clinical manifestations, diagnosis, and treatment of Haemophilus influenzae", section on 'Ampicillin resistance'.)
H. influenzae AOM is more commonly isolated in bilateral than unilateral AOM [89,90,99]. Otitis media caused by NTHi is frequently associated with concurrent conjunctivitis and milder symptoms (eg, lower fever, less inflamed tympanic membrane [TM]) than pneumococcal AOM [86,90]. NTHi infection is also associated with more complex otitis media, including increased risk for treatment failure, recurrence despite appropriate antibiotic therapy, and chronicity [59,99].
Moraxella catarrhalis — M. catarrhalis accounts for approximately 12 to 15 percent of bacterial middle ear isolates in children with AOM [6,78,84,85]. It is isolated more commonly in middle ear aspirates or otorrhea specimens in countries where children have been immunized with PCV. Virtually all strains produce beta-lactamase [6,66]. M. catarrhalis AOM typically is less severe than pneumococcal AOM.
Group A Streptococcus — Group A Streptococcus (GAS) occasionally causes AOM (2 to 10 percent of isolates) [2]. GAS AOM tends to occur in older children and to be more frequently associated with local complications (eg, TM perforation, mastoiditis) and less frequently associated with fever and systemic or respiratory symptoms than AOM caused by other organisms [100-102]. (See 'Tympanic membrane abnormalities' below.)
Staphylococcus aureus — S. aureus is an uncommon cause of AOM, but its prevalence appears to have increased after introduction of PCV7, particularly in children with spontaneous perforation of the tympanic membrane [2,68,103-105]. It is also often found isolated from acute otorrhea in children with tympanostomy tubes in place. Whether isolation of S. aureus from discharge in the external canal reflects pathogenicity or commensal bacteria is uncertain. (See "Tympanostomy tube otorrhea in children: Causes, prevention, and management", section on 'Pathogens'.)
Other bacteria — Anaerobic bacteria infrequently cause AOM. Enteric gram-negative bacilli such as Escherichia coli may cause AOM in the first months of life [106,107]. Pseudomonas aeruginosa has a special role in chronic suppurative otitis media. (See "Pseudomonas aeruginosa infections of the eye, ear, urinary tract, gastrointestinal tract, and central nervous system", section on 'Ear infections'.)
Viral pathogens — Microbiologic and epidemiologic data suggest that viral infection is frequently associated with AOM [60,108-111]. With advances in microbiologic techniques, including reverse transcriptase polymerase chain reaction, viruses are increasingly detected in the middle ear fluid of children with AOM [60,110]. The most frequently isolated viruses are respiratory syncytial virus (RSV), picornaviruses (eg, rhinovirus, enterovirus), coronaviruses, influenza viruses, adenoviruses, and human metapneumovirus. However, in an epidemiologic study, only influenza, RSV, and human metapneumovirus activity in the community were associated with an increase in AOM diagnoses [112].
Other pathogens
●Mycoplasma pneumoniae rarely has been isolated from middle ear fluids of children with AOM. (See "Mycoplasma pneumoniae infection in children", section on 'Clinical manifestations'.)
●Chlamydia trachomatis has been associated with otitis media in infants younger than six months of age. (See "Chlamydia trachomatis infections in the newborn".)
●Chlamydia pneumoniae has been isolated from some patients with acute and chronic otitis media [57].
Dual pathogen infection
●Dual bacterial infections – Dual bacterial infection, most commonly involving S. pneumoniae and H. influenzae, has been identified in children with persistent AOM and/or recurrent otitis media from multiple countries [42,113-115]. The persistence and recurrence of polymicrobial otitis media probably reflects biofilms in the middle ear space. In a prospective study, dual bacterial infection with S. pneumoniae and H. influenzae was more likely in children living in crowded living conditions with early colonization; nonvaccine serotypes were involved most frequently [42].
●Bacterial and viral infections – Bacterial and viral coinfection is common in children with recurrent AOM. In one series of 79 children with AOM and new onset otorrhea through a tympanostomy tube, both bacteria and viruses were isolated in 66 percent [60].
The frequency of mixed bacterial and viral infections has important clinical implications [116]. Mixed bacterial and viral infections may respond differently to antibiotic therapy than purely bacterial infections [117,118]. The presence of viruses may increase middle ear inflammation [119,120], decrease neutrophil function [121], and reduce antibiotic penetration into the middle ear [122].
PATHOGENS IN SPECIAL POPULATIONS
Young infants — Bacterial pathogens isolated from the middle ear aspirates of young infants with AOM typically are similar to those identified in older children (eg, S. pneumoniae and H. influenzae). In infants younger than two weeks, pathogens that cause neonatal sepsis (group B Streptococcus, enteric gram-negative bacilli, and S. aureus) also may be found. (See "Clinical features, evaluation, and diagnosis of sepsis in term and late preterm neonates", section on 'Etiologic agents'.)
Few studies have evaluated the microbiology of AOM in young infants after the introduction of pneumococcal conjugate vaccine (PCV). In an observational study of 182 infants <2 months of age from Israel who underwent tympanocentesis before (2005 to 2009) and after (2010 to 2014) the introduction of PCV, the proportion of S. pneumoniae and H. influenzae isolates decreased after the introduction of PCV (from 50 to 30 percent and 30 to 23 percent, respectively) and the proportion of culture-negative patients increased (from 19.6 to 35.6 percent) [123]. Among the 23 infants (13 percent) with concomitant serious bacterial infection, 19 had urinary tract infections which were generally caused by pathogens different than those isolated from middle ear fluid.
Resource-limited countries — In resource-limited countries, the most common bacterial causes of AOM are the same as in developed countries [124-126].
In addition, otitis media may be caused by Mycobacteria tuberculosis, Corynebacterium diphtheriae, and Clostridium tetani. Parasitic (Ascaris lumbricoides) and fungal (Blastomyces dermatitidis, Candida and Aspergillus species) middle ear infections may occur but are rare [124].
COMPLICATIONS AND SEQUELAE
Intratemporal complications
Hearing loss — Most patients with middle ear effusion have persistent or fluctuating conductive hearing loss. Fluid filling the middle ear space prevents the tympanic membrane (TM) from vibrating adequately, thereby diminishing movement of the ossicular chain. The hearing loss remains as long as fluid fills the middle ear space. The median hearing threshold is 25 dB, which is equivalent to putting plugs in the child's ears [127]. (See "Hearing loss in children: Etiology", section on 'Infection'.)
Despite treatment with appropriate antimicrobial agents, middle ear fluid may persist for weeks to months after the onset of signs of AOM. (See "Acute otitis media in children: Treatment", section on 'Clinical course without antibiotics'.)
Consequences and sequelae of prolonged middle ear effusion are discussed separately. (See "Otitis media with effusion (serous otitis media) in children: Clinical features and diagnosis", section on 'Hearing loss'.)
Sensorineural hearing loss is an uncommon consequence of AOM but may occur.
Balance and motor problems — Children with AOM may have balance, motor, or vestibular problems related to vestibular dysfunction or labyrinthitis [128-132]. (See "Causes of vertigo", section on 'Otitis media'.)
Tympanic membrane abnormalities
●Perforation – The increased pressure in the middle ear can result in central ischemia, necrosis, and spontaneous perforation of the TM, usually accompanied by otorrhea (picture 3) [133]. The risk of perforation is increased in children initially observed without antimicrobial therapy and in children with dual pathogen infections, including nontypeable H. influenzae and M. catarrhalis [102,134,135]. (See 'Group A Streptococcus' above.)
The frequency of spontaneous perforation is increased in Native American and Australian Aborigine children and in children in resource-limited countries [39]. AOM caused by group A Streptococcus is associated with higher rates of TM perforation than AOM caused by other pathogens [100-102].
The treatment of TM perforation associated with AOM is discussed separately. (See "Acute otitis media in children: Treatment", section on 'Tympanic membrane perforation'.)
●Myringosclerosis – Myringosclerosis (calcification of the connective tissue of TM, sometimes called tympanosclerosis) is a complication of frequent middle ear disease [136]. It is characterized by whitish plaques in the TM (picture 4A-B) and occasionally the middle ear. In most children, myringosclerosis is of no functional importance, but in some, the deposits may envelop the ossicles, resulting in a conductive hearing loss.
●Retraction or collapse – Chronic or recurrent decreased pressure in the middle ear in children with recurrent AOM may lead to retraction (atelectasis) or collapse of the TM (middle ear atelectasis) (picture 5).
Chronic suppurative otitis media — Unresolved or complicated AOM with perforation of the TM may lead to chronic suppurative otitis media (CSOM) or chronic otomastoiditis, which is defined as perforation of the TM with chronic purulent drainage from the middle ear cleft for more than six weeks (picture 6). Most often CSOM is the end stage of recurrent AOM episodes that begin in the first year of life. (See "Chronic suppurative otitis media (CSOM): Clinical features and diagnosis".)
Children with TM perforation and suppurative discharge that persists despite oral and/or topical antibiotics should be referred to an infectious disease specialist or otolaryngologist as soon as possible and a sample for a bacterial culture should be obtained to ensure optimal antimicrobial treatment. Children with perforation without drainage that persists for three months or longer should be referred to an otolaryngologist for further management [133]. Prevention of CSOM entails prompt and appropriate treatment of acute middle ear infection [39]. Chemoprophylaxis is not warranted. (See "Chronic suppurative otitis media (CSOM): Treatment, complications, and prevention".)
Cholesteatoma — A cholesteatoma is an abnormal growth of squamous epithelium in the middle ear and mastoid that may progressively enlarge to surround and destroy the ossicles. Recurrent AOM, which may lead to retraction pockets in the TM, is a risk factor for cholesteatoma.
Clinical features suggestive of acquired cholesteatomas include deep retraction pockets, as in panel A of the picture (picture 7), a white mass behind the TM (picture 8), focal granulation at the periphery of the TM (picture 9), new-onset hearing loss, and ear drainage for more than two weeks despite treatment. The diagnosis and management of cholesteatoma are discussed separately. (See "Cholesteatoma in children", section on 'Clinical features' and "Cholesteatoma in children", section on 'Surgical treatment'.)
Mastoiditis — Most episodes of AOM are associated with some inflammation of the mastoid because the mastoid air cells are connected to the distal end of the middle ear through a small canal or antrum (figure 2). In rare cases, resolution of the mastoid infection does not occur, and acute suppurative mastoiditis develops with pus filling the air cells.
The pathogenesis, epidemiology, and clinical features of mastoiditis in children are discussed separately. (See "Acute mastoiditis in children: Clinical features and diagnosis".)
Other intratemporal complications — Other intratemporal complications of AOM include [128]:
●Petrositis (extension of the infection into the petrous portion of the mastoid bone) (see "Acute mastoiditis in children: Clinical features and diagnosis", section on 'Complications')
●Labyrinthitis (extension of infection into the cochlear and vestibular apparatus) (see "Causes of vertigo", section on 'Otitis media')
●Facial paralysis (the facial nerve courses through the middle ear and mastoid); facial paralysis also may occur as a complication of acute mastoiditis or CSOM (see "Facial nerve palsy in children", section on 'Otitis media')
Intracranial complications — Intracranial complications of AOM are uncommon in resource-rich countries. However, they remain a concern in resource-limited countries where there is poor access to medical care [124,137]. Intracranial complications of AOM include:
●Meningitis (see "Bacterial meningitis in children older than one month: Clinical features and diagnosis", section on 'Clinical features')
●Epidural abscess (see "Intracranial epidural abscess", section on 'Clinical manifestations')
●Brain abscess (see "Pathogenesis, clinical manifestations, and diagnosis of brain abscess", section on 'Clinical manifestations')
●Lateral sinus thrombosis (see "Septic dural sinus thrombosis")
●Cavernous sinus thrombosis (see "Septic dural sinus thrombosis")
●Subdural empyema (collection of purulent material between the dura and the arachnoid membrane)
●Carotid artery thrombosis
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SUMMARY
●Definition – Acute otitis media (AOM) is defined by moderate to severe bulging (picture 1 and picture 2) of the tympanic membrane or new onset of otorrhea not due to acute otitis externa accompanied by acute signs of illness and signs or symptoms of middle ear inflammation. (See 'Introduction' above.)
●Epidemiology and risk factors – AOM occurs at all ages but is most prevalent between 6 and 24 months of age, after which it begins to decline. The incidence of AOM declined following the introduction of pneumococcal conjugate vaccines. (See 'Epidemiology' above.)
Viral upper respiratory infection is the most common predisposing factor for the development of AOM. The incidence of AOM in the United States is highest between 6 and 12 months of age and during the respiratory virus season. In addition to young age, risk factors for AOM include family history, day care attendance, exposure to tobacco smoke, and pacifier use. The risk of severe and recurrent AOM is increased among Native American children, Alaskan and Canadian Inuit children, and indigenous Australian and Greenlander children. Breastfeeding is protective. (See 'Risk and protective factors' above.)
●Pathogenesis – Inflammation of the upper respiratory tract predisposes to AOM via dysfunction of the Eustachian tube, leading to negative pressure and accumulation of middle ear secretions and impairment in host defenses (eg, normal mucociliary action). Microbial growth in the middle ear secretions may result in suppuration and clinical signs of AOM. (See 'Pathogenesis' above.)
●Microbiology – Streptococcus pneumoniae, nontypeable Haemophilus influenzae (NTHi), and Moraxella catarrhalis account for most of the bacterial isolates from middle ear fluid. The most common viral pathogens include respiratory syncytial virus, picornaviruses (eg, rhinoviruses, enterovirus), coronaviruses, influenza viruses, adenoviruses, and human metapneumovirus. (See 'Microbiology' above.)
In young infants (ie, <2 months of age), the most common bacterial causes of AOM are the same as they are in older children (eg, S. pneumoniae and H. influenzae); in those <2 weeks of age, AOM also may be caused by group B Streptococcus, enteric gram-negative bacilli, and S. aureus. (See 'Young infants' above.)
In resource-limited countries, the most common bacterial causes of AOM are the same as in developed countries. Additional bacterial pathogens include Mycobacteria tuberculosis, Corynebacterium diphtheriae, and Clostridium tetani. (See 'Resource-limited countries' above.)
●Complications and sequelae – Intratemporal complications of AOM include mild conductive hearing loss; vestibular, balance, and motor dysfunctions; TM perforation; inflammation of the mastoid and/or suppurative mastoiditis; petrositis; and labyrinthitis. Intracranial complications are rare in resource-abundant countries but more frequent in resource-limited countries; they include meningitis, epidural abscess, brain abscess, lateral sinus thrombosis, cavernous sinus thrombosis, subdural empyema, and carotid artery thrombosis. (See 'Complications and sequelae' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Jerome Klein, MD, who contributed to an earlier version of this topic review.
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