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18 Recurrent Otitis Media andHearing Loss inChildren
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Mastoiditis andHearing Loss inChildren
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19
AyşeKaraogullarindan, CemalCingi, andDilyanaVicheva
19.1 Introduction
Mastoiditis refers to inammation within the mastoid air cells of the temporal bone
[1]. Since the mastoid air cells are in communication with the middle ear cavity and
are adjacent to it, mastoiditis is present in nearly every case of acute otitis media,
both in children and adults, and in the majority of cases of chronic otitis media.
Typically, it is the middle ear-related symptoms that are most prominent, namely
pyrexia, otalgia and auditory impairment of conductive type, and mastoiditis is not
distinct from this clinical picture. In a number of cases, the infective process extends
beyond the mucosal lining of the middle ear cavity to affect the bone (osteitis) or
periosteum (periosteitis) of the mastoid region. The infection may directly invade
the bone by eroding cortical bone or spread haematogenously through the mastoid
emissary vein. Where this spread occurs, the diagnosis of acute (surgical) mastoiditis may be made. This condition is considered a complication of middle ear infection affecting the temporal bone [2].
Three categories of mastoiditis are recognised, namely acute, subacute and
chronic. Acute mastoiditis comprises two different conditions—incipient
A. Karaogullarindan (*)
Section of Otorhinolaryngology, Adana City Hospital, Adana, Türkiye
e-mail: draysekara01@gmail.com
C. Cingi
Department of Otorhinolaryngology, Faculty of Medicine, Eskişehir Osmangazi University,
Eskişehir, Türkiye
e-mail: cemal@ogu.edu.tr; ccingi@gmail.com
D. Vicheva
Department of Otorhinolaryngology, Medical University of Plovdiv, Plovdiv, Bulgaria
e-mail: vdilyana@gmail.com
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood
Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_19
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mastoiditis and coalescent mastoiditis. In the former, which may also be termed
‘acute mastoiditis with periosteitis’, pus collects in the spaces of the mastoid cells.
In the latter, also referred to as acute mastoid osteitis, the osseous septa, which
divide the air cells from each other, appear effaced. Abscesses may form in the
space and track into adjacent regions. In subacute mastoiditis, there is a longstanding infection affecting the middle ear and mastoid. Although the osseous
septa are destroyed by this process, the degree of inammation is low, and the
condition may also be referred to as masked mastoiditis [2]. Meanwhile, chronic
mastoiditis refers to a persistent purulent inammatory process of the mastoid
cells, with a duration from months to years. This condition is usually found in
association with chronic suppurative otitis media (CSOM) and is strongly linked to
cholesteatoma [2].
A. Karaogullarindan et al.
19.2 Definitions
Mastoiditis refers to purulent infective inammation of the mastoid air cells.
• Acute mastoiditis refers to purulent infective inammation of the mastoid air
cells, which lasts for a maximum of 1 month. These cases can be further classied depending on the pathological features [3, 4]:
• Incipient mastoiditis (i.e. with periosteitis) refers to a condition wherein there
is pus within the mastoid spaces but the osseous septa remain intact. If imagery
reveals the presence of uid within the mastoid cells, this nding lacks diagnostic specicity, as it may also be noted in paediatric cases of acute otitis media
(AOM) or otitis media with effusion (OME). To make the diagnosis, there must
be appropriate clinical signs, such as tenderness behind the ear and redness, and
the pinna should be swollen and protruded.
• Coalescent mastoiditis (synonymous with acute mastoid osteitis) features osse-
ous septal damage. Although appearances conrming the septa have been
destroyed do allow the diagnosis to be made, in the majority of paediatric cases,
imaging is not needed diagnostically. This condition may be complicated by
abscess formation, and purulent infection may track into nearby structures. The
most frequent site of abscess formation is subperiosteal [3].
• Subacute mastoiditis (sometimes termed ‘masked’) features destruction of the
osseous septa separating the mastoid cells but as a result of a long-standing
inammatory process of low intensity [5]. This condition is found either in children where OME persists or where there are repeated attacks of acute otitis
media without effective pharmacotherapeutic intervention.
• Chronic mastoiditis involves an infection that persists from months to years and
results in the formation of pus within the mastoid spaces.
Complicated mastoiditis is where the inammation within the mastoid is com-
plicated by further pathology within or outside the cranial cavity [3].
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251
19.3 Pathophysiological Mechanism
Acute mastoiditis usually develops as a complication of acute otitis media (AOM),
due to the contiguity of the middle ear cavity and mastoid spaces [6]. Thus, inammation that affects the mucosal lining of the middle ear can readily expand into the
mastoid. In most cases, resolution of mastoiditis occurs in conjunction with resolution of otitis media. If there is persistence of otitis media, pus builds up within the
mastoid [7].
The inammation and swelling of the antral mucosa mean that pathogenic infection cannot drain away from the mastoid and air cannot easily reach the space via
the middle ear cavity. Inammation may cause erosion of the antrum and allow the
infection to spread into several adjacent structures, which creates a high degree of
morbidity and may even endanger the patient’s life [2].
There are ve distinct stages to which mastoiditis may progress. The stages consist of the following [2]:
• Stage 1. The mucosal surfaces of the air spaces become hyperaemic.
• Stage 2. There is a transudated or exudated uid, which may be purulent, present
in the spaces.
• Stage 3. Osseous necrosis results from destruction of the septal blood supply.
• Stage 4. The walls of the mastoid cells break down and cavities develop lled
with abscesses.
• Stage 5. The inammation spreads to adjoining regions.
If an acute infective process within the mastoid cells persists, there may develop
osteitis in which the bone loses mass. This results in loss of the osseous trabecular
framework within the mastoid spaces and coalescence of the spaces. This is the
reason for the label ‘coalescent mastoiditis’.
In essence, coalescent mastoiditis is a collection of pus (empyema) within the
temporal bone. If the condition continues, drainage will either occur via the antrum,
in which case the empyema resolves, or a pathological drainage may occur, complicating mastoiditis. The latter refers to drainage to the mastoid surface, apex of the
petrous temporal bone or into the cranial cavity. When coalescent mastoiditis does
not resolve, there may be involvement of the adjacent structures, including those
within the temporal bone, such as the seventh cranial nerve, the labyrinthine complex or the venous sinuses [2].
19.4 Aetiology
19.4.1 Acute Mastoiditis
Since acute mastoiditis develops from acute otitis media, it is no surprise to nd that
the pathogens responsible are generally the same, namely Streptococcus pneu-
moniae, Haemophilus inuenzae and Streptococcal organisms in Group A, i.e.
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Streptococcus pyogenes [8]. These microbes are all capable of invasion and are
those most frequently identied in paediatric cases of acute mastoiditis.
The pneumococcal serotypes identied with the highest frequency in this condition are 19 (which accounts for above 50% of cases), followed by 23 and 3 [9]. As
rollout of the pneumoccal conjugated vaccine continues, this pattern may alter. It is
unusual to identify Pseudomonas aeruginosa, Gram-negative bacilli of aerobic type
or anaerobic bacteria, at least in acute cases. Recently, however, it has been reported
that acute mastoiditis secondary to Fusobacterium necrophorum is becoming more
common, with studies reporting its isolation in 8.5% of cases [10, 11]. If there is a
history of recurrent episodes of AOM with recent antimicrobial pharmacotherapy
and perforation of the eardrum, P. aeruginosa may be detected. Otherwise, it sel-
dom occurs. In rst-world countries, Mycobacterium tuberculosis seldom produces
inammation in the mastoid.
At the moment, many of the cases of acute mastoiditis secondary to S. pneu-
moniae are infected with multi-drug-resistant strains (MDRSP). Choice of pharmacotherapy needs to be guided by the following frequencies of drug-resistant
MDRSP: to penicillin (35–40%), to macrolides (30–35%) and to ceftriaxone (15%).
These frequencies may differ depending on the particular local prevalence [2].
A. Karaogullarindan et al.
19.4.2 Chronic Mastoiditis
Chronic mastoiditis typically develops from chronic suppurative otitis media and is
seldom caused by ineffective pharmacotherapy. In the majority of cases, the pathogens identied in chronic mastoiditis are the same as those responsible for chronic
suppurative otitis media. Thus, the likely pathogens are P. aeruginosa,
Enterobacteriaceae, Staphylococcus aureus (including methicillin-resistant strains)
and anaerobes [12]. In more than 50% of cases, there is more than one pathogen
isolated, typically an aerobe plus an anaerobe [2].
The most frequently identied anaerobes are Peptostreptococcus, Gram-negative
anaerobes with a bacillary morphology (such as pigment-bearing Prevotella,
Porphyromonas and Bacteroides spp.), as well as organisms from the Fusobacterium
genus [13, 14]. Recently published research highlights the growing prevalence of
mastoiditis secondary to Fusobacterium necrophorum within the preceding 20
years [15].
The ability to express a beta-lactamase is possessed by more than 50% of Gramnegative bacteria with a bacillary morphology, or members of the genus
Fusobacterium [16].
S. pneumoniae or H. inuenzae are seldom detected in cases of chronic mastoiditis. If P. aeruginosa is cultured, it may represent a contaminant introduced from the
ear canal at the time of sampling, as these bacteria are colonisers of the external
auditory meatus. A number of rarer pathogenic organisms are sometimes detected,
namely Blastomyces [17], M. tuberculosis, other Mycobacterial species not responsible for tuberculosis and Mycobacterium bovis [18, 19].
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19.5 Prognosis
Complete resolution of acute mastoiditis is the usual outcome provided there is no
involvement of the seventh cranial nerve or vestibule, nor extension into the cranial cavity.
In the majority of cases, there will be no cosmetic defect caused by surgery on
the affected ear provided the incision is carefully positioned and aps are created,
which apply posterior traction to the pinna when sutured into place.
Unless the ossicles are damaged, resolution of any conductive-type auditory
impairment may be anticipated. Hearing should be re-tested when ear discharge is
no longer present and the ear has recovered [11].
Mastoiditis of at least stage 3 is regarded as a complication of a middle ear infection. When mastoiditis extends beyond the mastoid to involve other structures, it is
considered complicated. There are several ways in which this can occur, for
example:
• The inammation extends into the sigmoid sinus, which then triggers thrombus
formation
• If the infection tracks into the occipital bone, osteomyelitis or a Citelli abscess
may develop
• The infection may extend superiorly, reaching the posterior cranial fossa, subdu-
ral cavity and the meningeal coverings of the brain
• If the infection tracks forward, it involves the root of the zygomatic bone
• In a lateral direction, an abscess may develop in the subperiosteum
• Where the infection extends inferiorly, a Bezold’s abscess may be formed
• Involvement of the petrous apex occurs if infection tracks medially
• The seventh cranial nerve and the labyrinth may be involved if the infection
tracks infratemporally
19.6 Diagnosis
19.6.1 History Taking andAuditory Impairment
Auditory impairment may be noted, as is the case with any condition affecting the
middle ear. There is no evidence from the history for recurrent middle ear infections
in above 80% of cases [2].
There may be specic signs indicating acute or chronic mastoiditis. Acute mastoiditis frequently causes pyrexia and is typically seen either during an episode of
acute otitis media or shortly thereafter. The clinical features vary depending on how
old the patient is and what stage acute mastoiditis has reached. Chronic mastoiditis
frequently results from incomplete antimicrobial pharmacotherapy for AOM and
may not come to the attention of a physician. An ear discharge that has been occurring for more than 3 weeks is strong evidence that a chronic infection has taken hold
in the mastoid.
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Pyrexia may be noted in 76% of cases [20], and the temperature is potentially
very elevated. Constant pyrexia is a potential feature of acute mastoiditis and probably originates from the middle ear inammation. Even where sufcient doses of
the correct antibiotic are being administered, pyrexia frequently does not stop in an
acute infection of the mastoid. If the pyrexia is spiking, there should be a suspicion
of thrombophlebitis in the signoid sinus.
Around two-thirds of patients (67%) complain of pain [20]. The pain is felt deep
within or posterior to the ear and usually becomes more intense in the evening. Pain
that does not remit is a clue to underlying mastoid involvement. However, assessing
this symptom may be problematic if the patient is very young. Patients may present
with systemic features, such as feeling lethargic or generally unwell, becoming irritable, not feeding properly or with diarrhoea [2].
A. Karaogullarindan et al.
19.6.2 Physical Examination
There are some signs indicative of acute mastoiditis, in particular [20]
• The ear drum may bulge and appear reddened.
• The ear drum perforates in 37% of cases, and ear discharge occurs in 50%.
• The skin overlying the mastoid is reddened, painful to touch and swollen.
• There is an area of uctuance behind the pinna.
• The pinna typically protrudes inferolaterally in patients under the age of 2years
and superolaterally in children over this age.
• The posterosuperior wall of the external auditory meatus sags in some 71% of
cases [20].
In cases of chronic mastoiditis, there may be features indicating the presence of
a complication, as where there is spread to adjacent structures, such as the periosteal
layer or an infratemporal structure, like the seventh cranial nerve. The following
appearances may be observed [2]:
• The eardrum may have normal appearances or appear inamed.
• There may be no external indications suggestive of mastoiditis.
When the neurological system is examined, there are generally no localising
signs. In cases that have become complicated, however, an abnormality in the cranial nerves may be noted. Potential ndings are as follows [2]:
• Sixth cranial nerve palsy
• Seventh cranial nerve palsy
• Pain in the distribution of the ophthalmic branch of the fth cranial nerve
In all cases of mastoid inammation (whether acute or chronic), the periosteum
may be coarsened, there may be abscess formation in the subperiosteum, a middle
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ear infection is present and the central portion of the eardrum may protrude forward
in such a way that it resembles a teat.
To note coarsening of the periosteum, the normal side should rst be compared.
The pinna may be protruded inferolaterally in children below the age of 2years or
superolaterally if the child is above that age. An abscess within the subperiosteum
pushes the pinna sideways and causes loss of the skin crease behind the ear. In cases
where a crease can still be seen, the abscess must be located laterally to the periosteal layer [2].
255
19.6.3 Tests
Any aspirate obtained from the interior of the mastoid at operation, or uid aspirated when performing myringotomy, requires laboratory investigation. The aspirate should be cultured aerobically and anaerobically, as well as for fungal pathogens
and Mycobacteria. Gram stain should be undertaken, as well as acid alcohol staining.
If there is an existing perforation of the eardrum, the external auditory meatus
should be cleaned and any uid freshly appearing aspirated for testing. The uid
sampled should originate in the middle ear cavity rather than the external auditory
meatus [2].
Venous blood should be sent for microbiological culture. A full blood count and
erythrocyte sedimentation rate should be obtained, which can assist in evaluating
how effectively antibiotics suppress the infection [2].
19.6.4 Computerised Tomography (CT)
It is routine practice to image the temporal bone using CT in cases of mastoiditis
[21]. Imaging in this modality possesses between 87 and 100% sensitivity to detect
mastoiditis. One danger is that CT may lead to overdiagnosis of mastoiditis, since
AOM invariably also affects the mastoid. If there are suspicions that the infection
has entered the cranial cavity or other complications have occurred, CT should be
undertaken without delay [2].
The imaging appearances that support a diagnosis of mastoiditis are blurring or
obliteration of the edges of the mastoid cavity and cortex, accompanied by blunting
or loss of the outline of the septa which usually separate the mastoid air cells, that
is, coalescent mastoiditis. If the air cells have a cloudy appearance, a bone scan
using technetium-99 can clarify whether destruction of bone is occurring. Both the
middle ear cavity and the mastoid frequently have a clouded appearance in the initial stages of an infection, and it is common to note cloudiness of the mastoid cells
in cases where AOM is the only diagnosis. Thus, a bone scan helps achieve diagnostic clarity [2].
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A. Karaogullarindan et al.
19.6.5 Magnetic Resonance Imaging (MRI)
The main use for MRI in cases of mastoiditis is where there is a clinical or radiological suspicion of extension of infection into the cranial cavity. Generally, however, MRI is not the preferred modality for imaging the mastoid.
MRI is, however, the most usual investigation to assess lesions where there are
contiguous soft tissue elements, especially within the cranial cavity. It can identify
build-up of uid outside the brain parenchyma and give warning of vascular complications. Furthermore, MRI is benecial when planning operative interventions [2].
19.7 Treatment
19.7.1 Tympanocentesis andMyringotomy
Prior to commencing antimicrobial pharmacotherapy, tympanocentesis and myringotomy may be undertaken. It is essential that microbiological culture of any aspirate
from the middle ear cavity be performed before prescribing. The most guaranteed
way to obtain the middle ear uid is by means of an operating microscope and suction traps, which have been developed with this purpose in mind. However, the procedure may also be undertaken using an otoscope, spinal needle and syringe [2].
19.7.1.1 Acute Mastoiditis
Medical treatment options in mastoiditis include antibiotics administered by the
intravenous route. The agent chosen depends on the results of laboratory testing of
any uid obtained from the middle ear cavity at operation. The principal purpose of
myringotomy and tympanocentesis is to procure a sample for microbiological analysis and to provide symptomatic relief in patients with AOM.The holes created
typically seal themselves in the space of days. Once a sample has been obtained,
whether through tympanocentesis or whilst grommets are being inserted +/− mastoidectomy, treatment may be initiated and adjusted if needed following the results
of microbiological analysis. If pyrexia ceases and there is a reduction in oedema
within 2–3days, antimicrobial treatment may be administered by mouth, as guided
by the results of laboratory testing [2].
Agents employed in the treatment of acute mastoiditis include vancomycin in
combination with one of ceftriaxone or cefepime (which possesses anti- pseudomonal
activity), or a penicillin and beta-lactamase inhibitor in combination (e.g. ampicillinsulbactam, piperacillin-tazobactam) or a carbapenem. Aztreonam in combination
with vancomycin may be employed in cases where the patient may react with anaphylaxis to the use of a beta-lactam agent [2].
In all cases of mastoiditis, antibiotics must be administered intravenously.
Nonetheless, antibiotic treatment is generally inadequate as monotherapy, especially as the condition develops, since there may be problems delivering pharmaceutical agents at the necessary concentration within the osseous tissues [22].
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