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Mastoiditis

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 About the Authors
Tal Marom
Dr Tal Marom obtained his medical degree at the Hebrew University in
Jerusalem, Israel. He did his residency training in Otolaryngology-Head
and Neck Surgery at the Edith Wolfson Medical Center (Holon, Israel),
affiliated to the Tel Aviv University Sackler School of Medicine. His research
fellowship in otitis media was conducted at the University of Texas Medical
Branch (Galveston, TX, USA). He currently works as a Clinical Lecturer at
the Department of Otolaryngology-Head and Neck Surgery, Assaf Harofe
Medical Center (Zrifin, Israel). His research interests include infections of
the head and neck, tumors of the aerodigestive tract and public health.

Johanna Nokso-Koivisto
Johanna Nokso-Koivisto obtained her medical degree at the University of
Helsinki, Finland. She did her residency training in Otorhinolaryngology
at Helsinki University Central Hospital (Helsinki, Finland) where she is
currently working as a specialist in Pediatric Otorhinolaryngology. She
obtained her PhD degree at University of Helsinki, Finland and conducted
research fellowship at the University of Texas Medical Branch (USA). Her
primary research interests include clinical virology and respiratory tract
infections, especially in children.

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 Chapter 6
Mastoiditis

Epidemiology 92
Tal Marom &
Microbiology 92 Johanna Nokso-Koivisto
Pathogenesis 93 Acute mastoiditis is a common complication of acute otitis
Clinical manifestations 94 media (AOM). During AOM, the infection may spread from
Diagnosis 95 the middle ear into the mastoid cavity, causing suppura-
Treatment 99 tive infection of the mastoid air cells, leading to bony ero-
sion and coalescence. It is more common in children, espe-
Prevention 101
cially in the age group of 1–4 years. Clinically, the patient
has a recent or current AOM, with redness, swelling and
tenderness in the retro-auricular area, and protruded or
displaced auricle. Diagnosis is made based on clinical signs
and symptoms. Computed tomography (CT) or magnetic
resonance imaging (MRI) are considered to confirm the
diagnosis in uncertain cases or whenever surgery is con-
sidered. First-line treatment of acute, uncomplicated mas-
toiditis includes drainage by myringotomy, with or without
ventilating tube insertion and antimicrobial therapy that
covers Streptococcus pneumoniae and Streptococcus pyo-
genes. In complicated or unresponsive cases, mastoidec-
tomy is warranted to drain the tympanomastoid cavity.
This chapter concentrates on acute mastoiditis; chronic
mastoiditis is not discussed since the pathophysiology,
treatment and prevention are different from the acute
form.

doi:10.2217/fmeb2013.13.295


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Marom & Nokso-Koivisto

Epidemiology
Mastoiditis used to be a common suppurative complication of AOM in the
past; however, its prevalence has dramatically declined after the widespread
use of antimicrobial therapy. Over the past decades, several publications
reported confounding results regarding the trend of acute mastoiditis
incidence in children. However, these observations were not based on
population-based studies [1]. Several large studies have shown that there
have been no significant changes in the incidence of acute mastoiditis during
the past decades [2–4]; the incidence of acute mastoiditis is reported to be
1.2–6.3/100,000 children per year.
The age clearly affects the incidence; the peak age of acute mastoiditis is in
children 1 to 4 years of age [1,4–6]. Among children less than 2 years of age,
the incidence of acute mastoiditis has been reported to be 13–15/100,000
children per year, with a peak incidence as high as 35/100,000 children in
the second year of life [2,6]. In contrast, in children aged 2–16 years, the
incidence of acute mastoiditis is much lower, 1.1–1.4/100,000 children per
year [6]. Up to a third of patients with acute mastoiditis may have a history of
recurrent AOM, but in general, affected children are otherwise healthy [5,6].
A Swedish study showed that changes in national AOM guidelines advocat-
ing ‘watchful waiting’ as an option in children with AOM did not increase
the incidence of acute mastoiditis, although a significant decrease in antibi-
otic prescriptions for otitis media were reported [6]. The widespread use
of 7-valent pneumococcal conjugate vaccine (PCV-7) did not decrease the
incidence of acute mastoiditis in the US [5]. Interestingly, a recent analysis
of an insurance claims database of a large, nationwide managed healthcare
plan from the US showed that while there were no significant changes in
acute mastoiditis rates in the years 2001–2008, mastoiditis rates signifi-
cantly decreased during 2009–2011, and especially after the nationwide
introduction of the 13-valent pneumococcal conjugated vaccine in 2010, in
parallel to the sharp decrease observed in AOM visit rates [7].

Microbiology
As acute mastoiditis is a complication of AOM, the causative bacterial
pathogens are similar to AOM. While AOM usually develops during or after
viral upper respiratory tract infection and is considered bacterial and viral
co-infection [8], acute mastoiditis is mostly a bacterial infection. The main
pathogens are Streptococcus pneumoniae (22–40%), followed by Strepto-
coccus pyogenes (7–14%). Other bacteria isolated from mastoiditis spec-
imens are Staphylococcus aureus, coagulase-negative Staphylococcus and
Haemophilus influenzae. Other infrequent bacteria are Pseudomonas aerug-
inosa and Fusobacterum necrophorum [4,6,9]. In about a third of the cultures,

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 Mastoiditis

there is no bacterial growth, probably due to a previous antimicrobial treat-

ment. In studies which included bacterial culture results also from pus from
the external ear canal in draining ears, the proportion of skin flora, for exam-
ple, P. aeruginosa, was over-represented. Therefore, bacterial cultures in
mastoiditis cases should be obtained directly from the middle ear, subpe-
riosteal abscess or the mastoid cavity itself.
The widespread use of the PCV-7 since 2000 has changed the pneumococ-
cal population in AOM, and also in mastoiditis. Prior to PCV-7 introduction,
S. pneumoniae serotype 19F was among the most common strains which
caused mastoiditis; the widespread application of PCV-7 has largely elimi-
nated this strain, along with serotypes 4, 6B, 9V, 14, 18C and 23F. However,
the infective niche has been rapidly filled by the previously minor S. pneumo-
niae serotype 19A, which has been found to possess a high rate of multidrug
resistance [10]. In a study by Ongkasuwan, a dramatic increase of acute
mastoiditis caused by S. pneumoniae serotype 19A was noted following
the advent of PCV-7 vaccine. In a 12-year period, 19A became the most
predominant serotype after it started from zero [11].

Pathogenesis
Acute mastoiditis usually occurs as a complication of AOM. During AOM,
the mucosal lining of middle ear and pneumatized cells in mastoid cav-
ity become inflamed. Usually, the inflammation in the mastoid resolves
once AOM resolves. However, if the inflammation persists, hyperemia and
edema may also obstruct the aditus ad antrum, the narrow channel which
connects between the middle ear and the mastoid cavity. This blockage
increases the pressure in the mastoid cavity and allows the progression of
infection; exudate is produced and accumulated within the mastoid cavity.
Subsequently, the reduced vascularization and ischemia of the bony septae
of the cells result in demineralization, breakdown and coalescence of the
septae. Coalescent mastoiditis can lead to the formation of abscess cavi-
ties and spread of infection to adjacent areas, resulting in extracranial or
intracranial complications (see Clinical manifestations).
Mastoiditis can develop rather quickly during AOM, often without a pro-
longed course. The median duration of AOM symptoms before hospital
admission has been reported to be 1–2 days [6]. About 30–50% of children
with acute mastoiditis do not have a history of a preceding AOM, while
3–29% of the patients have had recurrent AOM previously [5,6].

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Marom & Nokso-Koivisto
Figure 6.1 Clinical manifestations of acute mastoiditis.

Protruding of the left auricle, with a swelling and redness of the postauricular region.
On palpation, fluctuance was noted.

Clinical manifestations
The clinical spectrum of acute mastoiditis widely ranges from mild signs and
symptoms with spontaneous resolution, to progressive disease with poten-
tially life-threatening complications. In very young children, mastoiditis can
manifest as the presenting symptom of an AOM.
Local symptoms include ear pain, which may present as irritability in infants,
postauricular tenderness, erythema or swelling (with loss of the postauric-
ular crease), protruding auricle, fluctuance or palpable mass (Figure 6.1),
and displacement of the auricle (mostly downward and outward in children
younger <2 years, and upward and outward in children >2 years). Exami-
nation of the tympanic membrane (TM) usually reveals findings suggesting
concurrent or recent AOM (i.e., bulging, erythema, opacification, middle ear
effusion, perforation, otorrhea). However, the lack of AOM history does not
exclude the diagnosis of mastoiditis. Middle ear effusion may be absent if

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 Mastoiditis

the aditus ad antrum is obstructed, in the presence of a patent Eustachian

tube.
Systemic symptoms include fever, lethargy, malaise, irritability, poor feed-
ing, or diarrhea. Fever is non-specific, yet fairly sensitive, and may be pre-
dictive of complication or the need for surgical intervention. High-spiking
’picket-fence’ fevers may be indicative of sigmoid sinus thrombosis.
In a systematic review of the diagnostic criteria commonly utilized for acute
mastoiditis in children (65 studies published between 1980 and 2007), 42%
of the children had a history of otologic disease and at the time of admis-
sion; one half of the patients were on antibiotic therapy [12]. The mean
duration of symptoms suggestive of acute mastoiditis was 9.8 days (range
1–42 days). Local symptoms included postauricular swelling, with or without
fluctuation, which was present in an average of 81–85% of patients, sagging
or edema of the external ear canal (71%), otalgia (67%), otorrhea (53%)
and TM perforation (37%). Systemic symptoms included lethargy/malaise
(96%), fever (76%), irritability (71%) and headaches (31%).
Subacute mastoiditis, also referred as masked mastoiditis, should be consid-
ered in children with AOM that is not responding to antimicrobial therapy
and in children with signs of intracranial infection without any another rec-
ognizable focus of infection. It is characterized by nonspecific symptoms and
signs, such as fever, cough, ear pain and TM findings compatible with AOM.
Masked mastoiditis occasionally presents with an extracranial or intracranial
complication without preceding signs of AOM or mastoiditis.
Complications of mastoiditis are related to spread of infection or inflam-
mation from the mastoid to adjacent structures. Rarely, the complication
(i.e., cranial nerve palsy) is the presenting complaint. Box 6.1 summarizes
intracranial and extracranial complications of mastoiditis, and Figure 6.2
displays potential pathways of the infectious process from the mastoid cav-
ity to the surrounding structures. Intracranial complications are not rare
even in the modern era. In a recent study, 14% of children with mastoidi-
tis experienced intracranial complications [13]. Prompt early recognition and
treatment are essential, as the morbidity associated with such complications
can be high.

Diagnosis
The diagnosis of acute mastoiditis is usually made clinically in children with
characteristic findings. Laboratory tests and radiologic studies are helpful
tools in the course of mastoiditis treatment, and can support decision making
when current treatment strategy fails.

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Marom & Nokso-Koivisto

Box 6.1. Complications of acute mastoiditis.

Extracranial complications
Extratemporal
 Postauricular abscess.
 Bezold’s abscess.
 Luc’s abscess.
 Zygomatic abscess.
Intratemporal
 Facial nerve paralysis.
 Petrous apicitis.
 Labyrinthitis.
 Labyrinthine fistula.
 Sensorineural hearing loss.
Intracranial complications
 Meningitis.
 Epidural abscess.
 Subdural empyema.
 Brain abscess.
 Sigmoid (lateral) sinus thrombosis.
 Otitic hydrocephalus.
 Meningoencephalocele.
 Cerebrospinal fluid leak.

Laboratory work-up
Blood test results may not be specific: white blood cell count may be normal
or elevated and the erythrocyte sedimentation rate or C-reactive protein
may also be elevated. The importance of obtaining clinical specimens from
the middle ear cavity or pus for culture studies cannot be overemphasized.
Middle ear specimens can be obtained during myringotomy, ideally before
antimicrobial therapy is begun, but without delaying antimicrobial therapy
more than several hours. Middle ear specimens should be sent for gram
stain, aerobic and anaerobic culture and susceptibility testing for antimicro-
bials. Bacterial cultures should be obtained from the middle ear by incision
through an intact TM or by aspiration through a TM perforation, tympanos-
tomy tube, subperiosteal abscess or directly from the mastoid cavity, during
surgery, in order to avoid contamination from the external ear canal and

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 Mastoiditis
Figure 6.2 Complications of acute mastoiditis.

Brain abscess
Epidermal
abscess Meningitis,
subdermal
abscess
Labyrinthitis
Cerebellar
Superiostial abscess
abscess Facial nerve palsy
Septic thrombus

Jugular vein

Internal
carotid
artery

Bezold abscess

Sternocleidomastoid
muscle

Reprinted with permission from www.uptodate.com

improve culture result qualities. Bacterial culture may also be obtained from
cerebrospinal fluid, if lumbar puncture has been performed when meningitis
was suspected and from blood, if the patient’s temperature is ≥39◦ C.

Imaging studies
Box 6.2 summarizes CT and MRI findings in mastoiditis patients. Imaging
studies of the temporal bone are not necessary to make the diagnosis of

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Marom & Nokso-Koivisto

Box 6.2. Findings of acute mastoiditis and related complications in imaging

studies.
Computerized tomography (CT) studies
Opacification of the mastoid air cells and middle ear.
 Erosion of the walls of the mastoid cavity, resorption of bony septa (coalescent
mastoiditis); haziness or distortion of the mastoid outline.
 Subperiosteal abscess: along the external ear canal and the zygomatic arch; deep
to the temporalis muscle (Luc’s abscess); deep to the sternocleidomastoid
muscle (Bezold’s abscess).
 Epidural abscess: most commonly in the posterior fossa.
 Perisinus abscess: an epidural abscess over the sigmoid vein; MRI should be
complementarily performed.
 Subdural abscess
 Thrombosis of the sigmoid vein sinus, other deep dural sinuses and the internal
jugular vein (suspected if there is an increased density in the blood vessel).
 Petrous apicitis: bony resorption in a pneumatized petrous bone.
 Meningitis: gross dural thickening.
 Cerebral abscess: an area of low attenuation signifying cerebral edema, which
may show irregular enhancement.
Magnetic resonance imaging (MRI) studies†
Thrombosis of the sigmoid vein sinus, other deep dural sinuses and the internal
jugular vein: absence of a flow void on spin-echo sequences and filling defect on
gradient-echo or MR venography sequences.
 Meningitis: gross dural thickening.
 Cerebritis: focal ill-defined high T2 signal areas.
 Cerebral abscess: surrounded by edema, indicated by high T2 and
fluid-attenuated inversion recovery (FLAIR) signal. The necrotic center of an
abscess has restricted diffusion, leading to a high signal on diffusion weighted
imaging (DWI), which may help to differentiate it from a tumor, which usually has
a low central signal on DWI.
†
Indicated for diagnosis of intracranial complications.

acute mastoiditis in children with characteristic clinical findings, and are

also not required in the initial treatment of uncomplicated cases. However,
imaging studies may be necessary to confirm the diagnosis in children with
unusual symptoms (i.e., persistent otalgia or drainage without postauricular
swelling), determine the stage of disease which may influence the manage-
ment (acute mastoiditis with periosteitis vs coalescent mastoiditis), and

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 Mastoiditis
Figure 6.3 Computerized tomography scans in acute mastoiditis.

A B

(A) Contrast axial head computerized tomography scan demonstrating a subperiosteal

abscess in the left mastoid area (arrow), with an opacification of the mastoid cavity.
(B) Gadolinium axial T1-weighted magnetic resonance image demonstrating an
epidural abscess (arrow) secondary to right mastoiditis.

evaluate suspected complications. Indications for imaging may include clin-

ical findings suggestive of extracranial or intracranial complications, severe
illness or toxic appearance, and AOM cases which are not responding to
antimicrobials (possibly masked mastoiditis). CT and MRI are the preferred
imaging modalities, but are utilized differently. Bony changes, that is, dehis-
cence of the mastoid cortex or coalescence of the air cells, intracranial and
extracranial abscesses and vascular filling defects, suggesting of a thrombo-
sis, are best noticed with contrast-enhanced CT, while MRI with gadolinium
is recommended in patients with suspected intracranial complications, due
to its higher sensitivity for detection of extra-axial fluid collections and asso-
ciated vascular lesions. MRI is the gold standard modality for diagnosis of
intracranial complications [13,14]. Although the routine use of CT scan in
mastoiditis has been questioned [15], the determination of mastoid air cells
coalescence by CT scan is considered to be an important decision point in
the treatment of mastoiditis. Figure 6.3 displays characteristic findings of a
subperiosteal abscess (seen in CT) and an epidural abscess (seen in MRI).

Treatment
The treatment of mastoiditis depends upon the stage and the possibility
of complication(s). Box 6.3 shows treatment options in acute mastoiditis.
Surgical drainage and antimicrobial therapy have long been considered the
pillars of therapy. In an uncomplicated case, aspiration and/or drainage of

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Marom & Nokso-Koivisto

Box 6.3. Treatment options for acute mastoiditis.

 Myringotomy.
 Ventilating tube insertion.
 Incision and drainage of a subperiosteal abscess.
 Mastoidectomy (in severe cases or if no improvement within 48 h with
conservative treatment).
 Intravenous antimicrobial therapy, followed by oral therapy when clinical
improvement occurs.
 Topical antibiotic/steroid combinations (controversial).
 Systemic steroids (controversial).

the middle ear, for example, myringotomy, with or without ventilating tube
insertion provides therapeutic, as well as diagnostic values.
Empiric antimicrobial therapy administration should provide coverage for
the most frequent bacterial pathogens (S. pneumoniae and S. pyogenes).
Third-generation cephalosporin and/or clindamycin can be used in first-line
treatment and later the treatment should be adjusted according to bacterial
culture results and susceptibility tests. In many cases, antimicrobial therapy
which had already been used for AOM requires broadening of microbial
coverage to cover S. aureus. There are no randomized clinical trials to deter-
mine the optimal length of antimicrobial treatment in acute mastoiditis.
Based on prospective studies, intravenous treatment with antibiotic drugs,
such as third-generation cephalosporin (cefotaxime or ceftriaxone) and clin-
damycin for 7–10 days has been recommended, but shorter time has been
used in milder cases if the disease had been clearly improving. The total
recommended duration of antimicrobial therapy is 4 weeks [16,17]. Interest-
ingly, adequate antimicrobial therapy may fail to prevent the development
of complications of acute mastoiditis. In a series of 223 patients, 8.5% devel-
oped mastoiditis-related complications during antimicrobial therapy [18].
The role of steroids in uncomplicated mastoiditis cases is still controversial.
The rationale for this treatment is to decrease mucosal swelling and promote
natural drainage through the aditus ad antrum into the middle ear. Yet, their
clinical efficacy has not been proven, in addition to their side effects [19].
Patients should be monitored daily for clinical response. Mastoidectomy is
the surgical removal of the mastoid cortical bone and underlying air cells,
and it is indicated in order to externally drain the tympanomastoid cavity. If
no clinical improvement occurs within 48 h, surgical intervention should be
considered. A subperiosteal abscess necessitates external drainage, with or
without simple mastoidectomy [20]. Mastoidectomy should be considered

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 Mastoiditis

for children with postauricular fluctuance, mass or swelling (suggesting sub-

periosteal abscess), cervical fluctuance (Bezold’s abscess), imaging studies
with evidence of a rim-enhancing fluid collection, mastoid air cells coales-
cence, cortical bone erosion, intracranial involvement, high-spiking ’picket-
fence’ fever, or other focal neurologic signs. Mastoidectomy can also rarely
include thrombectomy and ligation of the draining veins in patients with
sinus vein thrombosis, with or without anticoagulant therapy [21,22].

Prevention
To date, there are no direct means to prevent mastoiditis. However, as acute
mastoiditis is an AOM complication, prevention and successful treatment of
AOM would theoretically decrease the incidence of mastoiditis. Prevention
and treatment of AOM is discussed in Chapter 2 – Acute otitis media.
Reduction in the exposure to pathogenic serotypes of the most common
bacteria in acute mastoiditis, S. pneumoniae, might have the greatest impact
on the incidence of mastoiditis. Although PCV-7 vaccine was effective against
invasive pneumococcal infections, the widespread use of PCV-7 vaccine did
not decrease the incidence of acute mastoiditis and did not seem to change
the role of S. pneumoniae as the most common pathogen in mastoiditis [5].
The more recent PCV-13 vaccine offers broader spectrum coverage against
S. pneumoniae, including the emerging serotype 19A. Recent evidence sug-
gests that mastoiditis cases have the greatest decrease during the first few
postmarket years of PCV-13, when compared with the 3 years preceding the
introduction of the vaccine [7,23]. Further studies are required to assess the
long-term effectiveness of PCV-13 in reducing pneumococcal-related acute
mastoiditis.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any
organization or entity with a financial interest in or financial conflict with
the subject matter or materials discussed in the manuscript. This includes
employment, consultancies, honoraria, stock ownership or options, expert
testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.

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Marom & Nokso-Koivisto

Summary
 The incidence of acute mastoiditis is stable despite the changes in AOM guidelines, bacterial
resistance and the introduction of PCV-7 vaccination. However, recent use of PCV-13 has been
associated with a substantial decrease in mastoiditis incidence rate, in parallel to the observed
decrease in AOM incidence rate.
 Characteristic signs of acute mastoiditis include fever, redness and swelling of the postauricular
region, with a protrusion of the auricle.
 Diagnosis of acute mastoiditis is based on clinical signs and symptoms, usually with a preceding
history of AOM.
 Imaging studies of the temporal bone are not necessary to make the diagnosis of acute mastoiditis
in children with characteristic clinical findings, and are not required for the initial treatment of
uncomplicated cases.
 The more conservative treatment of acute mastoiditis is emerging with the combination of
myringotomy, with or without ventilating tube insertion and intravenous antimicrobial therapy.
 Mastoidectomy should be considered in complicated mastoiditis or if conservative treatment fails.

Key terms
Acute mastoiditis: is a suppurative infection of the mastoid cavity with symptoms for
less than 1 month.
Acute mastoiditis with is an infection of the mastoid air cells with the presence of purulent
periosteitis: exudate.
Coalescent mastoiditis: is an infection of the mastoid cavity with destruction of the bony
septae between the air cells.

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