Pediatric Otorhinolaryngology: Diagnosis and Treatment, 1st Ed.


Otitis Media

David H. Chi and Dennis J. Kitsko

Otitis media (OM) is one of the most common infectious diseases in children, particularly in infants and toddlers. Approximately 30 to 35% of all visits for acute illness in the primary care setting in the first 5 years of life are for middle ear disease. Up to 40% of total office visits at 4 to 5 years of age will result in the diagnosis of some middle ear problem. This includes approximately 10% of children who present at well-child visits and are without any subjective complaint.1 Nearly half of all antibiotics prescribed in children less than 10 years old was for OM.2 The financial burden for medical and surgical intervention for OM is estimated at $5 billion yearly in the United States alone.3 But perhaps the impact on the day-to-day lives of families is far greater than any monetary figure. It can be associated with speech, language, and balance difficulties, which can contribute to further learning problems. The parental burden of dealing with a fussy, irritable child who sleeps poorly can be very frustrating. Also, parents may be forced to miss multiple days of work as daycare settings frequently forbid children with high fevers to attend; this is in addition to the time missed from work for physician visits.

For the sake of clarity, the following terms and their definitions will be used in this chapter. Otitis media will refer to nonspecific inflammation within the middle ear space. Acute otitis media (AOM) will refer to acute infection of fluid within the middle ear space, with associated otalgia and an erythematous or bulging tympanic membrane. Otitis media with effusion (OME) will be defined as fluid collection in the middle ear space in the absence of signs of acute infection mentioned above. Finally, middle ear effusion (MEE) will refer generally to fluid in the middle ear space, whether this fluid is associated with acute infection or not.



The vast majority of children will have at least one episode of AOM in childhood. Approximately 62% of infants will have AOM by 12 months of age, with this number rising to 84% at 3 years of age, and 95% by age 7. After age 7, children are much less likely to develop AOM.1 Many children will have recurrent episodes of AOM as well. Up to 20% of infants will have three episodes by their first birthday, and by age 7, 75% of children will have had at least three episodes.


Determining the incidence of OME is much more difficult because many children will present without any complaints. Furthermore, many episodes of AOM will “become” OME as ear pain and tympanic membrane erythema and bulging resolve, but MEE remains. Identifying the onset and interval to resolution of OME is challenging, as it requires very short observation intervals. This is particularly true given that approximately 65% of OME episodes will resolve in 1 month.4 Casselbrant et al found a 53 to 61% incidence of OME in 2- to 6-year-old daycare children followed monthly with pneumatic otoscopy and tympanometry. This number dropped to 22% in 5- to 12-year-old schoolchildren.4,5 Lous and Fiellau-Nikolajsen reported a similar 26% incidence in 7-year-old children who they followed-up for 1 year.6

Multiple studies in various countries have looked at the point prevalence of MEE, which includes both AOM and OME, with a great variety of ranges from 1 to 40%. Given the variability in race, sample sizes, age ranges, number of screenings, and screening tools, it is difficult to generalize these incidence data in a meaningful way. What is clear, though, is that almost all children developed MEE at some point during the first 3 years of life.7,8

Anatomy and Pathophysiology

The anatomic structures involved in regulating the middle ear system include the mastoid cavity, the middle ear cavity, the eustachian tube (ET), and the nose/nasopharynx and palate. The ET is perhaps the most important of these structures, particularly as it relates to the development of AOM and OME. The ET serves three important functions physiologically: (1) pressure regulation/ventilation and equilibration to atmospheric pressure, (2) protection of the middle ear from pathogens ascending from the nasopharynx via a gas cushion, and (3) clearance of secretions from the middle ear. The origin of middle ear disease is poor ET function and inability to regulate pressure. In infants, the ET is shorter and more horizontal than in an adult, and this is one anatomic factor that leads to poor pressure regulation.

ET dysfunction may occur spontaneously, particularly in infants, but is more commonly associated with antecedent events that cause either anatomic or, more commonly, functional obstruction. Anatomic causes include enlarged adenoids, nasal polyposis, foreign body, or tumor. Functional obstruction is associated with inflammation within the nasal cavity and nasopharynx, most commonly from a viral upper respiratory illness (URI) in children. Other causes include allergic rhinitis and gastroesophageal reflux disease (GERD). This inflammation leads to edema around the ET orifice, which is located in the nasopharynx, and subsequent inability of the ET to open in its usual passive fashion to regulate pressure. As negative pressure builds, secretions and pathogens can be aspirated from the nasopharynx into the middle ear space, creating MEE. This fluid may persist and not become infected, resulting in OME. If, however, the fluid becomes infected, either with viruses or more commonly bacteria, an AOM develops.

Certain populations have a much higher incidence of ET dysfunction and, subsequently, OM. Anatomically, those children with craniofacial abnormalities, Down syndrome, and cleft palate may have persistent ET dysfunction and difficulties with OM throughout their lives. Immunocompromised children are also at increased risk—this includes those with primary ciliary dyskinesia, immunoglobulin deficiencies, T- or B-cell defects, chemotherapy, or human immunodeficiency virus infections.



The most common bacteria isolated in AOM are Haemophilus influenzae (35 to 50%) and Streptococcus pneumoniae (25 to 40%). It was hoped that the introduction of the pneumococcal conjugate vaccine—PCV7—in 2000 would dramatically decrease the number of episodes of AOM, but the decrease has been reported at a modest 7.8%, with an increase in the number of infections from nonvaccine serotypes and Haemophilus infections.911 Moraxella catarrhalis is the third most common bacteria (3 to 20%) isolated, followed by group A Streptococcus and Staphylococcus aureus (1 to 10%). Also, although neonates and infants usually have the same bacteriologic pattern as older children, gram-negative bacteria such as Escherichia coliKlebsiella, and Pseudomonas are seen with a higher frequency. Anaerobic bacteria such as PeptostreptococcusFusobacterium, and Bacteroides are more commonly seen in chronic suppurative OM (persistent drainage via a tympanostomy tube or perforation) and in cases of cholesteatoma. A myriad of other bacteria have been recovered from the middle ear in rare cases, including MycoplasmaMycobacterium tuberculosis, group B Streptococcus species, and Neisseria and Chlamydia species.

Cultures in OME more commonly do not grow bacteria, and this “sterile” culture occurs in one-third of cases. Another one-third of the cultures will grow the three most common AOM bacteria (S. pneumoniaeH. influenzae, and M. catarrhalis), with Haemophilus being the most common. The final one-third is composed of nonpathogenic bacteria such as the normal skin bacterium S. epidermidis, as well as viruses.12

More recently, the role of bacterial biofilms in the pathogenesis of OM has been debated. A biofilm occurs when a community of bacteria interact together to surround themselves with a polysaccharide matrix, which protects them from a host's immune response. Because of its low metabolic rate, it is also resistant to antimicrobial therapy. Initially, it was thought that biofilms only existed on hard surfaces such as teeth and tympanostomy tubes. But research has shown that biofilms can also be found in the middle ear.13 These biofilms were identified in 48% of patients undergoing tympanostomy tube insertion even in the face of negative middle ear fluid cultures. Biofilms have also been found in the nasopharynx of children with OM. This suggests that these biofilms may act as a bacterial reservoir for repeated OM via the ET, and may help explain why adenoidectomy benefits some patients with OM. At this point, the existence of biofilms cannot be disputed. Their exact role in the pathogenesis of OM, particularly as it relates to treatment strategies, has yet to be clearly defined.


Before the advent of polymerase chain reaction, the incidence of viral AOM was unknown and largely underestimated, because isolating viruses in culture was technically challenging. Currently, it is thought that viruses alone account for approximately 20% of episodes of AOM and are present in approximately 20 to 30% of fluid in OME. Rhinovirus and respiratory syncytial virus are the most common, but influenza, parainfluenza, and adenovirus are also seen.14 The role of viruses in OM extends beyond their role in the middle ear directly. Viral URIs are often precursor events to episodes of OM. In one study, 70% of episodes of OM were associated with a viral URI, and viruses were isolated from MEE in 77% of these cases.15 This suggests that mixed bacterial and viral OM is common and perhaps viruses “set up” the middle ear space for bacterial infection, similar to the pathogenesis of sinusitis.



The most recent guidelines released by the American Academy of Pediatrics/American Academy of Family Physicians outline three components in diagnosing AOM: (1) history of acute onset, (2) confirmed presence of MEE, and (3) presence of signs and symptoms of acute inflammation.16 Common symptoms of AOM include ear pulling, poor sleep, fever, and irritability, although some children may have no symptoms. OME, as previously mentioned, is the presence of fluid in the middle ear without acute inflammation. This can be more challenging to diagnose and is often not accompanied by any symptoms, particularly in young children. If symptoms are present, the most common ones include hearing loss, fullness, otalgia (especially at night), and imbalance.

Physical Examination

Physical examination findings of acute inflammation in AOM include a bulging tympanic membrane (TM), erythema of the TM, or otorrhea associated with spontaneous perforation. The TM may be thickened and dull, and purulence may be visualized through the TM. However, caution must be taken when assessing redness of the eardrum. One study showed the predictive value of redness of the TM alone to be only 7%, and hyperemia of the TM alone is a common normal finding, particularly in a crying child.17 OME usually is seen as opacification of the TM with abnormal color, typically pink, yellow, amber, or blue. Bubbles or air–fluid interfaces may be visible, and the TM may be in a neutral or retracted position. Pneumatic otoscopy is a critical part of the otoscopic examination, particularly when determining whether MEE is present. This involves the application of positive and negative pressure to the TM. To properly perform pneumatic otoscopy, the largest speculum that adequately fits in the ear canal should be used and an airtight seal must be created within the cartilaginous ear canal. Decreased or absent mobility of the TM is suggestive of fluid and may be used to confirm MEE and OME. Other sources of poor mobility include scarring (myringosclerosis) or thickening of the TM, and obviously a perforation or tympanostomy tube will prohibit mobility. Myringosclerosis is seen as white plaques within the TM, and commonly occurs in a horseshoe pattern centrally around the pars tensa portion of the TM. This occurs with long-standing ear disease, either with or without the previous presence of a tympanostomy tube. Retraction, or atelectasis, of the TM is another common otoscopic finding, and may be associated with OME. In severe cases, hearing loss associated with ossicular chain erosion or cholesteatoma formation can occur. If available, binocular microscopy can also be a valuable tool in examining the TM and assessing for the presence of MEE. One study showed an 88% sensitivity and 89% specificity for binocular microscopy in identifying MEE, compared with 68 and 81%, respectively, for pneumatic otoscopy.18 Obviously, binocular microscopy will not be available in all diagnostic settings and may not be practical in every patient, particularly young children, therefore, pneumatic otoscopy remains the gold standard for identifying MEE.

Ancillary Testing

Immittance testing, or tympanometry, is an audiologic tool that can also be useful in diagnosing MEE. It is particularly useful in young children, those with small ear canals, and those patients in whom an airtight seal cannot be obtained for pneumatic otoscopy. Tympanometry involves placing a probe in the ear canal with an airtight seal. The probe emits a tone, and a curve is obtained by plotting the immittance of the middle ear as a function of pressure in the ear canal. A normal (or type A) tympanogram will have a sharp peak, which usually will occur near 0 daPa. A flat (or type B) tympanogram is classically associated with MEE, as compliance of the drum is poor. Other sources of flat tympanograms, however, include presence of a tympanostomy tube, or a false-positive result if a seal is not created with the probe. A type C tympanogram occurs when a peak is obtained, but this peak occurs at a pressure of 150 daPa or greater. This suggests high negative pressure, or a vacuum type effect, in the middle ear, and is much less specific in diagnosing MEE. Tympanometry is highly sensitive, with ranges around 80 to 90% reported in multiple studies, but its specificity is much lower, reportedly as low as 47%.18 It is particularly poor in children less than 1 year of age, and this may be due to the increased compliance of the ear canal in infants. This can be overcome to some degree by using a 1000 Hz probe tone instead of the usual 226 Hz tone. The role of other supplementary testing, including acoustic reflectometry and ultrasound, is less well defined and not readily available in most physicians’ offices.

Medical Treatment of AOM and OME


There has been controversy for quite some time about the need for antibiotic therapy in all cases of AOM. It has been shown that only a 12% increase in resolution rate was observed in children who received antibiotics versus clinical observation at 2 to 7 days.19 Furthermore, the incidence of meningitis, mastoiditis, and other suppurative complications are similar in those treated with antibiotics versus observation (0.17 vs. 0.59%, respectively). In fact, routine antibiotic usage may select out for more invasive, resistant bacteria. A scientific review of the best available studies was performed and new guidelines from the American Academy of Pediatrics (AAP) and American Academy of Family Physicians (AAFP) were introduced in 2004.16 This was the first set of guidelines from these academies that included observation as initial management in certain cases of AOM. The factors used to determine initial treatment include age, certainty of diagnosis, and severity of illness, and reliability of the caregiver/follow-up were the factors used to create this recommendation (Table 1.1). Certain diagnosis meets the three criteria mentioned previously in this chapter. Severe illness was defined as severe otalgia or fever greater than 39°C (102.2°F).


By definition, the “observation option” refers to observation for a period of 48 to 72 hours, and limiting management to symptomatic relief. This includes particularly the management of pain, another recommendation from the committee. The most important initial factor in determining whether observation is even an option in a child is the reliability of the caregiver. This not only relates to assurance of follow-up, but also their ability to recognize worsening severity of illness and to be able to provide them with prompt access to medical care if necessary. If there are serious concerns with any of these factors, then a physician may choose to initially treat a child with antibiotics empirically. When observation is chosen, a strategy should be in place to ensure that some follow-up occurs. This may include a scheduled clinic or phone follow-up, a parent-initiated visit if there is no improvement in 48 to 72 hours, or a safety-net antibiotic prescription given to parents to fill if there is no improvement in 48 to 72 hours. Other exclusion criteria for the observation option include immunodeficiency, genetic abnormalities, craniofacial anomalies, underlying persistent OME, and AOM in the past 30 days.

Table 1.1 Criteria for Initial Antibacterial Agent Treatment or Observation in Children with AOM


Certain Diagnosis

Uncertain Diagnosis

<6 mo

Antibacterial therapy

Antibacterial therapy

6 mo to 2 y

Antibacterial therapy

Antibacterial therapy if severe illness; observation optiona if nonsevere illness

≥2 y

Antibacterial therapy if severe illness; observation optiona if nonsevere illness

Observation optiona

aObservation is an appropriate option only when follow-up can be ensured and antibacterial agents started if symptoms persist or worsen. Nonsevere illness is mild otalgia and fever <39°C in the past 24 hours. Severe illness is moderate to severe otalgia or fever ≥39°C. A certain diagnosis of AOM meets all three criteria: (1) rapid onset, (2) signs of middle ear effusion and (3) signs and symptoms of middle ear inflammation.

Adapted from: American Academy of Pediatrics/American Academy of Family Physicians Subcommittee Guidelines on Management of Acute Otitis Media.

AOM, acute otitis media; mo, months; y, years.

All children under the age of 6 months should receive initial antibiotic therapy for AOM, regardless of certainty of diagnosis or severity of illness. The reason for this is the concern for serious infection in this very young age group and the diagnostic challenge in assessing worsening symptoms or signs of progression to suppurative complications. In the age of 6 months to 2 years, initial antibiotic therapy should be instituted if there is a certain diagnosis, or if there is an uncertain diagnosis in the presence of severe illness. If the diagnosis is uncertain and there is nonsevere illness, then observation is an option. In children older than age 2, observation is an option even in the presence of a certain diagnosis of AOM, as long as the patient has nonsevere illness. Initial antibiotic therapy should be instituted in the presence of severe illness (Table 1.1).

Although these guidelines are widely accepted, further research may give us a clearer picture of which patients should be treated initially and which can be observed. There have been problems cited with the studies that were used to show high spontaneous resolution rates in AOM. The definition of AOM may have included criteria that allowed inclusion of patients with OME, the antibiotics may have been inappropriate or at an insufficient dosage, and the sickest children and those less than 2 years of age may have been excluded/underrepresented.20 All these factors would make antibiotic therapy appear less efficacious. Another challenge is of getting parents to agree to observation, which can be difficult particularly given the empiric historic use in AOM. Practitioners have also not universally accepted this into their practice, and one study showed that although 83% of physicians felt observation was a reasonable practice, it was used in only a median of 15% of practices.21

Initial Antibiotic Therapy

The initial antibiotic for an uncomplicated, nonrecurring AOM is amoxicillin (Table 1.2). Amoxicillin has been shown to be effective against the most common AOM organisms, particularly S. pneumoniaeand nonbeta lactamase-producing H. influenzae. The dosage recommendation is 80 to 90 mg/kg/d versus the standard 40 mg/kg/d. This higher dose has been shown to be more effective, particularly against the increasing intermediate and highly resistant strains of S. pneumoniae that have emerged. In addition, amoxicillin is cost-effective and easy to take, with a low incidence of side effects. In patients with severe illness (severe otalgia or temperature >39°C), the recommendation is high-dose amoxicillin (90 mg/kg/d)/clavulanate (6.4 mg/kg/d). The challenge in determining appropriate initial antibiotic therapy is the changing landscape of the bacteriology of AOM. Nearly 50% of H. influenzae and 100% of M. catarrhalis are beta-lactamase–producing, and therefore resistant to amoxicillin alone. But there is also evidence to suggest that AOM caused by these bacteria are more likely to resolve spontaneously, and the combination of S. pneumoniae and amoxicillin-sensitive H. influenzae still represent the majority of AOM pathogens.

In penicillin-allergic patients without type I hypersensitivity, cefdinir, cefpodoxime, or cefuroxime can be used. Azithromycin or clarithromycin are alternatives in those patients with type I hypersensitivity, although studies suggest increasing resistance rates to these macrolide antibiotics. Other possibilities include erythromycin/sulfisoxazole or trimethoprim/sulfamethoxazole. Clindamycin is also effective if the pathogen is resistant S. pneumoniae. In the case of severe illness or the inability of the patient to tolerate oral medication, intramuscular ceftriaxone is also an option. The above protocols are designed not only for patients who are treated initially, but also for those in whom the observation option has failed after 72 hours. Table 1.3 outlines antibiotic guidelines from a combination of the AAP/AAFP and Centers for Disease Control and Prevention guidelines.

Table 1.2 AAP/AAFP Therapy Options for AOM in Varying Clinical Circumstances

At diagnosis when observation is not an option

Recommended: amoxicillin 80–90 mg/kg/d

Alternative for penicillin allergy: nontype I: cefdinir, cefuroxime, cefpodoxime; type I: azithromycin, clarithromycin

Clinically defined failure of observation option after 48 to 72 h

Recommended: amoxicillin 80–90 mg/kg/d

Alternative for penicillin allergy: nontype I: cefdinir, cefuroxime, cefpodoxime; type I: azithromycin, clarithromycin

Clinically defined failure of initial antibiotic treatment after 48 to 72 h

Recommended: amoxicillin/clavulanate (90 mg/kg/d of amoxicillin component, with 6.4 mg/kg/d of clavulanate)

Alternative for penicillin allergy: nontype I: ceftriaxone—3 d; type I: clindamycin

At diagnosis when observation is not an option

Recommended: amoxicillin/clavulanate (90 mg/kg/d of amoxicillin with 6.4 mg/kg/d of clavulanate

Alternative for penicillin allergy: ceftriaxone—1 or 3 d

Clinically defined failure of observation option after 48 to 72 h

Recommended: amoxicillin/clavulanate (90 mg/kg/d of amoxicillin with 6.4 mg/kg/d of clavulanate)

Alternative for penicillin allergy: ceftriaxone 1 or 3 d

Clinically defined failure of initial antibiotic treatment after 48 to 72 h

Recommended: ceftriaxone 3 d

Alternative for penicillin allergy: tympanocentesis, clindamycin

Adapted from: Pichichero ME, Casey JR. Acute otitis media: making sense of recent guidelines on antimicrobial treatment. J Fam Pract 2005;54(4): 313–322.

AAP, American Academy of Pediatrics; AAFP, American Academy of Family Physicians; AOM, acute otitis media; d, day(s); h, hour(s).

Table 1.3 Consistency of Guidelines for AOM

All recommend as first-line therapy

Amoxicillin, mostly at 80–90 mg/kg/d

All recommend as second-line therapy

Amoxicillin/clavulanate, mostly “ES” 80–90 mg/kg/d

Some recommend as second-line therapy

Cefdinir 14 mg/kg/d

Cefprozil 30 mg/kg/d

Cefuroxime axetil 30 mg/kg/d

Cefpodoxime 10 mg/kg/d

Ceftriaxone 50 mg/kg/d

Not recommended by any guideline Unless pathogen known to be sensitive; patient had severe allergic reaction to penicillin or amoxicillin; or combined with another antibiotic that is effective against additional organisms










Adapted from: Pichichero ME, Casey JR. Acute otitis media: making sense of recent guidelines on antimicrobial treatment. J Fam Pract 2005;54(4): 313–322.

AOM, acute otitis media; d, day(s); ES, extra strength.

The optimal duration of therapy for AOM is not completely certain. Evidence suggests fewer treatment failures in younger children with a standard 10-day course, and the current recommendation is 10 days in children younger than 6 years. A 5- to 7-day course may be appropriate in children older than 6 years of age without severe disease. Specific antibiotics have been approved for shorter courses even in younger children. Cefdinir and cefpodoxime have been approved for 5-day courses, and azithromycin has been approved for 1-, 3-, and 5-day courses.

Antibiotics for Treatment Failures

When initial antibiotic therapy fails, the patient should be started on high-dose amoxicillin/clavulanate if there is no allergy. If they have failed this therapy already, alternatives such as cefdinir, cefpodoxime, and cefuroxime can be considered. A 3-day course of intramuscular ceftriaxone can also be considered. In type I penicillin hypersensitivity patients, clindamycin is also an option because of its high (up to 95%) success against highly resistant S. pneumoniae.22 Finally, in the severely ill patient, tympanocentesis can be performed to make a bacteriologic diagnosis for culture-directed therapy.

Nonantibiotic Therapies


Symptomatic management of pain with analgesics is important in patients with AOM, regardless of whether or not they receive antibiotic therapy. Multiple options exist, with acetaminophen and ibuprofen being the most common and highly effective. Topical analgesia with benzocaine has also shown to be effective, though the benefits are short-lasting.23 Narcotic analgesics such as codeine and its derivatives can also be used, but must be used cautiously, particularly in younger children. Lethargy from the narcotic may mask the worsening symptoms of suppurative complications, and respiratory depression is also a side effect that needs to be monitored.


Although some small studies have shown short-term benefit with oral or intranasal steroid, the benefits have been marginal. A large study showed no benefit with oral steroid over antibiotic alone, and steroids are not routinely recommended in AOM.24

Antihistamines and Decongestants

Both large individual studies and meta-analysis of studies have shown no benefit in terms of early cure, symptom resolution, duration of effusion, or prevention of complication or surgery with antihistamines or decongestants.24These are not routinely recommended in AOM.

Alternative Therapies

Homeopathy, acupuncture, chiropractic treatment, and nutritional supplements have all been used for AOM, but there are no data suggesting a beneficial effect of these therapies. These alternative therapies are not currently recommended for AOM.



OME is common in children both with URIs and after AOM, and fluid may persist up to 1 month after an acute episode of AOM in 50% of cases. In a child without speech, language, or learning delays, observation of fluid is recommended for up to 3 months. If a child is at risk or OME persists beyond 3 months, audiologic evaluation should be done. If the child's hearing is normal (<20 dB), continued watchful waiting is recommended. If there is a moderate or worse conductive hearing loss (>40 dB) then surgical intervention is recommended. When the hearing falls in the mild conductive hearing loss range (21 to 39 dB), the duration and particularly the severity of symptoms related to the hearing loss must be addressed. If there is parental or teacher concern about the child's hearing, surgical intervention may be considered. Otherwise, observation at 3- to 6-month intervals is recommended until the fluid resolves, language delays occur, or structural abnormalities of the eardrum are observed. These recommendations are from the AAP/AAFP clinical practice guidelines for OME, also published in 2004.25

Medical Therapy

Little evidence exists to support the use of any medical therapy to shorten the duration of OME. The 2004 guidelines conclude that antihistamines and decongestants are ineffective in treating OME and they do not recommend their use, particularly from a risk−benefit standpoint. Antibiotics and corticosteroids are also not recommended. Although there may be short-term benefit of both antibiotics and steroids, these benefits become nonsignificant within several weeks of stopping them. In addition, their side effect profiles are led to a less than optimal risk−benefit ratio. Autoinflation of the eustachian tube, described by Politzer, has been shown to have limited short-term benefit in very small studies, but adherence to the procedure can be difficult in children.26 No definitive recommendation has been made regarding autoinflation.

Surgical Treatment of AOM and OME


Myringotomy, or an incision in the eardrum, may temporarily relieve pressure associated with an AOM and allow culture for bacteriology, but has not been shown to be as effective as antibiotic therapy, does not decrease duration of effusion, and does not prevent recurrent AOM. It also has been shown to be ineffective in the long-term management of chronic OME. Therefore, there is little role for myringotomy alone in OM.

Myringotomy with pressure equalization tube (PET) placement is the first-line surgical therapy for recurrent AOM, complicated AOM, as well as chronic OME.25 Children are in general considered candidates for PET placement if they have three to four episodes of AOM in 6 months or have four to six episodes in 1 year. Studies show that PETs reduce the frequency of AOM episodes by 56% and decrease the duration of OM.26,27 Although OM can still occur with a PET in place in the form of otorrhea, many of these episodes are not accompanied by any symptoms and can be treated with ototopical antibiotic drops without oral antibiotics. PET placement is also considered in a complicated AOM episode, such as AOM with mastoiditis, labyrinthitis, facial nerve paralysis, or other complications.

PET placement is also the most common initial surgical intervention in chronic OME. Indications for intervention, however, are somewhat more controversial. As mentioned previously, hearing loss, particularly as it relates to speech, language, or learning delays is usually the primary factor in determining whether PET placement is necessary. In a child with speech or language delays, particularly those at-risk patients with genetic abnormalities or other developmental delays, prompt PET placement is indicated. Otherwise, OME is observed for 3 months for spontaneous resolution. If the fluid persists and audiologic evaluation reveals moderate hearing loss (>40 dB) or speech or language delays develop, then PET placement is indicated at this time. With a normal audiogram, observation is recommended at 3- to 6-month intervals until resolution occurs, significant hearing loss develops, or structural damage of the TM is identified—if any of this occurs, PET placement should be considered. With mild (21 to 40 dB) hearing loss, a discussion with parents is necessary and either (1) a PET can be placed or (2) close observation at 3-month intervals can be continued.

The average length of time a PET stays in place is between 1 and 2 years with minor variations related to the type and model of tube inserted. An episode of tube otorrhea is not uncommon during this time and is often associated with a URI or exposure to water. Younger children (<2 to 3 years of age) have otorrhea more commonly associated with URIs, and the typical sinonasal bacteria (S. pneumoniaeH. influenzae, and M. catarrhalis) are usually cultured. In older children, (>3 years of age) otorrhea is more likely to occur with exposure to water, particularly when swimming, and the most common bacterial pathogens are Pseudomonas and S. aureus. Topical antibiotic therapy has been shown to be at least as effective as and perhaps more effective than oral antibiotics. Oral antibiotics are usually reserved for those patients with severe systemic symptomatology or those who have failed initial topical therapy. Aural toilet (i.e., suctioning) can also help clear the ear canal and allow the eardrops easier access to the middle ear space. This is even more important in those patients with acutely inflamed, edematous and narrow ear canals. Chronic or recurrent otorrhea is a rarer problem that can be more difficult to manage. If a patient has failed both topical and oral antibiotic culture-directed therapy in the presence of repeated aural toilet, consideration can be given to a variety of adjuvant therapies. This could include tube replacement, adenoidectomy, tube removal, intravenous (IV) antibiotic therapy, and mastoidectomy. Particularly in those patients with long-standing chronic otorrhea, a computed tomography (CT) scan can also be considered to evaluate for the presence of cholesteatoma.

There are other less frequently seen sequelae of PET placement. Early extrusion may occur, usually in the setting of an acute otorrhea episode. A tube may become blocked with cerumen, dried blood, or dried mucus which can often be cleared either with ototopical drops or manually in the office setting. Persistent perforation may occur after PET extrusion, with myringoplasty or tympanoplasty necessary to close the hole. A PET may not extrude spontaneously and be retained in the TM which may eventually need to be removed in the operative setting. Myringosclerosis (scarring of the TM), atrophy of the TM at the prior PET site, and retraction pockets can also occur after tube extrusion. Although these TM abnormalities can also occur without prior PET placement, they have been shown to be more common after PET placement.


Twenty-five percent of children who have had PETs will have a relapse of OM when the tubes extrude or become obstructed.28 In those instances where repeated PET placement is indicated, there is a role for adenoidectomy, as it decreases by 50% the need for further surgeries (i.e., a third set of PETs). The groups that benefit the most from adenoidectomy are those with chronic OME who are older than age 4 and those with recurrent AOM older than age 2 with a history of extruded PETs.29 Interestingly, the benefit from adenoid removal is independent of the size of the adenoid tissue, suggesting that not only adenoid size, but chronic inflammation, contributes to OM. Adenoidectomy with myringotomy alone was equivalent to PET placement alone in older children, but this is not recommended routinely because it is more invasive than PET placement alone. Adenoidectomy is not recommended routinely with a first set of PETs unless an indication such as chronic adenoiditis or chronic sinusitis coexists.25 Tonsillectomy is not recommended in the treatment of either AOM or OME, as it has shown limited evidence of benefit and poses significantly higher risks.

Complications of AOM


Acute Mastoiditis

Acute mastoiditis describes acute infection and inflammation within the mastoid cavity with bony destruction of the architecture of the air cells, or “coalescence.” Clinically, the child would have postauricular edema, erythema, and tenderness in the setting of an AOM. There is commonly protrusion of the pinna as well. A CT scan can confirm the presence of coalescence. Management is controversial, but IV antibiotic therapy alone is often the initial choice. If the child shows no improvement within 48 hours, the surgical options include myringotomy +/− PET placement and/or simple mastoidectomy. Another management strategy that is commonly employed is to perform a myringotomy and PET insertion initially in conjunction with IV antibiotics, with mastoidectomy performed if there is no improvement in 48 hours.

Subperiosteal and Bezold Abscesses

These occur when an acute mastoiditis erodes through the cortical bone either adjacent to the lateral surface of the mastoid cortex (subperiosteal) or through the mastoid tip into the neck (Bezold). This can most commonly be via direct bony erosion but may also occur hematogenously through mastoid emissary vessels. Purulence collects in these areas, with resultant fluctuance and erythema. Again, a CT scan can confirm the presence of an abscess and its precise location (Fig. 1.1). Management in these cases includes myringotomy +/− PET placement with incision and drainage of the abscess alone or in combination with simple mastoidectomy.


Figure 1.1 Axial computed tomography scan showing acute right mastoiditis with cortical bony erosion and subperiosteal abscess (arrow).

Petrous Apicitis (Gradenigo Syndrome)

Petrous apicitis occurs when infection spreads from the middle ear and mastoid medially to the petrous portion of the temporal bone, either directly or hematogenously via vascular channels. The classic triad in petrous apicitis is otitis/otorrhea, retrobulbar pain/headache, and abducens nerve (cranial nerve VI) palsy. A CT scan or a magnetic resonance imaging (MRI) examination can usually confirm the diagnosis, and initial management with IV antibiotic therapy alone is often successful.30 Petrous apicectomy, typically via a transmastoid approach, is usually reserved for antibiotic failures or infections with complications.


This occurs when inflammation in the middle ear spreads to the labyrinth, which includes the cochlea and semicircular canals. This may be via direct bacterial spread (suppurative labyrinthitis), but is also commonly caused by inflammatory mediators in the absence of the organisms themselves (serous labyrinthitis). Transmission can occur at the oval or round windows, or via microscopic bony labyrinthine defects. The diagnosis is made clinically with acute debilitating vertigo and sensorineural hearing loss (SNHL) in the setting of an AOM. An MRI examination, although not necessary, will also show labyrinthine involvement. IV antibiotics are recommended initially to both treat the infection and to try prevent meningitis. Conversely, labyrinthitis can also be a complication of meningitis; this is in part due to a normal communication channel between the extracranial labyrinth and intracranial meninges through the cochlear aqueduct. Myringotomy +/− PET placement drains the fluid and allows for culture-directed therapy, and vertiginous symptoms are managed in the usual fashion. Serous and suppurative labyrinthitis are treated similarly from a medical standpoint and it is rather difficult to distinguish them acutely. In general, however, serous labyrinthitis presents with milder vestibulocochlear symptoms than suppurative labyrinthitis and labyrinthine function is more likely to return in serous labyrinthitis.

Facial Nerve Paresis/Paralysis

The horizontal portion of the facial nerve runs through the middle ear space, and when AOM affects the facial nerve, either through the tiny vascular channels in the normal bony canal or directly secondary to dehiscence of the nerve, facial palsy can occur. This can be a partial weakness (paresis) or complete weakness (paralysis), with the former event more common. Management includes IV antibiotic therapy and wide-field myringotomy versus myringotomy with PET, with culture-directed therapy. A CT scan may be considered to rule out other intracranial or other extracranial involvement. More aggressive intervention is rarely indicated.


Meningitis/Otitic Hydrocephalus

Bacterial meningitis is the most common intracranial complication of AOM. Transmission of disease from the middle ear can be due to hematogenous spread or directly, via the oval and round windows, cochlear aqueduct, or other bony defects. Symptoms include high fever, altered level of consciousness, vomiting, and neck stiffness. There may be papilledema, Kernig and Brudzinski signs, bulging fontanelles, or cranial neuropathies on physical examination. Lumbar puncture is performed to confirm the diagnosis. A CT scan or an MRI examination is usually performed upfront to exclude tumor and mass effect, but they may also be used to look for other complications. Broad-spectrum antibiotic therapy with myringotomy +/− PET for culture is the treatment. Audiologic evaluation of these patients is recommended when neurologic status improves, as SNHL is very common, particularly with pneumococcal meningitis.

Although hydrocephalus is a common finding in bacterial meningitis, another entity has been described, known as otitic hydrocephalus. Lumbar puncture demonstrates high cerebrospinal fluid opening pressure with normal cytology, thereby excluding meningitis. The pathophysiology is thought to be due to nonobstructing thrombus of the transverse sinus, and MRI is useful to demonstrate the presence of a thrombus. Management includes antibiotic treatment of the underlying AOM and supportive measures to decrease intracranial pressure.

Sigmoid Sinus Thrombosis

This occurs when a septic thrombus occurs in the sigmoid dural sinus, usually as a result of direct extension of infection from the mastoid cavity. Clinically, it may present with “picket-fence” spiking fevers, headache, and photophobia. Abducens palsy, as well as swelling and tenderness over the mastoid process (Griesinger sign) have also been described. Either CT with contrast or MRI +/− venography can make the diagnosis (Fig. 1.2). Management includes IV antibiotic therapy and PET placement +/− mastoidectomy. If the choice to perform mastoidectomy is made, the bone directly over the sigmoid sinus should be decompressed. Surgical thrombectomy and anticoagulation are both controversial without strong evidence to support their benefit. This, combined with literature suggesting that recanalization usually occurs spontaneously in 4 to 6 weeks, suggests that a more conservative approach may be appropriate.31

Intracranial Abscesses (Epidural, Subdural, and Brain Abscesses)

Intracranial abscesses are defined by the space they occupy within the cranium. An epidural abscess is located between the bone and the dura mater, a subdural abscess is located between the dura and arachnoid maters, and a brain abscess is located intraparenchymally. The mortality associated with subdural and particularly brain abscess is much higher than that with epidural abscess. MRI is the imaging study of choice for these abscesses, but most can also be detected with contrast-enhanced CT.

Many epidural abscesses can be managed with IV antibiotic alone, close clinical observation, and interval imaging studies (CT or MRI) for comparison. When an epidural abscess is present in continuity with mastoiditis or sigmoid sinus thrombosis (Fig. 1.3), it may be decompressed via a transmastoid approach. If there is no improvement with antibiotic therapy, or if neurologic status deteriorates, surgical drainage either via craniotomy or burr holes should be performed.

Subdural abscesses tend to spread rapidly through the subdural space, partially contributing to their more aggressive clinical picture. Symptoms include fever, altered mental status, and headache. Neurosurgical drainage is always indicated, while otolaryngologic intervention should be performed if the patient is stable and deferred if the patient is unstable. Other measures to decrease cerebral edema should also be undertaken, as well as seizure prophylaxis.


Figure 1.2 Axial computed tomography scan showing thrombosis of the right sigmoid sinus. Comparison can be made to the normally enhancing left sigmoid sinus.


Figure 1.3 Axial computed tomography scan showing epidural abscess adjacent to a thrombosed right sigmoid sinus.

Brain abscess is a catastrophic complication of AOM, with a reported mortality of as high as 50%.32 Signs and symptoms may include fever, altered mental status, seizure, and focal neurologic deficits. These focal deficits depend on the location of the abscess within the brain parenchyma. The disease can have an indolent course, making diagnosis all the more difficult. Management is similar to that of subdural abscess.


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