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M. J. Herrera J and J. Alzerreca
considered an appropriate strategy for most children because
the effusion resolves spontaneously in most of them [10].
Hearing Aids
Other alternative is the use of hearing aids and osseous conduction hearing aids in children with craniofacial abnormalities, Down’s syndrome, and cleft palate. They have been
found to overcome the hearing loss associated with this condition. Childhood hearing loss can affect language development. Therefore, hearing aids may be considered as a
noninvasive option to treat OME [20].
Surgical Treatment
Ventilation Tubes (VT)
The use of ventilation tubes is widespread, with different
indication schemes. VT helps to ventilate the cavities of the
middle ear and balance the pressures on each side of the tympanic membrane, preventing re-accumulation of uid. After
this procedure, many patients do not need additional therapy
due to the growth and development of the eustachian tube
angle, which will allow for drainage [14].
Short-term VTs are used for rst-line treatment and fall
out after between 6 and 18months. Thus, the risk of complications is correspondingly lower. Long-term VTs stay in
place for 2years or more. Even though the complication rate
increases with the VTs’ duration of use, these devices are
still indicated when OME recurs in a child who has already
had short-term VTs. They are also recommended in children
with chronic eustachian tube dysfunction [14].
The current clinical practice guidelines for OME recommend surgical management for children with 3 or more
months of OME with persistent hearing loss or symptoms
that are likely attributable to OME, for recurrent or persistent
OME in children with developmental risks regardless of
hearing status or for OME with structural damage to the middle ear or tympanic membrane [15]. Also, the individual difculties related to the hearing loss, which vary from one
child to another and are not always correlated with the hearing threshold, need to be considered [6]. In children at risk of
language or learning disorders, rapid treatment is recommended to limit the impact of additional deafness. This concerns children with autistic spectrum disorders, perception
deafness unrelated to OME, a speech delay, a craniofacial
syndrome or malformation, blindness (or other visual disorders), a cleft palate, or a global development delay [15].
When OME is detected in an at-risk child, tympanostomy
tubes should be offered when the likelihood of spontaneous
resolution is low (type B tympanogram or persistence for
3months) [2].
In 2010, Browning etal. review of 10 randomized studies
show the effectiveness of ventilation tubes versus myringotomy or nonsurgical treatment in children with
OME. Randomized controlled studies are included. Tubes
installed after 12weeks of effusion with documented hearing
loss show benet in the rst 6months in hearing as does nonsurgical treatment. The studies showed a small difference in
relation to the decibels gained between those treated with
tubes and controls. At 12–18months, no differences were
found. There are no differences in language, behavior, cognitive development, or quality of life. Tympanosclerosis was
observed in one-third of the ears receiving tubes. Otorrhea is
common in infants but in children over 3years of age it
occurs in <2% of the ears in 2years of follow-up. No studies
evaluate benets in children with developmental or language
delays. Therefore, the tubes would be benecial only in the
short term in the hearing of healthy children [10].
Consequences for tympanic retractions and cholesteatoma are difcult to interpret from available evidence as the
ears with the most severe disease are usually those which
require ventilation tubes, so it is difcult to dissociate disease from treatment as cause of complications [3].
The tympanic membrane generally benets from tympanostomy tubes, avoiding posterosuperior retraction pockets,
ossicular erosion, adhesive atelectasis, and retraction pockets
that accumulate keratin debris [15]. A prospective study
shows that early tympanostomy tubes do not prevent the progression of OME toward tympanic retraction [30].
Concerning cholesteatomatous chronic otitis media, tubes
prevent the appearance of cholesteatoma on a population
level, but individually the absolute risk reduction is very
small [31]. There is insufcient literature to assess the possible benet of tubes on cholesteatoma prevention [3].
The use of tympanostomy with tubes decreased OME for
2years compared with watch and wait or myringocentesis
and improved hearing for 6months compared with watch
and wait [32].
Adenoidectomy
Adenoidectomy is currently utilized in cases of OME that
involve enlarged adenoids and is an important addition to
management in patients with OME.
The increase of adenoid hypertrophy cells can enhance
local inammation, resulting in abnormal physiological
function of eustachian tube and middle ear effusion. It is
found that many pathogenic microorganisms in the middle
ear effusion are like the bacteria in adenoid tissues [33].
Biolms contribute to the pathogenesis of OME [9].
Many therapeutic strategies have been attempted, and the
role of topical therapies is still being investigated. A review
of 30 articles shows that antibiotics were ineffective for eradicating biolm. Mupirocin irrigation, gentian violet, and thiamphenicol glycinate acetylcysteine effectively eradicated
21 Otitis Media withEusion: Pathophysiology, Clinical Picture andManagement
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biolms. Physical disruption, surfactants, and probiotics
were also shown to be benecial [34].
An animal experiment found that middle ear biolms
can be treated safely and effectively reducing the surface
area of biolm by washing the middle ear with saline solution or children’s shampoo. An hydrodebrider demonstrated
to be more effective at eradicating biolm than manual irrigation [35].
Adenoidectomy removes the physical obstruction of the
eustachian tube, restores the drainage of mucus, and equilibrates the pressure in the middle ear [8]. Adenoidectomy was
signicantly more effective in the treatment of OME when
large adenoids were in contact with the torus tubarius. The
viscosity of the middle ear effusion does not inuence the
effectiveness of adenoidectomy [36]. Adenoidectomy may
enhance the clinical effectiveness of TTs in OME, for at least
2years. Adenoidectomy is most benecial in children with
persistent OME aged ≥4years [18].
In 2010, Van den Aardweg etal. review shows that the
22% and 29% risk differences at 6months and 12months,
respectively, for children with persistent otitis media with
effusion in the trials that compared adenoidectomy with
unilateral tympanostomy tubes versus a unilateral tympanostomy tube alone, in which the non-operated ears were
used as the control, that shows a signicant benet of adenoidectomy as far as the resolution of middle ear effusion
in children with OME is concerned. The results of studies
of adenoidectomy with or without myringotomy versus
nonsurgical treatment or myringotomy only, and those of
adenoidectomy in combination with bilateral tympanostomy tubes versus bilateral tympanostomy tubes only,
showed a small benecial of adenoidectomy on the resolution of the effusion. The benet to hearing is small, and the
effects on changes in the tympanic membrane are unknown.
The risks operating should be weighed against these potential benets [37].
Adenoidectomy used as an adjunct to grommet insertion
reducing hearing loss by a further 4dB.As well as improving thresholds, there is a prolongation in the duration of
improvement in hearing of up to 18months. This extended
period creates a reduction in reinsertion rate of 21% [38].
Compared with simple tube insertion, tympanostomy
tubes combined with adenoidectomy can effectively shorten
the duration of middle ear effusion, reduce the recurrence
rate, and improve the curative effect. But it has no obvious
advantage in improving the postoperative hearing level [33].
The American guidelines recommend adenoidectomy for
the treatment of OME as a function of the child’s age. For
children under the age of 4years, adenoidectomy must only
be performed in cases of nasal obstruction or recurrent infections. In children over the age of 4years, it can be combined
with TT placement [2, 8].
Balloon Dilatation onEustachian Tube
The aim of this procedure is to improve the ventilatory and
pressure-equalizing function of the eustachian tube to treat
OME by widening the medial cartilaginous part of the eustachian tube.
A recent study shows that patients treated with dilatation
and grommet insertion had good outcomes, improving subjective symptoms and objective evaluations and achieved
good results in eustachian tube function and structure
(enlarged and effectively improves the active and passive
opening) [39].
Eustachian tube balloon dilatation combined with grommet insertion could be a treatment for refractory otitis media
with effusion [39].
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Inflammatory Mediators
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inthePathogenesis ofOtitis Media:
ABrief Review
TimothyT.K.Jung
22
Otitis media (OM) is a common childhood disease. OM can
be dened as an inammation or infection of the middle ear
cavity. Among many causative factors of OM, infection and
eustachian tube (ET) dysfunction are most important. These
causative factors stimulate middle ear epithelia and inammatory cells to secrete inammatory mediators (IMs) such
as cytokines, eicosanoids, platelet-activating factor (PAF),
tumor necrosis factor (TNF)-a, and nitric oxide. These IMs
increase vascular permeability and secretory activity resulting in middle ear effusion (MEE) [1]. Thus, IMs play a central role in the pathogenesis of OM.
Pathogenesis of OM has been studied in humans and various animal models. Various forms of OM have been studied
in longitudinal and parallel studies including acute purulent
otitis media (POM), serous otitis media (SOM), mucoid or
secretory otitis media (MOM), and chronic suppurative otitis
media (COM). When these forms of OMs are followed longitudinally, they seem to change in continuum and interrelated [2].
The purpose of this study was to better understand the
role of IMs in the pathogenesis of OM by nding levels of
IMs in samples of human middle ear effusion (MEE) and in
animal models of OMs and by studying the effect of the therapeutic use of inhibitors of IMs.
Methods
start with assaying samples of MEE in humans obtained at
the time of myringotomy and tympanostomy tube (TT)
insertions or in different types of animal models at different
time intervals. Many of the animal studies also examined
corresponding temporal bone histopathology.
Results
Lysozyme andLactic Dehydrogenase (LDH)
Both lysozyme and LDH have been used as an index of
inammation.
Human MEE
Levels of lysozyme and LDH were higher in mucoid MEE
than serous MEE [2].
Animal MEE
In POM model using chinchilla infected with pneumococcus, concentration of lysozyme and LDH were highest on
day 7 and decrease over time. In SOM model induced by
blocking eustachian tube in chinchilla and cat, levels of these
IMs were lower than POM [2].
Histopathology of the temporal bones showed inamma-
tions in mucoperiosteum corresponding to levels of IMs [2].
The topic of IMs in the pathogenesis of OM was searched in
the National Center for Biotechnology Information (NCBI)
and at the U.S. National Library of Medicine (NLM).The
articles were reviewed, organized, and discussed. Only common IMs studied in OM were included. Most of the studies
T. T. K. Jung (*)
Department of Otolaryngology-Head & Neck Surgery, Loma
Linda University School of Medicine, Jerry L.Pettis Veterans
Medical Center, Loma Linda, CA, USA
Inland Ear Head & Neck Clinic, Riverside, CA, USA
© 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_22
Eicosanoids, Prostaglandins (PGs),
andLeukotrienes (LTs)
Among the various IMs of OM, arachidonic acid (AA)
metabolites (eicosanoids) such as PGs and LTs appear to
play an important role in the pathogenesis of OM.To investigate the role of AA metabolites on the pathogenesis of OM,
concentrations of AA metabolites were measured in the
MEE from human and paralleling animal models of OM and
effects of inhibiters of AA metabolism, antibiotics, and tympanostomy tube (TT) on the outcome of animal models of
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T. T. K. Jung
OM were studied [3]. AA is released from membrane phospholipids by the action of phospholipase. This step is inhibited by corticosteroids. Once released, AA can be converted
to two metabolic pathways, one through cyclo-oxygenase
into PGs and the other through lipoxygenase into LTs. Most
of nonsteroidal anti-inammatory drugs (NSAIDS) like
aspirin or ibuprofen inhibit the activity of cyclo-oxygenase.
Human andAnimal MEE
PGE2 and PGF2a in human pooled MEE were measured by
radioimmunoassay (RIA) and found that mucoid effusions
had higher concentrations of PGs than serous effusion [4]. In
more extensive studies concentrations of major AA metabolites, both PGs and LTs were assayed and analyzed according to type of uids, age groups, and bacterial culture results.
It was found that AA metabolites were higher in younger age
group than from older age groups. Levels of LTs were generally higher in mucoid MEEs than in serous MEEs. LTB4 was
the only AA metabolite with higher levels in bacterial
culture- positive human MEE.
Eect ofInhibitors ofAA Metabolism
From the study of the therapeutic use of inhibitors of AA
metabolism, combination of penicillin and corticosteroid
was the best mode of therapy, followed by penicillin alone
and penicillin plus NSAID. Therapy with ibuprofen alone
induces more inammation and increased effusion probably
because of increased LTs due to inhibition of cyclooxygenase [3].
Eect ofLT andIts Inhibitor ontheClearance
oftheEustachian Tube
Using guinea pigs, this study demonstrated that LTC4
impaired mucociliary clearance function of the eustachian
tube in dose-dependent manner. This inhibition of mucociliary clearance function was prevented by pretreatment with
LT inhibitor. The ndings of this study suggest that LT plays
an important role in the pathogenesis of OME by impairing
eustachian tube clearance function. LT inhibitors may have
future prophylactic or therapeutic implications for OME [5].
dependent OME.PAF antagonist, WEB 2170, prevented the
development of OME.The ndings of this study suggest that
PAF plays an important role in the pathogenesis of OME [8].
Tumor Necrosis Factor-a (TNF-a)
TNF is produced by activated macrophages and has various
activities. It activates neutrophils, induces production of
intercellular adhesion molecules from lymphocyte, directs
tumoricidal action on certain tumor cell line, enhances production of interleukins such as interferon, interleukin (IL)-1,
IL-2, IL-6, and IL-8, and stimulates production of collagenase, prostaglandin, and pyrogen [9].
To clarify the role of TNF in experimental OME, OME
was induced by transtympanic injection of TNF in rats. MEE
was developed in 70% of specimens, and histopathological
changes such as subepithelial edema and marked inltration
of neutrophils were present in 100% at 24h after injection.
MEE was prevented by pretreatment with TNF antagonist,
TNF-soluble receptor type I (TNFsolRI) [10]. Another study
performed by same group showed that treatment with TNF
antagonist prevents MEE induced by pseudomonas lipopolysaccharide (LPS) in rats[11].
Nitric Oxide Metabolites
Free radicals such as nitric oxide (NO) seem to be important
in the pathogenesis of OME.This study measured concentrations of NO in human MEE.Type of MEE was determined at
the time of collection as SOM, MOM, and
POM. Concentrations of NO metabolites were highest in
MOM followed by SOM and POM.This study suggests that
NO is present in human MEE and may play an important role
in the pathogenesis of OME [12].
Review ofIMS, OM, andConnection toInner
Ear Function
Platelet-Activating Factor (PAF)
A biologically active phospholipid PAF is known to have
wide-ranging effects on acute inammation and allergy. It is
released from human neutrophils, platelets, eosinophils,
macrophages, mast cells, and vascular endothelial cells [6].
It has been identied in human MEE and has been suggested
to participate in developing OME and maintaining MEE by
stimulating vascular permeability and chemotaxis [7].
To test hypothesis that PAF can induce OME, PAF was
injected into the chinchilla bullae which induced dose-
Here is a review article dealing with the characteristics of
various inammatory mediators identied in the middle ear
during otitis media and in cholesteatoma. The role of each
inammatory mediator in the pathogenesis of otitis media
and cholesteatoma has been discussed. Further, the relation
of each inammatory mediator to the pathophysiology of the
middle and inner ear along with its mechanisms of histopathological change has been described. The mechanisms of
hearing loss including sensorineural hearing loss (SNHL) as
a sequela of otitis media are also discussed. The passage of
inammatory mediators through the round window membrane into the scala tympani is discussed. In an experimental
22 Inammatory Mediators inthePathogenesis ofOtitis Media: ABrief Review
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animal model, an application of cytokines and lipopolysaccharide (LPS), a bacterial toxin, on the round window membrane induced sensorineural hearing loss as identied
through auditory brainstem response threshold shifts. An
increase in permeability of the blood–labyrinth barrier
(BLB) was observed following the application of these
inammatory mediators and LPS[13].
Inammasome andOME
The nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inammasome is a critical molecule
mediating interleukin-1β (IL-1β) responses. However, the
role of the NLRP3 inammasome in otitis media has not
been fully examined. The purpose of this study was to assess
the expression of NLRP3, ASC (apoptosis-associated specklike protein containing a caspase recruitment domain and a
pyrin domain), and caspase-1in lipopolysaccharide-induced
otitis media. BALB/c mice received a transtympanic injection of either lipopolysaccharide or phosphate-buffered
saline. The mice were sacriced 24 h after injection.
Concentrations of IL-1β, NLRP3, ASC, and caspase-1in the
middle ear effusions were measured by enzyme-linked
immunosorbent assay. Temporal bones were processed for
histologic examination and immunohistochemistry.
The transtympanic injection of lipopolysaccharide signicantly upregulated levels of IL-1β, NLRP3, ASC, and
caspase-1 in the middle ear as compared with the control
mice. The proteins of NLRP3, ASC, and caspase-1 were
observed in inltrating inammatory cells induced by lipopolysaccharide in the middle ear cavity. Lipopolysaccharide
induces NLRP3 inammasome components in the middle
ear. The NLRP3 inammasome may play an important role
in the pathogenesis of otitis media. Modulation of
inammasome- mediated inammation may be a novel therapeutic strategy for otitis media [14].
Viral andBacterial Pathogens andIMs inMEE
Secretory otitis media (SOM) is characterized by persistence
of uid in the middle ear, often following an episode of acute
otitis media. The hypothesis is that failure to eliminate bacterial or viral pathogens may result in persistent low-grade
inammation. In this study, inammatory mediators in middle ear uids from 67 children with SOM were analyzed.
This was combined with determinations of viable bacteria by
culture along with detection of bacterial and viral genetic
material by real-time polymerase chain reaction (PCR). The
inammatory mediators found at the highest concentrations
(>30ng/mL) were stem cell growth factor-β (median 110ng/
mL), CXCL1, IL-16, IL-8, migration inhibitory factor,
CXCL10, and CXCL9. Among bacterial pathogens,
Moraxella catarrhalis and Haemophilus inuenzae dominated, regardless of detection methods, while rhinovirus
dominated among viral pathogens. Middle ear uid levels of
interleukin (IL)-1α, IL-17, IL-1β, broblast growth factor
basic, and tumor necrosis factor correlated strongly with the
presence of bacteria detected either by culture or PCR, while
IL-1RA, IL-3, IL-6, IL-8, CCL3, CCL4, and granulocyte
colony-stimulating factor correlated signicantly with realtime PCR values. CXCL10, CXCL9, CCL2, and TRAIL correlated signicantly with viral nucleic acid levels. To
conclude, persistence of viral and bacterial pathogens may
fuel persistent inammation in SOM. Bacteria caused a
broad inammatory response, while viruses chiey elicited
the interferon-induced chemokines CXCL9 and CXCL10
[15].
Discussion
The goal of this review is to nd the role of IMs on the pathogenesis of OM.Typical OM starts with viral upper respiratory infection followed by bacterial infection. It may start
with eustachian tube (ET) dysfunction creating negative
pressure in the middle ear. Frequently, OM may start with
the combination of both bacterial infection and ET dysfunction. Either bacterial infection or ET or both stimulate middle ear epithelia and inammatory cells to secrete
inammatory mediators (IMs) such as cytokines, eicosanoids, platelet-activating factor (PAF), tumor necrosis factor (TNF)-a, and nitric oxide. These IMs increase vascular
permeability and secretory activity resulting in middle ear
effusion (MEE) [1]. IMs can start, perpetuate MEE, and
cause sequelae such as sensorineural hearing loss.
Most of the studies of IMs in OM start with assaying samples of MEE from human or animal model of OM.Usually,
samples are divided by the type of uids such as SOM,
MOM, or POM either from human or experimental animal
models.
Next step is injecting IMs either transtympanic membrane
or through the top of the bullae and checking whether MEE
is produced or not. This step is followed by treating with
blockers of IMs being tested and checking whether formation of MEE is blocked or not. As much as possible histopathology of middle ear mucosa is examined.
The IMs that have been gone through these tests include
cytokines, prostaglandins, leukotrienes, platelet-activating
factor (PAF), tumor necrosis factor (TNF)-a, and nitric oxide.
No doubt there are more IMs involved in the pathogenesis of
OM, and more will be discovered and added to the list.
Goal of these studies is to nd better treatment of
OM. Finding how IMs induce OMs and inhibitors of IMs
may reduce or block OM can be used clinically to treat
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T. T. K. Jung
patients with OM.One example of this is the judicious use of
glucocorticoid with antibiotics to treat POM.This practice
came from extensive animal and human studies using glucocorticoid which blocks the formation of both LTs and PGs
from AA. It will be possible that more inhibitors of IMs
could be used to treat OM in the future.
Conclusion
This brief review demonstrates that various IMs such as
lysozyme, LDH, PGs, LTs, PAF, TNF, ILs, and NO are
involved in the pathogenesis of OM.These IMs were measured in the samples of MEE in human and animal models of
OME and histopathological effect studied. Effects of blockers of these IMs on the outcome of animal models of OM
were studied to discover better treatment for OM.One example of such nding was better outcome when OM was treated
with antibiotic in combination with glucocorticoids.
Goal of these studies is to nd therapeutic use of inhibitors of IMs. Further study is needed to determine if more of
these IM blockers can be implemented into the clinical
setting.
References
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2. Juhn SK, Paparella MM, Kim CS, Goycoolea MV, Giebink
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3. Jung TTK. Prostaglandins, leukotrienes, and other arachidonic
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4. Jakson RT. Autonomic stimulation, osmolarity and prostaglandin effects in the Eustachian tube. Ann Otol Rhino Laryungol.
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7. Cauwenberge P, Bernstein J.Inammatory mediators inmiddle ear
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Otorhinolaryngol. 2001;60:55–8.
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NJ, Jung TTK, Kim BH, Park SY, Lin J, Ondrey FG, Mains DR,
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Y, Makihara S, Nishizaki K. NLRP3 inammasome expression
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Wold A.Inammatory mediator proles in secretory otitis media
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org/10.1089/jir.2020.0075.
Retraction Pockets andAdhesive Otitis
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Media
MaríaJoséHerrera J andJavieraPardo
23
Denition
A retraction of the tympanic membrane occurs when a portion or the entirety of the membrane collapses within the
middle ear cavity, as a result of negative pressure from
impaired airow in this space.
The importance of retraction pockets lies in the loss of
the original histological and anatomical structure, which is
associated with the development of ossicular chain erosion,
cholesteatoma formation, and potentially life-threatening
complications from cholesteatoma. The development of
retraction pocket presumes a change in the histological
structure of the tympanic membrane, typically the loosening
of the elastic bers in the middle layer and reductions in
thickness and tensile strength and in the layer’s abilities to
maintain the shape and position of the tympanic membrane
and to return to its original thickness and strength. Retraction
pockets are considered sequels of abnormal pressure regulation in the middle ear; however, inammation or earlier perforations may also contribute to the development of
retraction pockets [1].
Prevalence
Retractions are much more common in children than in
adults. The incidence of atrophy increases from 4% at age
4years to 11% at age 16years [2]. In a study of 294 healthy
children between 5 and 16 years old, the prevalence of atelectasis of the eardrum was estimated at 14%–26% in the pars
accida and only 0.3%–3.7% in the pars tensa [3].
Re-examinations of children who had secretory otitis media
M. J. Herrera J (*)
Otolaryngologist Department of Otolaryngology,
Clínica Universidad de Los Andes,, Santiago, Chile
J. Pardo
Otolaryngologist Department of Otolaryngology,
Clínica Universidad de Los Andes, Santiago, Chile
e-mail: jpardo@clinicauandes.cl
noticed that 34% of the ears had developed different degrees
of attic retractions after 3–8years [4].
In 2011, Maw etal. used video-otoscopy to perform an
important longitudinal cohort study with 6908 healthy children, whose ages ranged from birth to 10years. They found
pars accida retractions in 9.6% of cases and pars tensa
retractions in 7.9%. Most of these retractions were mild, and
a few cases were severe [5]. The prevalence of retractions in
adults has been reported in a population sample as 9.6% for
pars accida and 7% for pars tensa [5].
Bilateral retraction pockets are often present. The association between pars tensa and pars accida abnormalities in the
same ear shows that pars accida retractions are frequently
associated with pars tensa abnormalities, but when abnormalities have been found in the pars tensa, the pars accida
has been completely normal [5].
Many studies have reached a similar conclusion: When
otitis media is present, the frequency of tympanic membrane
pathology is signicantly higher. Abnormalities in the tympanic membrane in ears without histories of otitis have been
present in 11% of cases. In children with a history of otitis,
the rates of abnormalities have been 46% and 92% (as found
with the use of a ventilation tube, or VT) for 8-year-olds. In
the same study, a high number of mild retractions that were
present during the initial examination at this age had substantially diminished at 10-year follow-ups [6].
Pathogenesis
Tympanic retraction is a sequel secondary to an inammatory process of the tympanic membrane, such as otitis media
with effusion or recurrent acute otitis media, and it is associated with the poor ventilation of the middle ear. Anatomically,
the tympanic membrane is formed by three layers of skin,
connective tissue, and mucosa. At the level of the pars tensa,
the lamina propria, corresponding to the middle layer, has
two layers: the stratum radiatum and the stratum circulare.
On one hand, in the posterosuperior part of the pars tensa, the
© 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_23
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M. J. Herrera J and J. Pardo
stratum circulare is poorly developed and more vascularized,
which makes it a weaker zone. On the other hand, at the level
of the pars accida, this zone has no annulus (Rivinus segment), and its lamina propria has few elastic and collagen
bers, which are also disorganized. This exacerbates the
weakness of this zone and increases the risk of retraction [7].
From a ventilation point of view, the middle ear is divided
into two compartments by the tympanic diaphragm: a posterosuperior compartment, which includes the superior epitympanum and mastoid, and an anteroinferior compartment,
which includes the mesotympanum, protympanum, hypotympanum, inferior retrotympanum, and inferior epitympanum (Prusak’s space). The ventilation of the posterosuperior
compartment depends on the tympanic diaphragm and its
isthmus, whereas the anteroinferior compartment is ventilated directly by the Eustachian tube. In addition, the inferior
epitympanum, which lies below the diaphragm and is independent of the superior epitympanum, is ventilated through
the posterior pocket of the Von Tröltsch fascia into the
mesotympanum.
Mastoid cells exhibit pneumatization, which occurs progressively from birth, from which age it eventually reaches
only the antrum and is completed in adolescence. The
mucosa of the mastoid is cuboidal, and its main function is
gas exchange. In contrast, the mucosa of the middle ear is
secretory, and its main function is mucociliary clearance.
When the middle ear mucosa becomes inamed, it tends
to reabsorb more gas, thus generating more negative pressure
[8]. In addition, the inamed mucosa tends to obstruct the
airways, both at the level of the isthmus and at the level of the
Eustachian tube. Obstruction at the level of the Eustachian
tube generates poor diffuse ventilation, which predisposes
the membrane to the generation of otitis media with effusion
and to the global retraction of the tympanic membrane. On
the other hand, altering segmental ventilation at the level of
the isthmus predisposes the membrane to focal retractions
and the formation of attic cholesteatomas.
At the cellular level, the inltration of the eardrum by
inammatory cells in cases of otitis media with effusion
destroys the lamina propria of the tympanic membrane,
through the secretion of collagenase and elastase, which also
generates atrophy [9, 10]. Atrophy is what predisposes the
membrane to the formation of retraction pockets.
Formation ofRetraction Pockets inthePars
Tensa
During otitis media with effusion, the chronic inammatory
process around the ossicular chain is more severe than in
other areas of the middle ear. Draining this area around the
ossicular chain is difcult, so the effusion tends to remain
there, and granulation tissue could form [11]. This tissue can
obstruct the superior retrotympanic airway, resulting in the
poor ventilation of the posterior retrotympanum. The anatomical passage through which this area drains into the inferior mesotympanum is easily blocked by mucosal folds and
by the infrastructure of the tympanic isthmus.
The iname area around the ossicular chain irritates the
eardrum and triggers the inltration of inammatory cells in
the squamous layer of the pars accida and the posterosuperior quadrant of the pars tensa of the tympanic membrane.
The inammatory process’s invasion into the tympanic
membrane plays an important role in the development of
retraction pockets and subsequent cholesteatoma formation,
through the destruction of the lamina propria and the stimulation of keratinocyte growth and proliferation [12–14].
Formation ofRetraction Pockets inthePars
Flaccida
Ventilation routes to the attic compartments are secured by
the tympanic isthmus and by the anterior route through the
incomplete tensor tympani fold in an anterior epitympanic
recess of normal size.
Selective epitympanic dysventilation syndrome occurs
when the tympanic isthmus of a complete tensor tympani
fold has been blocked, resulting in the complete isolation of
the epitympanum from the mesotympanum. This event
induces a gas decit and could be the basis for the selective
decrease of gas pressure in the attic, which leads to the development of an attic retraction pocket and its possibly evolving
into a cholesteatoma, even in subjects with normal Eustachian
tube function [14].
An incomplete tensor tympani fold prevents the development of extensive pathology around the malleus and the
attic, even in the presence of chronic otitis media [14]. In one
study, the blockage of the isthmus and a complete tensor
tympani fold were present in more than 96% of patients with
attical disease, whereas only present in 19% in the control
group [15].
The anterior epitympanic recess is important in the recurrence of otitis media with effusion. Complete control of the
retraction pocket was not achieved even with a tympanoplasty with cartilage or the reconstruction of the lateral wall
of the attic if there the surgery on the aeration of the anterior
epitympanic recess was insufcient [14, 16].
Clinic
Clinical evaluations of a retraction pocket allow for differentiation between a stable retraction pocket and an unsafe
retraction pocket, which progresses and is at risk of evolving
into a cholesteatoma. Retraction pockets can remain silent
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for a long time. Their clinical symptoms depend on their
extent and severity. Mild retractions are usually asymptomatic, and they may be associated middle ear effusion.
Retractions of the tympanum are incidentally diagnosed
during examinations. Their symptoms, such as otorrhea and
conductive hearing loss, as a result of a middle ear effusion,
splinting of the tympanic membrane, or ossicular chain erosion, are recurrent. Otalgia may be present because of
changes in middle ear pressure or infection [17]. Dizziness is
a very rare symptom [14].
Otorrhea is mostly intermittent and can be spontaneous or
can follow exposure to water. Hearing loss is mostly of the
mild conductive type but can reach up to 45–55dB in some
cases. No correlation has been established between hearing
threshold and retraction stages [14, 18]. But improvement in
audiometry exams has been found over time in mild retraction pockets [19].
Diagnosis
Diagnosis is clinical and requires a visual examination of
the tympanic membrane using an otoscope or microscope. A
retraction is dened as an intact tympanic membrane that
has been transformed into a very thin epidermal membrane
retracted toward the medial wall of the tympanic cavity
[14]. It is important to describe the severity of a retraction.
The description should include its position, its depth,
whether it is xed or mobile, the presence of discharge, the
accumulation of keratin, and the presence of bony erosion.
This could be carried out by using one of the published staging methods or by describing it with text, drawings, or photographs [20].
Descriptions ofRetractions
Retractions are localized to the pars accida and pars tensa;
they are marginal, nonmarginal, or bilateral [14]. The location can be made more specic by describing the involved
quadrant [1]. For adherence, the mobility of a retraction can
be tested via the Valsalva maneuver; via delicate suctioning,
which requires exercising caution so as not to disrupt the
pocket membrane [14]; or by using a pneumatic otoscope
[20].
In the pars tensa, descriptions should include the adhesion
to the ossicular structures, the facial recess, the sinus tympani, the promontory, and the area deep into the retrotympanum. In the pars accida, descriptions should include the
adhesion to the malleus.
For the external auditory canal’s status, descriptions
should include the presence of keratin accumulation at the
retraction pocket and granulations; any bone erosion in the
scutum and the posterosuperior quadrant; and the presence
of otorrhea.
Ossicular status includes the focal lysis of the incus, any
interruption of the incudostapedial joint, myringostapediopexy, and the lysis of the stapes.
Descriptions of the bottom of the retraction pocket should
include whether it is visible, any crusting, and the presence
of debris accumulation. If all the frontiers of the retraction
pocket can be seen, it is called a controllable retraction
pocket. This could be assessed by using an endoscope.
Descriptions of the neck of the retraction pocket should
include whether it stays large and wide enough and whether
it is capable of self-cleaning. A constricted neck results in
debris accumulation inside the pocket and runs the risk of
cholesteatoma formation [14].
In addition to their clinical uses, classication systems for
retractions are useful for research, where the behavior of
retractions can be studied. Also, any system must be validated and reproducible. All the currently used systems suffer
from a high degree of interobserver variability by an individual and between individuals [17, 21]. Grading a retraction
is considered a good protocol for the evaluation of its risk
factors, especially those for developing a cholesteatoma, and
helpful for making comparative assessments over time, once
the retraction has progressed. However, studies have lacked
a universally accepted or adopted staging system for retraction pockets. In addition, the functional decit has not been
included in any staging system [14], and none of these systems has a specic treatment method [1].
Retraction ofthePars Tensa
When the retraction compromises the pars tensa, it could be
seen as retraction pocket, atelectasis, or adhesive otitis
media. A retraction pocket is dened by a retraction of a
fragile portion of the tympanic membrane, such as the pars
tensa or the pars accida. Also, retraction pockets in both
portions can occur in the same ear. The collapse of the whole
membrane is called atelectasis. When the atelectatic membrane adheres to the middle ear oor, it is called adhesive
otitis media [14]. An instance of general retraction or atelectasis is not called a retraction pocket until specic sections
have been more retracted [1].
Retraction Pockets
A retraction pocket is a dynamic pathology with variable
outcomes, and it’s important to describe the stage of the
retraction. For pars tensa retractions, the Sadé classication
is the most popular [10], although others have been reported,
such as Charachon [22]. Dornhoffer’s staging is like the Sadé
classication except that stage 4 is assigned to retraction
pockets with invisible depths [1].
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