fisioterapia - fmrpusprca.fmrp.usp.br/wp-content/uploads/sites/176/2017/06...roth ja; cox jd; hong...
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![Page 1: FISIOTERAPIA - FMRPUSPrca.fmrp.usp.br/wp-content/uploads/sites/176/2017/06...ROTH JA; COX JD; HONG WK. Lung cancer, 3 ed,Blackwell publishing 1-468,2008. Title Câncer Pulmonar Author](https://reader033.vdocuments.pub/reader033/viewer/2022052800/5f0f12247e708231d4425867/html5/thumbnails/1.jpg)
Ft. Luciana G. FerreiraProf. Dr. Paulo R. B. Evora
FISIOTERAPIA - FMRPUSP
DISCIPLINA: PNEUMOLOGIA CLÍNICA E CIRÚRGICA
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Crescimento celular anormal,
incontrolável, que invade os
tecidos vizinhos e à distância.
(Uehara; 1998)
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Neoplasia Pulmonar. Carcinogênese
Epitélio
normalMetaplasia
escamosa Displasia
Neoplasia
Invasiva
= Maligna
Neoplasia Intraepitelial
= Pré-maligna
Ca. in situ
Moderada GraveLeve
Neoplasia
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Tipo mais comum de câncer no mundo;
• – 1.200.000 casos novos/ano (2000)
52% países desenvolvidos
Causa mais comun de morte por câncer no
mundo;
Geralmente de diagnóstico tardio
(INCA 2000 – 2010)
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Pico de incidência aos 60 – 70 anos de idade;
Aproximadamente 27.000 casos novos serão
diagnosticados no Brasil nesse ano:(INCA 2010)
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Homens
2º mais frequente nas regiões
Sul, Sudeste e Centro-Oeste;
3º mais frequente nas regiões
Nordeste e Norte
Mulheres
4º mais frequente nas
regiões Sul, Sudeste, Centro-
Oeste e Norte
5º mais frequente nas
regiões Nordeste
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(INCA, 2010)
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(INCA 2010)
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Susceptibilidade a produtos carcinogênicos
Mais importante: TABAGISMO (80 a 90% doscasos)
Comparados com os não fumantes, ostabagistas têm cerca de 20 a 30 vezes maisrisco de desenvolver câncer de pulmão.
Fumante passivo – risco para CA de pulmão éde 1,2 a 1,5 maior que o não fumante, que não éexposto ao fumo
(Uehara, 1998; INCA 2010)
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Agentes Ocupacionais – asbestos, sílica,
radônio, etc.
Predisposição Genética
• Risco para CA de pulmão é aumentado mais
de 5 vezes, se pelo menos um dos pais
morreu de CA de pulmão
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• Neoplasias Benignas: Hamartomas
• Neoplasias de Malignidade Intermediária: Carcinóides
• Neoplasias Malignas: Carcinomas Broncogênicos
Carcinomas Não Pequenas Células
• Epidermóide – 30%
• Adenocarcinoma – 30%
• Tipos mistos – 20%
• Grandes células – 4%
Carcinomas pequenas células (oat cell) – 14%
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Pequenas células
• Crescimento central;
• Pode estenosar brônquios por compressão
extrínseca;
• Endobrônquica;
• Pode ser acessível a broncoscopia ( central)
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Tumor
Brônquio
Fonte Direito
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Não pequenas células
• Adenocarcinoma
Mundo: mais comum 30 a 35%
Distribuição periférica
Metástase é mais comum
Acesso a broncoscopia é mais difícil
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Carcinoma bronquíolo-alveolar
É um subtipo do ADENOCARCINOMA.
Radiograficamente pode apresentar-se sob a
forma nodular ou de infiltrado difuso, bilateral,
do tipo preenchimento alveolar. A
expectoração abundante, em clara de ovo,
sugere fortemente o seu diagnóstico.
2% dos casos de neo pulmão
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Não pequenas células
• Epidermóide/ Carcinoma de células escamosas ( CEC)
É o mais comum no Brasil (2/3 casos)
Literatura mundial: 30%
Distribuição central, podendo estender-se para hilo e mediastino
Endobrônquico
Crescimento lento/metástases tardias
Pode ser acessível à broncoscopia ( central)
A citologia oncótica de escarro pode ser positiva.
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Não pequenas células
• Carcinoma de grandes células
10 a 20%
Periférico
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Carcinóides
Benignos
Carcinomas broncogênicos( > 90%)
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Assintomático
Sintomático ( 40% a 95%)
• Devido ao Tu. Primário 27%
• Devido a metástases 32%
• Efeitos paraneoplásicos ou sistêmicos 34%
(Carbone et al., 1970; Uehara, 1998)
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Tosse
Hemoptise
Dor torácica
Sibilo ou estridor
Dispnéia
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• Rouquidão e paralisia de diafragma;
• Derrame pleural;
• Coração: dispnéia, tosse, pulso paradoxal, estase jugular e
aumento da área cardíaca;
• Fígado: aumento do volume e nódulos hepáticos palpáveis;
• Supra-renal;
• Óssea;
• Sistema nervoso central: cefaléia, náusea, vômito, hemiparesias
• Síndrome de Pancoast;
• Síndrome da veia cava superior
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Localizado posteriormente no ápice do pulmão,
junto ao plexo braquial, causando sinais e
sintomas relacionados com a infiltração
neoplásica das raízes nervosas – C8, T1 e T2 –
dor intensa,
alteração na temperatura cutânea
atrofia da musculatura do ombro e da mão.
Incidência :4%.
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Síndrome de compressão/invasão
da veia cava superior
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Ocorrem em 10 a 20% dos pacientes – mais comum emcarcinoma indiferenciado de pequenas células
• Caquexia e anorexia;
• Manifestação músculo-esquelética;
• Síndromes hematológicas;
• Secreção inapropriada de hormônio antidiurético;
• Hipercalcemia;
• Síndrome de Cushing;
• Síndrome miastênica de Lambert-Eaton
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Radiografia de tórax;
Tomografia computadorizada de tórax;
Ressonância magnética;
Citologia do escarro;
Broncofibroscopia;
Biópsia por agulha transcutânea;
Mediatinoscopia;
Biópsia a céu aberto;
Toracocentese
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• Determina a extensão anatômica das
neoplasias;
• Indica melhor terapêutica;
• Compara resultados de tratamento;
• Indica prognóstico.
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Denoix (1949) – Sistema TNM
T Tamanho e posição do tumor
N Presença e localização de linfonodos
M Presença de metástases a distância
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• Tx: citologia +, tumor oculto;
• T1: < 3 cm, sem invasão
• T2: > 3cm, ou qualquer tamanho que invade pleura visceral ,
associado a atelectasia lobar ou segmentar ou pneumonite
obstrutiva. A mais de 2 cm da carina
• T3: qualquer tamanho com invasão da parede torácica, pleura
mediastinal, pericárdio sem envolver grandes vasos,traquéia,
esôfago. Ou a menos de 2 cm da carina
• T4: qualquer tamanho, que envolve coração, traquéia, grandes
vasos, esôfago, carina, Presença de derrame pleural maligno
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N1 metástases para lifonodos intrapulmonares
N2 metástases para lifonodos mediastinais
homolaterais
N3 linfonodos mediastinais contralaterais
ou extra-torácicos (supraclaviculares,
pré-escalênicos ou cervicais)
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M0 – nenhuma metástase conhecida
M1- presença de nódulo tumoral
metastático em outro lobo que não o do
tumor primário, metástases à distância
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T1: < 3 cm, sem invasão
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T1 NO MO
ESTADIO IA
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T2: > 3cm, ou qualquer tamanho que invade pleura visceral associado a atelectasia lobar ou segmentar ou pneumonite obstrutiva. A mais de 2 cm da carina
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T2 : 4cm/T2NOMO: Estadio IB
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T2
N1
T2N1MO: IIb
N1: linfonodos peribrônquico ou hilar ipsilateral
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T3
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N1: linfonodos peribrônquico ou hilar ipsilateralN2: linfonodos mediastinais ipsilateral e subcarinal
Estadio IIIa T3N1M0T1-3N2M0
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T3: qualquer tamanho com invasão da parede torácica, pleura mediastinal,pericárdio sem envolver grandes vasos,traquéia, esôfago. Ou a menos de2 cm da carina
Estadio IIb T3N0M0
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T4T4: qualquer tamanho, queenvolve coração, traquéia, grandesvasos, esôfago, carina, Presença dederrame pleural maligno
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Massa comprimindo veia cava
Derrame pleural
Estadio IIIb Qualquer TN3MO
T4qualquerNM0
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N1 N2N2
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Massa hilar
Adenopatia paratraqueal
N2: linfonodos mediastinais ipsilateral e subcarinalT2N2MO: IIIA
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N3
N3 - metástases em linfonodos hilares ou mediastinais
contralaterais, ou escalênico ou subclavicular,
ípsi ou contralateral
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Avaliação Radiológica
do Mediastino
Fator N
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Mediastinoscopia
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T4 M1
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Cerebral
– Uso de CT com contraste (RM)
Supra-renais
– Diferenciar de adenomas benignos (Biópsia)
– Usar US e CT com contraste
Hepática
– Enzimas TGO/TGP, FA. US abdome
Metástases Ósseas
– Mapeamento ósseo
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Estadiamento – Fator M
Cintilografia com TC-99m methylene diphosphonate (MDP)
RNM Cranio
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•A redução na mortalidade, no próximo século, dependerá
primeiramente, da efetividade dos esforços para reduzir a prevalência do
tabagismo;
•O estadiamento dos carcinomas não pequenas células é fator
fundamental no prognóstico. À medida em que progredimos no
estadiamento, menor será a sobrevida em cinco anos
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Doença localizada: quando o tumor é confinado a um
hemitórax e os linfonodos comprometidos são os
mediastinais, supraclaviculares ipsilaterais e hilares
contralaterais. Tumor que apresenta derrame pleural
ipsilateral, envolvimento de nervo laringoesquerdo,
obstrução de veia cava superior.
Doença extensa: doença avançada localmente e à
distância, incluindo envolvimento de pericárdio e
parênquima bilateral.
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• Tipo histológico• Estadiamento
• Idade
• Condição clínica
• Condição
cardiorrespiratória
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• Ressecção oferece o melhor tempo de
sobrevida (potencial) nos pacientes com
doença localizada
Controvérsia:
• Ressecção curativa na presença de linfonodos
mediastinais comprometidos
• Tratamento dos tumores localmente avançados
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Câncer do pulmão
Tratamento
Carcinoma de pequenas células
Quimioterapia e/ou radioterapia
Ressecção ? + Quimioterapia (T1NO, T2NO)
Demais carcinomas
Ressecção pulmonar – estágios I, II, e IIIa
Quimioterapia e/ou radioterapia adjuvante?
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• Ressecção em
cunha
• Segmentectomia
• Lobectomia
• Pneumectomia
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Como operar
1. Remoção completa do tumor e sua drenagem
linfática intrapulmonar (pneumonectomia
ou lobectomia)
2. Boa margem de segurança no coto brônquico
4. Linfadenectomia mediastinal (estadiamento)
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Pneumonectomia à esquerda
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Pneumonectomia à esquerda
Tardio
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Diagnósticos diferenciais
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Nódulo pulmonar
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Hamartoma
(benigno)
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RESSECÇÃO EM CUNHA
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Videotoracoscopia
RESSECÇÃO EM CUNHA
Biópsia de Congelação (patologista)
Benigno Maligno
Lobectomia + Esvaziamento
Mediastinal
Operação concluída
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UEHARA C; JAMNIK S & SANTORO IL. Câncer
de pulmão. Medicina, Ribeirão Preto, 31: 266-
276, abr./jun. 1998
Estimativa 2010/ incidência de câncer no
brasil.
http://www.inca.gov.br/estimativa/2010/
ROTH JA; COX JD; HONG WK. Lung cancer, 3
ed, Blackwell publishing 1-468,2008.