Tumor Otak
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Transcript of Tumor Otak
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Tumor Otak
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Tumor otak Definisi:
Tumor otak/tumor intra kranial:Massa yang timbul dalam ruang tengkorak dan menimbulkan proses desak ruang
Epidemiologi:- Insiden ± 10-17 per 100.000 orang.- Tumor otak primer ± 15/100.000 - Tumor otak sekunder ± 2-11/100.000- < 12 th : ± 2-3/100.000- 20-40% pada anak keganasan- ± 1,7% mengakibatkan kematian
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EtiologiPenyebab utama belum diketahui, biasanya ada faktor genetik, namun ada beberapa faktor yang berhubungan dengan perkembangan tumor, a.l.:
1. Herediter ; pd neurofibromatosis (von reckling housen), hemangioblastoma (von Hippel lindau), fakomatosis
2. Embrional; medulloblastoma, ependimoma, kraniofaringioma.
3. Virus onkogenik; ependimoma, meningioma, schwannoma diduga ada hubungan dengan infeksi kronis
4. Bahan karsinogen; hidrokarbon polisiklik, metilnitrosid
5. Radiasi6. Diet7. Dll
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Klasifikasi 1. Neuroepithelial:- Astrocyte astrocytoma- Oligodendrocyte oligodendroglioma- Ependymal cells ependimoma
choroid plexus Papilloma
Glioma - Neurons ganglioglioma/gangliocytoma
neuroblastoma- Pineal cells pineocytoma/pineoblastoma- Poorly defferentiated glioblastoma
multiforme- Embrionic cells medulloblastoma
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2. Meningen meningioma3. Nerve sheat cells neurofibroma
neurilemmoma/schwannoma4. Blood vessels hemangioma, hemangioblastoma5. Germ cells germinoma
teratoma6. Tumours of mal developmental origin:
- Craniopharyngioma- Epidermoid/dermoid cyst- Colloid cyst
7. Anterior pituitary gland- Pituitary adenoma- Adenocarcinoma
8. Metastases9. Lain-lain
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Untuk terjadi keganasan :
Diperlukan mutasi beberapa gen yg kompleks :•Oncogen : gen utk pertumbuhan (hiperaktif dr oncogen)•Gen suppresor tumor : gen menekan pertumb ( inaktif)•Gen utk apoptosis : kematian sel terprogram (inakif)• Gen utk perbaian DNA : inaktif• angiogenesis : molekul utk pertumbuhan vaskularisasi
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Tumor Otak1. Primer : dr SSP 50 - 80%- Glioma 50%
- astrositoma- glioblastoma multiforme- ependimoma- dll
- Meningioma 10-20%- Adenoma pituitari 10%- Neurinoma 5%- Kongenital 10%- Lain-lain 5%
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2. Sekunder : <50%A. Secara hematogen
70% multiple
B. Infiltratif : Ca nasofaring C. Melalui cairan likuor serebrospinalis ke
medulla spinalis . - Granuloma : Tuberkuloma
Sifiloma - kiste parasit: Kiste hidatik
Kiste sertiserkusis
-Dari paru 50%-Dari mamae 20%-Dari gastrointestinal 8%-Dari traktus urogenetalis 6%-dll
80% : Serebri17% : Serebellum3 % : batang otak ganglia basalis
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LokasiFrontal 22%Temporal 22%Parietal 12%Pituitari 10%Oksipital 4%Fossa posterior 30%
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LokasiDewasa:- Supratentorial 80-85% - Glioma- Infratentorial 15-20% - Metastase
- MeningiomaAnak2- Supratentorial 40% -
Meduloblastoma- Infratentorial 60% - Astrositoma-
serebelum
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Morfologi dan Sitologi TumorI. Benigna
Tumbuh lambat Batas jelas, tidak infiltratif Struktur sel reguler Mitosis lambat Deferensiasi struktur sel jelas
(parenkim, stroma tersusun teratur)
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II. Maligna Tumbuh cepat Sel tumor infiltratif sehingga batas tak jelas Selularitas meningkat Rasio inti dan sitoplasma tidak baik (inti >
sitoplasma) Formasi sel-sel raksasa Deferensi sel kurang baik Mitosis cepat Nekrosis Kiste
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PatofisiologiIsi tengkorak1. Jaringan otak (sel & cairan intra-
ekstrasel 80%):- Edema otak- Massa di otak
a. Herniasi sub falcineb. Herniasi tentorial- Lateral unkus lobus temporal- Sentral diensefalon
c. Foramen magnum tonsil serebelli
Herniasi
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Patofisiologi2. Likuor serebro spinalis (±10%)
Bila likuor bertambah desakan LCS keluar :- Melalui foramen magnum ke ruang
arakhnoid - Melalui foramen optikum orbita papil edema
3. Darah (±10%) Ganguan sirkulasi Permeabilitas kapiler Edema otak
Refleks cushing : tensi Bradikardia
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Gejala
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Gejala Efek MasaI. Gejala dan tanda peningkatan TIK (gx
umum):a. Nyeri kepala:- Terutama pada pagi hari (bangun tidur)- Karena peregangan struktur peka nyeri
(arteri besar, vena, sinus duralis, saraf otak 5,9,10, saraf servikalis 1-3)
b. Vertigo :- Terutama tumor infratentorial- Karena edema labirin
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c. Muntah- Proyektil- Tidak ada hub dg makan atau nyeri perut- Karena rangsangan pada inti batang otak
d. Gangguan kepribadian- Mudah lelah, tidak acuh, kurang perhatian,
menarik diri, lamban, masa bodoh- Dapat pula; tidak bisa diam, mudah marah,
emosi labil- Mengantuk, kesadaran menurun, stupor
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e. Kejang umum- Tu tumor supratentorial
f. Kepala membesar- Tu pada anak yang fontanella dan suturanya
belum tertutup
g. Papil bendung:- Dapat terjadi papil atrofi (sekunder) dengan
gangguan visus yang menetap
h. tanda-tanda vital- Peningkatan TIK trias cushing (bradikardia,
hipertensi sistolik, frekwensi pernafasan menurun)
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Gejala fokalSupratentorial LESI LOBUS FRONTALIS:
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Kelemahan tangan, kaki, atau wajah kontralateralAfasia motorik (hemisfer dominan)Perubahan kepribadian:
Tingkah laku anti sosialKetidak mampuan mengontrol diriKehilangan kemauanPenurunan intellegensiaDemensia bila korpus kallosum terlibat
Sindroma Foster-Kennedy (lesi di frontal bag basal)Anosmia ipsilatAtrofi papil ipsilatEdema papil kontralatPerubahan kepribadian
Gejala lobus frontalis
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Lesi LOBUS OKSIPITALIS- Gangguan lap pandang ; hemianopsia homonim
Lesi KORPUS KALLOSUM- Apraksia- Buta kata
Lesi LOBUS PARIETALIS Gangguan sensibilitas:
• Topognosis• Dua titik• Gerak pasif• Asterognosis• Ketajaman perabaan
Gangguan lapangan pandang (quadrianopsia homonim inferior)
Disorientasi kiri-kanan, finger agnosia, akalkulia, agrafia (gertsman syndrome lobus dominan di girus Supramarginalis)
Apraksia dan agnosia hemisfer non dominan girus Angularis
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Lesi LOBUS TEMPORALIS- Afasia sensorik Wirnicke- Gangguan lap pandang quadrianopsia
homonim superior
Lesi HIPOTHALAMUS:• Gangguan fungsi endokrin• Regulasi temperatur• Keseimbangan cairan dan elektrolit• dll
Lesi di SINUS KAVERNOSUS melibatkan N III,IV,VI.
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Gejala FokalInfratentoriala. Gejala lesi batang otak:- Lesi N Kranialis (III-XII)- Gangguan jaras motorik dan sensorik alternans- Penurunan kesadaran- Tremor- Gangguan gerak bola mata- Pupil tidak normal- Hiccup
b. Gejala lesi serebelum:- Gait ataksia- Intension tremor- Dismetria- Disartria- Nistagmus
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Diagnosaa. Anamnessa:- Nyeri kepala hebat- Mual, muntah- Kejang
b. Funduskopi- Papil edema ok TIK
c. EEG : abnormal fokus gelombang lambat
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d. Foto kepala:
1. TIK 2. Kalsifikasi glandula pinealis,
pendorongan pineale3. Destruksi tulang, hiperostosis,
osteolitik4. Perubahan sella tursika
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e. CT Scan : gambaran tumor hiperdense
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f. Arteriografi : lihat gambaran pembuluh darah di otakPerub posisi pemb darah normalArteri yg menyuplai darah utama ke otak (+)NeovaskularisasiDensitas jar tumor meningkatLama sirkulasi darah berubah
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g. MRI tumor (+)
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TerapiMenurunkan TIKOperasiRadiasiKemoterapiImunoterapiTx kombinasiTx gen
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Terapi
1. Menurunkan tekanan intra kranial
- Kortikosteroid 4 mg IV 3-4x
- Mannitol 6x 100 cc
- Hidrosefalus VP Shunt
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2. Operasi trepanasiTujuan:- Dx histologis yang tepat- Cytoreduction mengecilkan massa akibat tumor- Mendapat kesempatan tx yang lain- Terjadi perubahan sifat tumor
Komplikasi trepanasi;1. Perdarahan2. Edema otak3. Infeksi4. Kejang25. Hidrosefalus6. Gg-an endokrin meningkat
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3. RadioterapiDng sinar-X, gamma, & partikel lain
Radiasi diberikan dgn cara:1.Eksternal :
a. konvensional b. stereotactic radiosurgery2. brakhiterapi
Tumor ganas :- astrositoma, metastase- Medulloblastoma
Tumor jinak:- Pituitari adenoma- Kraniofaringioma
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Komplikasi :Selama terapi : edema otakMinggu-bulan : demielinisasiTahun : radionekrosis
Efek Samping :1.Efek samping lokal : perub kulit, rambut rontok,
dll 2.Efek samping sistemik : kelelahan, mual, sakit
kepala, kejang, perub selperub sel darah tepi, dlldarah tepi, dll
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4. Kemoterapi-sitostatika:
Kemoterapi bekerja pd sel yg sdg bermitosisPembelahan dng duplikasi & rekombinasi DNA
Kemoterapi dpt diberikan sbg :a. Prioritas utamab. Ajuvan terapi stlh radiasi atau pembedahanc. Radio sensitizer; disuntikkan segera sebelum /bersama
penyinaran
Tujuan kemoterapi :1. mencapai kesembuhan2. mencapai masa bebas peny yg lama3. memperbaiki kualitas hidup4. meningkatkan efek terapi lain5. memperkecil masa tumor sebelum pembedahan/penyinaran
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Kemoterapi sel tidak dapat menyelesaikan rekombinasiDNA
kehilangan bagian DNA sehigga tidak dapat
membelah diri sel tidak aktif
Hal yg membatasi kerja kemoterapi:- BBB- histologi yg heterogen- deferensiasi sel dlm berbagai stadium- neovaskularisasi yg abnormal- perubahan lingkungan antara in vitro & in vivo
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Indikasi kemoterapi:
Tumor otak yg efektif dng kemoterapi :Glioma pd anak2 Glioma derajat tinggiOligodendrogliomaEpendimoma yg rekurenEpendimoma pd anakMeningioma maligna yg rekurenMedulloblastomaGerminoma kel pineal
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Kontra indikasi kemoterapi
Absolut :Kasus terminalHamilSepsisKoma
Relatif :Umur <3 bln, atau lanjutDimensiaGagal organ beratTidak teratur kontrolTidak kooperatif
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Cara Pemberian KemoterapiIntra vena : terbatas krn otak mempunyai
BBBIntra-thecal : misal BCNU krn pny lipofilik
yg tinggi, sedangkan MTX tdk dianjurkan krn bs tjd iritasi meningen
Per oralIntra arterialIntraparenkim durante operasi
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Kemoterapi biasanya diberikan dg Kombinasi:- BCNU (bis chloretyl nitrosurea)- CCNU (chlorociclohexil nitrosurea)- Vincristine- Methotrexate- Procarbazine- Temozolamide (temodar)- Streptozotocin- Temoxifen (nolvadex)
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Kemoterapi yang dapat melalui BBB : BCNU CCNU Probarbazine Thiotepa Methotrexate dosis tinggi
Untuk memperlebar BBB :ManitolGliserol
*BBB = Blood-Brain Brain (Sawar darah otak)
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Efek Samping Kemoterapi :Kemoterapi membunuh semua sel yg sedang
membelah maka hal ini juga mempengaruhi jaringan normal.Merusak stem cellDepresi sumsum tulang
Sel darah putih menurun setlah 7-14 hari kemoterapi
Mual, muntah, dan anoreksiaRash, kulit kering dan rambut rontokMukosa pecah-pecahGangguan fertilitas
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PrognosisTumor metastase tergantung tumor primerPrognosa tumor primer tergantung:1. Usia2. Demensia3. Kejang4. Performans scale
Berdasarkan Karnofsky scale:- Bekerja dengan otak >80%- Berjalan 50-70- Tidak bisa jalan <40%Makin skala prognosa baik
5. Histologi6. Blood brain barrier
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ASTROSITOMA Semua umur sering 40-60 th Laki : wanita = 2 : 1 Lokasi : sering pd frontal, temporal, parietal, batang otak
jarang pd oksipital Pembagian mnrt lokasi :
- astrositoma serebri (grade I-II) subtipe fibrilari- astrositoma serebelum
subtipe pilositik & protoplasmik
Pd anak : - lokasi pd batang otak & serebelum- mrpk tumor intrakranial tersering- well differentiated
Pd dewasa :- lokasi hemisfir serebri- anaplastik
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Pembagian mnrt histologi & makroskopik o/ Kernohan grade I – IV
- low grade astrocytoma ( I – II )- malignant astocytoma ( III – IV )
Low grade - 14% TU primer intrakranial- umur 30 - 40 th- tumbuh lambat, difus, well
differentiated
Malignant- 40% TU- insiden puncak 55 th- tumbuh cepat ke lobus kontra lateral- daerah nekrosis kiste
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MENINGIOMA1/5 TU primer intrakranTU jinak, tumbuh lambat, asal dr granulasio
arakhnoidLaki : wanita = 1 : 2Usia insidensi Lokasi tersering sekitar sinus venosus
- parasagital 24% - supra sellar 10%- konveksitas 18% - fos post 8%- ala spenoid 18 % - tentorial 3%- sulkus olfakt 10%
Meningkatkan vaskularisasi tlg yg berdekatan, Hiperostosis & menekan jar otak sekitarnya
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Terapi : reseksi total
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TUMOR MEDULLA SPINALIS
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Tumor kanalis spinalis dan mielum 20% tu CNS/SSP
Tu. Mielum : • Servikal : 20%• Thoraks : 50%• Lumbal : 20%• kauda ekuina : 5%
Menurut tempat :• Ekstra dural• Intra dural : - Ekstra medullar
- Intra medullar
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Tumor kanalis spinalis dan mielum
Insiden : laki-laki = wanitaDewasa : 60% jinak, neurilemmoma
dan meningiomaAnak : 40% glioma dan sarcoma
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Ekstradural tumor
- Terbanyak : tumor metastase. dari : mammae, prostat, paru, thyroid,
GIT
- Sekitar tulang : Osteogenik sarkoma, Khordoma, Multiple mieloma, Malignant limfoma, Lipoma distruksi tulang
- Tumor dari ektra dural cepat kompresi pada medulla spinalis.
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Tumor intradural ekstrameduller (60%)
Asal:- Meningen meningioma- Radiks syaraf neurofibroma- Jaringan lemak lipoma- Pembuluh darah hemangioma- Metastase
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Tumor intradural intrameduller
± 15%Dapat berasal dari:
- Sel glial : - ependimoma - astrositoma - ganglioglioma
- Non glial : - hemangioma - paraganglioma - metastase - limfoma - dll
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Gejala klinis
Gejala MotorikTetraparese (C1 T2)C1- C4 gangguan otot pernafasanC5 motorik deltoid, sensorik
deltoidC6 gangguan bisepC7 gangguan trisepC8 – T2 gangguan otot interossei, syndroma horner
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Gejala Sensorik
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EPICONUS
CONUS
CAUDA EQUINA
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Sindroma epikonus L4-S2o Gangguan motorik:
- Ekstensi hip- Fleksi knee- APR –
o Gangguan sensorik ≈ dermatomo Gangguan autonomik : bladder
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Conus MedConus Med
Segment S3-CocSegment S3-CocCauda equinaCauda equina
Root L3-coccRoot L3-cocc
Spontaneus Spontaneus painpain
Bilateral simetrisBilateral simetris
Perineum pahaPerineum paha
suggestiveintramedulsuggestiveintramedullarlar
Unilateral simetrisUnilateral simetris
Idem prominentIdem prominent
Radicular in typeRadicular in type
Nerve root Nerve root involvementinvolvement
Sensorik defisitSensorik defisit Saddle bilateral Saddle bilateral discociation of discociation of sensation sensation
Saddle unilateralSaddle unilateral
no no
Motor lossMotor loss Simetris not markedSimetris not marked Asimetris more Asimetris more markedmarked
Reflex lossReflex loss Hanya APRHanya APR APR, KPRAPR, KPR
Bladder-rectal Bladder-rectal symtomssymtoms
Early markedEarly marked Late-less markedLate-less marked
Tropic changesTropic changes Decubiti commonDecubiti common Less markedLess marked
Sexual functionSexual function Erection – ejaculation Erection – ejaculation impairedimpaired
Less marked impairedLess marked impaired
Onset Onset Suddent bilateralSuddent bilateral Gradual-unilateralGradual-unilateral
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Diagnosa KlinisFoto vertebra (AP/LAT/Oblique)
- Pedikel rusak tu. Metastase- Diskus intervertebrae sempit HNP
Perspirasi test: batas tegas tumorLP: - Quickensted
- Ayala index - LCS: froin Syndrome: - prot - warna
xantochrom - sel N
Mielografi/kaudografi lokasi tumor hasil berbentuk khusus
CT ScanMRI
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FOTO VERTEBRA
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MIELOGRAFI
kjkmmn
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Terapi : Deksamethasone Operasi : laminektomi
Prognosa:- Lebih baik dari tumor intra kranial- Glioma intrameduller kurang agresif
dibanding glioma serebri
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TERIMA KASIH