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Managing Risk Factors inOtitis Media
https://t.me/medicina_free
JoshuaA.Stramielo andDanielaCarvalho
27
Introduction
morbidities, and socioeconomic practices (Table27.1). A
complete birth and medical history is the rst step to idenThe cumulative incidence of at least one episode of otitis
media (OM) by the age of 7years is reported to be 61–99%,
depending on the population [1–3]. Risk factors for otitis
media include a spectrum of nonmodiable and modiable
qualities specic to the patient. They can be described as
patient characteristics, genetic inuences, opportunistic
Table 27.1 Risk factors in otitis media: nonmodiable, potentially modiable, and modiable
Risk factors in otitis media
Nonmodiable Potentially modiable Modiable
Patient characteristics Genetic inuences Socioeconomic behaviors
Young age (2 yo, 4–5 yo) Monozygotic twins Second- and third-hand smoke
Male sex Family history, sibling with history of OM Obesity
Older sibling(s) Aerodigestive tract mucociliary disorders (primary
ciliary dyskinesia and cystic brosis)
Ethnicity (Native American, Canadian
Eskimo, and Australian Aborigine)
Cesarean section delivery Specic genotypes (ISL1 polymorph, A2LM1,
Lo Opportunistic morbidities
Immunodeciency (hypogammaglobulinemia and
leukocyte adhesion deciency)
SAMD9—MIRAGE syndrome)
Upper respiratory infection
Winter season
Cleft palate
Trisomy 21 (Down’s syndrome)
Craniofacial deformity
Adenoid hypertrophy
Environmental/food allergies
Gastroesophageal reux
tifying some of these risk factors. Frequent recurrence and
co- morbidities may prompt referral for other testing and in
some cases genetic testing. Regardless, educating parents
and patients of their risk factors and how to minimize them
is crucial to decrease the incidence of otitis media in
children.
Daycare
Short-term breastfeeding
Pesticide exposure in utero
J. A. Stramielo
Division of Otolaryngology Head and Neck Surgery, University of
California, San Diego, La Jolla, CA, USA
D. Carvalho (*)
Division of Otolaryngology Head and Neck Surgery, University of
California, San Diego, La Jolla, CA, USA
Rady Children’s Hospital, San Diego, San Diego, CA, USA
e-mail: dcarvalho@rchsd.org
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. V. Goycoolea et al. (eds.), Textbook of Otitis Media, https://doi.org/10.1007/978-3-031-40949-3_27
237
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J. A. Stramielo and D. Carvalho
Nonmodiable Risk Factors
Patient Characteristics
Risk factors for otitis media related to a patient’s characteristics are inherently nonmodiable. However, parent and
patient education is helpful in offering reassurance and
explaining why it does not necessarily portend serious underlying disorders. The rst of these risk factors include male
sex, which account for 51–55% of pediatric otitis media
cases, as well as young age, with a bimodal increased incidence at 6–18months old and 4–5years old [1, 3–7]. While
the slight male preponderance has been fairly consistent, no
explanations have been proven as to why otitis media is more
prevalent in males. Alternatively, it is widely accepted that
the risk of young age is related to short, relatively horizontal
eustachian tubes, which elongate and eventually develop a
30–40° upward angle toward the middle ear with increasing
age [8]. Having an older sibling at home is also a risk factor,
presumably due to earlier exposure to upper respiratory tract
infections, which is supported by further increased risk if a
room is shared with them [7].
Native American, Canadian Eskimo, and Australian
Aborigine ethnicities have an increased risk for otitis media,
compared to Caucasians [3, 7]. This is likely due to anatomical characteristics of the eustachian tube of these ethnicities.
Children with Black ethnic backgrounds have a decreased
risk [3, 5], though causality is unknown in all cases. Lastly,
children delivered via cesarean section have a slightly
increased risk of otitis media, as compared to nonoperative
vaginal delivery [9, 10]. The hypothesis is that there are differences in the gut biome of children born by cesarian section and via vaginal delivery [10]. Interestingly, patients born
via an operative vaginal delivery (dened as instruments
placed in the birth canal) have the same increased risk as
cesarean section [9]. Low birth preterm children are also at
an increased risk for otitis.
Potentially Modiable Risk Factors
Genetic Inuences
It is clear that genetics play a strong role in the risk for otitis
media as epidemiology studies have identied family history
of a sibling with prior otitis media as a risk factor [4, 7, 11].
Even more telling, this association is stronger between
monozygotic twins and triplets compared to dizygotic twins
and triplets, though this difference no longer remains signicant after 4years of age [11]. While genetic counseling is not
necessary for the majority of patients with otitis media,
advances in genomics and genetic therapies may prompt
genetic testing for patients with recurrent or severe disease.
Arguably, the otolaryngologist’s role in minimizing genetically inuenced risk factors for otitis media is identication
of the underlying cause, or more realistically, timely referral
for work-up. The presence of these risk factors may also
sharpen clinical acumen for the need of more aggressive preventive measures and more frequent follow-up to ensure
hearing is protected.
Ciliary Motility Disorders
Genetic diseases that lead to aerodigestive motility disorders
are important considerations for recurrent otitis media.
Primary ciliary dyskinesia is a rare (1:10,000–20,000 live
births) genetic disorder affecting the cilia of the upper respiratory tract which can lead to chronic rhinosinusitis, bronchiectasis, and otitis media. Clinical screening questionnaires
and expired nasal nitric oxide concentrations are potentially
cost-effective methods for identifying patients who warrant
formal genetic testing [12]. Historically, cystic brosis was
considered protective against otitis media due to well- aerated
temporal bones and overly tenacious nasal secretions making
translocation to the middle ear more difculty [13]. However,
recent review has noted increased incidence of otitis media
coinciding with increased identication of subclinical genotypes [14]. Interestingly, cystic brosis patients without otitis media were found to have a lower density of goblet cells
on postmortem analysis as compared to cystic brosis
patients with otitis media, yet most have inner ear damage
due to ototoxic drugs [13].
Immunodeciency
Immunodeciency is another important consideration.
Leukocyte adhesion deciency leads to a defect in transporting leukocytes to regions of tissue injury. A recent cohort
analysis identied an otitis media prevalence of 10–21% in
these patients. Suspicion is worked up with cytometric analysis of CD18 and CD11 expression of leukocytes, and diagnosis can be conrmed by the identication of a defect in the
ITGβ2 gene [15]. Similarly, a cross-sectional study of pediatric patients with hypogammaglobulinemia identied an
otitis media prevalence of 49%, which led to conductive
hearing loss in 73% of patients. This includes X-linked
agammaglobulinemia, common variable immunodeciency,
IgA deciency, and hyper-IgM syndrome [16].
Specic Genotypes
The ubiquity of genomics has also led to the identication of
specic genotypes with higher risk for otitis media with
unclear etiology, which includes ISL1 and A2LM1 polymorphisms and SAMD9 mutations [17–19]. ISL1 is part of the
insulin gene enhancer protein 1 homeodomain that regulates
the insulin gene. Specic polymorphisms of this gene relat-
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239
ing to different exons have been found to increase the risk of
otitis media [19]. The A2LM1 encodes the α-2 macroglobulinlike- 1 protein. A variant of which was identied in a Filipino
community to have a signicant odds ratio of 3.7 for OM
[18]. SAMD9, or sterile alpha motif domain containing 9,
encodes a protein of unknown signicance; however, mutations in this gene are responsible for MIRAGE (myelodysplasia, infection, restriction of growth, adrenal hypoplasia,
genital problems, and enteropathy) syndrome. MIRAGE
syndrome has been associated with increased risk of otitis
media. This may be related to cytopenias but has not been
investigated [17]. Of note, other mutations of SAMD9 can
also lead to normophosphatemic familial tumoral calcinosis
but has not been linked to otitis media [20].
Alternatively, some genotypes may be protective, such as
IFI44L minor homozygotes, who have a signicate incidence rate ratio of 0.77 compared to other allele combinations [21]. IFI44L is a protein-encoding gene for the
interferon-induced protein 44-like which has viral antiproliferative activity; however, the mechanism of this property is
unknown [22].
The prevalence of otitis media in children with Down’s
syndrome has been reported to be 81–83% [23, 24]. Temporal
bone studies have identied that Down’s syndrome patients
have smaller middle ear compartments and more collapsible
eustachian tubes due to immature development of eustachian
tube cartilage and the tensor veli palatini muscle [25]. These
patients can also have immunodeciencies that contribute to
their increase risk of otitis media [26]. Otitis media in
Down’s syndrome patients has been shown to commonly
cause signicant physical symptoms and hearing loss [27].
While tympanostomy tubes signicantly improve these
symptoms, it is common for their otitis media to stay unresolved requiring subsequent tubes for a majority of young
age [24, 27].
Opportunistic Morbidities
Several morphological morbidities have been identied as
risk factors for otitis media, which offers an opportunity for
potential medical or surgical intervention. Identifying these
risk factors and educating parents and patients offers better
informed perspectives of preventing OM.It may also obviate
the need for further testing and offer reassurance regarding
the overall health of the patient.
Upper Respiratory Infections
Likely the most common risk factor for otitis media is current or recent upper respiratory infection. In a prospective
cohort study of 294 children aged 1–3years, otitis media was
found to complicate upper respiratory infection 61% of the
time. While there were no associations with sex or ethnicity,
age was signicant with each increasing month of life after
1year reducing the risk of otitis media by 4%. Interestingly,
there was also a signicant difference in the incidence of otitis media by virus type with adenovirus and coronavirus
being the most associated with otitis media. The proposed
pathophysiology of this association is nasopharyngeal edema
leading to eustachian tube dysfunction, as well as increased
production of mucus in the middle ear [28]. Similarly, as
viral upper respiratory infections are most common in the
fall and winter seasons [29], so is otitis media [30]. Intranasal
steroids, antihistamines, and decongestants are not helpful as
treatment for otitis media [31], and this likely holds true for
prevention as well during an upper respiratory infection.
However, symptomatic care with oral hydration and nasal
saline irrigation are safe adjuncts [32]. Furthermore, yearly
inuenza vaccines have been linked to signicant reductions
in otitis media, and similarly, the pneumococcal conjugate
vaccine [33, 34].
Craniofacial Abnormalities
Extra vigilance should be practiced in patients with craniofacial abnormalities that can predispose to otitis media.
Patients with cleft palate ultimately have poor middle ear
ventilation due to poor function of the palatine muscles and
frequent velopharyngeal reux [35, 36]. Greater than 95%
of children with cleft palate have otitis media prior to palatal closure [37, 38], which can improve somehow along
with hearing status at about 6–12months after surgery [39].
However, pediatric patients with cleft palate have similar
long-term chronicity and audiological outcomes when
treated with tympanostomy tubes as compared to pediatric
patients without cleft palate [40]. Patients with other forms
of craniofacial deformity should also be considered to be at
an increased risk for otitis media. Specically, changes in
the relative positions of the mandible, skull base, middle
ear, sphenoid, and palate can increase the risk of otitis
media [41].
Adenoids
The adenoid tissue can act as a reservoir for otitis media
pathogens and can also cause eustachian tube dysfunction if
enlarged and encroaching onto the tori tubarius [42, 43].
Inammatory changes to the adenoids can also cause
increased inammation of the middle ear [44]. Interestingly,
Streptococcus pneumoniae is the most common adenoidal
pathogen in patients 7 years of age or younger and
Staphylococcus aureus is the most common in those older
than 7years of age. However, there is no association between
the risk of otitis media and the pathogen(s) colonizing adenoid tissue [45]. Adenoidectomy in the setting of hypertrophy has been shown to improve middle ear ventilation [46].
It may also decrease the number of repeated tympanostomy
tube in children older than 4years of age [47].
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J. A. Stramielo and D. Carvalho
Allergies
While the relationship between environmental allergies and
otitis media is complicated and controversial, immunological studies have identied IgE-mediated middle ear disease.
Furthermore, the middle ear mucosa is an extension or the
upper airway mucosa and has similar physiologic and
immune mechanisms, including inammation due to allergies. The prevalence of atopy, including allergic rhinitis in
patients with recurrent otitis, ranges from 24% to 89% [48].
Because of the multifactorial nature of OM, it is difcult
to measure the impact of allergy-related middle ear disease
in the setting of other known risk factors. However, allergy
testing can be considered for children with signs of atopia
[49]. Similarly, the impact of food allergies and the need for
avoidance practices remains controversial. Nonrandomized,
prospective studies have researched food allergy associations and impact of dietary avoidance among children with
OM with positive results [50, 51]. However, there remains a
dearth of denitive studies and subsequent consensus statements. While food allergy is a consideration and can be
tested, the risks and benets of dietary avoidance therapy
should be critically appraised specic to the patient and other
risk factors should be minimized.
GERD
Gastroesophageal reux in early childhood is another important concern, as it signicantly increases the risk for otitis
media [52, 53]. In fact, increasing the severity of reux
symptoms increases the risk of eustachian tube dysfunction,
hearing loss, and tympanostomy tube placement [52]. Part of
this may be related to pepsin or pepsinogen identied in
middle ear aspirates, putting even laryngopharyngeal reux
patients at risk. However, this connection has not been conrmed [54].
Modiable Risk Factors
Socioeconomic Practices
Lifestyle and access to healthy and clean food has important
implications beyond the incidence of otitis media but may
offer a tangible and evidence-based opportunity to educate
parents and improve social and environmental factors affecting the patient. One of the most important in this category is
exposure to second- and third-hand smoking. Passive smoke
exposure is a clear, reproducible risk factor across ethnicities
[4, 5, 18, 55–57]. The pathophysiology for this association
has not been established; however, second- and third-hand
smoke have been linked to signicant alterations in the respiratory microbiome, with exposed children more likely to
have inamed upper airways with pathogenic and polymicrobial ora [58, 59].
Obesity has a signicant role in increasing the risk of otitis media, though it is likely multifactorial. Obesity leads to
poor eustachian tube dysfunction secondary to an increase in
the Ostmann fat pad of the nasopharynx. There is also an
increased risk of acid reux, which is an independent risk
factor for otitis media. Most importantly, obesity also leads
to a local immune dysfunction of the middle ear with reduction in toll-like receptor-mediated expression of mRNA for
multiple cytokines [60].
Daycare
Daycare attendance has an odds ratio of 1.3–1.5 for otitis
media [61, 62]. However, an increasing number of caregivers
is not signicant [62], highlighting the increased microbial
transmission rates among young children, inherent to their
behavior. The risk is even higher when daycare attendance is
started prior to age 12months [63, 64], which emphasizes
the multifactorial nature of risk factors for otitis media.
While recommending removal from daycare may lead to signicant concerns, such as the effects on social development,
suggesting delaying admission and ensuring hygienic practices of the facilities, especially for patients with multiple
risk factors, may be better received.
Breastfeeding
Breastfeeding has repeatedly been shown to reduce the risk
of otitis media in infancy by 40–50% [65]. This risk reduction is most robust in infants who are breastfed ≥12months
as compared to those breastfed <6months [66, 67]. This ben-
et may be derived from milk fat globule membranes, or fat
globules, which transport high concentrations of phospholipids, gangliosides, and proteins [68]. Milk fat globule
membrane- supplemented formula signicantly reduces the
incidence of otitis media compared to nonsupplemented,
formula-fed infants [69]. Similarly, prospective research has
correlated pesticide exposure in utero to increased risk of otitis media in childhood, as compared to mothers who consumed an organic, pesticide-free diet [70]. Breastfeeding
position seems to cause different changes in negative pressure in the middle ear, and breastfeeding a child in the “at”
position might be related to increased risk of otitis media
[71, 72].
Common Misconceptions
Pacier use has had a long history of reported association
with increased risk for otitis media. However, signicant
correlations fail to remain signicant after multivariate logis-
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241
tic regression analysis [73]. Furthermore, other studies contradict this association, linking increased otitis media
prevalence with decreased pacier use [74]. This represents
sampling errors. Likely more important, otitis media within
the rst month of life increases the risk of recurrent otitis
media fourfold [75]. Given the clear reduction in sudden
infant death syndrome [76] and the paucity of denitive relationships to otitis media, pacier use should not be
discouraged.
Swimming can often be a confusing topic for parents and
caregivers of children with otitis media. While swimming
can increase the risk of otitis externa [77], it does not increase
nor decrease the risk of otitis media [78]. Similarly, there is
no increased risk for otitis media in patients with tympanostomy tubes 1month after placement and current tympanostomy tube guidelines do not recommend avoiding water
exposure [79, 80].
Eects ofSocial Distancing During
theCOVID-19 Pandemic
SARS-CoV2 (server acute respiratory syndrome coronavirus
2) and the subsequent COVID-19 (2019 novel corona virus
disease) pandemic has led to a radical change in daily life for
most people around the world. Social distancing, social isolation, and increased frequency of hygienic practices have
clearly mitigated the risk of contracting SARS-CoV2 and
developing COVID-19 [81]. As such, these practices have
simultaneously mitigated the risk of contact with other
viruses, subsequentially leading to a signicant 5–10 fold
reduction in the incidence of otitis media in children [82,
83]. Interestingly, this has also led to a signicant increase in
resolution of chronic otitis media with effusion [83]. Though
social distancing and isolation are likely not an appropriate
measure for most children given the need for social development, it does highlight the importance of ensuring hygienic
practices and a possible short-term adjunct for children
severely affected by otitis media.
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The rate of otitis media and other otologic problems is signicantly higher in children with developmental anatomic
issues such as Down syndrome or cleft palate, and physiologic issues such as primary ciliary dyskinesia or cystic
brosis (CF). Furthermore, other predisposing conditions
such as patients with sensorineural hearing loss or those
prone to febrile seizures must also be considered in their
overall clinical picture and otologic management.
Primary Ciliary Dyskinesia
Primary ciliary dyskinesia (PCD) is characterized by abnormal ciliary function impairing mucociliary clearance in the
airway and middle ear, causing respiratory tract infections
and otologic complications.
Pathophysiology
PCD is a genetically heterogenous disorder, which is predominantly inherited as an autosomal recessive trait
[1].“Primary” was adopted for the term PCD, to distinguish
it from secondary or acquired ciliary defects associated with
infection and inammation [2]. Ciliated epithelium covers
most areas of the upper respiratory tract, including nasal
mucosa, paranasal sinuses, middle ear, eustachian tube, and
pharynx, and the lower respiratory tract from the trachea to
the respiratory bronchioles. The normal ciliary axoneme is
structurally made of nine peripheral doublet microtubules
with attached dynein arms and radial spokes and two central
S. J. Wong
Pediatric Otolaryngology, Mount Sinai, NY, USA
D. Carvalho (*)
Rady Children’s Hospital, San Diego, San Diego, CA, USA
Division of Otolaryngology Head and Neck Surgery, University of
California, San Diego, La Jolla, CA, USA
e-mail: dcarvalho@rchsd.org
single microtubules. Cilia propel overlying mucus via a ciliary beat cycle is mediated by dynein arms. Patients with primary ciliary dyskinesia can encompass a wide range and
severity of axonemal defects [3–5], which ultimately impairs
ciliary beating and mucociliary clearance. In approximately
30% of cases, there still may be abnormalities in function,
despite normal ciliary structure [2].
Of note, Kartagener syndrome is part of the larger group
of disorders referred to as primary ciliary dyskinesias and is
characterized by the clinical trial of chronic rhinosinusitis,
bronchiectasis, and situs inversus, which randomly occurs in
approximately 50% of PCD cases.
Epidemiology
The estimated incidence of PCD is 1in 10,000–40,000 births
[6]. However, the prevalence of PCD in the United States is
difcult to determine, largely due to inadequacies of diagnostic methods [7].
Clinical Presentation
The diagnosis of PCD is based on a combination of clinical
phenotype, diagnostic tests such as nasal nitrous oxide measurement, inspection of mucosal cilia, and genetic testing. It
is manifested clinically by neonatal respiratory distress in
>80% of cases, evidence of chronic upper airway symptoms
(daily nasal congestion, episodic facial pain, and anosmia),
daily year-round wet cough starting soon after birth (nearly
100% of PCD patients), and early development of recurrent/
chronic middle-ear and sinus disease [1, 2, 8].
In children with PCD, the ciliary function of the eustachian tube and the middle ear mucosa is impaired leading to
mucous stasis and eustachian tube dysfunction. Recurrent
otitis media with effusion (OME) seems to affect at least
80% of children with PCD, particularly in the rst year of
life [1, 9–11].
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. V. Goycoolea et al. (eds.), Textbook of Otitis Media, https://doi.org/10.1007/978-3-031-40949-3_28
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S. J. Wong and D. Carvalho
Otologic Management
The utility of tympanostomy tubes in this patient population
is under some debate.
While OME in PCD patients can persist into adulthood,
the hearing loss generally thought to resolve by the age of 12
years regardless of intervention [9, 12, 13]. Furthermore,
several studies have found that tympanostomy tubes in PCD
often results in prolonged and offensive otorrhea, multiple
insertions, and permanent perforation [9, 13, 14]. Therefore,
the 2009 European Respiratory Society Consensus Statement
recommends managing OME in patients with PCD conservatively, with regular audiological assessment, hearing aids,
and hearing therapy, since treatment with tympanostomy
tubes can lead to signicant morbidity without a long-term
benet to hearing.
On the other hand, more recent systematic reviews have
shown benet of tympanostomy tubes for patients with
PCD.One 2009 literature review of eight studies found that
ventilation tube insertion improves hearing in primary ciliary
dyskinesia but may lead to higher rate of otorrhea (33%)
when compared to the general population (3.8–13.2%) [15].
The 2016 PCD Foundation Consensus Recommendations
advocate for tympanostomy tubes for children with PCD
who have hearing decits or speech delay and middle ear
effusions based on literature review ndings of signicant
hearing improvements post-tympanostomy tube placement
in children with PCD compared to those managed with medical therapy alone [8]. Overall, it should be noted that the
highest level of evidence found for the management of OME
in children with PCD was level IV [15].
Regardless, all PCD patients considering tympanostomy
tube placement should be counseled on the likelihood of
multiple insertions, postoperative otorrhea, and possibility of
permanent tympanic membrane perforation (up to 50% in
one study) [16]. Furthermore, otolaryngologists should
closely monitor these patients and always consider acquired
cholesteatoma as a potential cause of persistent otorrhea in
PCD given the poor eustachian tube function and multiple
tympanostomy tube insertions. Pediatric PCD patients
should visit a pediatric otolaryngologist at least once to twice
annually, while adult patients should have otolaryngology
care, as needed. An initial audiology assessment in all PCD
patients is suggested at diagnosis, with subsequent evaluations coordinated through their otolaryngologist [8].
Cleft Palate
Orofacial clefts are the most common congenital malformations of the head and neck region, and approximately threequarters of these patients have some form of cleft palate
deformity [17]. Both cleft lip and cleft palate (CP) occur
when tissues in the face and mouth do not fuse properly by
the second or third month of pregnancy. Presentation can be
varied, including with or without associated cleft lip, or be
syndromic or nonsyndromic. Several subtypes of CP can be
distinguished according to severity. At minimum, there can
be cleaving of the uvula. A more severe form is a cleft of the
soft palate. A submucous CP occurs when the cleft of the
hard palate is covered by mucosa and continues through the
soft palate. A complete CP is cleft of the hard palate, soft
palate, and uvula. Meanwhile, a cleft anterior to the incisive
foramen is also dened as a cleft of the primary palate. In all
cases, CP can be associated with anatomic abnormalities that
contribute to eustachian tube dysfunction [18].
Pathophysiology
Cleft palate results from the failure of the lateral palatine
processes to meet and fuse with each other. This can be the
result of (1) defective growth of the palatal shelves, (2) failure of the shelves to rise above the tongue, (3) lack of contact
between shelves (such as in an excessively wide head), (4)
failure to fuse, or (5) rupture after fusion of the shelves [18].
OME occurs in nearly all infants with an unrepaired cleft
palate under the age of 2years because of abnormal insertions of the tensor veli palatini, which causes limited ability
of the eustachian tube to open actively. Failure of the eustachian tube opening and equalization of the pressure within
the middle ear to that of the atmosphere leads to the accumulation of negative pressure and uid stasis within the middle
ear [19].
Epidemiology
The prevalence of CP alone is 0.5 per 1000 live births. The
overall incidence of cleft lip with cleft palate is 1 per 700 live
births. Sex differentiation (male:female ratio) for cleft lip
and palate is about 2:1, and 1:2 for CP alone [18].
Clinical Presentation
At the time of cleft palate repair, more than 90% of the middle ears contain mucoid material (“glue ear”) [20].
Approximately 75% of children with CP will have a history
of nontrivial OME.In these patients, middle ear disease persists longer and leads to an increased incidence of conductive
hearing loss, language delays, and cholesteatoma over that of
their peers [21]. Furthermore, most children with CP have
greater rates of acute otitis media (AOM). The incidence of
AOM in these children is not comparable to that of the general population until adolescence [22].
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In general, earlier age to cleft palate repair seems to correlate with a corresponding decrease in prevalence of middle
ear dysfunction and hearing loss [23]. However, although its
prevalence is reduced after surgical cleft palate repair, a signicant number (13–36%) of these children continue to suffer from middle ear disease and sequelae into adolescence
and adulthood [19, 24–27]. Severity or type of cleft palate
does not seem to correlate with otologic or audiologic outcomes [25].
Otologic Management
The inability to establish adequate eustachian function leads
to the near-universal recommendation that these children
receive early tympanostomy tubes to prevent otologic complications related to the conductive hearing loss [28].
In the short term, patients treated early with ear tubes
exhibit better audiometric results as well as better articulation and speech development compared with patients treated
conservatively, whereas no signicant differences have been
observed regarding mid- or long-term outcomes [29, 30].
However, patients who received tympanostomy tube placement prior to time of palate repair (typically 9–12months)
was associated with increased repeat tympanostomy tube
placement [31]. Thus, many doctors prefer to perform the
repair of cleft palate and ventilation tube surgery simultaneously when the child is near 1year old [31, 32].
The 2013 Clinical Practice Guidelines for tympanostomy
tube codeveloped by the American Academy of
Otolaryngology-Head and Neck Surgery Foundation (AAOHNSF), the American Academy of Pediatrics (AAP), and the
American Academy of Family Physicians (AAFP) advocate
for a more individualized approach [33]. Specically, that it
may be appropriate to offer tympanostomy tubes on an individualized basis for cleft palate infants with OME that persists after failing hearing tests [33] because resolving the
issue of middle ear effusion could facilitate the assessment of
hearing status. Hearing aids are an alternative to tympanostomy tubes when hearing loss is present. Regardless, it is
also recommended that clinicians evaluate children with
cleft palate for OME and hearing loss at the time at which
cleft palate is rst diagnosed. It is recommended that middle
ear status be assessed at 12–18months of age, considering
that this is a critical period in the development of language
skills, speech, balance, and coordination. By 18months of
age, delays in language and speech development are easily
identied. For children who do not receive tympanostomy
tubes, the follow-up schedule to monitor OME and hearing
loss until OME resolves should be more frequent than the
3–6-month intervals recommended for children without cleft
palate.
Meanwhile, palatoplasty is observed to decrease the frequency of middle ear disease and improve hearing compared
with untreated cleft palate [21]. The recovery rate of eustachian tube function after palatal surgery ranges from 40% to
86% [34, 35]. However, continued monitoring for OME and
hearing loss should continue throughout childhood, including after palate repair, because of a continued high prevalence of effusion and hearing loss [33].
Down Syndrome
Down syndrome is characterized by dysmorphic facies, at
nasal bridge, epicanthal folds, brachycephaly with anterior–
posterior attening of the skull, a simian crease, learning disabilities, and generalized hypotonia [36]. Children with
Down syndrome also experience an increased rate of recurrent AOM, OME, poor eustachian tube function, and stenotic
ear canals that can impede the assessment of the tympanic
membrane and middle ear status.
Pathophysiology
Down syndrome is genetically dened by a nondisjunction
mutation resulting in trisomy of chromosome 21.
Patients with Down syndrome have a range of otologic
problems including stenotic ear canals, increased incidence
of otitis media, chronic ear disease, secondary hearing loss,
as well as hearing loss caused by ossicular abnormalities and
inner ear dysplasia.
Specically, the high prevalence of serous otitis media in
these patients is thought to be due to several factors. The
major predisposing factors to otitis media in these children
are thought to be the result of defective eustachian tube cartilage and musculature. In addition to histologically abnormal cartilage, the diameter of the eustachian tube is
signicantly smaller compared to the general population.
Hypotonicity and muscular defects of the tensor palatini and
dilator tubae have also been described. These produce stasis
within the eustachian tube and allows easier ascent of bacteria from the nasopharynx [36].
Patients with Down syndrome also have midface and
nasopharyngeal anatomy that predisposes them to chronic
ear disease. Midface hypoplasia seen in many of these
patients involves the nasopharynx and the eustachian tube
openings. The bony connes of the nasopharynx are smaller
in children with Down syndrome, and therefore even smallto medium-sized adenoids may give rise to eustachian tube
dysfunction in these patients [37].
Finally, children with Down syndrome suffer from
increased number of upper respiratory infections, thought to
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