Prof. Dr. Lucio A. Castagno Otorrinolaringologia [email protected] .
Transcript of Prof. Dr. Lucio A. Castagno Otorrinolaringologia [email protected] .
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Prof. Dr. Lucio A. CastagnoOtorrinolaringologia
www.clinicadrcastagno.com.br/Arquivos
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Fisiologia do equilíbrio
Humanos usam 3 sistemas:
1. Visual2. Proprioceptivo3. Vestibular
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3. Vestibular Informa posição da cabeça no espaço.Aceleração angular (rotatória).Aceleração linear.
3 canais semicircularesSáculo Utrículo.
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Fluidos vestibularesPerilinfa: labirinto ósseo;
similar ao líquido extracelular (-K e +Na).
Endolinfa: interior do labirinto membranoso; similar ao fluido intracelular (+K e – Na).
Ambos fluidos em continuidade a cóclea.
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Receptores vestibulares
Estrutura receptora Órgão Estímulo detectado
Otólitos:
Sáculo
macula Gravidade e aceleração linear vertical
Utricule macula Gravidade e aceleração linear horizontal
Canais semicirculares:
Horizontal (lateral)
Posterior
Superior
ampola Aceleração angular (rotacional)
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Macular hair cellsin the utricle.
At rest the utriclecilia stand upstraight.
Tilting of the headallows pull fromgravity to pull onthe gelatinous capand bend the haircells.
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A mácula utricular é horizontal, enquanto a mácula sacular é vertical. A orientação da despolarização nas máculas é indicaca pelas setas, permitindo a detecção de aceleração linear em qualquer plano direção.
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Estímulos opostos simétricos = equilíbrio
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Canais semicircularesDetectam aceleração angular (=
rotatória).As células ciliadas situam-se em
uma membrana (crista) embebida em uma cúpula gelatinosa (ampola).
Aceleração movimenta a endolinfa e também os cílios na ampola do canal semicircular.
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Canais semicircularesRespondem a aceleração angular (rotatória) no plano
do canal.Funcionam aos pares (excitação em um lado é
acompanhada de inibição no outro).
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Reflexos Vestibulares1) Reflexo vestibulo-ocular: quando sua cabeça vira
para a direita, seus olhos movem-se para esquerda visando manter a fixação na imagem original.
Outras conecções produzem náuseas quando há conflito na informação vestibular e visual.
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Avaliando pacientes com distúrbios do equilíbrio
1. Anamnese 2. Exame clínico3. Eletronistagmografia (vectonistagmografia)4. Videonistagmoscopia5. Posturografia Dinâmica
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1. Anamnese
Anamnese é o mais importanteDecrição completa dos sintomasVertigem (=rotatório) ou tontura?Início, duração, agravantes, hipoacusia,
tinitus, pressão aural, limitação funcional.
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2. Exame clínicoExame cardiovascular geralExame de pares craneanosCoordenação cerebelar (disdiadocosinesia):
index-nariz e marchaPropriocepção / Vestibulospinal
Teste de RombergReflexos tendinosos profundosPropriocepção
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2. Exame clínicoPresença de nistagmo:
Direção (componente rápida)Rotatório (=torsional)Efeito inibidor da fixação ocular
Óculos de Frenzel
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2. Exame clínicoProvas de provocação:
HiperventilaçãoDix-HallpikeProva calórica
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3. Exames complementares
Eletronistagmografia (vectonistagmografia)VideonistagmoscopiaPosturografia Dinâmica
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EletronistagmografiaRegistra o movimento reflexo dos olhos devido a
diferença de potenciais bioelétricos entre a córnea e a retina.
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NistagmoA fase lenta do nistagmo é induzida pelo movimentos da
endolinfa dentro do labirinto membranoso; a fase rápida é a correção do SNC (retorno a posição inicial).
A fase lenta representa a atividade vestibular.
A intensidade do nistagmo é medida pela “velocidade angular da componente lenta” nos aparelhos de eletronistagmografia.
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EletronistagmografiaProva calórica: 30 e 44ºC (água/ar); única que testa
labirinto isoladamente
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EletronistagmografiaProva calórica
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VideonistagmoscopiaVideocamara infravermelho registra
diretamente o movimento ocular
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Posturografia Dinâmica
Avalia o reflexo vestíbulo-espinhal:
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Sempre diferencie vertigem (=alucinação de movimento) de “tontura”.
80% das vertigens tem origem periférica no
labirinto !
80% das vertigens tem origem periférica no
labirinto !
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TONTURA (não vestibular)
Distúrbio Achados ManejoPré-síncope vagal Calor; stress Evitar precipitantes
Hipotensão ortostática
Queda >20mmHg ao levantar
Remover medicação
Pré-síncope cardíaca Arritmia Antiarrítmicos; marcapasso
Hipoglicemia Baixa glicemia Glicose
Pânico Ansiedade extrema Anti-serotonina
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VERTIGEM: Periférica x Central
Periférica CentralNáuseas – vômitos Graves Moderados
Desequilíbrio Moderado Grave
Hipoacusia Comum Rara
Oscilopsia Moderada Grave
Sintomas associados Auditivos Neuro-visuais
Compensação Rápida Lenta
LABIRINTOPATIAS
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DÚVIDAS
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Prof. Dr. Lucio A. CastagnoOtorrinolaringologia
www.clinicadrcastagno.com.br/Arquivos
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“LABIRINTOPATIAS”Vertigem posicional paroxística benignaDoença de MénièreNeuronite vestibular
CinetoseSíndromes cervicaisSíndrome multisensorial do idosoEnxaqueca vestibular
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1- VPPB: Vertigem posicional paroxística benignaVertigem fugaz (minutos)
secundária a movimentação da cabeça.
Possível náuseas e vômitos.Desequilíbrio.Sem sintomas auditivos.Causado pelo deslocamentos
dos otólitos utrículares para a ampola do canal semicircular posterior (cupulolitíase).
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VPPB: DiagnósticoAnamneseExame ORL
MANOBRA DE DIX-HALLPILE
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VPPB: TratamentoAuto-limitadoReabilitação labiríntica (Manobra de Epley)Depressores vestibulares
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2- Neuronite Vestibular (labirintite aguda)Vertigem súbita e intensa (horas)Nistagmo (fase lenta -> labirinto afetado)Sem sintomas audiológicosAuto-limitada em 2-3 semanasIVARS prévia -> inflamação do nervo ou núcleo
vestibular
Tratamento:Depressores vestibulares
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Labirintopatias: Princípios de tratamentoFase aguda ou sub-aguda:
Equilibrar estímulos de ambos labirintos (bloqueio do labirinto sadio)
Depressores vestibularesAnsiolíticosAntieméticos
Fase crônica (>4-6 semanas):Compensação cerebelar central
Exercícios de reabilitação labiríntica
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Labirintopatias:Depressores vestibularesFase aguda Posologia
Diazepam 10mg q8h IM ou IV
Dimenidrato+B6 (Dramin B6) 50mg/50mg q8h IM
Prednisona 20mg q8-12h VO
Fase subaguda Posologia
Betaistina (Labirin) 24mg q12h VO
Cinarizina (Stugeron) 75mg qD VO
Flunarizina (Vertix) 10mg qD VO
Dimenidrato (Dramin) 50mg q8h VO
Meclizina (Meclin) 25mg q8h VO
Ginkgo biloba (Tebonin) 120mg q12h VO
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3- Doença de Ménière
Hipoacusia flutuante
Vertigem recorrente (horas ou dias)
Zumbidos (tinitus)
“Pressão nos ouvidos”
Prosper Ménière (1799-1862)
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DOENÇA DE MÉNIÈREHistórico1861 - Prosper
Ménière: descreve síndrome de surdez, tinitus e vertigem causada por lesão no labirinto
1938 – Hallpike e Cairns: patologia da hipertensão (hidropsia) endolinfática
Hidropsia endolinfática
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CócleaCaracol com 2 3/4
voltas ao redor de um coluna óssea
Três canais:Escala Vestibular Escala TimpânicaEscala Média
Perilinfa Endolinfa
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Órgão de Corti
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FisiologiaFisiologia
PerilinfaPerilinfa – similar ao LCR (alto Na+, baixo – similar ao LCR (alto Na+, baixo K+)K+)
EndolinfaEndolinfa – produzida na – produzida na Stria VascularisStria Vascularis (baixo Na+, alto K+); escala media(baixo Na+, alto K+); escala media
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Células ciliadasdo Órgão de Corti
Outer Hair Cells (células ciliadas externas)
Inner Hair CellInner Hair Cell (célula ciliada interna)(célula ciliada interna)
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DOENÇA DE MÉNIÈRE
Labirinto membranoso normal Labirinto membranoso dilatado (hidropsia endolinfática)
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DOENÇA DE MÉNIÈREEpidemiologia
Predomínio em brancos1/1000 da população20-50 anos (raro em crianças)Bilateral em 40%
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DOENÇA DE MÉNIÈREEtiologia
MÉNIÈREMÉNIÈRE ? ?
MÉNIERE ?MÉNIERE ?
MENIÈRE ?MENIÈRE ?
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DOENÇA DE MÉNIÈREEtiologia Multifatorial
1) Anatômico: redução de pneumatização do mastóide e hipoplasia do aqueduto vestibular
2) Genético: 7.7% hereditário
3) Imunológico: deposição de imunocomplexos no saco endolinfático
4) Viral ?
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DOENÇA DE MÉNIÈREEtiologia Multifatorial
5) Vascular: associado a enxaqueca
6) Psicológica: obsessivo; neurótico
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D.MÉNIÈRE: PatofisiologiaD.MÉNIÈRE: Patofisiologia
HidropsiaHidropsia endolinfáticaendolinfática(=hipertensão) leva a (=hipertensão) leva a distorção da membrana de Reissner no distorção da membrana de Reissner no labirinto membranoso labirinto membranoso
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D.MÉNIÈRE: PatofisiologiaD.MÉNIÈRE: Patofisiologia
Hipertensão endolinfática pode Hipertensão endolinfática pode causar causar microrupturas na membrana microrupturas na membrana de Reissnerde Reissner..
Essas rupturas são confirmadas em Essas rupturas são confirmadas em vários estudos histológicos.vários estudos histológicos.
Review Article: Minor, Lloyd et al, Meniere’s Disease, Current Opinion in Neurology 17(1) Feb2004
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D.MÉNIÈRE: PatofisiologiaD.MÉNIÈRE: Patofisiologia
Review Article: Minor, Lloyd et al, Meniere’s Disease, Current Opinion in Neurology 17(1) Feb2004
MICRORUPTURAS NA MEMBRANA DE
REISSNER
HIPERTENSÃO ENDOLINFÁTICA
Crises VERTIGEM
HIPOACUSIA
TINITUS
Cicatrização HIPOACUSIA FLUTUANTE (melhora
audição)
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Vincent van Gogh(Holanda 1853-1890)
Auto-retrato com orelha enfaixada (1890)
Noite Estrelada (1889)
DOENÇA DE
MÉNIÈRE ?
DOENÇA DE
MÉNIÈRE ?
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PatofisiologiaPatofisiologia
O que causa a hidropsia?O que causa a hidropsia?
– Obstrução do ducto ou saco endolinfático.Obstrução do ducto ou saco endolinfático.
– Alteração na absorção da endolinfa Alteração na absorção da endolinfa (“síndrome de (“síndrome de mal absorção da endolinfa”?)mal absorção da endolinfa”?)
– Lesão imunológica no ouvido interno Lesão imunológica no ouvido interno (níveis (níveis elevados de Ig na endolinfa)elevados de Ig na endolinfa)
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DOENÇA DE MÉNIÈREDiagnósticoAnamnese
AudiometriaEletrococleografiaEletronistagmografiaCT-ouvidos
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DOENÇA DE MÉNIÈREQuadro clínico
Hipoacusia + vertigem + tinitus
Enfermidade crônica “dinâmica”Estágio I: vertigem; assintomático nas
remissões.Estágio II: hipoacusia sensorial para sons
graves (flutuante -> permanente); sem vertigem.Estágio III: surdez; vertigem->desequilíbrio.
(AAOHNS 1972, 1985 e 1995)
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DOENÇA DE MÉNIÈREAudiometria
a) Hipoacusia em freqüências graves (tinitus de baixa freqüência= graves)
b) Hipoacusia em graves e agudos (melhor audição em 2kHz)
c) Hipoacusia em todas as freqüências
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Cóclea: Freqüências
Agudos = janela oval e turno basal
Graves = apex
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DOENÇA DE MÉNIÈRETratamento
Empírico; etiologia desconhecida
Efeito placebo
Vertigem desaparece após anos (70% dos casos)
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Hipócrates(Grécia, Cós, 460-370 AC)
“Primun non nocere” (“primeiro não faça mal”)
Pai da medicinaMedicina X ReligiãoEscolas gregas de medicina:
Cnido: diagnósticosCós: prognósticos; tratamento
passivo (ag, cron, crise, endêmico, epidêmico, reagudização, resolução... Hipócrates! )
“Primun non nocere” (“primeiro não faça mal”)
Pai da medicinaMedicina X ReligiãoEscolas gregas de medicina:
Cnido: diagnósticosCós: prognósticos; tratamento
passivo (ag, cron, crise, endêmico, epidêmico, reagudização, resolução... Hipócrates! )
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DOENÇA DE MÉNIÈRETratamentoCrise aguda: cinarizina/flunarizina;
diazepam
Manutenção: restrição sal; diuréticos (furosemide/hct); betaistina; cinarizina/flunarizina; corticóides
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DOENÇA DE MÉNIÈREPrescrição
1. Restrição de sódio2. Hidroclorotiazida (DrenolR) 25-50mg qD 2-
3m3. Betaistina (LabirinR) 24mg q12h 2-3s4. Flunarizina 10 mg (VertixR) qD 3-4 s5. Dimenidrato 100mg (DraminR) q6h prn
Obs: Diversos outras drogas também podem ser usadas e a posologia é muito variável de acordo com a intensidade do quadro clínico. A prescrição acima representa apenas uma entre várias alternativas.
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DOENÇA DE MÉNIÈRETratamento cirúrgicoAblativo: destruição do neuroepitélio do
ouvido interno; injeção intratimpânica de gentamicina (90% controle da vertigem e 25% risco de surdez coclear).
Cirúrgico:a) Conservador: drenagem saco endolinfático;
secção do nervo vestibular.b) Destrutivo: labirintectomia; cocleosaculotomia.
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DOENÇA DE MÉNIÈRESumário
Etiologia multifatorialHidropsia endolinfáticaDiagnóstico: vertigem, hipoacusia e
zumbidosDoença crônica (longos períodos de
remissão)Tratamento clínico (cirurgia apenas em
vertigem severa incapacitante)
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CASO CLÍNICO 1JB, fem., 48anos:
episódios vertiginosos há 5 meses (duração dias); hipoacusia flutuante e “pressão” OE; tinitus OE contínuo.
ENG normalCT e IRM normais
AUDIOMETRIA
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Caso 1Diagnóstico é ?
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Caso 1Diagnóstico é ?
Doença de MÉNIÈRE OE
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CASO CLÍNICO 2RH,masc.,50 anos:
tontura, hipoacusia flutuante e tinitus OE há 5 anos; crises de vertigem (duração horas).
Cofose OD secundária a cirurgia de decompresão do saco endolinfático há 10 anos.
AUDIOMETRIA
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Caso 2Diagnóstico é ?
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Caso 2Diagnóstico é ?
Doença de MÉNIÈRE BILATERAL
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CASO CLÍNICO 3JM, masc., 76 anos:
vertigem fugaz (minutos) ao virar na cama, com náuseas e vômitos, há 3 semanas; ausência de tinitus e “pressão”; hipoacusia progressiva bilateral há cerca de 10 anos (não flutuante).
AUDIOMETRIA
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Caso 3Diagnóstico é ?
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Caso 3Diagnóstico é ?
VERTIGEM POSICIONAL PAROXÍSTICA BENIGNA
... Nem tudo é sempre Doença de Ménière !
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Charles Robert Darwin (Inglaterra 1809-1882)
“A Origem das Espécies” (1859)Viagem de 5 anos no HMS BeagleDoença de Ménière
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www.clinicadrcastagno.com.br/Arquivos
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Elizabeth J. Rosen, M.D.Jeffery T. Vrabec, M.D.
5/24/00
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LabyrinthitisInflammatory process involving the inner ear
infectious vs. non-infectiousgeneralized vs. circumscribedacquired vs. congenitalisolated vs. systemic
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PathogenesisMeningogenic
spread through IAC or cochlear aqueductTympanogenic
spread through round or oval windowsHematogenic
spread through vascular channels
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Bacterial InfectionsToxic Labyrinthitis
sterile inflammationbacterial toxins
penetrate perilymphatic spaces
mild hearing loss or mild vestibular loss
usually resolves without sequelae
Suppurative Labyrinthitisbacterial invasion of
the inner earintense inflammatory
reactionprogresses along four
pathologic stagesmedical emergency
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Suppurative LabyrinthitisPresentation--acutely ill patient with severe
vertigo, N/V, profound hearing lossLook for signs of associated meningitis or
otitis mediaHospitalization, hydration, vestibular
suppressants, IV antibiotics
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Bacterial LabyrinthitisMeningogenic
S. pneumoniaeN. meningitidisH. influenzae
TympanogenicS. pneumoniaeH. influenzaeM. catarrhalisPseudomonasProteusAnaerobes
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Bacterial MeningitisIncidence of post-meningitic hearing loss is
10-20%Hearing loss occurs early in the course of
meningitisMost often bilateral, severe to profound, and
permanentManagement = Antibiotics +/- Steroids
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SyphilisCongenital Syphilis
primary maternal infection = 70-100% transmission
early congenital syphilis symmetrical, flat, profound SNHL
late congenital syphilis asymmetric, fluctuating, variable severity
SNHL lower discrim scores than expected with PTA
Acquired Syphilis secondary or tertiary disease
hearing loss similar to late congenital infection
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SyphilisDiagnosis
non-specific screening testsspecific confirmatory tests
TreatmentPenicillin+/- Steroids
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SyphilisTemporal Bone Findings
Early congenital/Acute acquired round cell invasion of CN VIII, nerve fiber loss degeneration of organ of Corti and spiral ganglion fibrinous exudate and hemorrhage
Late congenital/Late acquired obliterative endarteritis round cell osteitis gumma formation
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Viral InfectionsMay present as congenital syndrome, systemic
illness, or isolated inner ear infectionDefinitive infection has been identified only
with CMV and mumps virusSuspects include: rubella, rubeola, influenza,
varicella-zoster, EBV, poliovirus, RSV, adenovirus, parainfluenza, herpes simplex
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CytomegalovirusMost common congenital infection in U.S.
1% of all live births
Infection via transplacental transmission, passage through infected birth canal, ingestion of infected breast milk
40% transmission rate with primary maternal infection; .15%-1.0% transmission rate from seropositive mothers
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Cytomegalovirus90% asymptomatic at birth
10-15% develop SNHL variable in severity risk factors include periventricular calcifications,
high maternal antibody titers
10% symptomatic at birth90% with cytomegalic inclusion disease65% with SNHL
bilateral, severe to profound, permanent
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CytomegalovirusDiagnosis
viral culture specific antibody testing
Treatment acyclovir, gancyclovir, foscarnet vaccine
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CytomegalovirusTemporal Bone Findings
Hematogenic Spread stria vascularis endolymphatic spaces
Meningogenic Spread CN VIII, cochlear aqueduct perilymphatic spaces
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RubellaDecrease in incidence since introduction of
rubella vaccineTransmission to fetus associated with
primary maternal infection First trimester = 90% symptomatic Second/Third trimester = 25-50% symptomatic
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RubellaCongenital Rubella Syndrome
triad of cataracts, heart deformities, SNHL
Hearing Loss 50% of symptomatic infants 10-15% of asymptomatic infants variable in severity, “cookie-bite” pattern on
audiogram, permanent
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RubellaDiagnosis
viral culture specific antibodies
Treatment vaccination antepartum screening auditory rehabilitation
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RubellaTemporal Bone Findings
Scheibe malformationcollapse of Reissners membranetectorial membrane abnormalitiesatrophy of stria vascularis
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MumpsTriad of parotitis, orchitis, meningo-
encephalitisPrimarily affects children and young adultsHearing loss in .05% of cases
presents as parotitis is resolving 80% unilateral, maximal in HF, severe to profound,
permanent associated tinnitus and aural fullness
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MumpsDiagnosis
viral culture specific antibodies
Treatment vaccination auditory rehabilitation
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MumpsTemporal Bone Findings
Hematogenic spread infection of stria vascularis and endolymph degeneration of organ of Corti, tectorial membrane
and cochlear neurons
Meningogenic spread spread through CN VIII or cochlear aqueduct into
perilymph degeneration of modiolar neural elements fibrosis/ossification of perilymph spaces
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MeaslesTriad of rash, conjunctivitis, Koplik spotsHearing loss seen in less than 1 per 1,000
cases variable in severity unilateral or bilateral worse in high frequencies permanent
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MeaslesDiagnosis
viral isolation specific antibodies
Treatment vaccination auditory rehabilitation
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MeaslesTemporal Bone Findings
cochlear degenerationatrophy of stria vascularisabnormalities of tectorial membranemacular degeneration
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Varicella-ZosterPrimary infection = chicken pox
Reactivation = zosterRamsay Hunt syndrome
vesicles on pinnae or EAC facial weakness/paralysis SNHL
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Varicella-ZosterDiagnosis
clinical presentation culture of vesicular fluid
Treatment antiviral therapy steroids analgesics
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Varicella-ZosterTemporal Bone Findings
facial nerve inflammationvestibulocochlear nerve inflammationdestruction of organ of Cortieventual fibrosis and ossification
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Herpes SimplexHSV-1
reactivation within spiral ganglion causing SSNHL
HSV-2 encephalitis with spread along CN VIII to perilymph
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Human Immunodeficiency VirusPresentation may include sudden hearing
loss, tinnitus or vertigoMechanisms include direct infection of
labyrinth with HIV, opportunistic infection, neoplasm, or drug ototoxicity
Most common finding is mild SHNL
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Human Immunodeficiency VirusTemporal Bone Findings
isolation of CMV, adenovirus, HSV-1invasion with pneumocystis, cryptococcushair cell inclusions, viral-like particles
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Protozoal InfectionsToxoplasmosis
Congential infection triad of chorioretinitis, hydrocephalus, intracranial
calcifications first trimester infection associated with severe
manifestations third trimester infection associated with highest
transmission rate 75% are asymptomatic at birth up to 85% later present with hearing loss
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ToxoplasmosisDiagnosis
maternal infection IgG seroconversion or rise in titers
fetal infection mouse inoculation or PCR of amniotic fluid umbilical cord blood IgM or quantitative IgG
Treatment combination therapy with pyrimethamine and
sulfonamide 70% reduction in transmission reduction in sequelae
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Fungal InfectionsOccur in immunocompromised hostsReported pathogens include Mucor,
Cryptococcus, Candida, Aspergillus, and Blastomyces
Meningogenic, Tympanogenic, Hematogenic spread to the labyrinth
Treat with appropriate antifungals
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Acute Cochlear LabyrinthitisISSNHLDefinition
30 dB deficit3 contiguous frequenciesover a 3 day period
Mechanismviral infection
30-50% report recent URI
vascular compromisemembrane rupture
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ISSNHL90 % unilateralvariable in severitysudden in onsetpainlessassociated with tinnitus or aural fullnessassociated vestibular dysfunction
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ISSNHLDifferential Diagnosis
autoimmune, trauma, neoplasm, ototoxic meds, vascular accidents
Labs CBC, ESR, glucose, FTA-ABS
Imaging CT, MRI
Auditory/Vestibular Testing audiogram, ENG
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ISSNHLTreatment
Steroid therapy (Wilson, 1980) double blind, controlled study compared oral steroid to placebo recovery rate of 61% in treatment group recovery rate of 32% in control group moderate hearing loss showed most
improvement with steroid therapyAntiviral therapy
interferon acyclovir
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ISSNHLPrognosis
30-70% have partial/complete recoveryGood prognostic factors:
< 40 y/o present within 10 days of onset mild hearing loss steroid therapy for moderate hearing loss no vestibular symptoms
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Acute Vestibular LabyrinthitisDiagnostic Criteria (Coatis)
1. Acute, unilateral peripheral vestibular d/o without associated hearing loss
2. Occurs most frequently in middle age3. A single episode of severe prolonged vertigo4. Decreased caloric response in the involved
ear5. Resolution of symptoms in 6 months
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Acute Vestibular LabyrinthitisDifferential Diagnosis
Meniere’s disease, vestibular schwannoma, labyrinthine fistula, cerebellar infarction, multiple sclerosis, dysequilibruim of aging
Auditory/Vestibular Testing audiogram (by definition should be normal) ENG
Imaging CT, MRI
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Acute Vestibular LabyrinthitisTreatment
Supportive hydration vestibular suppressants antiemetics
PrognosisRecovery/Compensation within 6 months
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Conclusion
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Case Presentation23 y/o man presents to ENT clinic reporting
complete loss of hearing in the right ear that he noticed upon awakening yesterday morning.
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Case PresentationAdditional History
no otalgia, no otorrheano associated vertigo+ right tinnitus
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Case PresentationPast Medical History
nonePast Surgical History
inguinal hernia repair age 17Medications
noneAllergies
NKDA
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Case PresentationPhysical Examination
normal EAC and TM bilaterallyneurologic exam normalWeber to leftRinne: left AC>BC, right no response
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Case PresentationWork-Up
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Case PresentationWork-Up
Audiogram
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Case PresentationWork-Up
AudioLabs
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Case PresentationWork-Up
AudioLabsImaging
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Case PresentationDifferential Diagnosis
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Case PresentationDifferential Diagnosis
infectious labyrinthitis viral late congenital/acquired syphilis
autoimmune labyrinthitisvascular accident
traumaneoplasm
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Case PresentationTreatment
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Case PresentationTreatment
oral steroid taper
anti-viral meds
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Case PresentationFollow-up ?
Prognosis ?
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Case PresentationFollow-up
repeat audio 2 weeks after presentation, steroid taper should be finished
repeat audio 6 weeks after presentation
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Case PresentationGood Prognostic
Factorsless that 40 y/opresentation within
10 days of onsetno vestibular
symptoms
Poor Prognostic Factorsevere to profound
loss on initial audiogram
associated with less that 20% chance of recovery regardless of intervention