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Role ofPneumococcal Conjugate Vaccines
The prevalence and resistance proles of microorganisms
have changed in recent years due to the advent of pneumococcal conjugate vaccines and the frequent use of antibiotics.
A relative increase in beta-lactamase-producing strains of H.
inuenzae and M. catarrhalis has been observed, as has vari-
ation in rates of penicillin resistance across different strains
of S. pneumoniae. [26]
The introduction of universal pneumococcal vaccination
through conjugate vaccines has changed the microbiology of
OM, interfering with the proportions of the most commonly
implicated bacteria and changing the prole of pneumococcal strains isolated from the middle ear. Before the advent of
the rst (7-valent) pneumococcal conjugate vaccine, serotypes covered by this vaccine were detected in approximately
65% of cases [27]. Prospective studies performed after its
introduction have documented reductions of up to 45% in
pneumococci identied in the middle ear and a concomitant
increase in the isolation of non-typeable H. inuenzae. The
advent of vaccination with the 7-valent pneumococcal vaccine was also followed by a change in serotype prole; serotypes not present in the vaccine, mainly 19A, became
predominant among pneumococci isolated from the middle
ear and nasopharynx [28–30]. The prevalence of pneumococci has become even lower after the introduction of the
13-valent conjugate vaccine, while the detection of H. inu-
enzae and M. catarrhalis continues to rise [3]. Some studies
conducted after the introduction of the 13-valent vaccine
documented a decrease both in the general incidence of
AOM and in the incidence of episodes caused by the serotypes covered by the vaccine. Unfortunately, more recent
studies have already identied a higher prevalence of pneumococcal serotypes not present in the 13-valent vaccine in
the middle ear of children with AOM [31].
The Role ofBacteria inCOME
For many years, the effusion present in the middle ear of
patients with COME was presumed to be sterile. The relative
failure to grow bacteria from these effusions, combined with
the ineffectiveness of antibiotic therapy, appeared to corroborate the “sterile effusion” theory and suggest a minor or
absent role of bacteria in the etiopathogenesis of this
condition.
During the second half of the twentieth century, the rst
studies that conrmed the presence of bacteria in the middle
ear of children with AOM and COME were published. These
rst authors found a 30% culture positivity rate as well as a
signicant number of white blood cells [32]. Subsequently,
several authors documented culture positivity rates ranging
from 18 to 45% in effusion specimens from patients with
protracted courses of OM.The advent of PCR nally allowed
signicant advances and clearly demonstrated that the degree
of bacterial and viral involvement in the various presentations of otitis media had been grossly underestimated, especially in COME. Early studies using the PCR technique
detected bacteria in up to 80% of effusions from ears with
COME [10, 33, 34].
The concept of a continuum of disease states linking the
various forms of otitis media with increasingly competent
detection of pathogenic microorganisms in the middle ear
helps to understand the existence of a causative role for bacteria in AOM and COME.As noted above, the key otopathogens remain the same, but with a clear predominance of H.
inuenzae, followed by S. pneumoniae and M. catarrhalis. It
is now known that most cases of AOM are self-limited and
thus resolve spontaneously, but patients sometimes present
with recurrent forms (rAOM) or progress to chronic conditions such as COME [35, 36]. Several studies carried out in
the last 25 years have conrmed the presence of bacterial
communities—in the form of biolms—living in the nasopharynx, middle ear, and even in tympanostomy tubes. These
ndings are consistent with the low efcacy of systemic antibiotics, prescribed at conventional doses, in the management
of rAOM and COME [37, 38].
The Role ofBacteria inChronic Otitis Media
Signicant microbiological differences can be observed in
the chronic forms of OM, especially in chronic suppurative
otitis media (CSOM) and when there is cholesteatoma. P.
aeruginosa and S. aureus represent the two most commonly
isolated aerobic species from samples of patients with
CSOM and chronic otitis media with cholesteatoma, followed by Enterobacteriaceae such as E. coli, K. pneumoniae,
and Proteus sp. Unlike the classic otopathogens that colonize
the mucous membranes of the upper respiratory tract, P.
aeruginosa and S. aureus are found mainly in the external
auditory meatus, from where they can reach the middle ear.
P. aeruginosa is intrinsically resistant to several antibiotics
and can evade immune defenses by producing several virulence factors [39]. The role of other species, including fungi,
is difcult to assess because they are also present in the
external auditory meatus as part of its normal microbiota
[40].
Several studies carried out from the 1970s through the
2000s assessed the presence of anaerobic microorganisms in
middle ear uids. In general, these studies reported more frequent isolation of anaerobic species in CSOM and chronic
OM with cholesteatoma; however, in approximately half of
the cases, the isolates were found in combination with other
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aerobic and anaerobic species. Several genera of
gram- positive and gram-negative anaerobic bacteria have
been isolated from middle ear effusions, especially
Peptostreptococcus sp., Prevotella, Porphyromonas,
Bacteroides, and Fusobacterium. Interestingly, many of
these species are beta-lactamase producers, and their hydrolytic activity on penicillins and cephalosporins can be measured directly in the middle ear effusions of these patients.
The use of antibiotics with adequate coverage against anaerobes and combinations of penicillins and beta-lactamase
inhibitors may be useful for the treatment of these polymicrobial infections [41].
The Role andRelevance ofBiolms
The term “biolm” was rst used in 1975 in reference to
mixed colonies of bacteria detected in an aquatic environment. Bacteria have the ability to avoid destruction and
extinction by existing in two modes in nature: planktonic
(free-living) and sessile (grouped into biolms). Currently,
both modes are believed to form part of the life cycle of a
bacterium. When in planktonic form, bacteria are able to
reproduce rapidly and are associated with acute infections.
In the form of biolms, they tend to be less aggressive but are
able to survive in adverse conditions [42]. A biolm represents a complex organization of bacteria that attach themselves to a surface (biological or nonbiological) in order to
live in the form of organized structures in which they can
share nutrients and communicate cooperatively. Biolms are
produced by the bacteria themselves as a means of protection, nutrition, and growth [43]. The bacteria are contained
within a structure composed of polysaccharides, proteins,
and nucleic acids called the glycocalyx, or, more appropriately, exopolysaccharides or extracellular polymeric sub-
stances (EPS). The vast majority of bacteria live in biolms,
and all otopathogens have this ability [44].
To form a biolm, bacteria must rst adhere rmly to a
surface, and then enter a maturation stage in which they
organize themselves into microcolonies within an EPS
matrix. In this state, they are able to communicate with one
another (via so-called quorum sensing), share nutrients and
oxygen, and eliminate waste products of their metabolism
through open channels that play the role of a primitive circulatory system. In addition, biolms protect bacteria from
changes in pH, temperature, humidity, and exposure to ultraviolet light. Biolms found on mucosal surfaces are physiologically different from those formed on inert surfaces and
are modulated by the host’s immune responses. Host cells
may even be incorporated into the composition of the polysaccharide matrix [45].
Specically in the eld of otolaryngology, several acute,
recurrent, and chronic infections affect the pharyngeal and
palatine tonsils, paranasal sinuses, and ears. Biolms cause
the majority of recurrent and chronic infections and their
importance in rAOM and COME is well documented.
Bacterial communities in biolms have the ability to disperse bacteria in planktonic form into their surroundings
(dispersion), which explains the pathogenesis of recurrent
acute infections [42, 45].
The presence of otopathogens in biolm form in the nasopharynx has been proven, and some authors suggest that episodes of AOM and rAOM occur when bacteria leave the
biolm in the region of the pharyngeal tonsils and, in the
presence of Eustachian tube dysfunction, migrate to the middle ear [46]. In support of this theory is the fact that children
with rAOM have more biolms on their pharyngeal tonsils
than those with AOM (97.6% versus 27.7%) [47].
The identication of bacteria in biolms by conventional
culture methods is difcult, but the evolution of PCR techniques, with an increase in both sensitivity and specicity,
has allowed the detection of S. pneumoniae, H. inuenzae,
and M. catarrhalis in metabolically active forms in effusion
specimens from patients with COME. Subsequently, biolms were identied in the middle ear of children with
COME, with effusions being 100% positive on PCR testing,
even though only 22% of specimens were culture-positive
[34, 48]. These ndings conrmed the role of bacteria in biolms in the development and maintenance of chronic infectious processes in the middle ear, contributing decisively to
the near extinction of the early concern that molecular techniques were mostly detecting the genetic remains of nonviable bacteria (“fossilized remains”).
Biolms are also present in cholesteatomas, and recurrent
episodes of otorrhea are probably attributable to their presence. Strains of Pseudomonas aeruginosa present in cholesteatomas have been demonstrated to form biolms [49].
The emergence of new antibiotic-resistant strains of otopathogens, especially S. pneumoniae, can be explained at
least in part by the existence of biolms, insofar as they function as a “reservoir” of microorganisms capable of interrupting complete healing and causing reinfections. Although
some antibiotics are able to penetrate biolms, phenotypic
changes in bacteria, which decrease their metabolic rates and
their ability to divide, make these organisms particularly
drug-resistant [45, 50]. On the other hand, resistance to host
defense mechanisms occurs due to bacterial aggregation
within polysaccharide structures that make them too large to
undergo phagocytosis and reduce their accessibility to the
humoral immune system. It is important to bear in mind that
a strain of a bacterium can be very susceptible to a particular
antibiotic when it is in its planktonic (free-living) form and
highly resistant when within a biolm [51]. In addition to
these mechanisms, cooperation among the bacteria that constitute the biolm can also interfere with the action of antibiotics. One example is the production of beta-lactamases by
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M. catarrhalis, which protects pneumococci and
Haemophilus from the action of amoxicillin by inactivating
the drug [52].
Implications ofBiolms fortheTreatment
ofOtitis
Current management strategies for rAOM and COME
involve antibiotic therapy (with only relative success) and
removal of the effusion through a tympanostomy, along with
the placement of a tympanostomy tube. In addition to other
benets, evacuation of the effusion performs biolm removal.
Adenoidectomy is also effective in the treatment of rAOM
and COME, as the pharyngeal tonsils are well known to be
rich in biolms containing one or more otopathogens [53]. In
episodes of chronic otitis with cholesteatoma, topical antibiotics (when there is discharge) and surgical removal of the
cholesteatoma are the cornerstones of treatment.
In some ear infections, ares occur due to the formation
of granulation tissue, which, in turn, surrounds the tympanostomy tube and causes persistent discharge. In these cases,
the scar tissue and the tube must both be removed and a new
tube placed if necessary [54, 55]. Tympanostomy tubes
coated with silver oxide or antibiotics decreased the incidence of otorrhea, possibly due to an anti-biolm effect [56].
The Upper Respiratory Tract Microbiome
andIts Relationship withOtitis Media
Microbiological and molecular techniques have always correlated otitis media with the presence of classic otopathogens, as well as with some other species associated with this
condition, but without denitive proof of their pathogenic
role. More recently, the possibility of detecting microorganisms has expanded considerably with the evolution of DNA
sequencing techniques, especially the use of 16S rRNA gene
sequencing for bacterial detection and identication, which
can be applied directly to clinical specimens [57].
With about 1500 base pairs, the 16S rRNA gene is an integral part of the ribosome and is present in all bacteria, being
composed of highly conserved regions (i.e., with the same
nucleotide sequence present in all species) interspersed with
variable regions, which, once characterized, allow identication of the species. The evolution of sequencing techniques,
especially with the advent of NGS, now allows for the complete and simultaneous sequencing of all species present in a
given clinical sample, thus providing crucial data on its constituent microbiome. The relative abundance of each species
in the analyzed sample can also be assessed. Use of these
methods has also made it possible to follow the evolution
over time of one’s normal and pathogenic microbiota since
the initial colonization after birth, to compare their variations
throughout the life course or even during the emergence of
disease states, and, in the latter case, to assess whether the
normal microbiota is being replaced by new, potentially
pathogenic species [58].
Studies have tried to correlate the microbiota of the upper
respiratory tract, especially the nasopharynx and pharyngeal
tonsils, with that found in the middle ear. The results suggest the presence of certain bacterial genera, such as
Dolosigranulum, Corynebacterium, Lactococcus,
Cutibacterium (Propionibacterium), and Staphylococcus, in
an amount inversely proportional to that of classic otopathogens, such as pneumococci, Haemophilus, and Moraxella.
The inverse also seems to hold true; that is, the presence of
increased colonization by classic otopathogens, especially
in the pharyngeal tonsils, seems to be associated with a
smaller number and reduced variety of the species mentioned above. Furthermore, in children with otitis media,
there seems to be a signicantly reduced diversity of other
bacterial species in nasopharyngeal and pharyngeal tonsil
samples when compared to healthy controls. Interestingly,
molecular techniques point to the existence of a normal
microbiota in the middle ear, which is no longer considered
a sterile site [4, 59]. Unfortunately, studies based on traditional bacteriological techniques fail to disclose bacteria in
middle ear samples from healthy individuals, casting doubt
on the results of molecular methods, whose identied bacterial sequences could have been the result of inevitable contamination of the reagents used in the process rather than the
actual presence of the detected organisms in the clinical
sample [60, 61].
At any rate, it now seems undeniable that some bacterial
species may play a protective role when present in the upper
respiratory tract. Two of these genera, Dolosigranulum and
Corynebacterium, are found in signicantly increased proportions in the nasopharynx of children without OM, suggesting that they are part of a normal and protective
microbiota [62].
In summary, new molecular methods have conrmed the
importance of the so-called otopathogens as causative agents
of OM. These same studies also provide evidence of the
abundant presence of certain bacterial genera, such as
Alloiococcus and Turicella, in middle ear uid samples from
children with AOM or rAOM; these are also present in signicant amounts in the outer ear but are practically absent in
the nasopharynx. These potential pathogens act as adjuvants
within biolms formed by classic otopathogens, facilitating
the persistence of these species in the middle ear and hindering their elimination either by the immune system or by antimicrobial therapy, a hypothesis that warrants further
investigation [22, 63].
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Conclusions andRecommendations
Ongoing, global monitoring of the bacteria involved in the
pathogenesis of OM is essential for the development of vaccines and the establishment of new therapeutic strategies.
Improvement of vaccines against the organisms that cause
middle ear infections is essential for the prevention of otitis
media in its acute, recurrent, and chronic forms [10].
Finally, it is beyond question that greater knowledge
regarding biolm function is essential for the development
of new therapeutic options [43, 64]. These options can target different stages of biolm formation (adhesion, maturation, quorum sensing, and dispersion), bearing in mind that
different bacterial species and strains can employ different
methods in the development of their biolms and that the
genetic exchange that occurs between communities within
biolms can increase and modify existing resistance mechanisms [42].
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Otitis Media withEffusion:
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Pathophysiology, Clinical Picture
andManagement
MaríaJoséHerrera J andJoséAlzerreca
21
Overview
One of the most frequently diagnosed middle ear diseases is
otitis media with effusion (OME), which is dened as the
presence of uid behind an intact tympanic membrane, without any acute signs or symptoms [1].
First described by Mawson in 1976, it was originally
referred as seromucous otitis media, a condition that have
received multiples synonyms over the past such as nonsuppurative otitis media or ear uid [1].
It occurs mostly in children and about 90% of them have
had at least one episode of OME before school age, being the
most frequent cause of acquired hearing loss in preschool
children [2].
The vast majority of OME cases resolve spontaneously in
less than 3 months from its onset without producing any
hearing impairment. However, at least 25% of OME episodes can last longer and may be associated with hearing
loss, balance difculties, ear discomfort, and behavioral and
sometimes social concerns [1, 2].
Incidence andPrevalence
OME is a disease predominantly seen in children, with an
incidence of 0.6% between the adult population. Almost
50–90% of children will have at least one episode of OME
by the age of 5years, with a peak in the rst year of life and
a per year prevalence of 15–30% [1, 2].
Having an early age rst OME episode may be the primary event that predisposes a child to recurrent and chronic
otitis media by setting up an inammatory process in the
middle ear and eustachian tube.
There is no difference in prevalence between gender, but
there are studies that determine a higher prevalence in Native
American and Inuit population. Also, some American Indian
and Eskimo communities have reported a low prevalence of
OME [1].
About 4 episodes of new onset OME occur annually in
young children with a mean duration of 17–20days per episode, with 13–21% having bilateral involvement. Recurrence
in OME is also common, with an estimated rate of 50%
within 24months [1, 2].
At least 40% of ear uid episodes can last longer than
30 days, and sometimes becoming a reason for outpatient
visits to pediatricians, accounting for almost 11% of ofce
consultations in primary care practices [2].
Etiology
It has been suggested that the etiology of OME is multifactorial and that different conditions can contribute to the appearance and persistence of OME.
There are several theories and determined risk factors for
the development of OME.These conditions can be categorized as:
Eustachian Tube Dysfunction
The eustachian tube connects the middle ear to the nasopharynx via a 24-mm length bony cartilaginous tube which main
function is to allow adequate ventilation of the middle ear. In
children, the eustachian tube is wider and more horizontaloriented. This difference with the eustachian tube of and
adult increases the possibility of an upper respiratory tract
infection to rise to the middle ear [1, 3].
Apart from the anatomical differences of the eustachian
tube in children, there are other causes of dysfunction such
as obstruction for hypertrophied adenoids or inammation
secondary to upper respiratory infections [1, 2].
M. J. Herrera J (*) · J. Alzerreca
Department of Otolaryngology, Clínica Universidad de Los Andes,
Santiago, Chile
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
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M. J. Herrera J and J. Alzerreca
Craniofacial Abnormalities
Any condition or syndrome that affects the anatomy of the
middle third of the face or the skull base can be a risk factor
for OME. Most common examples of this condition are
Down’s syndrome and cleft palate abnormalities, since this
kind of syndromes can present with abnormal muscle insertion of the soft palate leading to an inadequate opening of the
eustachian tube during swallowing [2].
Acute Otitis Media Sequelae
Up to 45% of children diagnosed with acute otitis media
were found to have a middle ear effusion at 1month and 10%
at 3months after the initial diagnosis [3, 4].
Gastroesophageal Reux Disease (GERD)
Pepsin-related association with middle ear effusion is
well studied. Pepsin found in middle ear effusion is
thought to arise as a result of reux; however since not all
effusion have pepsin, it is unlikely a factor for all cases of
OME [5, 6].
Allergies
Allergies may predispose to OME by generating edema
around the eustachian tube or as a primary mucosal disease
of the middle ear. Some studies have found up to 63% of
positive skin test on children with OME [7].
tion with an increased number of mucus cells. This factor
contributes to a higher exudate production that lls the middle ear space.
Some researchers have studied the presence of biolms in
the middle ear cavity estimating that almost 65% of chronic
infections involve biolms. This structure of bacterial and
fungal origin is formed from polysaccharides, proteins, and
nucleic acids, that give protection against antibodies, phagocytosis, and antibiotics, perpetuating the presence of effusion
or infection in time [9].
Many other factors are considered to play a role in the
pathogenesis of OME, and they include GERD, pollution,
allergies, which in theory alter the middle ear mucosa in the
same way as previously exposed.
Clinical Presentation
Children with OME may present as an asymptomatic patient
and be detected on routine screening, since children rarely
complain about hearing loss, making diagnosis of OME
more difcult.
OME can produce a variety of clinical scenarios, but physicians should always be aware of a hearing disorder, a
delayed language acquisition, difculties at school, and
behavioral and/or sleep disorders [1].
Other symptoms that may indicate the presence of OME
include clumsiness, bumping into things, or balance issues,
and it is very common that these patients are assessed for a
neurological disorder initially [2].
Also, any children with nasal obstruction, snoring, or
mouth breathing should be assessed for OME, since adenoid
hypertrophy is related with middle ear effusion.
Pathogenesis
The pathogenesis of OME is mainly considered to be initiated by an inammatory reaction against a rhinopharyngeal
infection. This inammatory process leads the production of
cytokines and the secretion of a protein and inammatory
mediators’ rich exudate. Also, there is a vasodilatation process that is responsible for an increased gaseous exchange
with an endotympanic pressure drop consequently. This
pressure changes in the middle ear affects the tympanic
membrane mostly in its pars accida which is the most fragile area, sometime developing a retraction at this site [1, 8].
If the middle ear pressure drops continues without correction, tympanic atelectasis progresses to the pars tensa and
may lead to a complete atelectasis of the tympanic
membrane.
Also, when a prolonged inammation of the middle ear
mucosa is present, it is common to observe cell differentia-
Diagnosis
The diagnosis is essentially clinical. The probability of OME
is dened by the balance between symptoms and signs and
the review of the medical history and possible risk factors.
Due to the multiple factors that must be considered in the
diagnosis, there is considerable interobserver variation.
Another consideration is the signicant difference in diagnosis between pediatricians and otolaryngologists [1, 2, 8].
Otoscopy is diagnostic in around 78% of cases, with 95%
specicity, when performed by an otolaryngologist [1, 2, 8].
The medical history should consider epidemiological factors such as age, gender, race, and seasonality. Risk factors
considered are the age of the rst AOM, bilaterality, history
of allergic rhinitis and family history of OME, childcare
assistance, and parental smoking. In adults, the risk factors
are the history of allergy and radiation therapy of the head
and neck [1, 8].
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Most cases are asymptomatic, with hearing loss being
the most frequent symptom. Because children do not usually report hearing loss, the diagnosis is usually late,
resulting in language delay or deterioration of school performance. Screening at school entrance can trigger a referral to the otolaryngologist who ends up diagnosing an
OME [2].
The head and neck examination should be complete
because it may reveal predisposing anatomical factors or airway inammation. The examiner should determine the presence of craniofacial dysmorphias, upper respiratory
infections, complications, or other ear pathologies [1, 8]. In
the examination of the tympanic membrane in recent OME,
a translucent membrane and middle ear with aqueous liquid,
sometimes with air bubbles or an airuid level, are usually
observed. In chronic OME mucosal effusion is observed, the
membrane is thickened, opaque, and without inammation
[1]. Microscopic examination helps to increase accuracy and
should be used when the diagnosis is unclear. The use of the
ngerboard can also contribute to the diagnosis of driving
hearing loss [1].
The accuracy of diagnosed OME by otoscopy is difcult
to measure because the gold standard—the true condition of
the middle ear—can only be documented by myringotomy
or tympanocentesis. There is consensus that the diagnosis
can be challenging, and even experienced otolaryngologists
require the use of adjuvant diagnostic methods such as the
microscope or tympanometry to better discern the presence
of middle ear uid in difcult cases [10, 11].
Determining membrane mobility is important, and pneumatic otoscopy is recommended but there is great interobserver variability. Actually, visible light pneumatic otoscopy
is considered as the best currently available diagnostic tool
for otitis media. A systematic review for diagnosing OME
showed a sensitivity of 94% and specicity of 80% [12]. The
Clinical Practice Guideline of the American Academy of
Otolaryngology 2016 strongly recommends the use of pneumatic otoscope to document the presence of middle ear effusion to diagnose otitis media with effusion in a child and to
assess for OME in a child with otalgia, hearing loss, or both
with the pneumatic otoscope [2].
However, pneumatic otoscopy has various limitations.
The speculum must create an adequate seal against the external auditory canal to obtain tympanic membrane movement,
which is seldom possible with the standard disposable speculum. Also, sufcient training is required for effective pneumatic otoscopy, but there is frequently a gap in training for
most clinicians. The implementation of pneumatic otoscopy
by primary care physicians in their practice has not been
optimal, leading to a lack of resident training and a perception that pneumatic otoscopy is difcult [11].
Recently, an otoscope sensitive to shortwave infrared
(SWIR, 1–2μm) wavelengths of light with the objective of
improving middle ear disease diagnoses has been described.
SWIR otoscopy provides two fundamental advantages over
conventional visible light-based pneumatic otoscopy. First, a
SWIR otoscope could help identify middle ear effusions
based on the strong light absorption by middle ear uid in the
SWIR spectral region. Second, due to a longer wavelength,
SWIR light can penetrate deeper through tissue, enabling a
better view of middle ear anatomy behind the tympanic
membrane [11].
The differentiation of OME versus OMA is the determining factor in the therapeutic decision. For this, it is important
to determine the presence of tympanic effusion and signs of
acute inammation. Paradise suggested a useful algorithm to
differentiate OME from OMA based on the presence of otalgia, otorrhea, and the degree of erythema and gloom of the
tympanic membrane, classifying them as suppurative and
nonsuppurative. Kempthorne created a clinical severity scale
for each entity based on the presence of signs found in otoscopy [1].
The tympanometer provides more objective information.
The presence of a smaller amplitude or a wider or absent
pick are associated with a greater probability of effusion. An
OME will show a B-curve and absence of stapedial reection
[1]. Clinicians should obtain tympanometry in children with
suspected OME for whom the diagnosis is uncertain after
performing pneumatic otoscopy [2]. The acoustic reectometer is another instrument used to determine the probability
of effusion, but its pressure is questioned.
Pure tonal audiometry will show mild to moderate driving
hearing loss. It is essential to evaluate the impact of OME on
the child’s hearing, given the disorder’s frequent occurrence
during the language acquisition period. Around 50% of children with OME have a loss of more than 20dB, 20% have a
loss of more than 35dB, and 5–10% have a loss of more than
50dB.A hearing loss greater than 50dB must be considered
as a possible inner ear damage [11, 13–15]. Ideally, the hearing assessment should include tonal audiometry with air and
bone conduction and age-appropriate vocal audiometry. If an
audiometric examination is impossible, auditory evoked
potentials or the auditory steady state response is recommended [3, 8].
It is important to obtain a hearing test prior to surgery
when a child becomes a candidate for tympanostomy tube
insertion. To conrm the indication of surgery and to discard
sensorineural hearing loss [1, 3], reevaluation at 3–6months
intervals, until the effusion is no longer present, signicant
hearing loss is identied, or structural abnormalities of the
eardrum or middle ear are suspected, is recommended [2].
Children who are at risk for developmental difculties
would likely be disproportionately affected by hearing problems from OME.Clinicians should determine if a child with
OME is at increased risk for speech, language, or learning
problems from middle ear effusion because of baseline sen-
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M. J. Herrera J and J. Alzerreca
sory, physical, cognitive, or behavioral factors and should
evaluate at-risk children for OME.
At-risk patients are patients with permanent hearing loss,
speech and language delay or disorder, autism spectrum disorder and other developmental disorders, syndromes or
craniofacial disorders that include cognitive, speech, or language delays, and visual impairment or cleft palate [2].
The use of nasal endoscopy should be used in cases of
associated nasal obstruction or prolonged or unilateral OME
to conrm adenoid hypertrophy. Flexible nasal endoscopy
also enables the differential diagnosis of a rhino pharyngeal
tumor, and it should be used more routinely in areas with
high HIV prevalence due to the increased risk of nasopharyngeal anomalies such as lymphoma [3]. It is important to
screen for an associated palatal disorder or craniofacial dysmorphism that are risk factors for the onset, persistence, and
recurrence of OME [1, 8]. The cavum radiography may help
only when you cannot do a nasal endoscopy.
Among the predisposing factors of OME, allergy plays a
crucial role in the etiology of OME.Many publications show
that OME is associated with allergy. Allergies may predispose to OME by causing edema around the eustachian tube
or primary mucosal disease in the middle ear. Allergy can
induce an inammatory reaction in the middle ear cavity and
increase the susceptibility to infection by microbes. Skin
tests of children with OME were found to be negative in
37.1% and positive in 62.9% of cases [16, 17]. The presence
of atopy or allergic rhinitis represents an important risk factor for OME, so it seems important to diagnose and treat it
[13, 14, 18]. Studies on interventional strategies to reduce
these risk factor and the impact on OME and evaluate the
impact of treatment of allergic rhinitis and rhinosinusitis on
OME are needed [19].
GERD has been associated with OME, and pepsin and
H.Pylori have been found in middle ear uid [3]. In a recent
study, at long-term follow-up, the prevalence of OME in
adults was higher in the GERD group. The same study found
that allergic rhinitis, asthma, or chronic rhinosinusitis
showed increase in the risk of developing OME than those
without these conditions [6].
In the case of a persistent OME, it is recommended to
explore the most frequent risk factors such as GERD and all
causes of nasopharyngeal obstruction.
Treatment
Treatment should be individualized and aimed at managing
predisposing factors. The goal is to reverse hearing loss and
prevent an OMC with permanent sequelae and complications
by eliminating the effusion in the middle ear [1].
Treatment will depend on the patient’s history and age,
the type of OME, the presence and degree of hearing loss,
bilaterality, and duration of the effusion.
An OME secondary to an IRA can last 1–2months and
resolve spontaneously without the need for treatment. When
secondary to an AOM, the effusion slowly disappears after
the treatment of the AOM. Fifty percent have effusion after
2weeks, 20% after 4weeks, and 10% after 8weeks. These
cases also do not require additional treatment [8]. So, OME
generally resolves spontaneously with watchful waiting.
Clinician decisions for the correct interventional treatment of OME for a specic patient include a variety of factors such as comorbidities, severity of hearing loss,
unilaterally or bilaterally, effusion duration, age, social factors, costs, adherence to treatment, and familial assistance
with treatment. A patient-focused approach should be
adopted when assessing hearing disability. How the child is
coping socially and at school is more important than the
results of audiometry investigations. Although most OME
patients will warrant a conservative management approach,
all physical and social factors should be examined to provide
a patient-centered treatment plan that optimizes outcomes
for the patient [20].The recommendation is to watchful waiting for 3months from the date of effusion onset(if known) or
the date of diagnosis [2, 8, 15].
Medical Therapy
Antibiotics
Venecamps and cols review randomized controlled trials
comparing oral antibiotics with placebo, no treatment, or
therapy of unproven effectiveness in children with
OME. They present evidence of both benets and harms
associated with the use of oral antibiotics to treat children up
to 16years with OME.Although evidence indicates that oral
antibiotics are associated with an increased chance of complete resolution of OME, they found evidence that these children are more likely to experience diarrhea, vomiting, or skin
rash. The impact of antibiotics on short-term hearing was
uncertain, and low-quality evidence did not show that oral
antibiotics were associated with fewer ventilation tube insertions. They found no data on the impact of antibiotics on
speech, language, and cognitive development or quality of
life [13]. The recommendation is against the use of antibiotics for OME [2].
A study investigated the therapeutic effect of erythromycin, clarithromycin, azithromycin, and roxithromycin on a
histamine-induced animal model of OME. They recommended the use of macrolide antibiotics, as they show anti-
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bacterial and anti-inammatory efcacy on OME [21]. The
international recommendation guidelines do not recommend
the use of macrolides in the treatment of OME [3].
Decongestants andAntihistamines
Its use is based on reducing the congestion of the eustachian
tube. A systematic review of 2010 found no benet on
hearing, but some benets in improvement of nasal and ocular allergic symptomatology. They found more adverse
effects (11%) in treated versus untreated subjects. They recommended against using antihistamines, decongestants, or
both for treating OME [22].
Mucolytics might relieve the symptoms of OME but do
not have proven for long-term efcacy [8]. Mucolytics can
be used as support in the watchful waiting period because
these agents have low cost and are safe [3].
Corticoids
Local inammation that causes eustachian tube dysfunction
in OME could be treated with systemic and/or intranasal
corticoids.
In the Cochrane Review of 2011, the analyses of 12 studies shows that there was no evidence of benet for systemic
steroid treatment for OME or hearing loss associated with
OME in the longer term [23]. Furthermore, systemic corticoids are associated with a range of adverse reactions, such
as diarrhea, nausea, hyperactivity, and epistaxis [8].
Compared with systemically administered steroids, intranasal steroids have limited side effects. Patients with OME
and allergic rhinitis may benet for topical intranasal steroids, targeting the inammatory component of allergic rhinitis. More prolonged treatment protocols and long-term
clinical outcomes will require critical assessment (7). There
may be a short-term benet of topical intranasal steroids in
children with adenoidal hypertrophy, although the magnitude of the effect is small, and dosing in one report was
higher than recommended [22].
In the 2011 review, no evidence of benet from treatment
of OME with topical intranasal steroids, alone or in combination with an antibiotic, was found [23].
The recommendation is against the use of these medications for OME [2, 8].
Table 21.1 Medical treatment of OME [3, 4]
Treatment Recommended
Oral or nasal steroids No
Oral antihistamines No
Antibiotics No
Mucolytics No
Decongestants No
Autoination Yes (limited evidence)
pressure in the nose. This can be achieved by forced exhalation with closed mouth and nose, blowing up a balloon
through each nostril or using an anesthetic mask. The aim is
to introduce air into the middle ear, via the eustachian tube,
equalizing the pressures and allowing better drainage of the
uid. Studies of this technique are small of limited treatment
duration and had short follow-up, and no double-blind trials
have been performed [8, 24].
A literature review found a trend toward rapid improvement of the symptoms. The audiometry and tympanometry
results were not statistically signicant. But, because of the
low cost and absence of adverse effects it is reasonable to
consider autoination while awaiting natural resolution of
OME [25] (Table21.1).
In children, the EarPopper® shows to be a safe and effective treatment option for hearing loss from persistent OME,
and reduces the rate of ventilation tube insertion [26]. Another
study of 320 children with OME (unilateral and bilateral)
showed tympanometric resolution at 3months in a nasal balloon autoination (Otovent®) group versus no nasal balloon
autoination group. The study concludes that the treatment
shows to be feasible, safe, and effective in clearing effusions
and in improving important ear symptoms [27]. The use of
Otovent® in cleft palate children accelerates the improvement
of middle ear status and hearing thresholds at 6months [28].
In adults, the combined treatments including medication
and the use of a modied Politzer device (Streamsys) show
to be more effective than medical treatment alone. Younger
age, smaller air bone gap, and higher tubomanometry value
are good predictors for treatment success too [29].
PPIs
Although the link between gastroesophageal reux disease and
OME is increasingly well documented, there is no evidence
regarding the treatment of reux and OME.It is not recommended to use anti-reux medication for OME at this time [6].
Autoination
The use of autoination balloons is also an option.
Autoination (Politzer maneuver) is a technique consists in
the eustachian tube which is partially reopened by raising
Immunization
Medical therapy should be attempted before a surgical solution, but there is nothing proven for it. Active observation is
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