PENYAKIT PARENKIM PARU - drAlf
Transcript of PENYAKIT PARENKIM PARU - drAlf
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PENYAKIT PARENKIM PARU
DEPT PULMONOLOGI DAN KEDOKTERAN RESPIRASI
FK UNAIR/RS AIRLANGGA/
RSUD DR. SOETOMO SURABAYA
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PNEUMONIA
EDEMA PARU
KANKER PARU
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PNEUMONIA
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DEFiNISI
Pneumonia adalah suatu peradangan
akut parenkim paru yang disebabkan oleh
mikroorganisme. ( selain Mtb)
Non mikroorganisme : (bahan kimia, radiasi,aspirasi bahan toksik, obat-obatan dan lain - lain) : Pneumonitis
PDPI (2014). Pneumonia komunitas. Pedoman Diagnosis & Penatalaksanaan di Indonesia
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MEKANISME PERTAHANAN PARU
1. filtrasi partikel di hidung,
2. pencegahan aspirasi dengan refleks epiglotis,
3. refleks batuk,
4. sistem pembersihan oleh lapisan mukosiliar,
5. respon imun.
Dalam keadaan normal, saluran pernapasan bagian
bawah mulai dari trachea sampai alveoli selalu
dalam keadaan steril.
PDPI (2014). Pneumonia komunitas. Pedoman Diagnosis & Penatalaksanaan di Indonesia
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patogen berhasil menembus mekanisme
pertahanan paru
Inflamasi
Substitusi udara di dalam alveoli (air spaces) oleh cairan eksudat
(= KONSOLIDASI)
Shunting
Kuliah dr. Soedarsono, Sp.P (K) ,SMF Pulmonologi dan Ilmu Kedokteran Respirasi FK Unair
InhalasiAspirasi Hematogenous Langsung
Patogenesis
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Tanda & Gejala
• Demam mendadak, bisa sampai menggigil
• Batuk, mula-mula mukoid lalu purulen
• bisa terjadi hemoptisis
• Nyeri pleuritik, ringan sampai berat apabila
proses menjalar ke pleura (terjadi pleuropneumonia)
• Tanda & gejala lain yang tidak spesifik :
mialgia, pusing, anoreksia, malaise, diare, mual & muntah
PDPI (2014). Pneumonia komunitas. Pedoman Diagnosis & Penatalaksanaan di Indonesia
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Pemeriksaan fisik
• Sisi hemitoraks yg sakit tertinggalInspeksi
• Sisi hemitoraks yg sakit tertinggal
• Fremitus raba / suara meningkatPalpasi
• RedupPerkusi
• Suara napas bronkovesikuler – bronkial
• Ronki basah halus, yang kemudianmenjadi ronki basah kasar pada stadium resolusi
Auskultasi
PDPI (2014). Pneumonia komunitas. Pedoman Diagnosis & Penatalaksanaan di Indonesia
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Pemeriksaan penunjang
1. Pemeriksaan dahak
2. Darah
3. Foto toraks PA / lateral
4. Analisa gas darah
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1. Pemeriksaan Dahak
Sebelum di berikan antibiotik
• Spesimen dahak langsung ( Hapusan Gram, Kultur)
• Aspirat pipa endotrakeal
• BAL
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2. Pemeriksaan darah
Peranan Petanda Infeksi
Procalcitonin (kadar > 2ng/ml) infeksi bakterial berat, sepsis, syok septik, MODS.
(mendukung diagnosis, prediktor komplikasi dan peningkatan angka kematian, panduan pemberian dan
penghentian antibiotic)
C-reactive protein (nilai normal 3mg/l) kadar 10 mg/l merupakan indikasi inflamasi.
(spesifitas rendah, kadar CRP >100 mg/l menentukan prognosis dan kebutuhan ventilasi mekanik)
• Umumnya lekositosis ( leukopenia viral)
• Hitung jenis bergeser ke kiri ( shift to the left)
• LED dapat juga tinggi
• Kultur darah dapat positif pada 20-25 % penderita yang tidak diobati
• Analisa Gas Darah : Hipoksemia & hipokarbia dan Asidosis respiratorik pada
stadium lanjut
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3. Foto toraks
• Abnormalitas radiologis pada pneumonia disebabkan karena
pengisian alveoli oleh cairan radang berupa : infiltrat/ opasitas /
peningkatan densitas ( konsolidasi ) disertai dengan gambaran
air bronchogram.
• Bila di dapatkan gejala klinis pneumonia tetapi gambaran
radiologis negatif, maka foto toraks harus diulang dalam 24-48
jam untuk menegakkan diagnosis.
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Foto Thorax Normal
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Gambaran Radiologis Pneumonia Lobaris
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Gambaran radiologis bronkopneumonia
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Gambaran radiologis pneumonia interstitialis
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Adanya Infiltrat Pada Fototorak !!!
Disertai 2 Gejala Berikut :
• Demam 380c
• Lekosisitosis > 10.000 / Mm3
• Sputum Purulen
• Batuk, Sesak, Nyeri Dada
• Pemeriksaan Fisis : Tanda Konsolidasi
SECARA KLINIS DIAGNOSIS PNEUMONIA DAPAT
DITEGAKKAN BILA DIPENUHI BATASAN SBB :
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Demographics History & Laboratory
Physical find.
Age = years (male) Neoplasia (+30) pH < 7.35 (+30)
Age = years – 10 (female) CHF (+10) BUN >10.7 (+20)
Nursing home resident (+10) Renal disease (+10) Na < 130 (+20)
Liver disease (+20) Glucosa> (+10)
Cerebrovasc. Dis. (+10) Hct<30% (+10)
Pulse ≥ 125 (+10) PO2<60 (+10)
BP ≤ 90 mm/Hg (+20) Effusion (+10)
Temp < 350C or ≥400C (+15)
Altered mental status (+20)
Perhitungan skor risiko berdasar PSI
SETTING RUMAH SAKIT
The Pneumonia Patient Outcomes Research Team (PORT)
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DERAJAT SKOR RISIKO CAP
Risiko Klas risiko Total skor Perawatan
Rendah I Tidak diprediksi Rawat jalan
Rendah II 70 total skor Rawat jalan
Rendah III 71-90 tot. skor Rwt inap / rwt jln
Sedang IV 91-130 tot. skor Rawat inap
Berat V > 130 tot. skor Rawat inap
Mortaliti : I (0,1%) ; II (0,6%); III (2,8%) ; IV ( 8,2%) ; V (29,2%)
Lanjutan PSI……
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PDPI merekomendasikan menggunakan PSI
kriteria yang di pakai untuk indikasi rawat
inap CAP
• PSI > 70
• PSI < 70 jika di jumpai salah satu kriteria :
- RR >30/ min
- Pa O2/FiO2 < 250 mmHg
- CXR menunjukkan infiltrat multilobus
- tekanan Systolic < 90 mmHg
- tekanan Diastolice < 60 mmHg
- Pneumonia pada pengguna NAPZA
PDPI (2014). Pneumonia komunitas. Pedoman Diagnosis & Penatalaksanaan di Indonesia
FiO2 = 21 + (4 x lpm)
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SETTING RUMAH
SAKIT
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PENILAIAN SEVERITAS PNEUMONIA SETTING
FASKES PRIMER
CRB 65
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Alasan diberikan terapi antibiotik secara empirik :
Mortaliti pneumonia yang tinggi
penundaan antibiotik > 4 jam setelah px MRS meningkatkanmortality
Sulitnya menemukan kuman patogen meskipun dg metode invasif
30-60% kuman tidak teridentifikasi
Keterbatasan tes-tes diagnostik untuk identifikasi kuman patogen
PENATALAKSANAAN
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Penatalaksanaan CAP dibagi
menjadi :
Pasien rawat jalan
Pasien rawat inap
Pasien rawat inap intensif
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1. Rawat Jalan
Pasien TANPA riwayat AB 3 bulan sebelumnya.
-lactam
or -lactam + -lactam inhibitor
OR New macrolide (azithromycin, clarithromycin)
Pasien dengan komorbid atau mempunyai riwayat pemakaianantibiotik 3 bulan sebelumnya.
respiratory fluoroquinolone (Levo 750, moxi) OR
-lactam + -lactam inhibitor OR
-lactam + macrolide
PDPI (2014). Pneumonia komunitas. Pedoman Diagnosis & Penatalaksanaan di Indonesia
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2. Rawat Inap non Intensif
Respiratory fluoroquinolone (Levofloxacine 750 mg, moxifloxacine)
OR
-lactam + new macrolide
PDPI (2014). Pneumonia komunitas. Pedoman Diagnosis & Penatalaksanaan di Indonesia
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29PDPI (2014). Pneumonia komunitas. Pedoman Diagnosis & Penatalaksanaan di Indonesia
• Paling sedikit 1 dari 2 gejala mayor (membutuhkan ventilasi mekanik dan vasopressor > 4 jam (syok septik)
Atau
• 2 dari 3 gejala minor tertentu (PaO2/FiO2<250 mmHg, foto toraks kelainan bilateral, TD sistolik < 90 mmHg)
3. INDIKASI PERAWATAN RUANG INTENSIF: Pneumonia Berat
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Perbaikan klinis
EVALUASI : 48 - 72 jam
Suhu kembali normal
hari 2 - 4
RHONKI (-)
Hari 7 ( 60-80%)
Leukosit kembali normal
hari 4
Perbaikan X-ray.
2 mgg ( 50.6 %)
4 mgg ( 66.7 %)
Jangan rubah Tx antibiotik < 72 jam,
kecuali jika KLINIS MEMBURUK
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BILA TIDAK RESPONS TERHADAP TERAPI EMPIRIK
DIAGNOSIS SALAH DIAGNOSIS BENAR
FAKTOR
PENDERITAFAKTOR OBAT
FAKTOR
KUMAN - Gagal jantung - Emboli -Keganasan -Sarkoidosis -Reaksi Obat -Perdarahan
- Kelainan lokal- Respon yg –tidak adekuat
- Komplikasi
- Salah pilih obat
- Salah dosis/carapemberian -Komplikasi- Reaksi obat
- Resisten -Kuman patogenlain -
Non bakterial(jamur, virus)
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KOMPLIKASI
1. Efusi pleura
2. Empiema
3. Abses paru
4. Syok septik
5. Perikarditis
6. Atelektasis
7. Meningitis
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PULMONARY EDEMA
DEPARTEMEN PULMONOLOGI
DAN ILMU KEDOKTERAN RESPIRASI FK UNAIR/RS AIRLANGGA/
RSUD DR. SOETOMO SURABAYA
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DEFINITION
fluid moving Hukum Starling
Extravasation of fluid from the pulmonary vasculare
into the interstitium and alveoli of the lung
NDF : Net Driving Force
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1. Membrane permeability increase
2. Hidrostatic pressure microvasculer increase
3. Perimikrovaskuler hidrostatic pressure decrease
4. microvasculer oncotic pressure decreases
5. perimicrovasculer oncotic pressure increases
PATOGENESIS
5. lymphatic drainage problem
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CARDIOGENIC
NON-
CARDIOGENIC
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Cardiogenic Pulmonary Edema Non-Cardiogenic Pulmonary Edema
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CARDIOGENIC PULMONARY EDEMA
Left Atrial Pressure (25-30 mmHg) -Lung Microcirc. – Transvasc. Fluid flow into the Lung Interstitium Flooding of the Alveolar Spaces by Edema Fluid
Capacity of the Interstitial Space exceeded Edema Fluid moves through the Visceral Pleura Pleural Effusions
NON-CARDIOGENIC PULMONARY EDEMA
• DECREASED PLASMA ONCOTIC
PRESSURE
• INCREASED NEGATIVITY OF INTERSTITIAL
PRESSURE
• ALTERED ALVEOLAR-CAPILLARY
MEMBRANCE PERMEABILITY(ARDS)
• LYMPHATIC INSUFFICIENCY
• OTHERS: HIGH-ALTITUDE, NEUROGENIC,
NARCOTIC OVERDOSE
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Cardiogenic Pulmonary Edema NonCardiogenic Pulmonary Edema
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HAPE ( High Altitude Pulmonary Edema)
* One Of Non Cardiogenic Pulmonary Edema
*Hipoksia Vasokonstriction Of Pulmonalis
Vein Tekanan Pulmoner Meningkat
Tekanan Kapiler Paru Meningkat
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DIAGNOSIS Sesak Akut
Peningkatan Tekanan Vena Jugular ( Kardiogenik)
Awal Ronkhi Basah Halus Di Bagian Basal Paru
S3 Pada Auskultasi Jantung
Hipoksemia
Pemeriksaan Penunjang Radiologis, Echocardiografi, RFT, EKG, Biomarker Kardiologi (BNP)
SWAN-GANZ CATHETERS
• PULMONARY-ARTERY WEDGE PRESSURE:
CARDIOGENIC : HIGH, > 18 MMHG
NON-CARDIOGENIC: NORMAL OR LOW, <=18 MMHG
• Monitoring Cardiac Output
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Algorithm for the Clinical Differentiation
between Cardiogenic and Noncardiogernic Pulmonaruy Edema
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Definition of ARDS
acute onset
bilateral infiltrates on chest radiography
pulmonary-artery wedge pressure <= 18mmHg
or absence of clinical evidence of left atrial hypertension
CLINICAL FEATURE OF ARDS
-- SEVERE TAKIPNEU -- RAPID ONSET -- SEVERE DYSPNEU
-- DECREASE PULMONARY COMPLIANCE -- ARTERIAL HYPOXEMIA
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1. DEPEND ON ETIOLOGY
Kardiogenik Atasi Faktor Kardiogenik (Nitrat, Ace-inhibitor, Inotropik), Jangan Lupa DIURETIK
Penurunan Tekanan Onkotik Naikkan Kadar Protein
Reekspansi Paru Pencegahan Dengan Melakukan Tindakan Secara Perlahan
HAPE Turunkan Dari Ketinggian, Deksametasone, Azetazolamide
Infeksi Antibiotik
2. RESPIRATORY SUPPORT Ventilator Adequate Oxygenation
3. GENERAL SUPPORTIVE CARE Adequate Nutrition (Oral, Parenteral)
Prevent Overfeeding (KBH) – CO2 Production >
Hypokalemia, Hypophosphatemia
Sedatives – Hypnotics
Gastric Stress & Ulcers
MANAGEMENT
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CARCINOMA
BRONCHOGENIC
LAKSMI WULANDARI
DIVISI ONKOLOGI
SMF ILMU PENYAKIT PARU
FAKULTAS KEDOKTERAN UNIVERSITAS AIRLANGGA
RSUD DR. SOETOMO - SURABAYA
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DEFINISI : Tumor Ganas Paru Primer Yang Berasal Dari Saluran Nafas
Penegakan Diagnosis Membutuhkan Sarana Yang Tidak Sederhana, Memerlukan Kolaborasi
Multidisipliner Kerjasama Ahli Paru, Ahli Radiologi Diagnostic, Ahli Patologi Anatomi, Ahli
Radioterapi, Ahli Bedah Thoraks, Ahli Rehabilitasi Medik, Dll
ETIOLOGI
Konsep Terkini Kanker Adalah Penyakit Gen Adanya Ketidakseimbangan Antara Fungsi
Onkogen Dan Tumor Supressor Gen Dalam Proses Tumbuh Dan Berkembangnya Sebuah Sel.
Perubahan / Mutasi Gen Menyebabkan Hiperekspresi Onkogen Dan/ Kurang/ Hilangnya Fungsi
Gen Tumor Supressor, Sehingga Sel Tumbuh Dan Berkembang Tak Terkendali.
Memerlukan Proses Lama Dan Multistep.
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The Hallmark of CancerSelf sufficiency in growth signal
Tissue invasion& metastasis
Sustainedangiogenesis
Insensitivity toanti-growth signals
Evadingapoptosis
Self-sufficiency ingrowth signals
Limitless replicativepotential
Hanahan D, et al. Cell 2000; 100: 57-70
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PREVENTION
• Lebih Dari 36 Jenis Bahan Yang Dikandung Asap Rokok
Bersifat Karsinogen.
• Faktor Risiko Yang Lain : Perokok Pasif, Pajanan Asbes,
Radon Dan Polusi Udara.
• Radon Merupakan Gas Radioaktif Yang Secara Alamiah
Terdapat Di Alam Terutama Daerah Dengan Kandungan
Granit Yang Tinggi.
• Polusi Udara Berupa Pembuangan Asap Kendaraan
Bermotor Dan Sisa Gas Industri.
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WHO :
LEVELS of PREVENTION
PRIMER : PREVENSI ELIMINASI / BLOCKING KARSINOGEN
SEKUNDER : DIAGNOSA DINI
TERTIER : TERAPI KURATIF
QUARTER : PENANGANAN PALIATIF
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Smoking-Related Cancers
• Bladder • Lung
• Cervical • Mouth
• Esophageal • Pancreatic
• Kidney • Throat
• Laryngeal
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TATA LAKSANA
KECURIGAAN :
LAKI : ratio LK / W = 5:1
USIA > 40 TH : 84.2 % (Sby)
PEROKOK : > 80 %
PAPARAN INDUSTRI
GEJALA KLINIK :
BATUK >2 Mgg,
BATUK DARAH,
SESAK,
BB TURUN > 4kg/6bln
EXPERTISE
DOKTER
UMUM
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KONFIRMASI / SKRINING
A/B/C RUJUK
D : SKRINING ULANG BILA INDIKASI TETAP ADA / 4-6 bln
X-RAY
( + )
X-RAY
( - )
CYTOLOGY
( + )A B
CYTOLOGY
( - )C D
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NSCLC DIAGNOSIS
Physical examination Detect signs
Visualize and sample mediasturial lymph nodes
Detect position, size, number of tumors
Detect chest wall invasion mediastinal lymphodenopathy
distant metastases
Lymph node staging
Detect changes in hormone production,
and hematological manifestations of lung cancer
Precise location of tumor obtain biopsy
Chest X-ray
CT scan
PET scan
Laboratory analysis
Bronchoscopy
Mediastinoscopy
FNA Cytology
NCCN Guidelines 2000
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GEJALA
INTRA-PULMONAL
GANGG.MUCUCIL
ULSERASI
OBSTRUKSI
RADANG
INTRA - TORAKAL
EKSTRA - PULMONAL
MEDIASTINAL
INVOLVEMENT
EKSTRA-TORAKAL
NON - METASTATIK
NEUROMUSK.
ENDOKRIN
JAR.IKAT & TLG
VASKULER
METASTATIK
GAMBARAN KLINIK
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GEJALA INTRAPULMONAL BATUK LAMA / BERULANG : 70-90%
BATUK DARAH : 6 - 51%
NYERI DADA : 42-67%
SESAK NAFAS : 58%
MEKANISME :
GANGGUAN GERAKAN SILIA,
ULSERASI MUKOSA,
RADANG BERULANG,
OBSTRUKSI SAL.NAFAS
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INTRATORAKAL
EKSTRAPULMONAL
PENYEBARAN TUMOR KE MEDIASTINUM :
N.FRENIKUS :---->DIAFR.
N.REKURENS :---->CH.VOCALIS
S.SIMPATIK :----> Sindr.HORNER
ESOFAGUS :----> DISFAGI
V.CAVA SUP. :----> Sindr.V.C.SUP.
JANTUNG :----> Gg.FUNGSI
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EKSTRAPULMONAL NON METASTATIK
NEUROMUSKULER:
Myo / Neuro / Encephalopathia
ENDOKRIN & METABOLIK:
Syndr. Cushing / IADH / Karsinoid
gynecomastia / hyperpigmentasi
JAR.IKAT dan TULANG:
Clubbing fingers
VASKULER & HEMATOLOGIK
Anemia / purpurae / thrombo-phlebitis
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METASTATIK EKSTRAPULMONALSATU-SATUNYA TUMOR yang mampu
LANGSUNG AKSES ke SIRKULASI
ARTERIIL
Terutama :
OTAK,
HATI dan
TULANG
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PEMERIKSAAN RADIOLOGI
Mutlak dibutuhkan untuk menentukan lokasi tumor primer
dan metastasis.
TNM staging .
Foto thoraks, PA/ lateral, CT scan thoraks, brain scan,
bone scan, bone survey, USG abdomen.
Positron Emission Tomography (PET), Magnetic
Resonance Imaging (MRI)
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PEMERIKSAAN KHUSUS Bronkoskopi Tujuan Diagnostic Untuk Mengambil Jaringan Dengan
Menggunakan Endobronchial Ultrasound (EBUS) Yang Dapat Menunjukkan
Secara Tepat Lokasi Tumor Yang Menempel Di Dinding Luar Bronkhial.
Transbronchial Needle Aspiration (TBNA)
Transbronchial Lung Biopsy (TBLB), Jika Lesi Kecil Dan Lokasi Agak Perifer.
Transthoracal Needle Aspiration ( TTNA), Jika Lesi Di Perifer Dan Ukuran > 2
Cm.
Biopsy Transthoracal ( Transthorastic Biopsy)
Video Assisted Thoracoccopy Surgery (VATS)
Sitologi sputum
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NSCLC stages
Stage 0
Stage IA
Stage IIB
Stage IIIB
Stage IV
Lymph nodes
Main
bronchus
Contralateral
lymph node
Metastasis
to distant
organs
Invasion of
chest wall
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TNM DEFINITION in NSCLC
T TUMOR PRIMER
TX Tumor primer tidak dapat ditentukan dengan hasil radiologi
dan bronkoskopi tetapi sitologi sputum atau bilasan bronkus
positif ( ditemukan sel ganas)
T0 Tidak tampak lesi atau tumor primer
TIS CARSINOMA IN SITU
T-1 Ukuran terbesar tumor primer ≤ 3 cm tanpa lesi invasi
intrabonkus yang sampai ke proksimal bronkus lobaris
• T1a : ukuran tumor primer ≤ 2 cm
• T1b : ukuran tumor primer > 2 tetapi ≤ 3 cm
T-2 Ukuran terbesar tumor primer > 3 cm tetapi ≤ 7 cm, invasi
intrabronkus dengan jarak lesi ≥ 2 cm dari distal karina, berhubungan dengan atelektasis atau pneumonitisobstuktif pada daerah hilus atau invas ke pleura viseral
• T2a : ukuran tumor primer > 3 tetapi ≤ 5 cm
• T2b : ukuran tumor primer > 5 tetapi ≤ 7 cm
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T-3 Ukuran tumor primer > 7 cm atau tumor menginvasi dinding
dada termasuk sulkus superior, diafragma, nervus phrenikus,
menempel pleura mediastinum, perikardium. Lesi
intrabronkus ≤ 2 cm distal karina tanpa keterlibatan
karina. Berhubungan dengan atelektasis atau pneumonitisobstruktif di paru. Lebih dari satu nodul dalam satu lobusyang sama dengan tumor primer.
T-4 Ukuran tumor primer sebarang tetapi telah melibatkan atau
invasi ke mediastinal, trakea, jantung, pembuluh darah besar,
karina, nervus laring, esofagus, vetebral body. Lebih dari satu
nodul berbeda lobus pada sisi yang sama dengan tumor
primer (ipsilateral).
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TNM DEFINITIONS in NSCLCN METASTASIS KE KELENJAR GETAH BENING (KGB)
N0 Tidak ditemukan metastasis ke KGB
Nx Metastasis ke KGB mediastinal sulit dinilai
dari gambaran radiologi
N1 Metastasis ke KGB peribronkus (#10), hilus
(#10), intrapulmonary (#10) ipsilateral
N2 Metastasis ke KGB mediastinum ( #2)
ipsilateral dan atau subkarin (#7)
N3 Metastasis ke KGB peribronkial, hilus,
intrapulmonari, mediastinum kontralateral dan
atau KGB supraklavikula
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TNM DEFINITIONS in NSCLC
M METASTASIS KE ORGAN LAIN
M0 Tidak ditemukan metastasis
Mx Metastasis sulit dinilai dari gambaran
radiologi
M1a Metastasis ke paru kontralateral, nodul di
pleura, efusi pleura ganas, efusi perikardium
M1b Metastasis jauh je organ lain ( otak, tulang,
hepar, ginjal atau KGB leher, aksila,
suprarenal, dll)
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STAGING SCLC
BATAS :
SUDAH / BELUM TERLAMPAUI IPSILATERAL HILAR NODES
LIMITED EXTENSIVE
TX NON SURGICAL
CHEMO SURV ; CURE(-)
DBL
AMAT
CEPAT
Tumor confined to
hemithorax of origin and/or
the mediastinum and
supraclavicular nodes
Tumor not confined to
hemithorax of origin
Distant metastasis
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Strategies to Fight Lung Cancer
Prevention
Surgery
Radiation therapy
Chemotherapy
Targeted therapy
Immunotherapy
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Surgery for Lung Cancer
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TNM STAGING NSCLC
N-0 N-1 N-2 N-3
T-1 I A II A III A III B
T-2 I B II B III A III B
T-3 II B III A III A III B
T-4 III B III B III B III B
ALL M-1 = IV OPERABLE
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SURGICAL OPTION:
MAJOR CONSIDERATIONS
FITNESS for
SURGERY1. AGE
2. PULM.FUNCTION
3.CARDIOVASC.FITNESS
4. NUTRITION & PERFORMANCE
STATUS
OPERABILITY1. DIAGNOSIS & STAGING
2. ADJUVANT THX.
3. SURG.PROCEDURES AVAILABLE
4. LOCALLY ADV.DISEASE
5. SMALL C.L.C.
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Stereotactic Body Radiotherapy
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Chemotherapy
Reduce cancer burden,
largely by killing rapidly
dividing cells
Results in collateral damage
to healthy tissue, causing
unwanted side effects in :
► Circulatory system
► Immune system
► Digestive system
► Others
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KEMOTERAPIPERSYARATAN :
PERFORMANCE scale/skala tampilan: KARNOFFSKY > 70 = ECOG / WHO 0-1
MEMAKSAKAN KEMOTERAPI PADA KONDISI YANG TIDAK MEMENUHI
SYARAT MEMPERCEPAT KEMUNDURAN PENDERITA
KARNOFFSKY WHO / ECOG KETERANGAN
90 – 100 0 AKTIVITAS N
70 – 80 1 MASIH AKTIF danDAPAT MENGURUS DIRI
50 – 60 2 CUKUP AKTIF namunKADANG PERLUBANTUAN
30 – 40 3 KURANG AKTIF, PERLURAWATAN
10 – 20 4 TIDURAN, BUTUHRAWAT INAP
0 – 10 - TIDAK SADAR
REGIMEN CHEMOTHERAPY
• FIRST LINE : PLATINUM DOUBLED 4 – 6
SERI
• SECOND LINE : DOSETAKSEL,
PEMETREXED, ERLOTINIB, GEFITINIB
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The Advantage of Targeted Therapy
Interact with specific molecules (part of the pathways used by cancer cell to grow and spread) as their target
Cause little or no collateral damage to normal cells
Fewer and less toxic side effects
Some can even be given orally
But unfortunately also limited by some drug resistance issues
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PENENTUAN MODALITAS TERAPI
HISTO PATH NSCLC SCLC
SURGERY SURGICAL CASE NON SURGICAL
CHEMO / & RADIASI CURATIVE?
PALLIATIVE
MAIN THERAPY
HORMONAL
BIOLOGICAL
RESPONSE
MODIFIER (BMR)
GENE TX
? ?
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RESPONSE EVALUATION CRITERIA in SOLID
TUMORS (RECIST) MEASURABLE LESION:
> 20 mm ( CONVENTIONAL X-RAY) or
> 10 mm ( SPIRAL CT)
MAX. 5 LESIONS / ORGAN
MAX. 10 TOTAL
SUM of the LONGEST DIAMETER (LD) =
TOTAL OF ALL LD’s IDENTIFIED AS TARGET LESIONS
TARGET
LESION
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RESPONSE CRITERIA
WHO 1979
COMPLETE RESPONSE (CR):
DISAPPEARANCE of ALL TARGET LESIONS
PARTIAL RESPONSE (PR):
> 30 % REDUCTION in the SUM of LD
PROGRESSIVE DISEASE (PD)
> 20 % INCREASE in the SUM of LD , OR
APPEARANCE OF > 1 NEW LESION(S)
STABLE DISEASE (SD)
PD < SD < PR
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REALITA
TREATMENT of NON
SURGICAL NSCLC
THERAPEUTIC
PLATEAU / CEILING
BENEFIT:
OBJECT.RESP.RATE :
25-40%
MEDIAN SURV : 8-10
mo
1 YR SURV RATE: 30-
40%0 5 10 15 20 25 30
Months0.0
0.20.4
0.60.8
1.0
Survival by Treatment GroupAll Randomized Cases
Cis/PaclitaxelCis/GemcitabineCis/DocetaxelCarbo/Paclitaxel
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PERAWATAN PALIATIF
Tujuannya : meningkatkan kualitas
hidup penderita dan meminimalkan
gejala/ keluhan
Cardinal principles :
autonomy, do good, do no harm,
justice
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INFORMATION
THE RIGHT TO
INFORMATION
CONCERNING
THEMSELVES
OBLIGATION TO
PRESERVE BOTH
PHYSICAL & EMOTIONAL
WELL-BEING
DO NOT
GIVE
FALSE
HOPE
DO NOT
DESTROY
HOPE
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CHEMOTHX IN St. IV
NSCLC
IMPROVES SURVIVAL
PALLIATES SYMPTOMS
IMPROVES QUALITY of LIFE
BOTH IN 1st LINE & 2nd LINE
SETTING
ACCP LUNG CANCER GUIDELINE COMM 2003
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91
TERIMA KASIH