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Complicationsof
Chronic
Otitis
Media1Chunfu
DaiThree
categorieson
an
anatomic
basis2Extratemporal
extracranialBezold
abscessSubperiosteal
abscessIntratemporalMastoiditis,
labyrinthitis,
sensorineural
hearing
loss,petrositisFacial
paralysis,
cholesteatoma,
labyrinthine
fistulaIntracranialEpidural
abscess,
lateral
sinus
thrombosis,
otitichydrocephalus,meningitis,
brain
abscess,
subdural
abscessCauses3Hyper-function
of
immune
systemInfant,
olderStrong
bacteriaDamaged
structurescholesteatomaUnreasonable
interventionsDrug
resistant,Poor
drainageTransmission
coursePathways
of
spreadDirect
extension
ofinfection
to
structure(bone
erosion)Hemogenous
routine(microbiologic
an
hostfactors)Bacteria
gain
access
tointracranial
throughunsealed
gap,
innerear45Bezold
abscessDefinition:Erosion
the
tip
of
themastoid
boneInfects
the
soft
tissueofthe
neck,Deep
to
thesternocleidomastoid
muscleDiagnosisEar
infectionMass
in
the
neckFever,
neck
stiff,
otorrheaCT
scan6Bezold
abscessTreatmentAntibioticAbscess
cavity
should
beevacuatedAn
external
drainageshould
be
placedMastoidectomyAntrum
drainage
required,via
epitympanum
tothemiddle
ear7Supperiosteal
abscessDefinition:
Bone
erosion,via
osteitis
or
necrosis,leads
to
a
dehiscenceintothe
postauricular
soft
tissue.DiagnosisFever,
pain
and
otorrheaFollowed
by
appearance
ofthe
postauricular
mass,displacing
the
auricleanteriorlyCT
scan8Supperiosteal
abscess9ManagementsAntibioticDrainage,
using
postauriclar
incisionAfter
achieving
effective
drainage
of
the
mastoidinfection,
the
site
of
suppuration
can
be
addressedNecrotic
tissues
require
debridementLabyrinthitisClassificationsCirvumscribed
labyrinthitis(fistula
of
labyrinth)Communication
of
middle
earwith
perilymphatic
spaceSerous
labyrinthitisToxin,
inflammatory
mediaSuppurative
labyrinthitisBacteria10Fistula
of
labyrinthIncluding
bone
erosion,exposure
of
the
endostealmembrane
and
a
true
fistulainto
the
fluid
compartmentof
the
inner
ear.It
occurs
in5-10%
ofcaseswith
cholesteatomaLateral
semicircular
canal
isthe
most
common
location(90%)Mechanism
of
bone
erosionOsteolysisresorptive
osteitis11Fistula
of
labyrinthDiagnosisVertigo
(intermittent
orconstant)Hearing
lossFistula
test
(only50%of
patientsarepositive)CT
scan
maydemonstrate
evidenceof
fistula,
however,small
fistula
canbeoverlooked12Fistula
of
labyrinthManagementsSurgical
inverventionmastoidectomyRemoval
cholesteatoma
matrix
atthe
primary
operation,
fistulaclosed
with
temporal
fasciaLeaving
cholesteatoma
matrixundisturbed.
9-12
months
later,second
operation
is
performed.antibiotic13Serous
labyrinthitisOccurs
from
inflammation,rather
than
infectionCaused
by
bacterial
toxins,inflammtory
mediatorsInflammatory
cells
rather
thanbacteria
are
found
in
thelabyrintine
fluidsVertigo,
sensorineural
hearingloss14Suppurative
labyrinthitisBacteria
infiltrates
the
fluid
spaceof
inner
earVestibular
symptomsAcute
phase
of
inflammation:Vertigo,
nauseaThe
phase
of
central
compensation:imbalance
or
unsteadinessRecovery
phase:
severeperturbation,
patients
experiencesabrief
sensation
of
vertigo.15Suppurative
labyrinthitisSymptoms
associated
withcochleaPermanent
sensorineuralhearing
lossTinnitus16Suppurative
labyrinthitis17InterventionsAntibioticAddress
the
problem
of
the
underlyingCOMand
cholesteatomaElectrolyte
(due
to
vomiting)PreventionEarly
and
effective
treatment
of
the
COM
andcholesteatomaPetrous
apicitisThe
most
medial
andanterior
portion
ofthetemporal
bone30%
of
temporalboneswith
pneumatization
of
thepetrous
apexProximity
to
the
posteriorand
middle
cranial
fossae18Petrous
apicitis19Classic
triad
(Gradenigo’s
syndrome)Deep
ear
and
retroorbital
pain
(irritation
ofthetrigeminal
nerve)Aural
dischargeIpsilateral
abducents
nerve
palsyPetrous
apicitisManagementsAntimicrobials
directedagainst
the
most
likelypathogens.If
hearing
present
in
theaffected
ear,
otic
capsuleshould
be
preserved
whileeffective
drainage
achievedretrolabyrinthine,infralabyrinthine,infracochlear
approachs
cangain
access
to
the
petrousapex20Petrous
apicitisManagementsThe
affected
ear
isdeadear,
translabyrinthine
ortranscochlear
approachesafford
greater
access
tothe
petrous
apex21Intracranial
complicationsOverviewIt
is
less
frequently,
due
toImproved
access
to
medical
careandmedicationBroad
spectrum
antibioticPathways
of
spreadDirect
extension
of
infection
tointracranial
structure
(bone
erosion)Hemogenous
routine
(microbiologican
host
factors)Bacteria
gain
access
to
intracranialthrough
unsealed
gap,
inner
ear22Epidural
abscess23Epidual
space
is
a
potential
space
betweentheperiosteum
and
outer
dural
layer,
the
tough
duraoften
will
limit
the
spread
of
infection.diagnosisNo
specific
symptoms
and
signs
to
an
epiduralabscess,Pulsative
otic
dischargeHeadache
(associated
with
the
size
of
abscess)CT
reveals
bone
erosion,
abscessMRI
can
detect
dural
thickening
and
inflammationEpidural
abscess24ManagementsSurgical
exploration
and
drainageBone
overlying
the
temgen
tympani,
sigmoid
sinus,and
posterior
fossa
dura
must
be
thinned,epidural
space
should
be
visualized,non
inflamed
dura
is
encountered.Medical
treatmentAntibioticSigmoid
sinus
thrombosisPathwayDirect
extension
of
mastoidinfectionRetrograde
thrombosisAntergrade
thrombosis.25Sigmoid
sinus
thrombosis26DiagnosisClinical
presentation:high,
spiking
fevers,Headache,
Intracraninal
high
pressureactive
ear
diseaseAcute
phase
of
thrombosis,
absence
of
flowsignal
in
MR
venography
imagesSigmoid
sinus
thrombosis27ManagementsSurgical
explorationMastoidectomy
to
expose
the
sigmoid
sinusA
needle
may
be
used
to
aspirate
the
sinus,
if
free-flowing
blood
returns,
then
no
additional
surgery
isneeded.
If
no
blood
returns,
then
open
anddraining
the
sinus
are
indicated.In
the
face
of
ongoing
septic
pulmonary
emboli,internal
jugular
vein
ligation
can
be
performed.Sigmoid
sinus
thrombosis28ManagementsMedical
treatmentAntibioticsAnticoagulation
(in
individual
cases,
in
the
face
ofpropagating
thrombosis)MeningitisAmong
intracranial
complications
ofCOM,
meningitis
is
one
of
themostcommon,
it
account
for
50%
of
theintracranial
complications.In
COM,
bacterial
contaminationmay
occur
via
bone
erosionwithepidural
abscess/granulationformation
or
retrogradethrombophlebitis
of
emissary
veins.29Meningitis30DiagnosisSymptoms
ofCOMHigh
fever,
headache,
vomitingNeck
stiffness
and
altered
mental
statusCT
or
MRI
will
document
meningeal
enhancementLumbar
puncture
and
examination
of
the
CSFismandatory
(CFS
leukocytosis
and
low
glucose,elevated
level
of
protein
and
lactate,
bacteria
culturepresent
positive)Meningitis31ManagementsUrgent
antibiotic
(culture
and
sensitivity
reports
fromthe
CSF
samples
can
further
direct
antibiotic
therapyAdjunctive
therapy
(dexamethasone
can
reduce
theneurologic
and
auditory
squelae
of
bacterialmeningitisReduce
the
high
intracranial
pressureMastoidectomy
(removal
lesion
and
achievement
ofdrainage)Brain
abscess62%
of
abscesseswerelocated
in
the
temporalobeand
34%
in
thecerebellumDirect
extension
alongpreformed
pathways
orperivascular
channels
is
morelikely
route
of
infection.The
thin
bone
of
tegmen
maybe
more
easily
violated
thanthe
bone
overlyingtheposterior
fossa
dura,
given
theincreased
frequency
oftemporal
lobe
versuscerebellar
abscess.32Brain
abscess33phasesInitial
phase:
localized
microfoci
and
cerebritisor
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