Panel 8
Panel 8
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-- Head and Neck Surgery
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Abstract
Background and Objectives. Although serious complications of
otitis media (OM) such as brain abscess are rare, sequelae
of OM such as tympanic membrane perforation and atelectatic tympanic membrane are quite common. Inner ear
sequelae can cause hearing loss and speech and language
problems. The objectives of this article are to provide a
state-of-the-art review on recent articles on complications
and sequelae of OM in different anatomic locations, from
the tympanic membrane to intracranial sites, as well as hearing loss and speech and language development.
Data Sources. Primarily PubMed supplemented by Ovid
MEDLINE and the Cochrane Database.
Review Methods. All types of articles related to OM complications and sequelae published in English between January
2007 and June 2011 were identified. A total of 127 relevant
quality articles are summarized and included in this report.
Results. Key findings are summarized based on the following
major anatomic locations and categories: tympanic membrane;
cholesteatoma; ossicular problems; mucosal sequelae; inner ear
sequelae; speech and language development; extracranial areas,
including mastoiditis and facial nerve paralysis; intracranial complications; and future research goals. New information and
insights were gained to prevent complications and sequelae.
Conclusion and Implications for Practice. Over the past 4 years,
progress has been made in advancing the knowledge on the
complications and sequelae of OM, which can be used to
prevent and treat them effectively. Areas of potential future
research have been identified and outlined.
Otolaryngology
Head and Neck Surgery
148(4S) E122E143
American Academy of
OtolaryngologyHead and Neck
Surgery Foundation 2012
Reprints and permission:
sagepub.com/journalsPermissions.nav
DOI: 10.1177/0194599812467425
http://otojournal.org
Received May 17, 2012; revised October 11, 2012; accepted October
19, 2012.
1
Department of Otolaryngology, Loma Linda University, Loma Linda,
California, USA
2
Division of Pediatric Otolaryngology, University of Pittsburgh, Pittsburgh,
Pennsylvania, USA
3
Department of Audiology, Karolinska University Hospital, Stockholm,
Sweden
4
Division of Audiology, Cincinnati Childrens Hospital Medical Center,
Cincinnati, Ohio, USA
5
Department of Otolaryngology, University of Lund, Lund, Sweden
6
Department of ORL-HNS, Gazi University, Ankara, Turkey
7
House Ear Institute, Los Angeles, California, USA
8
Division of Audiology, Ohio State University, Columbus, Ohio, USA
9
Department of Otolaryngology, Ajou University, Suwon, Korea
10
Division of Audiology, University of Pittsburgh, Pittsburgh, Pennsylvania,
USA
11
Department of Otolaryngology, University of Porto, Porto, Portugal
Keywords
otitis media, tympanic membrane perforation, atelectasis of
TM, cholesteatoma, hearing loss, speech and language, facial
nerve paralysis, mastoiditis, cranial complications
Corresponding Author:
Timothy Jung, MD, PhD, Department of Otolaryngology, Loma Linda
University School of Medicine, Loma Linda, CA 92354, USA
Email: ttkjung@gmail.com; timothy.jung@va.gov
Jung et al
E123
the short- and long-term research goals identified at the previous meeting of this panel have been met; (3) to identify
deficiencies in our understanding of the complications and
sequelae of OM in specific sites related to the TM (including cholesteatoma), middle ear, inner ear, and intratemporal
and intracranial sites, as well as the impact of OM on sound
transmission in the middle ear (including TM and ossicles)
on hearing and speech and language; (4) to define and prioritize research goals that address deficiencies in our knowledge for investigation during the next 4 years; and (5) to
identify the short- and long-term goals for the future and
methods by which they can be accomplished.
Methods
Articles came primarily from PubMed supplemented by
Ovid MEDLINE and the Cochrane Database.
All types of articles related to OM complications and
sequelae published in English between January 2007 and
June 2011 were identified. A total of 127 relevant quality
articles are summarized and included in this report. All articles in English with a keyword of otitis media, complications, or sequelae were evaluated and included. Articles
considered new and significant were included.
Discussion
Key findings are summarized based on the following major
anatomic locations and categories: TM; cholesteatoma; ossicular problems; mucosal sequelae; inner ear sequelae; speech
and language development; extracranial areas, including mastoiditis and facial nerve paralysis; intracranial complications;
and future research goals.
Tympanic Membrane
Perforation. Von Unge et al1 evaluated a model for studies
on sequelae after acute otitis media (AOM) in the
Mongolian gerbil. The middle ears of 16 Mongolian gerbils
were inoculated with type 6a Streptococcus pneumoniae.
Half of the animals were treated with antibiotics on days 4 to
6, when otoscopy was performed as well. After 1, 2, 3, or 4
weeks, the animals were sacrificed and their TMs were examined. On days 4 and 6, AOM was produced in approximately
80% of the animals, and perforations prevailed in approximately 30% at the study end points. Clinical signs of AOM
and edema of the TM had already started to reduce after 1
week and often resolved within 2 weeks. The mechanical stiffness of TM remained relatively unharmed in the nonperforated
ears. The antibiotic treatment seemed to reduce the duration of
edema but not the perforation rate.
Santa Maria et al2 reported keratinocyte growth factor
(KGF) 1, fibroblast growth factor (FGF) 2, and FGF10 in
the healing TM following perforation in rats. The TMs of
rats were perforated and sacrificed at time points over a
14-day period. KGF1, FGF2, and FGF10 play important
roles in TM healing following perforation. KGF1 and
FGF2 appeared to be involved in the proliferation and
migration of keratinocytes. The role of KGF1 appeared to
be exclusively connected to an increased proliferation and
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tympanometric measurements, significantly reduced magnitudes of maximum admittance were observed in control and
saline groups. The TM of the STS group appeared thinner
than that of the control group (P \ .05) and with a reduced
calcium deposition. The authors showed that STS has a preventive role in the development of MS in the experimental
animal model.
Song et al12 investigated the effect of caffeic acid phenethyl ester (CAPE) on the prevention of experimentally
induced MS. Thirty-five Sprague-Dawley rats were divided
into 3 groups; group 1 received no treatment, group 2
received intraperitoneally administered saline, and group 3
received intraperitoneally administered CAPE. The TMs
were examined on the 15th day after treatment. Group 1
showed extensive MS, and group 2 showed a similar occurrence of MS. Group 3 had reduced MS. The lamina propria
of the pars tensa was thicker and more sclerotic in groups 1
and 2. The authors concluded that systemic CAPE was
effective in the prevention of sclerotic lesions in myringotomized rat TMs.
Acute OM. Dai and Gan13 developed an OME model in
guinea pigs, in which middle ear transfer functions could be
measured. Evidence of OME was assessed by otoscopy,
tympanometry, histology, and measurement of the volume
of fluid in the middle ear. Vibrations of the umbo and round
window membrane were measured with a laser Doppler vibrometer at a frequency range of 200 to 40 kHz in 3 groups
3, 7, and 14 days after injection of lipopolysaccharide
(LPS). Changes in displacement of the umbo and round
window membrane in response to an 80-dB sound pressure
level (SPL) in the ear canal were measured across the frequency range. Displacement of both the umbo and round
window membrane was reduced at all time points following
LPS injections. Furthermore, the change of the displacement
transmission ratio (DTR) from the TM to the round window
occurred mainly in chronic OME ears. This study provides
useful data for analyzing the change of middle ear transfer
function in OME ears.
Basic science of TM/gas exchange. Knutsson et al14 located
progenitor/stem cells in the human TM. Human TMs
obtained at translabyrinthine surgery were investigated
using immunohistochemistry and immunofluorescence to
detect the progenitor/stem cell markers a6-integrin, b1integrin, and cytokeratin 19 (CK19). a6-Integrin was
detected in the basal layer of the keratinizing epithelium in
the umbo, in the annular region, and along the malleus but
not in the intermediate portion of the pars tensa. b1-Integrin
and CK19 were found in the same locations, not only in the
basal layer but also in the suprabasal layers of the keratinizing epithelium. The authors concluded that possible progenitor cells are found in the umbo, in the annular region, and
along the malleus.
Redmond et al15 compared phenotypic and genotypic
profiles of human TM (hTM) derived from hTM tissue
explants with epithelial and mesenchymal reference cells.
Epithelium-specific ets-1 (ESE-1), E-cadherin, KGF1/FGF7,
KGF2/FGF10, fibroblast growth factor receptor (FGFR) 1,
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Cholesteatoma
Congenital or acquired. Persaud et al19 reviewed the etiopathogenic theories of congenital and acquired cholesteatoma. Congenital cholesteatoma is explained by the
persistence of fetal epidermoid formation. Acquired cholesteatoma may develop by various mechanisms: immigration,
basal hyperplasia, retraction pocket, and/or trauma (iatrogenic or noniatrogenic). Chronic inflammation seems to
play a fundamental role in multiple etiopathogenic mechanisms of acquired cholesteatoma. The authors recommend
that early treatment of inflammatory conditions might
reduce the sequelae by preventing the development of
hyperplastic papillary protrusions.
Welkoborsky et al20 reported a study designed to evaluate
the cell-to-cell and epithelium-stroma interaction of acquired
cholesteatoma. Surgical specimens of 54 patients who underwent primary surgery for an acquired cholesteatoma of the
middle ear were examined by histopathology and DNA
image cytometry (DNA-ICM). Immunohistochemical investigations included expression of proliferation markers (proliferation cell nuclear antigen and MIB-1) along with cell
surface markers reflecting the cell-to-cell interaction (ie,
a1b6-integrin, E-cadherin, I-CAM = CD54) and the
epithelial-to-stroma interaction (ie, a-v and b3-integrin
chains, V-CAM = CD106, CD44v6, and fibronectin). Cell
surface markers and cell adhesion molecules were equally
expressed in both groups except a1b6-integrin and fibronectin, which were significantly overexpressed in pediatric
cholesteatomas.
The authors concluded that pediatric and adult cholesteatomas do not show differences at a cellular level. The
observed clinically more aggressive behavior of pediatric
cholesteatoma is likely due to other secondary factors such
as more intense inflammation, disturbed middle ear ventilation, or the diminished calcium salt content of pediatric
bone.
Basic science of cholesteatoma. Kwon et al21 analyzed gene
expression profiles in cholesteatoma using an oligonucleotide microarray. In all, 1327 upregulated or 767 downregulated genes that were over 3 times more prominent in
cholesteatoma than in skin were identified by 5 samples of
microarray data. Among these up- or downregulated genes
in cholesteatoma, 291 genes were identified in 3 of 5 samples as upregulated expression more than 3-fold in density,
and 191 genes were downregulated more than 3-fold in density. Reverse transcriptase PCR of 21 selected genes
revealed that those expression levels were higher in cholesteatoma than in skin. The authors suggested that microarray
analysis may be a useful tool to identify some candidate
genes related to the pathogenesis of cholesteatoma.
Hamajima et al22 investigated the role of the inhibitor of
DNA binding (Id1) in the hyperproliferation of keratinocytes. Keratinocytes were transfected with Id1, and the
responses of keratinocytes to Id1 were studied by using cellular and molecular biologic methods. Id1 significantly
increased the promoter activity of nuclear factor (NF)kB,
which, in turn, upregulated the expression of cyclin D1 and
keratin 10 in keratinocytes. Specific NF-kB inhibitors (pyrrolidine dithiocarbamate, PDTC) or a dominant-negative
inhibitor (IkBaM) abrogated the Id1-induced cell proliferation and keratin 10 production, whereas p65, a subunit of
the NF-kB heterodimer and an enhancer of NF-kB activity,
strengthened the Id1-induced cell proliferation and keratin
10 production. The authors identified that Id1 contributed to
the hyperproliferation of keratinocytes via enhancement of
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on the tympanic membrane (11%), 1 on the tympanic portion of the facial canal (6%), and 1 just under the skin of
the external auditory canal (6%). By retrospective videotape
analysis, it was observed that the main cause of residual
cholesteatomas in the epitympanum and sinus tympani was
incomplete removal of the matrix under an indirect surgical
view because of insufficient drilling.
In a review of 1531 surgeries (1183 patients), Kaylie et al30
revealed that smokers had more cholesteatomas and required
more canal wall-down surgeries than nonsmokers.
Furthermore, they required more revision surgeries and had
overall worse hearing outcome than nonsmokers.
Zhang et al31 investigated identification of Id1 in acquired
middle ear cholesteatoma. Two hundred sixty-four ears with
COM that had undergone ear surgery were included.
Fourteen middle ear cholesteatoma specimens were collected
for immunohistochemical analysis of abnormal proliferation
of keratinocytes. The inhibitor of the DNA-binding (Id1)
gene, which is involved in controlling cell cycle progression,
was abundantly expressed in cholesteatoma epithelium. In
vitro studies indicate that Id1 regulated the expression of NFkB, cyclin D1, proliferating cell nuclear antigen, and cell
cycle progression of keratinocytes. The authors concluded
that chronic inflammation in the ossicular chain area (OCA)
is closely related to the formation of cholesteatoma. The Id1/
NF-kB/cyclin D1/proliferating cell nuclear antigen signaling
pathway is involved in the abnormal proliferation of keratinocytes in acquired cholesteatoma.
Ossicular Problems
Gluth et al32 reviewed the results of malleostapedotomy for
incus replacement in 7 individuals who had undergone malleostapedotomy in the setting of quiescent COM and a
mobile stapes. They investigated surgical results and hearing
outcomes by preoperative and postoperative pure-tone
audiometry. Improvement in the air-bone gap was noted in
6 of 7, with an average closure of 17 dB. In 5 of 7, the airbone gap was closed to 20 dB or less, and in 3 of 7, the airbone gap was closed to 10 dB or less. The authors suggested
that malleostapedotomy is a potentially safe and effective
alternative to placement of a total ossicular replacement
prosthesis (TORP).
Hamilton33 investigated systematic preservation of the
ossicular chain in laser-assisted cholesteatoma surgery. In
this study, ears were categorized into 2 groups based on the
state of the ossicular chain at the end of surgery. Patients
with a continuous ossicular chain were allocated to group
A. Patients with a disrupted chain and an intact stapes
superstructure onto which an ossiculoplasty had been performed were placed in group B. Ultimately, it was concluded that the fiber-guided laser allows the cholesteatoma
surgeon to preserve the ossicular chain in a systematic
manner that is both safe and of benefit to the patient.
Mucosal Sequelae
Ebmeyer et al34 reported that TNF-a deletion alters apoptosis as well as caspase 3 and 4 expression during otitis
Jung et al
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substantial enough that many physicians would consider vaccination to prevent OM (score 5.1). The authors reported that
OM remains a significant burden for clinical practice, despite
awareness of shortcomings, and antimicrobial therapy
remains the most frequent treatment for OM.
Urschel38 reported a brief insight into primary immunodeficiencies in cases of otitis media. All patients suffer from
recurrent, prolonged, and/or unusual infections leading to
local sequelae, failure to thrive, developmental delays, and
systemic infections with severe courses. A stepwise diagnostic approach is proposed to facilitate early and accurate
diagnosis, as well as effective and timely therapy to
improve the patients outcome.
Yamamoto-Fukuda et al39 analyzed the expression of
keratinocyte growth factor and its receptor in noncholesteatomatous COM (NC-COM) and cholesteatomatous COM
(C-COM). The subepithelial tissue from 18 patients with
NC-COM and 70 patients with C-COM was processed for
immunohistochemistry for KGF and KGFR. Keratinocyte
growth factor was positive in 28% of NC-COM specimens and 88% of C-COM specimens. Thirty-seven (60%)
C-COM specimens were positive for KGFR, whereas 0%
of the NC-COM specimens were positive. The Ki-67
labeling index (LI) was significantly smaller in NC-COM
than in C-COM. B-cell LI was almost similar in the 2
groups. T-cell LI was significantly higher in C-COM than
in NC-COM. T-cell LI in NC-COM was higher in KGFpositive tissues. The authors concluded that coexpression
of KGF and KGFR explains the pathologic difference
between C-COM and NC-COM and that KGF may play
an important role in cholesteatoma.
Using noninvasive optical interferometry for the
assessment of biofilm growth in the middle ear, Nguyen
et al40 identified the presence of a biofilm with 86% sensitivity and 90% specificity with a novel classification
algorithm for acquired low coherence interferometry data.
Streptococcus pneumoniae is the most common pathogen
associated with otitis media.
Han et al41 reported a role for Toll-like receptor 2
(TLR2) in the immune response to S pneumoniae infection
in mouse otitis media. Nineteen of 37 TLR2/ mice had
bacteremia and died within 3 days after the challenge, compared with only 4 of 32 wild-type (WT) mice that died. Of
those that survived, more severe hearing loss in the TLR2/
mice was indicated by an elevation in auditory-evoked
brainstem response thresholds at 3 or 7 days after inoculation. The histological pathology was characterized by
effusion and tissue damage in the middle ear. At both 3
and 7 days postchallenge, the TLR2/ mice had higher
blood bacterial titers. By 3 days postchallenge, the
mRNA accumulation levels of NF-kB, TNF-a, IL-1b,
MIP1a, Muc5ac, and Muc5b were significantly lower in
the ears of TLR2/ mice. The authors concluded that
TLR2/ mice may produce relatively low levels of proinflammatory cytokines following pneumococcal challenge,
thus hindering the clearance of bacteria from the middle
ear and leading to sepsis and a high mortality rate. They
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demonstrated that moderate to severe hearing loss was present in 32% of 47 Aboriginal children and 7% of 120 nonAboriginal children aged 12 months or older. Furthermore,
they found that Aboriginal children who failed TEOAE at
age 1 to 2 months were 2.6 times more likely to develop
OM subsequently than those who passed. They suggested
measurement of TEOAEs at age 1 to 2 months to identify
children at risk of developing OM in a routine health service
setting in view of the frequently silent nature of OM in
Aborigines.
In a study by Hunter et al,53 hearing screening in Native
American infants and toddlers was reported. Infants were
prospectively assessed with pneumatic otoscopy, distortion
product otoacoustic emissions (DPOAEs), and tympanometry. In the newborn period, 23.5% of infants failed hearing
screening in at least 1 ear. Hearing screening failures
increased to 29.9% from 2 to 5 months of age. Only 1 of 366
infants was identified with sensorineural hearing loss, and
thus essentially all of the hearing screening failures reflected
either a middle ear origin or other temporary problems. The
authors suggested that behavioral assessment is needed after
6 months of age, when high rates of OME persist in this
population.
Rosenfeld et al54 analyzed tympanostomy tube outcomes
in children at risk and not at risk for developmental delays.
Fifty-five percent children had at least 1 condition placing
them at risk for developmental delays. After tube insertion,
89% caregivers stated that their childs life was much
better. Speech and language was much better for 55%,
more often in at-risk children. Learning or school performance was much better after tubes for 55%, more often
in at-risk children. Improved hearing was reported by 84%
with no relationship to at-risk status. Caregivers reported
favorable outcomes regardless of their childs at-risk status,
but children at risk for delays had better reported outcomes
for speech, language, learning, and school performance.
Daudia et al55 reported long-term middle ear ventilation
with myringotomy and tympanostomy tube (MT). They retrospectively studied 45 patients with COM and hearing loss,
associated with adhesive otitis media in 7, TM retraction in
17, and TM perforation in 3. The mean improvement in airbone gap was 14 dB. Complications included blockage
(16%), perforation after extrusion (9%), granulation (5%),
and infection (4%). The authors concluded that MT provides
an effective option for management of intractable MEE and
eustachian tube dysfunction.
Spielmann et al56 reported a follow-up after BMT.
Twenty percent of their patients required further MT insertion within the study periods. Children with abnormal clinical findings or a mean hearing threshold greater than 20 dB
were significantly more likely to require further intervention. The authors recommended 1 postoperative review with
audiometry 3 months after surgery.
Revai et al57 investigated tympanometric findings in
young children while they had upper respiratory tract infections (URIs) with and without AOM. The peak day for an
abnormal tympanogram was day 2 of the URI. An abnormal
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Chianese et al61 showed spectral gradient acoustic reflectometry (SGAR) compared with tympanometry in diagnosing OME among 786 healthy children. The SGAR results
were available for 3096 otoscopic examinations in 647 children. Tympanometric results were available for 2854 otoscopic
examinations in 597 children. Using the recommended SGAR
pass or fail cutoff, 53% of the ears in which effusion was present would have been considered effusion free. Only 10% of
the ears without effusion would have been considered to have
effusion. The area under the receiver operating characteristic
curve was 0.78 for SGAR and 0.83 for tympanometry. The
authors concluded that SGAR is slightly less discerning than
tympanometry in predicting OME in children younger than
2 years.
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Future Research
In the previous postsymposium meeting in 2007, a set of
recommendations were provided that called for future studies to use a variety of research designs with varied populations; to design research that is hypothesis driven; to
include reliable and valid measures of OME, hearing, and
development; to include mediating and moderating measures that may affect the relationship between OME and
developmental outcomes; and to provide adequate information in research reports, including power for nonsignificant
findings, so that research synthesis may be completed.
Several of these goals were met. Most of the studies were
designed to examine specific hypotheses and used outcome
measures to examine these effects. Populations included
both middle-class and less advantaged groups, but in only 1
study was a clinical sample included. Many of the investigators examined hearing at the time of the developmental
assessment to ensure that when outcomes were measured,
their samples had hearing in the normal range.
However, hearing during the time when children experienced OME was included as an independent variable in
only 2 studiesHooper et al74 and Paradise.75 Aside from
SES, only Feagans et al76 and Hooper and colleagues considered other environmental variables to account for
development.
Our recommendations for future studies are to more consistently apply the suggestions made previously. We encourage investigators to use more specific measures that may be
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Extracranial Complications
Mastoiditis. Benito and Gorricho77 reviewed the cases of
mastoiditis over 10 years (1996-2005) at the Nino Jesus
University Children Hospital in Madrid. Of the 215 children
(aged 0.6-17 years) with mastoiditis, 67% were younger
than 3 years and 69% were males. The number of cases
doubled in 1999, with the same percentage of admissions in
the pediatric service, and tripled in 2005 compared with
1996. Surgical treatment has increased from 4% to 33% in
the past years and grew to 70% in 2005. Most cases (80%)
had received prehospital antibiotic therapy, but individual
pathogens and current complications of periostitis or subperiosteal abscess formation were equally distributed between
the 2 groups. The authors detected S pneumoniae in 29%
and a significantly high rate of S aureus (16%). Fifty-four
percent of cases had negative cultures. There was a progressive increase in the incidence of acute mastoiditis and an
increase in surgical treatments. Most cases of acute mastoiditis had responded well to medical management alone. The
authors concluded that tympanocentesis for middle ear culture may become more valuable and more frequently used
in cases of antibiotic treatment failures, and surgical therapy
may be necessary more often in the future.
Kvaerner et al78 studied the variation and characteristics
of acute mastoiditis in 399 children aged 0 to 16 years in
Norway. The study was based on a registry with complete
data on hospitalization for acute mastoiditis and cortical
mastoidectomy in Norway during 1999-2005. The incidence
of acute mastoiditis in children younger than 2 years ranged
Jung et al
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of the walls of former air cells. The authors point out that
their observations closely match the histopathological find ber die normale und
ings by Wittmaack (Wittmaack K: U
die pathologische Pneumatisation des Schlafenbeins. Jena,
Germany: Gustav Fischer; 1918), who developed the concept of the normal pneumatization process of the temporal
bone and the pathogenesis of aberrant pneumatization.
Mallur et al90 determined the clinical characteristics and
treatment outcomes of an unusual cluster of intracranial
complications seen in AM. They performed a retrospective
review of pediatric patients treated for AM in a tertiary care
hospital from March 2006 to March 2007. Eleven children,
6 months to 10 years of age (mean age, 3.8 years), were
treated for AM confirmed by computed tomography, which
identified asymptomatic intracranial complications in 8 of
the 11 patients: these were sigmoid sinus thrombosis (4
patients), epidural abscess (4), perisigmoid abscess or bony
erosion (2), and tegmen mastoideum dehiscence (1). All
patients required operative intervention with tympanomastoidectomy, although only 2 patients required neurosurgical
intervention, consisting of evacuation of epidural abscess
and sigmoid sinus thrombosis, respectively. Although
uncommon, intracranial complications of AM may present
without clinical signs or symptoms. Computed tomography
of the temporal bone with contrast is essential for identifying asymptomatic complications. Mastoidectomy remains
the mainstay of surgical treatment.
Pang et al91 studied 79 episodes of AM, managed in 76
patients in a pediatric population, in a review of 11 years of
experience in management. Prehospital treatment was commenced by the family practitioner or district hospital doctor
in 53 of 79 patients. In 33 episodes, a previous history of
acute otitis media was noted (42%). Complications were
found in 30 episodes (38%), and 36 episodes (46%) required
surgical treatment. The authors suggested that children with
acute mastoiditis should be managed in centers where
timely and complete medical and surgical treatment is
available.
Thompson et al92 conducted a retrospective cohort study
by using the UK General Practice Research Database.
Children aged 3 months to 15 years between 1990 and 2006
were included. Risk of mastoiditis within 3 months after
otitis media diagnosis and the protective effect of antibiotics
were determined. There were 2,622,348 children within the
General Practice Research Database; 854 had mastoiditis,
only one-third of whom (36%) had antecedent otitis media.
Mastoiditis incidence remained stable between 1990 and
2006 (approximately 1.2 per 10,000 child-years). Risk of
mastoiditis, after otitis media, was 1.8 per 10,000 episodes
(139 of 792,623) after antibiotics compared with 3.8 per
10,000 (149 of 389,649) without antibiotics and increased
with age. Antibiotics halved the risk of mastoiditis. General
practitioners would need to treat 4831 otitis media episodes
with antibiotics to prevent 1 child from developing mastoiditis. If antibiotics were no longer prescribed for otitis
media, an extra 255 cases of childhood mastoiditis would
occur, but there would be 738,775 fewer antibiotic
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Jung et al
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conjunction with steroid therapy is the mainstay management of facial paralysis due to chronic otitis media without
cholesteatoma, and it is therefore not necessary to decompress the facial nerve in cases of facial paralysis in noncholesteatomatous chronic otitis media.
Intracranial Complications
Isaacson et al110 investigated pediatric otogenic intracranial
abscesses. An inpatient database was queried for the following diagnostic codes from 2000 to 2008: petrositis (383.2),
acute mastoiditis (383), labyrinthitis (386.3), facial paralysis
(Bells palsy) (351.0), facial nerve disorder unspecified
(351.9), other facial nerve disorders (351.8), subperiosteal
abscess (383.01), Gradenigos syndrome (383.02), meningitis (320), extradural or subdural abscess (324.9), intracranial
abscess (324.0), thrombosis of intracranial venous sinus
(325), and otic hydrocephalus (348.2). Forty patients were
identified with an otogenic intracranial complication. Thirty
patients had evidence of an intraparenchymal, epidural, subdural, or petrous apex suppurative complication of otitis
media. Eighty percent of patients had a canal wall-up mastoidectomy, 10% patients had a craniotomy without a mastoidectomy, and 10% patients were managed with
intravenous antibiotics with or without pressure equalization
tubes. The authors showed that in selected cases, patients
with intracranial abscesses can be managed with intravenous
antibiotics without mastoidectomy. The use of canal wall-up
mastoidectomy is an acceptable alternative to radical mastoidectomy when surgical intervention is necessary.
Lin et al111 investigated the prevalence of chronic otitis
media and its complication rates in teenagers and adult
patients. Complications secondary to COM were identified
in a total of 115 patients. The incidence of COM in adults
decreased per year (R2 = 0.845; P \ .001) from 1998 to
2007. The mean age of patients with COM increased from
44.67 to 49.43 years (linear regression; R2 = 0.896; P \
.001). The prevalence of COM decreased considerably.
However, the annual extracranial complication rate (R2 =
0.109; P = .352) and intracranial rate (R2 = 0.382; P = .057)
have not decreased during the past 10 years. The authors
concluded that the complication rate for COM has remained
steady in the past 10 years, regardless of the overall reduction in the prevalence of COM with the use of antibiotics. A
high index of suspicion and imaging studies for early identification are recommended. Pneumococcal vaccination is
recommended, particularly for elderly patients who are
treated conservatively because of relatively poor general
health conditions.
Mustafa et al112 studied complications of COM with
cholesteatoma during a 10-year period in Kosovo. Among
91 patients (60.4% men and 39.6% women), 1 or 2 complications were recorded. Extracranial (EC) complications
were observed in 57.1%, and intracranial (IC) complications were seen in 31.9%. Eleven percent had multiple
complications. For the IC cases, meningitis (19.7%) and
perisinus abscess (15.3%) were the most common complications. The most often isolated pathogen from ear swabs
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Disclosures
Competing interests: None.
Sponsorships: None.
Funding source: None.
References
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