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23/04/2017 pukul 22.00 WIB

Practice Essentials

Otitis media (OM) is any inflammation of the middle ear (see the images
below), without reference to etiology or pathogenesis. It is very common in
children.

Acute otitis media with purulent effusion behind a bulging tympanic

membrane.
View Media Gallery
Chronic otitis media with a retraction pocket of the pars flaccida.
View Media Gallery
There are several subtypes of OM, as follows:
Acute OM (AOM)
OM with effusion (OME)
Chronic suppurative OM
Adhesive OM

Signs and symptoms

AOM implies rapid onset of disease associated with one or more of the
following symptoms:
Otalgia
Otorrhea
Headache
Fever
Irritability
Loss of appetite
Vomiting
Diarrhea
OME often follows an episode of AOM. Symptoms that may be indicative of
OME include the following:
Hearing loss
Tinnitus
Vertigo
Otalgia
Chronic suppurative otitis media is a persistent ear infection that results in
tearing or perforation of the eardrum.
Adhesive otitis media occurs when a thin retracted ear drum becomes sucked
into the middle ear space and stuck.
See Clinical Presentation for more detail.

Diagnosis

OME does not benefit from antibiotic treatment. Therefore, it is critical for
clinicians to be able to distinguish normal middle ear status from OME or
AOM. Doing so will avoid unnecessary use of antibiotics, which leads to
increased adverse effects of medication and facilitates the development of
antimicrobial resistance.
Examination
Pneumatic otoscopy remains the standard examination technique for patients
with suspected OM. In addition to a carefully documented examination of the
external ear and tympanic membrane (TM), examining the entire head and
neck region of patients with suspected OM is important.
Every examination should include an evaluation and description of the
following four TM characteristics:
Color A normal TM is a translucent pale gray; an opaque yellow or
blue TM is consistent with middle ear effusion (MEE)
Position In AOM, the TM is usually bulging; in OME, the TM is
typically retracted or in the neutral position
Mobility Impaired mobility is the most consistent finding in patients
with OME
Perforation Single perforations are most common
Adjunctive screening techniques for OM include tympanometry, which
measures changes in acoustic impedance of the TM/middle ear system with
air pressure changes in the external auditory canal, and acoustic
reflectometry, which measures reflected sound from the TM; the louder the
reflected sound, the greater the likelihood of an MEE.
See Workup for more detail.

Management

Most cases of AOM improve spontaneously. Cases that require treatment may
be managed with antibiotics and analgesics or with observation alone.
Guidelines from American Academy of Pediatrics
In February 2013, the American Academy of Pediatrics (AAP) and the
American Academy of Family Physicians (AAFP) released updated guidelines
for the diagnosis and management of AOM, including recurrent AOM, in
children aged 6 months through 12 years. The recommendations offer more
rigorous diagnostic criteria to reduce unnecessary antibiotic use.
According to the guidelines, management of AOM should include an
assessment of pain. Analgesics, particularly acetaminophen and ibuprofen,
should be used to treat pain whether antibiotic therapy is or is not prescribed.
Recommendations for prescribing antibiotics include the following:
Antibiotics should be prescribed for bilateral or unilateral AOM in
children aged at least 6 months with severe signs or symptoms
(moderate or severe otalgia, otalgia for 48 hours or longer, or
temperature 39C or higher) and for nonsevere, bilateral AOM in
children aged 6 to 23 months
On the basis of joint decision-making with the parents, unilateral,
nonsevere AOM in children aged 6-23 months or nonsevere AOM in
older children may be managed either with antibiotics or with close
follow-up and withholding antibiotics unless the child worsens or does
not improve within 48-72 hours of symptom onset
Amoxicillin is the antibiotic of choice unless the child received it within
30 days, has concurrent purulent conjunctivitis, or is allergic to
penicillin; in these cases, clinicians should prescribe an antibiotic with
additional beta-lactamase coverage
In February 2016, the American Academy of OtolaryngologyHead and Neck
Surgery Foundation, the AAP, and the AAFP issued updated guidelines for the
assessment and management of OME
See Treatment and Medication for more detail.
Background
Otitis media (OM) is the second most common disease of childhood, after
upper respiratory infection (URI). OM is also the most common cause for
childhood visits to a physician's office. Annually, an estimated 16 million office
visits are attributed to OM; this does not include visits to the emergency
department.
OM is any inflammation of the middle ear, without reference to etiology or
pathogenesis. It can be classified into many variants on the basis of etiology,
duration, symptomatology, and physical findings.
Acute OM (AOM) implies rapid onset of disease associated with one or more
of the following symptoms:
Otalgia
Fever
Otorrhea
Recent onset of anorexia
 Irritability
Vomiting
Diarrhea
These symptoms are accompanied by abnormal otoscopic findings of the
tympanic membrane (TM), which may include the following:
Opacity
Bulging
Erythema
Middle ear effusion (MEE)
Decreased mobility with pneumatic otoscopy
AOM is a recurrent disease. More than one third of children experience six or
more episodes of AOM by age 7 years.
OM with effusion (OME), formerly termed serous OM or secretory OM, is MEE
of any duration that lacks the associated signs and symptoms of infection (eg,
fever, otalgia, and irritability). OME usually follows an episode of AOM.
Chronic suppurative OM is a chronic inflammation of the middle ear that
persists for at least 6 weeks and is associated with otorrhea through a
perforated TM, an indwelling tympanostomy tube (TT; see the image below),
or a surgical myringotomy.

Various tympanostomy tube styles and sizes.

View Media Gallery

Pathophysiology
The most important factor in middle ear disease is eustachian tube (ET)
dysfunction (ETD), in which the mucosa at the pharyngeal end of the ET is
part of the mucociliary system of the middle ear. Interference with this mucosa
by edema, tumor, or negative intratympanic pressure facilitates direct
extension of infectious processes from the nasopharynx to the middle ear,
causing OM. Esophageal contents regurgitated into the nasopharynx and
middle ear through the ET can create a direct mechanical disturbance of the
middle ear mucosa and cause middle ear inflammation.
In children, developmental alterations of the ET, an immature immune system,
and frequent infections of the upper respiratory mucosa all play major roles in
AOM development. Studies have demonstrated how viral infection of the
upper respiratory epithelium leads to increased ETD and increased bacterial
colonization and adherence in the nasopharynx. [1]
Certain viral infections cause abnormal host immune and inflammatory
responses in the ET mucosa and subsequent microbial invasion of the middle
ear. The host immune and inflammatory response to bacterial invasion of the
middle ear produces fluid in the middle ear and the signs and symptoms of
AOM.
Although interactions between the common pathogenic bacteria in AOM and
certain viruses are not fully understood, strong evidence indicates that these
interactions often lead to more severe disease, lowered response to
antimicrobial therapy, and OME development following AOM.

Etiology
A multitude of host, infectious, allergic, and environmental factors contribute to
the development of OM.

Host factors

Immune system
The immature immune systems of infants or the impaired immune systems of
patients with congenital immune deficiencies, HIV infection, or diabetes may
be involved in the development of OM. [2] OM is an infectious disease that
prospers in an environment of decreased immune defenses. The interplay
between pathogens and host immune defense plays a role in disease
progression.
Patel et al found higher interleukin (IL)6 levels in patients with OM who also
had influenza and adenoviral infections, whereas IL-1 levels were higher in
patients who developed OM following URI. [3] In another study, Skovbjerg et al
found that middle ear effusions with culturable pathogenic bacteria were
associated with higher levels of IL-1 , IL-8, and IL-10 than sterile effusions. [4]
Familial (genetic) predisposition
Although familial clustering of OM has been demonstrated in studies that
examined genetic associations of OM, separating genetic factors from
environmental influences has been difficult. No specific genes have been
linked to OM susceptibility. As with most disease processes, effects of
environmental exposures on genetic expression probably play an important
role in OM pathogenesis.
Mucins
The role of mucins in OME has been described. Mucins are responsible for
gel-like properties of mucus secretions. The middle ear mucin gene
expression is unique compared with the nasopharynx. Abnormalities of this
gene expression, especially upregulation of MUC5B in the ear, may have a
predominant role in OME.
Anatomic abnormality
Children with anatomic abnormalities of the palate and associated
musculature, especially the tensor veli palantini, exhibit marked ETD and have
higher risk for OM. Specific anomalies that correlate with high prevalence of
OM include cleft palate, Crouzon syndrome or Apert syndrome, Down
syndrome, and Treacher Collins syndrome.
Physiologic dysfunction
Abnormalities in the physiologic function of the ET mucosa, including ciliary
dysfunction and edema, increase the risk of bacterial invasion of the middle
ear and the resultant OME. Children with cochlear implants have a high
incidence of OM, especially chronic OM and cholesteatoma formation. One
study described a relationship between laryngopharyngeal reflux and chronic
OM (COM); the authors concluded that reflux work-up should be performed as
part of COM investigations, and, if reflux is confirmed, reflux treatment should
be initiated in addition to treatment of primary disease. [5]
Other host factors
Vitamin A deficiency is associated with pediatric upper respiratory infections
and AOM.
Obesity has been linked to an increased incidence of OM, although the causal
factor is unknown. Speculations include alteration of intrinsic cytokine profile,
increased gastroesophageal reflux with alterations of the oral flora, and/or fat
accumulation; all of these have been linked with an increased incidence of
OM. Conversely, OM may increase the risk of obesity by altering the taste
buds. [6]

Infectious factors

Bacterial pathogens
The most common bacterial pathogen in AOM is Streptococcus
pneumoniae, followed by nontypeable Haemophilus influenzae and Moraxella
(Branhamella) catarrhalis. These three organisms are responsible for more
than 95% of all AOM cases with a bacterial etiology. [7]
In infants younger than 6 weeks, gram-negative bacilli (eg, Escherichia coli,
Klebsiella species, and Pseudomonas aeruginosa) play a much larger role in
AOM, causing 20% of cases. S pneumoniae and H influenzae are also the
most common pathogens in this age group. Some studies also
found Staphylococcus aureus as a pathogen in this age group, but
subsequent studies suggested that the flora in these young infants may be
that of usual AOM in children older than 6 weeks.
Many experts had proposed that the MEE associated with OME was sterile
because cultures of middle ear fluid obtained by tympanocentesis often did
not grow bacteria. This view is changing as newer studies show 30-50%
incidence of positive results in middle ear bacterial cultures in patients with
chronic MEE. These cultures grow a wide range of aerobic and anaerobic
bacteria, of which S pneumoniae, H influenzae, M catarrhalis, and group A
streptococci are the most common.
M catarrhalisinduced AOM differs from AOM caused by other bacterial
pathogens in several ways. It is characterized by higher a proportion of mixed
infections, younger age at the time of diagnosis, lower risk of spontaneous
perforation of the tympanic membrane, and an absence of mastoiditis. [8]
Further evidence for the presence of bacteria in the MEE of patients with OME
was provided by studies using polymerase chain reaction (PCR) assay to
detect bacterial DNA in MEE samples that were determined to be sterile with
standard bacterial culture techniques. In one such study using PCR assay,
77.3% of the MEE samples had positive results for one or more common AOM
pathogens (eg, S pneumoniae, H influenzae, M catarrhalis).
In chronic suppurative OM, the most frequently isolated organisms include P
aeruginosa, S aureus, Corynebacterium species, and Klebsiella pneumoniae.
An unanswered question is whether these pathogens invade the middle ear
from the nasopharynx via the ET (as do the bacteria responsible for AOM) or
whether they enter through the perforated TM or a TT from the EAC.
The role of Helicobacter pylori in children with OME has been increasingly
recognized. [9] Evidence that this agent might be responsible for OME comes
from its isolation from middle ear and tonsillar and adenoidal tissue in patients
with OME.
Alloiococcus otitidis is a species of gram-positive bacterium that has been
discovered as a pathogen associated with OME. [10, 11] This organism is the
most frequent bacterium in AOM, as well as in OME. It has also been detected
in patients who had been treated with antibiotics, such as beta-lactams or
erythromycin, suggesting that these agents may not be sufficiently effective to
eliminate this organism. Further investigation is needed to reveal the clinical
role of the organism in OM.
Viral pathogens
Because acute viral URI is a prominent risk factor for AOM development, most
investigators have suspected a role for respiratory viruses in AOM
pathogenesis.
Many studies have substantiated this suspicion by showing how certain
respiratory viruses can cause inflammatory changes to the respiratory mucosa
that lead to ETD, increased bacterial colonization and adherence, and,
eventually, AOM. Studies have also shown that viruses can alter the host-
immune response to AOM, thereby contributing to prolonged middle ear fluid
production and development of chronic OME.
The viruses most commonly associated with AOM are respiratory syncytial
virus (RSV), influenza viruses, parainfluenza viruses, rhinovirus, and
adenovirus. Human parechovirus 1 (HPeV1) infection is associated with OM
and cough in pediatric patients. [12] OM developed in 50% of 3-month follow-up
periods that yielded evidence of HPeV1 infection but in only 14% of the
HPeV1-negative periods; in recurring OM, the middle ear fluid samples were
positive for HPeV in 15% of episodes.

Factors related to allergies

The relation between allergies and OM remains unclear. In children younger

than 4 years, the immune system is still developing, and allergies are unlikely
to play a role in recurrent AOM in this age group. Although much evidence
suggests that allergies contribute to the pathogenesis of OM in older children,
extensive evidence refutes the role of allergies in the etiology of middle ear
disease.
The following is a brief list of evidence for and against the etiologic role of
allergy in OM:
Many patients with OM have concomitant allergic respiratory disease
(eg, allergic rhinitis, asthma)
Many patients with OM have positive results to skin testing or
radioallergosorbent testing (RAST)
Although mast cells are found in the middle ear mucosa, most studies
fail to show significant levels of immunoglobulin E (IgE) or eosinophils
in the MEE of patients with OM
OM is most common in the winter and early spring, yet most major
allergens (eg, tree and grass pollens) peak in the late spring and
early fall
Most patients with concomitant OM and allergy show no marked
improvement in middle ear disease with aggressive allergy
management, despite marked improvements to nasal and other
allergy-related symptoms

Environmental factors
Infant feeding methods
Many studies report that breastfeeding protects infants against OM. The best
of these studies indicates that this benefit is evident only in children who are
breastfed exclusively for the first 3-6 months of life. Breastfeeding of this
duration reduces the incidence of OM by 13%. The protective effects of
breastfeeding for the first 3-6 months persist for 4-12 months after
breastfeeding ceases, possibly because delaying onset of the first OM
episode reduces recurrence of OM in these children.
Passive smoke exposure
Many studies have shown a direct relation between passive smoke exposure
and risk of middle ear disease. [13] A systematic review of 45 publications
dealing with OM and parental smoking showed pooled odds ratios of 1.48
(95% confidence interval [CI] of 1.08-2.04) for recurrent OM, 1.38 (95% CI of
1.23-1.55) for MEE, and 1.3 (95% CI of 1.3-1.6) for AOM. [14]
Group daycare attendance
Daycare centers create close contact among many children, which increases
the risks of respiratory infection, nasopharyngeal colonization with pathogenic
microbes, and OM.
Many researchers have used meta-analysis to confirm that exposure to other
young children (including siblings) in group daycare settings is a major risk
factor for OM.[15] A meta-analysis reported that care outside the home
conferred a 2.5-fold risk for OM. Other critical reviews of studies on OM and
group childcare show heightened odds ratios of 1.6-4.0:1 for center care
versus home care.
Children who attend daycare centers frequently acquire antibacterial-resistant
organisms in their nasopharynx, leading to AOM that may be refractory to
antibacterial treatment. American Academy of Pediatrics and American
Academy of Family Physicians' guidelines recommend high-dose amoxicillin-
clavulanate as the antibiotic of choice in the treatment of AOM in children who
attend daycare.
Socioeconomic status
Socioeconomic status encompasses many independent factors that affect
both the risk of OM and the likelihood that OM will be diagnosed. [16]
In general, lower socioeconomic status confers higher risk for environmental
exposure to parental smoking, bottle-feeding, crowded group daycare,
crowded living conditions, and viruses and bacterial pathogens. Compared
with children from middle-income and high-income families, children from
lower socioeconomic groups use health care resources less frequently, which
decreases the likelihood that OM cases will be diagnosed.
Epidemiology
United States statistics

OM, the most common specifically treated childhood disease, accounts for
approximately 20 million annual physician visits. Various epidemiologic
studies report the prevalence rate of AOM to be 17-20% within the first 2
years of life, and 90% of children have at least one documented MEE by age
2 years. OM is a recurrent disease. One third of children experience six or
more episodes of AOM by age 7 years.

International statistics

Incidence and prevalence in other industrialized nations are similar to US

rates. In less developed nations, OM is extremely common and remains a
major contributor to childhood mortality resulting from late-presenting
intracranial complications. International studies show increased prevalence of
AOM and chronic OM (COM) among Micronesian and Australian aboriginal
children.

Age-related demographics

Peak prevalence of OM in both sexes occurs in children aged 6-18 months.

Some studies show bimodal prevalence peaks; a second, lower peak occurs
at age 4-5 years and corresponds with school entry. Although OM can occur at
any age, 80-90% of cases occur in children younger than 6 years. Children
who are diagnosed with AOM during the first year of life are much more likely
to develop recurrent OM and chronic OME than children in whom the first
middle ear infection occurs after age 1 year.

Sex-related demographics

Several studies have now shown equal AOM prevalence in males and
females; many previous studies had shown increased incidence in boys.

Race-related demographics

For some time, the prevalence of OM in the United States was reported to be
higher in black and Hispanic children than in white children. However, a study
that controlled for socioeconomic and other confounding factors showed equal
incidence in blacks and whites. Hispanic children and Alaskan Inuit and other
American Indian children have higher prevalence of AOM than white and
black children in the United States.
Prognosis
US mortality is extremely low in this era of antimicrobial therapy (< 1 death per
100,000 cases). In developing nations with limited access to primary medical
care and modern antibiotics, mortality figures are similar to those reported in
the United States before antibiotic therapy. A study that examined the causes
of death in Los Angeles County Hospital from 1928-1933, years before the
advent of sulfa, showed that 1 in 40 deaths was caused by intracranial
complications of OM.
Morbidity from this disease remains significant, despite frequent use of
systemic antibiotics to treat the illness and its complications. Intratemporal
and intracranial complications of OM are the two major types.
Intratemporal complications include the following:
Hearing loss (conductive and sensorineural)
TM perforation (acute and chronic)
Chronic suppurative OM (with or without cholesteatoma)
Cholesteatoma
Tympanosclerosis
Mastoiditis
Petrositis
Labyrinthitis
Facial paralysis
Cholesterol granuloma
Infectious eczematoid dermatitis
Intracranial complications include the following [17] :
Meningitis
Subdural empyema
Brain abscess
Extradural abscess
Lateral sinus thrombosis
Otitic hydrocephalus
The prognosis for almost all patients with OM is excellent [18] ; the exceptions
are patients in whom OM involves intratemporal and intracranial complications
(< 1%).
Data on cognitive and educational outcomes of OM in the literature are
limited. [19]The impact of OM on child development depends on numerous
factors. OM in infants younger than 12 months predisposes to long-term
speech and language problems. OM has also been reported to negatively
affect preexisting cognitive or language problems. Careful follow-up and early
referral are key to management.
Patient Education
Patient education topics should include the following:
Avoiding risk factors
Appropriate use of antibiotics
Understanding the implications of antibiotic-resistant bacteria in OM
Education for health care providers should focus on the following topics:
Antibiotic-resistant bacteria and the need to avoid overprescribing
antibiotics
Importance of pneumatic otoscope examination to distinguish AOM
from OME
Treatment differences between AOM and OME
For patient education resources, see the Ear, Nose, and Throat Center, as
well as Earache.