慢性中耳炎的并發(fā)癥課件

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