a12. hepatoma (hcc)

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    ANATOMI HATI

    T.D. 2 LOBUS : KANAN & KIRI.

    LOBUS KIRI SEG. LATERAL .SEG. MEDIAL .

    BATAS LIG . FALSIFORMIS.

    LOBUS KANAN SEG. ANTERIOR .SEG. POSTERIOR.

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    This is the external surface of a normal liver.

    The color is brown and the surface is smooth.

    A normal liver is about 1200 to 1600 grams.

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    Surgical Treatment of HCC Budi Irwan 5

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    METABOLISME GARAM EMPEDU,PIGMENEMPEDU

    METABOLISME KARBOHIDRAT

    PEMBENTUKAN UREA,PENYIMPANAN

    PROTEIN(ASAMAMINO),METABOLISME

    LEMAK,KETOGENESIS SINTESIS

    KOLESTEROL,DAN PENIMBUNAN LEMAK

    PENIMBUNAN VITAMIN DAN MINERAL METABOLISME STEROID

    DETOKSIFIKASI

    GUDANG DARAH DAN FILTRASI

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    KHS (KARSINOMA

    HEPATOSELULAR),HEPATOMA PRIMER DR

    SEL HEPATOSIT

    KARSINOMA

    KOLANGIOSELULAR,HEPATOMA PRIMER

    YANG BERASAL DARI EPITEL SALURAN

    EMPEDU INTRAHEPATIK KARSINOMA CAMPURA HEPATOSELULAR

    DAN KOLANGIOSELULAR

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    TIPE MASSIF,PD SATU LOBUS DAN HANYA

    SATU NODUL SAJA

    TIPE NODULER,PALING SERING

    DIJUMPAI,HATI MEMBESAR,NODUL YG

    BANYAK (IRREGULER)

    TIPE DIFFUS,UMUMNYA SEL HATI MASIH

    DALAM BATAS NORMAL TETAPI TERISI OLEHSEL KARSINOMA YG DIFFUS

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    TUMOR HATI PRIMER ( HEPATO CELLULAR

    CARCINOMA ) AS, JARANG DISTRIBUSI DENGAN ANGKA KEJADIAN

    TERTINGGI DI ASIA TIMUR,SUB SAHARA

    AFRIKA DAN MELANESIA,

    JARANG DITEMUKAN PADA USIA MUDA

    INSIDENS MENINGKAT PADA USIS TUA

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    Hepatocellular carcinoma (HCC) a primarymalignancy of the liver, hepatocellularorigin HCC is a major cause of death from cancerin Eastern Asia and sub-Saharan Africa HCC causes 662,000 deaths per year,about half of them in China. Males >> females Age of 30 to 50.

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    HBV

    70-90% of chronic cases in cirrhosis Treatment decrease risk

    HCV 1-3% of HCV develop HCC

    Treatment decrease risk Co-infection Aflatoxins (Aspergillus fumigatus)

    4 fold increased risk HCC

    Alcohol >50-70g/day Synergist with HCV and HBV

    Nonalcoholic Steatohepatitis?

    El-Serag, H.B. and K.L. Rudolph, Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. Gastroenterology, 2007. 132(7): p. 2557-76.Brunetto M.R., O.F., Koehler M., et al., Effect of interferon-alpha on progression of cirrhosis to hepatocellular carcinoma: a retrospective cohort study.

    International Interferon-alpha Hepatocellular Carcinoma Study Group. Lancet, 1998. 351(9115): p. 1535-9.

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    Obesity

    Diabetes Mellitus

    Hemochromatosis Alpha-1 antitrypsin deficiency

    Autoimmune hepatitis

    15-50% of HCC in the US have noestablished risk factors

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    15/43Thorgeirsson, S.S. and J.W. Grisham, Molecular pathogenesis of human hepatocellular carcinoma. Nat Genet, 2002. 31(

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    HCC with cholangiolar features, moderately

    differentiated

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    Hepatic Fibrosis

    Cirrhosis Liver Cancer

    Healthy Liver

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    Hepatic Fibrosis

    Cirrhosis Liver Cancer

    Healthy Liver

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    KANKER HATI

    20% infeksi kronis 80%Infeksi HCV: kronis

    berakhir dengan sirosis

    25% sirosis berakhir

    dengan kanker hatiatau gagal hati

    Kelompok Risiko Tinggi HCV:

    Pengguna Narkoba Suntik

    Penerima Transfusi

    Pasien terpapar alat medis

    yang tak steril

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    Here is another example of macronodular cirrhosis. Viral hepatitis (B or

    C) is the most common cause for macronodular cirrhosis. Wilson's

    disease and alpha-1-antitrypsin deficiency also can produce a

    macronodular cirrhosis.

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    METASTASE TUMOR HATI DIAFRAGMA PERI PORTAL LIMPH NODE

    PARU - PARU

    TULANG

    ADRENAL

    OTAK

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    D/ SUBKLINIS HEPATOMA,STAD.DINI,TANPA

    GEJALA DAN TANDA FISIK YG JELAS

    D/NON INVASIF

    D/PATOLOGIS

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    1. Clinis2. Imaging3. Blood level of alphafetoprotein4. Needle biopsy

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    RIWAYAT ALKOHOL ATAU SIROSIS

    RASA SAKIT ATAU TIDAK ENAK

    TERABA MASSA

    BERAT BADAN MENURUN

    ASITES

    JAUNDICE

    ANOREKSIA,PERUT GEMBUNG

    LETIH,BERAT BADAN MENURUN,

    PERDARAHAN

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    DIAGNOSA

    AFP MENINGGI 50 90 % . TUMOR KECIL BISA NORMAL / SDKT . AFP JUGA BISA ME PADA SIROSIS HATI .

    TIDAK BERMAKNA.

    MONITOR KEBERHASILAN RESEKSI

    KURATIF.AFP

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    PARA NEOPLASTIC COMPLIKASI :HIPOGLISEMIA

    HIPERKALSEMIA

    ERITROSITOSIS

    HIPERTROFI PULMONARI

    OSTEOARTROPATI

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    CT Scan MRI Preferred USG Nuclear Medicine Angiography Less usefull Plain film

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    BIOPSI

    USG . STAGING .

    STAGING SYSTEM HCC ( AJCC )

    KLASIFIKASI TNM

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    TNM SISTEM,OKUDA,MORPHOLOGY,MET,VI

    OKUDA SISTEM, BILLIRUBIN,ALB,ASC

    CLIP (CANCER OF THE LIVER ITALIAN

    PROGRAM),CHILD PUGH

    JIS SCORE (JAPAN INTEGRATED STAGING)

    BCLC(BARCELONA CLINIC LIVER CANCER)

    ,CHILD PUGH,PH,BILLIRUBIN

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    STAGE GROUP

    - STAGE I T 1 N0 M0

    - STAGE II T2 N0 M0

    - STAGE III T3 N0 M0

    T 1-3 N1 M0

    - STAGE IVa T4 Any N M0

    - STAGE IVb Any T Any N M1

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    PENATALAKSANAAN :

    TERAPI DEFINITIF

    OPERASI

    HANYA 10 30 % MASIH OPERABLE HANYA 50 70 % YANG CURATIVE

    KRITERIA NON OPERATIF :

    ADA PENYAKIT EKTRA HEPATIK

    GANGGUAN FUNGSI HATI BERAT MASA TUMOR YANG MASIF

    V. PORTA ATAU V. CAVA SUDAH TERLIBAT

    KONTRA INDIKASI RELATIF

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    HEMANGIOMA

    ABSESS HEPAR

    TUMOR METASTASE

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    TERAPI OPERASI

    RESEKSI

    TRANSPLANTASI HATI

    TERAPI NON OPERATIP

    RFA (RADIO FREKWENSI ABALATIO) INJ.ETANOL MRNI (95%),INTRA TUMOR

    PERKUTANTAS

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    KEMOEMBOLISASI ARTERI HEPATIK

    PERKUTANERAPI OPERASI

    KEMOTERAPI SISTEMIK

    RADIOTERAPI

    TAMOXIPEN

    INJ.ASAM ASETAT PERKUTAN

    SORAFENIF (95%)

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    Treatment modality

    1. Livertransplantation

    2. Hepatic resection3. Thermal ablation

    (Radiofrequency,microwave,la

    ser)

    4. Cryotherapy

    Limitations

    1.Donor avaibility, Three orfewer lesions, none > 3 cm ,

    Solitary lesion < 5 cm2.Minimal or no cirrhosis, threeor fewer lesions

    3.Three or fewer lesions, each