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Silent Otitis Media andSubtle
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Complications
Rafaelda CostaMonsanto andMichaelM.Paparella
32
Introduction
Otitis media (OM) is a ubiquitous health problem in the
United States that is associated with signicant morbidity
[1]. OM is increasingly impacting upon public health: it is
the primary reason for visits to the Emergency Room, the
second ranking reason for visits to a physician’s ofce, the
number one reason for antibiotic prescriptions in childhood
(accounting for greater than 40% of all outpatient use of oral
antibiotics), the primary reason for hearing loss in children
and the third leading cause of hearing impairment in people
of all ages, the primary reason for the use of general anesthesia in the pediatric population (for the purpose of inserting
tympanostomy tubes) and is a signicant cause of vestibular
impairment [2–6]. The direct and indirect cost of medical,
surgical, and rehabilitation management of OM is approximately 5 billion dollars in the United States alone [6, 7]. The
chronic form of otitis media (COM) has an extremely high
disease burden: it results in over 3 million disability-adjusted
life years lost and results in 28,000 deaths yearly, mostly
associated with intracranial complications [8, 9]. Over 60%
of patients with COM have signicant hearing impairment,
accounting for a prevalence of up to 200 million people
worldwide [1, 10]. More recently, a systematic review demonstrated that COM associates with a 40–60% prevalence of
vestibular impairment, resulting in delayed acquisition of
developmental milestones, abnormalities in several vestibular function tests, and increased risk of falls as compared
with controls [11, 12].
Throughout the decades, many authors have described
that chronic otitis media required the presence of a perforation of the tympanic membrane in association with persistent
middle ear inammation and otorrhea [13]. However, in a
groundbreaking study published in 1979, Paparella etal. [5]
introduced the concept of silent otitis media, demonstrating
that even patients with an intact tympanic membrane could
present “undetected or undetectable” clinically intractable
chronic tissue (Fig.32.1). Such hypothesis was later consistently corroborated by human temporal bone and clinical
studies demonstrating similar ndings [5, 14, 15]. As the
diagnosis of this condition may be delayed because of the
mild symptomatology and absence of a tympanic membrane
perforation, the disease can progress through signicant time
periods without adequate diagnosis or treatment, which—in
turn—could result in severe complications and sequelae.
Numerous studies have described the presence of intractable tissue pathology behind an intact eardrum. Meyerhoff
et al. [3] studied 123 temporal bones with chronic otitis
media. Only 24 of these patients (36 ears) had symptoms of
otological disease recorded on their charts, and—of these—
only 19.5% had an associated tympanic membrane perforation. In another study [16], 144 temporal bones with chronic
R. da CostaMonsanto (*) · M. M. Paparella
Department of Otolaryngology, Head and Neck Surgery,
University of Minnesota, Minneapolis, MN, USA
e-mail: rdacosta@umn.edu
© 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_32
Fig. 32.1 A representative human temporal bone horizontal section
showing signs of silent otitis media: the tympanic membrane is intact,
although a retraction pocket is seen in the posterior aspect of the drum.
In the middle ear, mucoid-purulent effusion permeated by brosis is
seen
279
280
Resolution
CO
Sequelae
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R. da CostaMonsanto and M. M. Paparella
otitis media were divided into two groups: 28 with perforated and 116 with nonperforated tympanic membranes. The
authors observed that the prevalence of granulation tissue,
ossicular erosion, middle ear effusion, cholesterol granuloma, and tympanosclerosis were not signicantly different
between ears with and without tympanic membrane
perforation.
Silent otitis media is a common nding in children.
Paparella etal. [5] studied 111 infant ears; 54 of these showed
histological evidence of otitis media. Of these, 20 cases presented with clinical manifestations, while 34 did not and
were identied as silent otitis media. Mehta [17] examined
60 temporal bones of stillborns and neonates who died of
causes other than septicemia for evidence of otitis media. He
found 23.3% had silent otitis media.
Pathophysiological Mechanisms: The“Otitis
Media Continuum”
Paparella etal. [18], in 1970, were the rst authors to hypothesize and demonstrate that otitis media occurs in a continuum of mucoperiosteal changes that nally result in chronic
inammatory disease and clinically intractable tissue
changes in the middle ear cleft (such as brosis, bony erosion, cholesterol granuloma, and cholesteatoma) (Fig.32.2).
In their study, the authors demonstrated progressive tissue
changes that followed obstruction of the eustachian tubes of
squirrel monkeys. These patterns have been also observed in
clinical studies over the years. Collectively, the data suggest
that the “acute” forms of otitis media (such as purulent,
serous, and mucoid otitis media), when unresolved, may
progress over time to more advanced degrees of pathological
middle and inner ear changes [19]. As the disease advances
OME
SOM
POM
MOM
M
Fig. 32.2 Continuum of otitis media and interaction of its various
forms. OME otitis media with effusion, POM purulent otitis media,
SOM serous otitis media, MOM mucoid otitis media, COM chronic otitis media, OM otitis media
to the chronic, end stages of the continuum, the risks of inner
ear sequelae also increase, resulting in sensorineural hearing
loss and peripheral vestibular impairment [20]. The continuum of otitis media pathologic tissue changes was consistently seen in the otitis media temporal bone collection at the
University of Minnesota, even in specimens with an intact
tympanic membrane. Meyerhoff etal. [14] reproduced the
series of events leading to silent otitis media in animals:
using 38 chinchillas who received intratympanic bacterial
inoculation, the authors later found the presence of effusion,
mucosal edema, granulation tissue, hyperemia of the subepithelial space, hemorrhage in the middle ear space, and abundant polymorphonuclear leukocytes in the middle ear cleft
despite the presence of a normal or subnormal tympanic
membrane.
Paparella etal. [4] performed a longitudinal morphometric study of the middle ears of cats with otitis media in different time points (ranging from 1 week to 6 months). The
authors showed the series of events following obstruction of
the eustachian tube: at 1 week, a thin effusion could be
observed in the middle ear cleft, possibly resulting from the
negative middle ear pressure causing vascular transudate
[21]. In the following weeks, a distinct metaplasia of the
middle ear mucosal lining could be seen: the epithelium
became cuboid, with enlargement of the blood vessels; also,
goblet cells (who are not seen in a healthy middle ear
mucosa) were seen in the epithelium. The middle ear effusion became increasingly thicker, being intensely stained by
hematoxylin and eosin possibly due to a high protein content
secondary to active secretion of the goblet cells. There is also
an increasing concentration of inammatory cells in the middle ear, polymorphonuclear leukocytes being the most frequent cell type. Months after the eustachian tube blockage,
progressive development of intractable tissue changes
occurred, including granulation tissue and brosis. These
series of events, which are highly consistent with the concept
of “otitis media continuum,” were also demonstrated by following studies. Yoon etal. [22] observed a signicant trend
toward the development of these clinically intractable tissue
changes in the later stages of the continuum (mucoid and
chronic otitis media), further corroborating that time and the
severity of the middle ear inammation are pivotal factors in
the development of these changes.
Although the pathophysiological mechanism resulting in
otitis media and its subtypes are multifactorial, it has been
demonstrated that obstruction of the middle ear ventilation in
isolation can both initiate and perpetuate the cellular abnormalities that result in otitis media. This obstruction to the
ventilation pathways may occur in different locations of the
temporal bone, including the bony and cartilaginous eustachian tube, protympanum, mesotympanum, isthmus, attic,
aditus ad antrum, and/or isolated groups of mastoid air cells
[15]. In a study that included a total of 229 temporal bones
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281
with otitis media, obstruction of the epitympanum and mastoid antrum by pathological tissue (granulation tissue, residual mesenchyme, cholesterol granuloma, or cholesteatoma)
was seen in 44 (19.2%) [23]. Palva and Johnsson [24] also
demonstrated the patterns of ventilation within the mesotym-
panum and epitympanum, showing that the presence of brosis and granulation tissue secondary to otitis media can result
in selective dysventilation. The decreased ventilation to specic parts of the middle ear can also result in the continuum
of changes described by Paparella and colleagues [3].
Monsanto et al. [25] showed that the volume of the
epitympanum and the area of the posterior tympanic isthmus
are signicantly decreased in human temporal bones with
chronic otitis media. The authors hypothesized that the ventilation blockage caused by the tissue changes can result in
negative pressure and hypodevelopment of the epitympanum
and mastoid, being one potential pathophysiological mechanism involved with retraction pockets and cholesteatoma formation. Similar ndings were later described in computed
tomography studies [26].
In children, questions have been raised regarding the role
residual mesenchyme in the pathogenesis of otitis media.
Guggenheim etal. [27] commented on whether the residual
mesenchyme would provide a predisposition toward or if it
would act as a protective immunologic mechanism against
development of otitis media. Kasemsuwan etal. [28] evaluated the temporal bone specimens of children who were
younger than 5years old and observed that the peak incidence of unresolved mesenchyme occurred between the ages
of 4 months and 1 year. Furthermore, they observed that
bones who had residual mesenchymal had a much higher
prevalence of histological signs of otitis media. Considering
the high association between mesenchyme and otitis media,
as well as the observation that the highest prevalence of mesenchymal tissue was within the ages of peak incidence of
otitis media, the authors argued that the presence of mesenchymal tissue in the middle ear would most likely contribute
with the development of otitis media.
Subtle Complications ofOtitis Media
The clinical symptoms of silent otitis media are frequently
mild, and some patients may present only with intermittent
aural fullness or tinnitus. As the disease might progress over
signicant periods of time (even decades) without adequate
diagnosis or treatment, the risks of silent otitis media resulting in acute complications or sequelae might be even higher
than in normal cases of acute or chronic otitis media presenting with tympanic membrane perforation [29]. Among the
most frequent subtle complications are sensorineural hearing
loss, labyrinthitis, vestibular impairment, and endolymphatic
hydrops [5, 20, 30]. Although the exact pathophysiological
mechanisms leading to these inner ear changes are still
unknown, they most likely result from the passage of inammatory mediators and bacterial products to the middle ear
through the semipermeable round window membrane [31,
32]. This hypothesis was raised following observations that
proteins, toxins, pharmaceutical substances, and even whole
bacteria can penetrate the round window membrane during
episodes of otitis media [33].
Endolymphatic Hydrops
Endolymphatic hydrops is a histopathological nding that
has been associated as a causative mechanism of Meniere’s
disease. Paparella etal. were the rst authors to describe a
potential association between otitis media and secondary
endolymphatic hydrops [34]. In their studies, the authors
described the presence of signicant cochlear hydrops in 20
temporal bones with chronic otitis media. The authors also
hypothesized that the presence of an intact tympanic membrane would favor the development of inner ear sequelae,
including endolymphatic hydrops, as the inammatory
mediators would be concentrated in the hypoventilated middle ear environment. However, studies dedicated to evaluating the pathophysiological mechanisms involved with the
development of endolymphatic hydrops secondary to otitis
media are very scarce in the literature.
Labyrinthitis
Although labyrinthitis can occur through meningogenic,
hematogenic, or tympanogenic origins, otitis media has been
described as one of the most frequent causative agents [29,
30]. The association between otitis media, labyrinthitis, and
meningitis has been receiving a renewed interest after a
study revealed an unexpected positive relationship between
abnormal tympanometry and mortality rates in children with
nontraumatic coma [35].
Three different types of labyrinthitis have been described:
serous, suppurative, and ossicans. Serous labyrinthitis
refers to the presence of “serous,” proteinic material in the
labyrinth, with brous or granular precipitate in the inner ear
in the absence of bacteria, viruses, or inammatory cells
[30]. The serous labyrinthitis is most likely secondary to a
change in the concentration of protein in the endolymphatic
and perilymphatic uids due to an inammatory process.
Kaya et al. [30] showed in a human temporal bone study
involving patients with silent otitis media that serous labyrinthitis resulted in signicant loss of outer hair cells in the
basal and middle cochlear turns and increased degrees of
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cochlear hydrops. However, authors showed that serous labyrinthitis did not result in loss of cochlear inner hair cells,
spiral ligament brocytes, and spiral ganglion neurons.
Suppurative labyrinthitis, on the other hand, refers to the
presence of an active bacterial infection of the inner ear,
resulting in conspicuous inner ear changes [36]. Studies
from the otopathology laboratory at the University of
Minnesota recently showed some of these cochlear changes
secondary to suppurative labyrinthitis [36]. In their studies,
the authors found not only loss of outer hair cells but also
signicant damage to the inner and outer hair cells, spiral
ganglion cells, stria vascularis, and signs of severe endolymphatic hydrops in bones with suppurative labyrinthitis.
Labyrinthitis ossicans refers to the process of deposition
of new bone in the cochlea following suppurative labyrinthitis
or meningitis. Labyrinthitis ossicans is a critical problem that
may affect patients with inner ear complications of otitis
media, as it frequently results in complete deafness and could
result in impossibility to perform a cochlear implant.
Therefore, patients with labyrinthitis and meningitis must be
carefully evaluated for the presence of progressive hearing
loss, as delays in the diagnosis might result in irreversible
deafness. The group at the University of Minnesota studied
temporal bone specimens with labyrinthitis ossicans
(Fig. 32.3), demonstrating signicant abnormalities of the
cochlear architecture, with critical damages to all cellular and
neural structures of the cochlea and signs of severe endolymphatic hydrops [37]. Paparella etal. [38] reported that silent
otitis media can also result in tympanogenic labyrinthitis and
complete cochlear deafness. The authors also hypothesized
that the absence of a tympanic membrane perforation can
increase the chances of inner ear complications secondary to
otitis media, as the infection is conned to a cavity with minimum or no drainage. Kaya etal. [39] also evaluated the sensorial epithelium of the peripheral vestibular system secondary
to labyrinthitis: while all three types of labyrinthitis showed
losses of vestibular hair cells (Fig.32.4), loss of transitional
and dark cells were seen only in the suppurative and ossicans
group. The authors nally argue that labyrinthitis secondary to
otitis media can signicantly affect vestibular function.
Sensorineural Hearing Loss
In 1972, Paparella etal. [38] were the rst authors to demonstrate a concrete association between chronic otitis media
and sensorineural hearing loss. The authors studied 279
cases of chronic otitis media and revealed that the otopathologic ndings (loss of cochlear hair cells in the basal turn of
the cochlea) were tonotopically consistent with the highfrequency hearing loss seen in most patients with the disease
[38, 40]. Furthermore, they hypothesized that the round window membrane was the portal of entry from the middle to
inner ear, which was later corroborated by experimental
studies (Fig. 32.5) [41–43]. The passage of inammatory
mediators and bacterial toxins through the round window
membrane results in serobrinous precipitates and inammatory cells in the perilymph of the scala tympani of the
basal turn [40]. In a study of sensorineural hearing loss in
chronic otitis media involving six centers from ve countries, all centers showed signicant levels of sensorineural
hearing losses in patients with chronic otitis media. Through
the following decades, studies continued to support these
early observations [44, 45]. More recently, clinical studies
showed that even a single episode of uncomplicated acute
otitis media can result in permanent sensorineural hearing
loss affecting the extended high frequencies, as demonstrated
in long follow-up studies [46, 47].
Vestibular Impairment
Fig. 32.3 A representative human temporal bone from a donor with
signs of chronic otitis media behind an intact tympanic membrane. The
cochlea is seen at the midmodiolar level, showing intense brosis and
cochlear ossication within the cochlear turns
The association between otitis media and vestibular symptoms has been a matter of great controversy [12]. Frequently,
the presence of vestibular symptoms in patients with otitis
media are immediately associated with a perilymphatic stula or other causes of dizziness, such as metabolic diseases
or benign paroxysmal vertigo [12]. Nonetheless, growing
evidence indicate that otitis media, most frequently chronic
and silent otitis media, can cause vestibular impairment even
in the absence of perilymphatic stula: studies revealed that
the prevalence of vestibular symptoms in patients with COM
ranged from 40% to 60%, and these symptoms frequently
associate with abnormal results in vestibular function tests
(caloric tests, cervical vestibular evoked myogenic potential
(cVEMPs), and rotatory chair) [12].
The rst author to evaluate potential causes for vertigo
and vestibular symptoms in patients with silent otitis media
ab
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Fig. 32.4 (a) A representative human temporal bone specimen show-
ing signs of serous labyrinthitis in the vestibule. (b) Squared area of the
sensorial epithelium of the saccule from the top image seen under a
higher magnication. The sensorial epithelium shows cellular disorganization, with areas of loss of vestibular hair cells (*)
the presence of saccular edema and an abnormal neuroepithelium, while no signicant abnormalities were seen in the
utricle and semicircular canals. Monsanto etal. [52], in 2016,
were the rst authors to reveal a signicant loss of vestibular
hair cells type I and II in the saccular and utricular macula
(more intense) and loss of type I cells in the anterior and
posterior semicircular canals (less intense). Also, the authors
found a signicant loss of dark cells in the COM group as
compared with controls. A later follow-up study from the
same authors revealed that the cochlear changes secondary
to otitis media initiated at an earlier stage and seemed to be
more severe as compared with the vestibular losses [20].
Clinical studies showed similar ndings: a systematic review
demonstrated that over 30% of patients with different types
of otitis media experience some sort of symptom attributable
to vestibular dysfunction [12]. In children with otitis media
Fig. 32.5 A human temporal bone specimen with purulent otitis
media, sectioned horizontally at the level of the round window membrane. Several inammatory cells are seen in the round window niche
(*), with an adjacent inammatory inltrate in the basal turn of the
cochlea
with effusion and chronic silent otitis media, children were
described as “clumsy” and had a higher tendency to fall as
compared with children who did not have otitis media [53].
Additionally, a 30-year cohort has demonstrated that the
prevalence of self-reported dizziness in adulthood was signicantly higher among people who had a history of otitis
was Paparella etal. [34] In their observations, the authors
noted that some patients with otitis media have uctuating
sensorineural hearing loss, tinnitus, and episodic dizziness or
media in the past as compared with people who did not,
showing that otitis media do lead to permanent (although
potentially subclinical) peripheral vestibular damage [54].
vertigo, which were consistent with symptoms caused by
endolymphatic hydrops. Based on these observations, the
authors performed an otopathologic study in 194 temporal
bones specimens with otitis media, revealing a 40% preva-
Severe Complications
lence of endolymphatic hydrops. Later, clinical studies
showed that some patients with chronic otitis media tend to
develop Meniere’s disease over time [48–50].
Histopathological examinations of the vestibular structures in bones with otitis media are very scarce. Kodama
etal., in 1988 [51], demonstrated eosinophilic deposits in the
endolymphatic and perilymphatic compartments, being
more concentrated in the saccule. The authors also showed
Although in most cases silent otitis media result in subtle
changes and mild symptoms, they might also result in severe
complications. In this regard, meningitis is considered the
most typical intracranial complication of otitis media [9, 29,
55, 56]. Although several otolaryngological societies dedi-
cated to proposing diagnostic guidelines and the widespread
use of antibiotics, intracranial complications of otitis media
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R. da CostaMonsanto and M. M. Paparella
are still very common, especially in underdeveloped countries [9]. Among the reasons for the high incidence of otogenic meningitis, we can highlight the fact that in children,
the symptomatology of acute and chronic otitis media can be
highly unspecic [57]. Moreover, Pichichero et al. [58]
revealed that the diagnostic accuracy of pediatricians and
general practitioners for detecting otitis media was lower
than 50%. Therefore, it seems that many cases of meningitis
in children could be prevented if an adequate diagnosis and
treatment of otitis media was made [35].
Djeric et al. [59] evaluated 16 temporal bones from 8
children who died of otogenic meningitis. The authors found
signs of chronic inammation of the round window membrane, with inammatory cell inltration within the membrane and the adjacent scala tympani. All cases had
suppurative labyrinthitis, with a signicant number of bacteria and inammatory cells in all cochlear turns and the
vestibule. Most interestingly, the tympanic membrane was
intact in all 16 specimens. Yildirim-Baylan etal. [56] also
found an 82% prevalence of bacteria embedded within a
brous matrix in the middle ear of infants with tympanogenic meningitis who had silent otitis media. The authors
also comment that clinicians must be aware that an intact
tympanic membrane does not necessarily preclude the presence of pathologic changes in the middle ear cleft that could
result in severe intracranial complications. The authors discussed on potential pathways for the spread of these bacteria
to the central nervous system, of which the most likely
would be through the round window membrane. In this
regard, Schachern etal. [60] revealed ndings that corroborate this hypothesis: in an animal study, they compared
chinchillas with and without grafted round window membranes that were inoculated with Streptococcus pneumoniae.
The authors demonstrated that none of the animals who
received round window membrane grafts had signs of active
labyrinthitis. Non-grafted animals, however, frequently
showed bacteria in the cerebrospinal uid, suggesting meningitis of tympanogenic origin. Thus, the authors further
corroborate the round window membrane as the most likely
route for spread of infection from the middle to the inner ear
and central nervous system.
Treatment ofSilent Otitis Media
Considering the risks of hearing loss, vestibular impairment,
and intratemporal and intracranial complications, patients
with a suspected silent otitis media must be adequately followed and diagnosed for optimal prevention and treatment
strategies [56]. In children at the initial stages of the otitis
media continuum, patients can be adequately treated by tympanostomy tubes [5]. In patients with a suspected chronic
silent otitis media with the presence of intractable tissue in
the middle ear, surgical treatment is recommended [61].
Prof. Michael Paparella has proposed the use of the “exible
approach” to treat chronic silent otitis media [62]. Although
the surgical procedure will be discussed in detail in a different chapter, this approach proposes an endaural approach
aimed to perform an exploratory tympanotomy, removal of
tissue pathology, opening of the ventilation spaces in the
middle ear and mastoid, and treatment of ossicular pathology
as necessary. The exible approach has been extensively
used by many surgeons in the past four decade, with excellent hearing and functional results [15].
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Complications ofOtitis Media Limited
https://t.me/medicina_free
toWithin theTemporal Bone
DianeBiju, AishanPatil, ShailaSidam, AditiGovil,
KanchanGupta, VishalTyagi, Rosemariede Souza,
andChrisde Souza
33
Intratemporal Bone Complications
Complications are different from sequelae. Sequalae are limited to the mucoperiosteum, while complications extend
beyond it. An example of a sequelae is tympanosclerosis. An
example of a complication is a perforation of the tympanic
membrane or a brain abscess. Acute otitis media can exist
behind an intact tympanic membrane. The inammation may
involve the entire middle ear cleft or rarely the middle ear
cavity alone. In the era that was before the widespread availability and use of antibiotics, infections of the middle ear
cavity rapidly spread to involve the entre middle ear cleft and
thus were able to cause complications. Chronic otitis media
presents in two forms: (a) cholesteatoma and (b) perforations
D. Biju
Holy Spirit Hospital, Mumbai, India
A. Patil
Vascular Surgery, Borders General Hospital,
Melrose, Scotland, UK
S. Sidam
All India Institute of Medical Sciences,
Bhopal, Madhya Pradesh, India
A. Govil
Lilavati Hospital and Research Centre, Mumbai, India
BJ Medical College, Ahmedabad, India
K. Gupta
Lilavati Hospital and Research Centre, Mumbai, India
V. Tyagi
Holy Family Hospital, Holy Spirit Hospital, Mumbai, India
Department of ENT, VN Desai Hospital, Mumbai, India
R. de Souza
Internal Medicine, BYL Nair Hospital and TNM College,
Mumbai, India
C. de Souza (*)
Faculty SUNY, Brooklyn, NY, USA
LSUHSC, Shreveport, LA, USA
Lilavati Hospital, Holy Family Hospital, Holy Spirit Hospital,
Mumbai, India
of the tympanic membrane. In the era of the understanding of
otologic diseases, the surgical management of cholesteatomas was evolving. While cholesteatomas themselves are not
infectious, they harbor infections which allowed infections
to spread through the channels created by cholesteatomas.
Chronic otitis media also presented in the form of perforations. These perforations rarely healed and allowed egress of
infection into the middle ear cavity and middle ear cleft
through frequent attacks of otitis media. In general, it was
chronic otitis media (with cholesteatoma or with perforations) that was primarily associated with complications.
Acute otitis media could and did cause complications, especially if the infection was a particularly virulent one.
Tympanic Membrane Perforation
Tympanic membrane perforations of the tympanic membrane are the single most common complication of otitis
media. Perforations develop in the presence of either acute or
chronic ear disease. The pathogenic pathway that causes perforations are excessive pressure on the TM, resulting either
from pressurized purulent matter in the middle ear or from
long-standing eustachian tube dysfunction which in turn
causes atelectasis. The resulting perforation usually occurs
in the pars tensa and can vary considerably in size.
Most perforations heal spontaneously. There are a few
patients who present with chronic perforation. A patient with
a chronic perforation classically presents with a conductive
hearing loss. Hearing loss will depend on the type and location of the perforation and the status of the ossicular chain.
Diagnosis of a perforation can be conrmed by direct visualization with otomicroscopy or otoendoscopy. The treatment
of perforations is through surgery. The results of tympanoplasty for chronic TM perforations are excellent.
© 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_33
287
288
https://t.me/medicina_free
D. Biju et al.
Acute Mastoiditis
Mastoiditis is the acute inammation of mastoid air cells
which are epithelium-lined bone septations that are continuous with the middle ear cavity.
Coalescent Mastoiditis [1–3]
Coalescent mastoiditis with presence of a subperiosteal
abscess occurs when the air cells in the mastoid that are separated from each other by multiple septa break down and form
a single pus-lled cavity. This in turn causes the infection to
spread to the periosteum resulting in a subperiosteal abscess.
Although this much dreaded complication has declined considerably, the mortality of mastoiditis sequela in children
remains 10% [4].
Acute mastoditis is a clinical diagnosis. The pathognomonic triad of symptoms of acute mastoiditis are (1) severe
unrelenting otalgia, (2) postauricular swelling indictive of a
subperiosteal abscess, and (3) fever. Otorrhea and hearing
loss are also present. The most common presenting sign,
postauricular tenderness, is seen in a majority of cases. In
addition, protrusion of the pinna and postauricular erythema
and swelling are classic ndings. On otoscopy, bulging of the
posterosuperior wall of the external auditory canal and a
bulging erythematous tympanic membrane can be seen.
Induration over the mastoid is often a sign of an impending sub-periosteal abscess.
Temporal bone computed tomographic (CT) scanning is
the imaging modality of choice, and a loss of bony trabeculae in a single inamed pus lled cavity is the commonest
nding (Fig.33.1). CT scans of the temporal bone can also
pick up other conditions like Bezold’s abscess and venous
thrombosis.
The natural progression of acute otitis media to coalescent mastoiditis follows a well-described sequence of stages
[5].
Stage 1. At rst, there is hyperemia and edema of the muco-
periosteal lining of the pneumatized mastoid air cells.
This results in obstruction of the narrow aditus which in
turn disrupts aeration (ventilation and drainage).
Stage 2. The thickened mucous membrane and impaired cili-
ary function prevent drainage of secretions of the middle
ear through the eustachian tube. The exudates in the early
stages of the infection are serous.
Stage 3. They become purulent once inammatory cells
invade. These series of events result in venous stasis, local
acidosis, and dissolution of calcium from the bony septae.
Osteoclastic activity in the inamed periosteum softens
and dissolves the bony partitions, causing the small air
cells to coalesce into larger cavity that results in.
Stage 4. Coalescent mastoiditis
Histological examination shows that areas of coalescent bone erosion are combined with adjacent areas of
bone deposition. The healing processes cause the normal
mucoperiosteum to be replaced with maturing granulation tissue. Osteitis occurs in the areas of bone destruction
which results in the production of dense, compact bone
resulting in a sclerotic contracted mastoid bone.
Masked Mastoiditis
Acute mastoiditis has frequently been reported in patients
with a well-aerated tympanic cavity and normal appearing
tympanic membrane and present with minimal symptoms.
This has been termed masked mastoiditis and is attributed to
Fig. 33.1 CT scan demonstrating coalescent mastoiditis (white arrow).
This can be easily compared to the opposite mastoid which is clearly
uninvolved. a CT scan coronal view of the temporal bone. b CT scan
ba
coronal sections of the te with coalescent mastoiditismporal bone.
white arrow points towards the affected side
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