+++
Epidemiology
and Genetics
++
Acute otitis media has been a disease burden for children since
the beginning of time. Examination of Egyptian mummies revealed
perforations of the tympanic membranes and destruction of the mastoid.4 Before
the introduction of antimicrobial agents, AOM was a frequent reason
for hospitalization of infants and children; in 1932, AOM, mastoiditis,
and intracranial complications were the admitting diagnoses for
27% of pediatric admissions to Bellevue Hospital in New
York City.5 The introduction of the sulfonamides
in 1936, penicillin in the 1940s, and the many broad-spectrum antimicrobial
agents in the 1950s substantially reduced hospitalizations for suppurative
complications of AOM.
++
Previous longitudinal studies are a rich source of information
about the disease in specific populations but three factors are
likely to further alter the epidemiology of otitis media in the
United States since 2000: (1) introduction of the 7-valent conjugate
pneumococcal vaccine (PCV7) in the United States in 2000, and later
in countries throughout the world, which has reduced the number
of episodes of vaccine-type pneumococcal acute otitis media (AOM) and
decreased the incidence of severe and recurrent disease; (2) publication
of management guidelines by the American Academy of Pediatrics (AAP)
and the American Academy of Family Physicians (AAFP) in 2004, which
presented uniform criteria for diagnosis, choice of antimicrobial
agents, and recommendations for use or withholding of antimicrobial
agents for children with AOM2; and (3) programs
developed by the Centers for Disease Control (CDC) and advocacy
groups to inform physicians and consumers about the appropriate
use of antimicrobial agents for common diseases such as AOM and
avoidance of use of these agents for trivial, usually viral, respiratory
infections to decrease the selection of multidrug-resistant bacteria.
+++
Incidence of
Otitis Media
++
Otitis media is a disease of infancy and early childhood. Acute
otitis media (AOM) is the most frequent reason that children visit
health care facilities in the first 3 years of life and has been
one of the most frequent reasons that physicians prescribe antimicrobial
agents for infants and children. The peak age-specific attack rate
of AOM occurs between 6 and 18 months. Children who have had little
or no experience with otitis media by age 3 are unlikely to have
subsequent severe or recurrent disease. On average, children have 1.2
and 1.1 episodes of AOM in the first and second years of life, respectively.6 By
age 3, children may be categorized into three groups based on diagnoses
of AOM: approximately one third have had no episodes of AOM; one
third have had one or two episodes; and one third have had three
or more episodes.5
++
Otitis media with effusion (OME) is even more common than AOM.
Up to 90% of school age children have OME at some time.
In the first year of life, > 50% of children experience
OME, increasing to > 60% by 2 years of age. Most episodes
resolve spontaneously within 3 months but about 30% of
children have recurrent episodes of OME, and 5% to 10% of
these episodes persist for 1 year or longer.2
++
The more severe suppurative complications are infrequent in developed
countries where access to medical care is readily available, although
these complications are still a frequent cause of morbidity in developing
countries. It is unclear whether early prescribing of antibiotics has
been responsible for decreasing the incidence of mastoiditis in
developed countries.
+++
Risk Features
for Acute Otitis Media
++
Age at first episode of acute otitis media (AOM) is significantly
associated with recurrent episodes. Males have a higher incidence
of single and recurrent episodes of AOM than do females.6
++
Genetic predisposition to AOM is suggested by the aggregation
of cases in families. A meta-analysis by Uhari and colleagues identified
an increase in risk if any other member of the family had had AOM.7 Severe
and recurrent disease may be associated with genetically determined features,
such as skull configuration, or by overt or subtle immunologic defects.
Studies of the incidence of otitis media in twins indicate that
there is a strong genetic component to the amount of time with otitis
media with effusion and the number of episodes of AOM; there was
a strong correlation between members of monozygotic twins compared
with dizygotic sets.8
++
Selected racial groups, many in developing countries or hostile
environments, appear to be otitis prone. Native Americans and Alaskan
and Canadian Inuit infants and children have a high incidence of
severe AOM and suppurative complications. A prevalence study of
an Apache community found the presence of draining ear or perforation
in 8.4% of patients of all ages.9 Several
survey studies indicate that African American children have less
otitis media than white children11,12but it is
unclear if this is explained by underdiagnosis in the African American
community due to less access to medical care, or to difference in
the position of the bony eustachian tube among races.12 Several
surveys of African American children indicated that they had less otitis
media than white children. AOM in the first year of life occurred
in significantly more white Cleveland children than black children.10 In
Boston, persistent middle ear effusions were more frequent in white
children than in black children.11 The predominance
of ear disease in white children in these studies was not readily
explained: One possibility was less access to medical care in the
African American community, resulting in fewer diagnosed episodes
of AOM; a second hypothesis was suggested by the studies of skulls
of different racial groups by Doyle, with identification of differences
in the position of the bony eustachian tube.12
++
The increased number of infants and young children in daycare
groups has resulted in an increase in respiratory infections, including
AOM. Children in daycare not only have more episodes of AOM than
children in home care but have more surgical procedures; a study
of Pittsburgh children who were observed from birth noted that myringotomy
and tympanostomy tube placements were performed in 21% of
children in group daycare and in only 3% of children in home
care by the second year of life.13 The more children
in the daycare group, the more exposures to respiratory pathogens
brought to the daycare from the household of each child.
++
Breast-feeding has been documented to prevent nasopharyngeal
colonization14 as well as respiratory infections
including AOM.6 Among the possible reasons for
the beneficial effect of breast feeding are the presence of various
immunoglobulins, B and T cells, macrophages and neutrophils, and
nonimmune factors including interferon and glycoproteins. Oligosaccharides
in breast milk that correspond to the pneumococcal carbohydrate
receptor suggest that breast milk may protect against otitis media
by blocking attachment of bacterial pathogens to respiratory mucosa.15
++
Altered host defenses may play a role in recurrent and severe
AOM. Among the host issues are anatomic defects (cleft palate, cleft
uvula, submucous cleft); alteration of normal physiologic defenses
(patulous eustachian tube); congenital or acquired immunologic deficiencies
(decreased or absent immunoglobulins, chronic granulomatous disease); malignant
neoplasmas that may alter the anatomy of the upper respiratory tract;
and drugs that suppress immune processes. An increased incidence
of AOM also occurs in children with Down syndrome16 and
in children with AIDS.17 An increased incidence
of acute otitis media occurs in children with Down syndrome.16 Children
with AIDS have a higher age-specific incidence of acute otitis media
beginning at age 6 months compared with uninfected children or children
who initially were positive for HIV antibody but who seroreverted.17
++
Environmental factors, including passive cigarette smoking and
environmental pollutants, have come under increased scrutiny as agents
responsible for structural and physiologic changes in the respiratory
tree. Smoke exposure can result in goblet cell hyperplasia and mucus
hypersecretion in the respiratory tract, ciliostasis, and decreased
mucociliary transport. The availability of a biochemical marker,
cotinine, has made documentation of exposure to tobacco smoke more
reliable than history alone. Etzel and colleagues demonstrated that
high concentrations of serum cotinine were associated with increased
incidence of acute otitis media and increased duration of middle
ear effusion after an acute episode.18 The Committee
on Environmental Health of the American Academy of Pediatrics reviewed
the effects of ambient air pollution on the health of children.19 Although
there are no data relevant to environmental pollutants on eustachian
tube function or middle ear disease, invasive pneumococcal infections
in children and adults are associated with levels of sulfur dioxide
used as a marker for air pollution and higher ragweed pollen counts.20
++
The middle ear system includes the nasopharynx, the eustachian
tube, the middle ear space, and the adjacent structures, including
the mastoid air cells and inner ear (see Fig.
369-1). The middle ear is a narrow box or cleft: the vertical
and anterior-posterior diameters measure about 15 mm; the transverse
diameter measures 2 to 6 mm; and the tympanic membrane diameter
is 10 mm (eFig. 243.1). The size
of the middle ear cavity and the ossicles are the same at birth
as in the adult. In infancy, the eustachian tube is short, wide,
and in a straight position, permitting easy access of nasopharyngeal
flora into the middle ear space. With increasing age, the eustachian tube
elongates, narrows, and assumes an oblique position, corresponding
to a decrease in the incidence of otitis media as age increases.
++
++
The pathogenesis of otitis media includes microbial pathogens
(viral and bacterial infection); host factors (immature or impaired
immunology, familial predisposition, sex, and race); anatomic and
physiologic dysfunction (eustachian tube dysfunction, cleft palate,
or submucous cleft); and environmental factors (breast-feeding,
smoking in households, and daycare attendance). The physiology of
the eustachian tube is key to understanding the pathogenesis of
acute otitis media. The normal physiologic functions of the eustachian
tube include pressure regulation or ventilation of the middle ear,
which equilibrates gas pressure in the middle ear with atmospheric
pressure; protection of the middle ear by anatomic, immunologic,
and mucociliary defenses; and clearance or drainage of secretions
produced within the middle ear via mucociliary activity and muscular
clearance. In acute otitis media and otitis media with effusion,
one or more of these eustachian tube functions is impaired.
++
The normal physiologic functions of the eustachian tube include
pressure regulation or ventilation of the middle ear, which equilibrates
gas pressure in the middle ear with atmospheric pressure; protection
of the middle ear by anatomic, immunologic, and mucociliary defenses;
and clearance or drainage of secretions produced within the middle
ear via mucociliary activity and muscular clearance. In acute otitis
media (AOM) and otitis media with effusion, one or more of these
eustachian tube functions is impaired.
++
Most episodes of AOM involve the following sequence of events:
++
1. Congestion of the mucosa of the upper respiratory
tract, including the nares, nasopharynx, and eustachian tube (ET),
usually due to respiratory viral infection;
2. Swelling of the mucosa of the ET, resulting in obstruction
of the narrowest portion of the tube, the isthmus;
3. Obstruction of the ET tube, which results in negative middle
ear pressure and accumulation of secretions formed normally by the middle
ear mucosa; the mucosa secretions have no egress and fill the middle
ear space;
4. Viruses and bacteria that colonize the upper respiratory tract
are aspirated or insufflated into the middle ear and multiply in
the middle ear fluid, causing a suppurative infection, acute otitis
media.
++
Although appropriate antimicrobial agents sterilize the middle
ear infection, fluid may persist in the middle ear for weeks to
months. The mean duration of middle ear effusion after an episode
of AOM is approximately 23 days, with 10% persisting after
12 weeks (eFig. 243.2).
++
++
Our understanding of microbiology of acute otitis media (AOM)
has been documented by needle aspiration (tympanocentesis) of the
middle ear abscess. The results of many studies have been uniform
in demonstrating the dominance of Streptococcus pneumoniae and
nontypable Haemophilus influenzae and a minor role
for Moraxella catarrhalis. Respiratory viruses
alone or combined with bacterial pathogens are present in many middle
ear fluids of children with AOM.
++
Disparate results of cultures of middle ear fluids have been
reported in 20% to 30% of children with bilateral
AOM.21,22 Most often there is sterile fluid in
one ear and a bacterial pathogen in the other ear, but various results have
been reported, including different pathogens in the two ears, two
bacterial pathogens (or pneumococcal serotypes) in one ear, and one
or none of the pathogens in the other ear.
++
Our understanding of the microbiology of AOM is undergoing change
based on recognition of new microbiologic phenomena such as biofilms
and new microbiologic techniques such as polymerase chain reaction
(PCR). The introduction of the pneumococcal conjugate vaccine (PCV7),
has led to a decrease in number of episodes of AOM due to vaccine
serotypes with resultant increased proportion of nonvaccine pneumococcal
serotypes and nontypable H influenzae.
++
Although there are 90 antigenically distinct serotypes of S
pneumoniae, relatively few types are responsible for most
AOM. In recent surveys, the most common types responsible for AOM
in order of decreasing frequency were types 19F, 23, 14, 6B, and
3.1 PCV7 includes the major serotypes responsible
for invasive disease and AOM but lacks coverage for type 3, which
is included in a 13-serotype investigational conjugate vaccine (Wyeth Vaccines).
++
H influenzae was first identified as an important
pathogen of acute otitis media (AOM) in the 1940s; for reasons that
remain unclear, earlier studies identified the pathogen in few cases or
not at all. Studies of children with AOM since the introduction
of PCV7 suggest that nontypable H influenzae may
replace the pneumococcus as the most frequently isolated pathogen
of AOM.23,24 Although H influenzae was
considered to be restricted in importance to AOM in preschool children,
the organism has been found of equal importance in older children,
adolescents, and adults. H influenzae is the primary
pathogen in the unique conjunctivitis–acute otitis media
syndrome.25
++
M catarrhalis has been identified in up to 27% of
middle ear fluid aspirates of children with AOM but most studies
suggest an incidence of less than 10%.26
++
During the preantibiotic era, otitis media due to group A streptococcus
(GAS) was frequently associated with scarlet fever and was often
of a destructive form. GAS was the most prevalent organism in cultures
taken at myringotomy for acute otitis media (AOM) and the most frequent
cause of mastoid infection.27 In recent years,
AOM due to GAS is uncommon. A recent survey of the experience of
investigators in Beersheva, Israel, identified GAS in 3.1% of
11,311 episodes of AOM28
++
A variety of microorganisms have been infrequently identified
in AOM as the sole focus of infection or part of a systemic or respiratory
illness. Mycoplasma pneumoniae has been documented
as a cause of bullous myringitis but has rarely been associated
with AOM. Chlamydia pneumoniae has been identified
in patients with pharyngitis, bronchitis, and pneumonia but infrequently
with otitis media. Diphtheritic otitis media may accompany diphtheritic
croup and nasopharyngitis; complications are frequent, including
destruction of the tympanic membrane and ossicles and invasion of
contiguous structures including the mastoid air cells, the temporal
bone, and the labyrinth. Mycobacterium tuberculosis is
characterized by a painless, watery otorrhea through single or multiple
perforations of the tympanic membrane. When acute otitis media occurs
as the only apparent focus of tuberculous infection, the disease
is usually due to ingestion of infected cow’s milk. Acute
or chronic otitis media has been reported due to nontuberculous
mycobacterial infections including Mycobacterium fortuitum,
Mycobacterium avium intracellulare, and Mycobacterium
chelonae. Acute otitis media due to Clostridium
tetani may occur as a sequela of chronic suppurative otitis
media; the organism is present in the external ear canal and gains
access to the middle ear through the perforated tympanic membrane.
Fungi are frequently associated with external otitis but rarely
cause acute otitis media; there are case reports of Candida and Aspergillus species
in immunodeficient patients who developed chronic suppurative otitis
media.
++
The clinical history suggests that viral infection frequently
is the initial event in the development of AOM (see Chapter 241). Respiratory viruses have been isolated from the nasopharynx of
up to 50% of children with AOM.29 Viruses, viral
antigens, and virus presence by polymerase chain reaction have been
identified in middle ear fluids alone or in combination with bacterial pathogens. Pitkaranta
and colleagues analyzed middle ear fluids of Finnish children with AOM
and found evidence of rhinovirus RNA in 22% of patients,
respiratory syncytial virus in 18%, and coronavirus in
7%.30 Combined viral and bacterial infections
may be more severe than bacterial infection alone; Chonmaitree and
coworkers noted that a higher proportion of patients with virus
and bacteria in middle ear fluids failed to clear the bacteria 2
to 4 days after initiation of therapy compared with the group who
had bacteria alone.31
++
Children with acute otitis media (AOM) have rapid onset of nonspecific
signs and symptoms including fever, irritability, headache, apathy, anorexia,
vomiting, and diarrhea. Fever occurs in one third to two thirds
of children with AOM but temperatures of 40°C or more are unusual unless
accompanied by invasive bacterial disease or foci elsewhere.
++
Specific signs of AOM include the following: Patients may experience
otalgia or ear pain. In infants, pulling at the ear or irritability may
be the only sign of ear pain. Otalgia may also result from external
otitis or from disease in the temporomandibular joint, teeth, or
pharynx. Earache is not universal in AOM; about one fifth of children
in a pediatric practice with AOM did not complain of ear pain, and most
of the children were older than age 2.32
++
The pain is due to pressure of the increasing suppuration in
the middle ear and is relieved when the pressure leads to ischemia
of the central vessels in the capillary bed of the tympanic membrane.
Persistent ischemia leads to necrosis of the tympanic membrane,
with rupture and discharge of the contents of the middle ear abscess
and virtual elimination of the otalgia. Otorrhea or discharge from
the middle ear occurs, following rupture of the tympanic membrane.
Parents often report that a child who had cried with pain was relieved and
bloody pus was observed on the pillow or pajamas. However, the tympanic
membrane is so vascular that the site of perforation may not be
evident within 24 hours, and the resealed membrane may result in
reaccumulation of the purulent middle ear fluid.
++
Hearing loss is a frequent sign in young infants and may be expressed
by verbal children or detected by a parent who sees the child not responding
to spoken voice.
++
Purulent conjunctivitis has been associated with acute otitis
media due to nontypable H influenzae. The conjunctivae
are injected with pain; there is tearing or purulent discharge associated
with signs and symptoms of AOM.23
++
Swelling about the ear may be due to malignant external otitis
media with spread of the infection to the contiguous skin and soft
tissues. Rarely, a diabetic or immunocompromised patient may present
with pseudomonal otitis externa that spreads via the fissures of
Santorini to affect the skull base, and may present with pain and
cranial nerve palsies. This condition is known as malignant
otitis externa and carries a high mortality rate if not
appropriately treated. Postauricular swelling may indicate disease
of the mastoid, including periostitis or subperiosteal abscess.
++
Less common signs and symptoms of acute otitis media include
vertigo, nystagmus, and tinnitus.
++
Otitis media with effusion may be silent in its presenting symptomatology
and may be an incidental finding. There may be subjective symptoms
such as mild balance disturbance, especially in younger children,
or a change in a child’s behavior. The major symptom and
concern is hearing loss (see Complications and Outcomes).
++
The diagnosis of acute otitis media (AOM) is based on three elements:
(1) abrupt onset of signs and symptoms of middle ear inflammation;
(2) presence of middle ear effusion identified by any of the following:
bulging of the tympanic membrane (TM), limited or absent mobility
of the tympanic membrane, or otorrhea; and (3) signs or symptoms
of middle ear inflammation such as erythema of the TM or otalgia.2
++
Normal and abnormal findings on otoscopic examination are shown
in Figure 243-1. The otoscopic examination
should include evaluation of the position, color, and degree of
translucency and mobility of the tympanic membrane. The normal eardrum
should be in the neutral position. Mild retraction of the TM usually
indicates the presence of negative middle ear pressure, an effusion,
or both. Severe retraction of the TM identifies high negative pressure
associated with middle ear effusion (MEE). Fullness or bulging of
the TM is caused by increased middle ear pressure or MEE.
++
++
The normal TM has a ground-glass appearance and is translucent.
++
The otoscopist should be able to look through the TM and visualize
the middle ear landmarks. A blue or yellow color identifies MEE
seen through a translucent TM. A red TM may indicate inflammation
but may also identify engorgement of the blood vessels of the TM
caused by crying, sneezing, or nose blowing. The diagnosis of AOM
is often made with some uncertainty, particularly in infants and young children
due to difficulty with adequate examination of the TM for confirmation
of MEE.
++
Pneumatic otoscopy is the most feasible and cost-effective
method for diagnosis of AOM and otitis media with effusion. Mobility
of the TM is identified by pressure applied to the rubber bulb attached
to the pneumatic otoscope. The normal or air-filled middle ear is
identified by a brisk movement inward with slight positive pressure and
outward with slight negative pressure. MEE or high negative pressure
within the middle ear dampens movement of the TM. Movement of the
TM is best seen in the posterosuperior quadrant of the TM.
++
Tympanometry and acoustic reflectometry can supplement
penuamtic otoscopy (see Chapter 369). Tympanometry
involves varying the pressure in the external canal accompanied
by a probe tone. A graphic presentation, the tympanogram, provides
information on middle ear pressure and the presence of an air-filled
or fluid-filled middle ear space.1 Because tympanometry and
pneumatic otoscopy require a seal in the external canal for a few
seconds, they may be difficult to perform in the young infant who
is irritable due to ear pain. Acoustic reflectometry accompanied
by spectral gradient analysis determines the probability of MEE
by measuring the response of the eardrum to a frequency sweep in the
audible range of 1.8 to 4.4 kHz and provides information on the
probability of an air- or a fluid-filled middle ear space.33
++
MEE can also be demonstrated by needle aspiration, tympanocentesis,
observation of fluid in the external canal, or evidence of pus on
the pillow or bedding of the child as a result of tympanic membrane
perforation.
++
The otoscopist should be able to look through the TM and visualize
the middle ear landmarks. A blue or yellow color identifies MEE
seen through a translucent TM. A red TM may indicate inflammation
but may also identify engorgement of the blood vessels of the TM
caused by crying, sneezing, or nose blowing. Mobility of the TM
is identified by pressure applied to the rubber bulb attached to the
pneumatic otoscope. The normal or air-filled middle ear is identified
by a brisk movement inward with slight positive pressure and outward
with slight negative pressure. MEE or high negative pressure within
the middle ear dampens movement of the TM. Movement of the TM is
best seen in the posterosuperior quadrant of the TM.
++
Pneumatic otoscopy is the most feasible and cost-effective method
for diagnosis of acute otitis media and otitis media with effusion
but can be supplemented by tympanometry and or acoustic reflectometry.
Tympanometry involves varying the pressure in the external canal
accompanied by a probe tone. A graphic presentation, the tympanogram,
provides information on middle ear pressure and the presence of
an air-filled or fluid-filled middle ear space.1 Because
tympanometry and pneumatic otoscopy require a seal in the external
canal for a few seconds, they may be difficult to perform in the
young infant who is irritable due to ear pain. Acoustic reflectometry
accompanied by spectral gradient analysis determines the probability
of middle ear effusion by measuring the response of the eardrum
to a frequency sweep in the audible range of 1.8 to 4.4 kHz and
provides information on the probability of an air-filled or a fluid-filled
middle ear space.33 Middle ear effusion can also
be demonstrated by needle aspiration, tympanocentesis, observation
of fluid in the external canal, or evidence of pus on the pillow
or bedding of the child as a result of tympanic membrane perforation.
++
Infants and children who are diagnosed with acute otitis media
(AOM) traditionally have been treated with an antimicrobial agent
with efficacy against the three major bacterial pathogens: S
pneumoniae, nontypable H influenzae, and M
catarrhalis. An option of withholding therapy and observing
the child may be considered for the child who has uncomplicated
AOM with mild to moderate signs and symptoms and/or uncertain
diagnosis and is older than age 2.
++
Selection of antimicrobial agents is based on clinical and microbiology
efficacy, acceptability (eg, taste and texture) of the oral preparation,
absence of side effects and toxicity, and convenience of dosing
schedule and cost. As of September 2008, 19 drugs have been approved
by the US Food and Drug Administration for treatment of acute otitis
media. Two types of ear drops, ofloxacin otic and ciprofloxacin
with dexamethasone, are approved for acute otorrhea in children
who have tympanostomy tubes in place.
++
Many children with a diagnosis of AOM do not benefit from antimicrobial
agents, including those whose diagnosis is uncertain, those whose
AOM is due to a viral pathogen, and those who have AOM due to a
bacterial pathogen that resolves spontaneously. Data from double
tympanocentesis studies (aspiration at the time of diagnosis of
AOM and 3 to 5 days later) in children treated with placebo revealed that
approximately 50% of children who had nontypable H
influenzae in the initial culture had sterile cultures
in the later aspirate, and approximately 20% of children
who had S pneumoniae in the initial culture had
sterile cultures in the second aspirate.34,35 In
many Western European communities, the practice is to withhold antimicrobial
agents initially from children diagnosed with AOM. Although a number
of clinical trials support an initial observation period, most of
these studies have significant flaws in design and execution.2 The
2004 Clinical Practice Guideline suggested criteria for children
with AOM who may be initially observed rather than treated with
an antimicrobial drug. This includes children older than age 6 months
whose diagnosis is uncertain, and children older than age 2 years who
do not have severe disease (defined as moderate to severe otalgia
or fever equal to or greater than 39°C in whom follow-up can be ensured
and antibacterial agents started if symptoms persist or worsen).
AOM is a treatable disease in all other children2(Table 243-1).
++
++
Selection of antimicrobial agents is based on clinical and microbiology
efficacy, acceptability (eg, taste and texture) of the oral preparation,
absence of side effects and toxicity, and convenience of dosing
schedule and cost. As of September 2008, 19 drugs have been approved by
the US Food and Drug Administration (FDA) for treatment of AOM.
Two types of eardrops, ofloxacin otic and ciprofloxacin with dexamethasone,
are approved for acute otorrhea in children who have tympanostomy
tubes in place.
++
The drugs of choice for patients who are being treated initially
or who have failed initial management with antibacterial agents
are listed in Table 243-2. Amoxicillin is
the drug of choice for treatment of AOM in patients with a temperature
less than 39°C and/or severe otalgia because it continues
to be effective, safe, and relatively inexpensive. A dosage of 80
to 90 mg/kg/d in 2 doses provides concentration
of the drug in the middle ear sufficient to inhibit susceptible
and intermediate nonsusceptible strains of S pneumoniae and
many resistant strains. Following administration of antibacterial
agents, clinical stabilization should occur during the initial 24
hours, and clinical improvement by 48 to 72 hours. If initially
febrile, defervescence usually is observed within 48 to 72 hours.
If initial therapy fails (lack of clinical improvement), or the
child has a temperature greater than 39°C, and/or moderate
or severe otalgia at presentation, the American Academy of Pediatrics (AAP)
recommends amoxicillin clavulanate, cefuroxime axetil, or a single
dose of intramuscular ceftriaxone.2 A macrolide
(erythromycin plus sulfisoxazole, azithromycin, or clarithromycin) is
the preferred for therapy of acute otitis media in children who
are allergic to β-lactam antimicrobial agents.
Duration of therapy is based on data from clinical trials and tradition.
The AAP recommends a 10-day course for the oral antimicrobial agents,2 except
for azithromycin, which is approved for 1-, 3-, and 5-day courses.
The FDA has approved shorter courses of other selected drugs; efpodoxime
and cefinir are approved for 5-day courses.
++
++
The clinical course of the child who is treated with an effective
antimicrobial agent results in significant resolution of acute signs and
symptoms within 48 to 72 hours. Persistent ear pain or systemic
signs, including fever, indicate a need for reevaluation for persistent
AOM or foci elsewhere. The child may need change in antimicrobial
therapy or a myringotomy. The myringotomy results in immediate relief
by draining the abscess and provides information about the pathogen.
Myringotomy should be considered for the child who is toxic, who
has severe suppurative or nonsuppurative complications (eg, mastoiditis or
facial nerve palsy), who fails to improve on repeated antibiotic
therapy, or who has an underlying immunodeficiency.
++
AOM may be associated with severe pain as the middle ear abscess
expands and presses against the tympanic membrane. The 2004 American
Academy of Pediatrics Clinical Practice Guideline recommended that
assessment of pain be included in management of acute otitis media
and recommended acetaminophen or ibuprofen for mild to moderate
pain and codeine or analogs or myringotomy for severe pain.2
++
Antihistamines have not been shown to be of any value in management
of AOM and may prolong the duration of middle ear effusion.36 Similarly,
nasal and oral decongestants administered alone or in combination
with an antihistamine may provide symptomatic relief from the effects
of nasal congestion but are ineffective for treatment of AOM or
otitis media with effusion (OME).2 A short course
of systemic corticosteroid therapy is of uncertain efficacy in management
of OME in children and is not recommended
for infants and children with OME because of its unproven efficacy
and potential side effects.2
++
Surgical management of AOM includes tympanocentesis (needle aspiration
of the middle ear infection), myringotomy (an incision in the anterior-inferior
quadrant of the tympanic membrane that drains the middle ear abscess),
and adenoidectomy. Myringotomy should be considered when the child
has acute mastoiditis, labyrinthitis, facial paralysis, or an intracranial suppurative
complication such as meningitis. Myringotomy and placement of a
tympanostomy tube is extensively used for children with persistent
otitis media with effusion and recurrent acute otitis media.3 Adenoidectomy
for management of severe and recurrent AOM and OME has been shown
to be of value in selected children age 2 and older but remains
controversial.2
+++
Acute Otitis
Media Associated with Tympanostomy Tubes
++
In a child with tympanostomy tubes, acute otitis media (AOM)
may still occur, presenting as a discharging ear, usually without
pain or fever. Although this may occur as a result of contaminated
water penetrating the tympanostomy tube to enter the middle ear
space (eg, bath water, pool water), it is much more likely to occur
as a result of a concurrent upper respiratory tract infection. Treatment
with antibiotic eardrops is usually effective, although systemic
antibiotics (amoxicillin ± clavulanate) may also be indicated, especially
if there is a tenacious exudate that may interfere with appropriate
administration of the eardrops. A recent advance has been the introduction
of quinilone antibiotic eardrops (Floxin, Ciloxan), which are extremely effective,
well tolerated, and nonototoxic. An antibiotic and steroid combination
eardrop (Cipro HC) may be utilized if desired. However, for antibiotic
eardrops to be effective, they must penetrate the tympanostomy tube
to reach the middle ear space. Most formulations require at least
7 drops per application to penetrate into the middle ear space.
Tragal pumping is important to improve penetration. A proportion
of children with recurrent ear discharge may have bacterial colonization
of the tympanostomy tube itself, usually because of a bacterial
biofilm, which may be extremely resistant to bacterial eradication.
In such circumstances, removal of the tympanostomy tube may be required.
+++
Otitis Media
with Effusion
++
The likelihood of spontaneous resolution of otitis media with
effusion (OME) varies depending upon the cause and duration. After
an episode of acute otitis media (AOM), 75% to 90% of
residual OME resolves within 3 months, and about 25% of
OME of unknown duration in 2- to 4-year-old children resolves within
3 months. If OME is asymptomatic it is likely to resolve spontaneously
and intervention is unnecessary. The laterality, duration, and presence
and severity of associated symptoms should be documented at periodic
reevaluations (every 3 to 6 months). Hearing should be evaluated
if the effusion persists for 3 months or longer, and at any time
that language, learning problems, or a significant hearing loss
is suspected (see Complications and Outcomes below). Children who
are otherwise well should be reevaluated at 3- to 6-month intervals
until the effusion is no longer present, significant hearing loss
is identified, or structural abnormalities of the middle ear are suspected.
Medical therapies including antihistamines, decongestants, antimicrobials,
and corticosteroids are not beneficial. There is no clear evidence
showing a benefit of allergy management for treatment of OME.
++
Surgical treatment with tympanostomy tubes has been recommended
to avoid developmental sequelae due to hearing deficits caused by
persistent OME in early childhood. However, a large randomized controlled
study that included children with bilateral effusions for > 90 days,
or unilateral effusions for > 135 days showed no developmental benefit
of early treatment compared to observation with surgical treatment
only when bilateral effusion persisted > 6 months and unilateral
effusion > 9 months.41 Despite these observations,
existing recommendations still suggest that surgery can be considered
for children with OME lasting 4 months or longer, or if there is
recurrent or persistent OME in children at risk for inadequate follow-up,
and in those in whom structural damage to the tympanic membrane
or middle ear exists. Tympanostomy tubes are recommended as the
initial surgery. Adenoidectomy should not be performed unless a
distinct indication exists. If repeat surgery is performed, adenoidectomy
plus myringotomy, with or without tube insertion, is recommended.
+++
Complications
and Outcomes
++
Hearing loss is the most common complication of otitis media
and can be conductive, sensorineural, or both. Some degree of conductive
hearing loss is present whenever fluid fills the middle ear space.
In acute otitis media, the loss is usually between 15 and 40 dB;
the average loss due to acute otitis media or otitis media with
effusion is 27 dB.38 Hearing returns to normal
thresholds with resolution of the middle ear effusion. Negative pressure
in the middle ear, in the absence of middle ear effusion, can also
be a cause of hearing loss. Reversible or irreversible sensorineural hearing
loss can occur during acute otitis media (AOM) or otitis media with
effusion (OME). Reversible sensorineural loss is due to increased
tension and stiffness of the round window membrane. Permanent sensorineural
hearing loss is most likely due to the spread of infection or products
of inflammation through the round window membrane into the labyrinth,
development of a perilymphatic fistula in the oval or round window,
or suppurative complications such as labyrinthitis or meningitis.
Hearing testing is recommended when OME persists for 3 months or longer,
or at any time that language delay, learning problems, or a significant
hearing loss is suspected (see Chapter 369).
+++
Effect of Otitis
Media on Development of the Child
++
Middle ear effusion and the resulting conductive hearing loss
may result in decreased perception of language, impaired development
of speech and language, lower scores on tests of cognitive abilities,
and poor performance in school. Many studies have been performed
relating experience with AOM and OME and developmental outcomes,40 but
the differences in design of the studies and inconsistencies of
the results limit conclusions about the effect of otitis media on development.
Paradise and colleagues found that early placement of ventilating
tubes in children with prolonged time spent with middle ear fluid did
not measurably improve developmental outcomes at age 3 years.41
+++
Suppurative
Complications
++
Chronic suppurative otitis media (CSOM) occurs when episodes
of recurrent acute otitis media are untreated or inadequately treated;
a perforation of the tympanic membrane persists and there is chronic
infection of the middle ear and mastoid. The hallmark of CSOM is
a purulent, mucoid, or serious discharge through the persistent
perforation. CSOM is a major health problem in many developing countries
but is of particular concern in regions and populations with limited
access to medical care, including the Inuits of Alaska, Canada,
and Greenland; Australian Aborigines; and Native Americans.
++
Extension of infection from suppurative AOM into the mastoid
air cells is frequent; the mastoid infection resolves with treatment
of AOM but in some cases may progress to an acute periosteitis or
osteitis. Labyrinthitis may follow the spread of infection from
the middle ear into the cochlear and vestibular organs, resulting
in sensorineural hearing loss and/or vertigo.
++
Intracranial complications of otitis media include meningitis,
epidural abscess, subdural empyema, brain abscess, dural sinus thrombosis,
and otitic hydrocephalus. Suppurative meningitis and other intracranial
complications usually follow invasive bacterial infection but may
also occur as a result of spread from the middle ear mastoid infection
through the dura. The pus can proceed to accumulate between the dura
of the brain and the cranial bone (epidural abscess) or the potential
space between the dura and the arachnoid (subdural empyema) or progress
to the meninges to cause meningitis.
+++
Nonsuppurative
Complications
++
Nonsuppurative complications of acute otitis media include facial
paralysis, avascular necrosis of the long process of the incus with
an associated conductive hearing loss, atelectasis of the middle
ear (with and without a retraction pocket), adhesive otitis media,
tympanosclerosis, and cholesteatoma. Cholesteatomas consist of keratinized
squamous epithelium and may accumulate within the middle ear and expand,
resulting in necrosis of surrounding tissues. Cholesteatomas may
be a sequela of recurrent otitis and may develop from epithelium
that has migrated through a perforation of the tympanic membrane
or from epithelium deposited from alternating infection and healing.
++
Although the facial nerve normally travels in a bony canal in
its complicated course through the middle ear, up to 55% of
individuals have small areas where the bony covering is incomplete,
particularly in the area of the oval window. Inflammation may cause
edema of the exposed facial nerve as it passes through the middle
ear, compromising its venous return within the surrounding bony
canal and resulting in peripheral facial nerve palsy. Although full
recovery of facial nerve function can be expected in virtually all
cases, it is usually recommended that the patient have insertion
of a tympanostomy tube and be started on systemic antibiotic therapy.
A tympanostomy tube not only serves to drain pus but also allows
for antibiotic and steroid eardrops to be placed directly into the
middle ear space.
++
Cholesteatomas may be due to chronic negative
middle ear pressure that retracts a portion of the tympanic membrane,
inhibiting the natural epithelium migration of desquamated squamous debris.
This can then become wet, and infected, producing foul-smelling
otorrhea and/or an expansile mass lesion that can cause
local bony erosions. In a patient with a history of chronic otorrhea,
pneumatic otoscopy may demonstrate retraction of the TM or granulation
tissue or debris within a retraction pocket. However, the diagnosis
of cholesteatoma is best made with otomicroscopy using an operating
microscope. Computed tomography scanning of the temporal bone may
provide further information on the size of the lesion. Aside from
otorrhea, symptoms may include conductive hearing loss due to ossicular
erosion, sensorineural hearing loss or disequilibrium due to vestibular
involvement. Treatment is surgical.
++
Parents may reduce exposure of the infant to transmission of
infectious agents and decreasing risk factors for acute otitis media
by adhering to a few techniques: breast-feeding, making the home
a smoke-free environment; discouraging pacifier use, using family
or small-group out-of-home daycare, and maintaining simple but effective
hygienic procedures such as appropriate hand-washing.
++
The rationale for chemoprophylaxis to prevent AOM is that a modified
dose of antimicrobial agents administered during the respiratory season
will decrease the rate or intensity of colonization of the upper
respiratory tract by bacterial pathogens.37 The
physician must weigh the benefits of decreased risk of infections
against the risk of development of resistant bacteria and possible
adverse events of the drug. The principles of chemoprophylaxis apply
to its use for prevention of new episodes of acute otitis media: (1)
the patient is at risk if infection occurs; (2) the bacteria are
known and are consistent causes of disease; (3) the microorganisms
are unlikely to develop resistance to the drug used for a prolonged
course; (4) the drug is well tolerated and can be administered in
a convenient dosage and form; and (5) the drug has limited side
effects or toxicity. There is an abundant literature about use of
chemoprophylaxis to prevent new episodes of acute otitis media,
and most studies identify benefits.1,37 Candidates
to consider for prophylaxis include children who have had three
episodes of AOM in 6 months or four episodes in 12 months. Both
amoxicillin and trimethoprim-sulfamethoxazole have been used in various
clinical trials, but when the two drugs have been compared, amoxicillin
has had superior results. Half of the therapeutic dose is administered
in 1 dose/day; the drug is provided during the respiratory
season, usually from the fall through early spring. Occasional episodes
of acute otitis media may occur in the child who is on chemoprophylaxis;
therapy for these children should include an alternative agent such
as parenteral ceftriaxone or amoxicillin-clavulanate.
++
The 7-valent pneumococcal conjugate vaccine (PCV7) is immunogenic
in infants beginning at age 2 months and has demonstrated efficacy
in prevention of invasive disease as well as pneumonia and otitis
media.38,39 PCV7 employs a diphtheria toxin mutant
(CRM 197) as the protein carrier (Prevnar, Wyeth Vaccines) and has
been distributed in the United States since 2000. The vaccine includes
serotypes responsible for the vast majority of episodes of invasive
disease and acute otitis media: serotypes 4, 6B, 9V, 14, 18C, 19F
and 23F. The vaccine was effective in preventing 97.4% of
cases of vaccine serotype invasive disease in fully vaccinated California
infants.38 Clinical trials in Northern California38and
Finland39 established the efficacy of PCV7 for
prevention of pneumococcal acute otitis media. The vaccine reduced
the number of episodes of otitis media and number of otitis media
visits by 7.0% and 7.8%, respectively, and reduced
the number of procedures for placement of ventilating tubes by 23%.
Children who received the pneumococcal vaccine had more episodes
of AOM due to nonvaccine pneumococcal serotypes and nontypable H
influenzae (eTable 243.1). The reasons why PCV7 was more effective
in preventing invasive pneumococcal disease than in preventing vaccine
serotype pneumococcal otitis is uncertain, but higher concentrations
of serum antibody may be necessary to prevent the local mucosal
diseases such as acute otitis media and pneumonia.
++