CPG มะเร็งตับและท่อน้ำดี

·π«∑“ß°“√√“¬ß“π°“√«‘π‘®©¬— ¡–‡√ßÁ µ∫—
ª∞¡¿Ÿ¡®‘ “°™Èπ‘ ‡πÈ◊Õ

√“™«∑‘ ¬“≈¬— 欓∏‘·æ∑¬å

§≥–º®âŸ ¥— ∑”

1. 𓬷æ∑¬å摇™∞  —¡ª“∑“π°ÿ ≈ÿ
2. 𓬷æ∑¬æå ß…åæ√’ –  ÿ«√√≥°ÿ≈
3. ·æ∑¬Àå ≠‘ß¿“ππ‘ ’ ∂“«√—ß°Ÿ√
4. 𓬷æ∑¬å™«≈µ‘ ‰æ‚√®πå°≈ÿ
5. 𓬷æ∑¬å‰æ‚√®πå ®√√¬“ߧ¥å °’ ÿ≈
6. 𓬷æ∑¬åπƒ¡≈ §≈“â ¬·°â«
7. ·æ∑¬Àå ≠ß‘ π√‘ —™√å ‡≈‘»ª√–‡ √∞‘  ¢ÿ
8. 𓬷æ∑¬§å ≥‘µ Õ∏ ‘ ÿ¢

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·π«∑“ß°“√√“¬ß“π °“√µ√«®∑“ß欓 ‘∏«‘∑¬“
°“√«π‘ ®‘ ©—¬¡–‡√Áßµ—∫ª∞¡¿Ÿ¡‘®“°™‘Èπ‡πÕ◊È

∫∑π”

°“√µ√«®™‘Èπ‡πÈ◊Õ®–„Àâ°“√«‘π‘®©—¬∑’Ë·πàπÕπ „π°“√«‘π‘®©—¬ πÕ°®“°√–∫ÿ™◊ËÕ‚√§¡–‡√Áß
¬ß— §«√µÕâ ß∫Õ°™π¥‘ ¬Õà ¬ ‡°√¥ ¢π“¥¢Õß°âÕπ °“√≈°ÿ ≈“¡‰ª¬—ßÀ≈Õ¥‡≈Õ◊ ¥ ·≈–À√Õ◊ À≈Õ¥π”È ‡À≈Õ◊ ß¡’
À√◊Õ‰¡à √«¡∂÷ß°“√‡ª≈’ˬπ·ª≈ßµà“ßÊ∑Ë’‡°‘¥°—∫ à«π¢Õßµ—∫∑Ë’‰¡à„™à¡–‡√Áß ·≈–¢Õ∫¢Õß°“√ºà“µ—¥«à“æâπ
®“°¢Õ∫¢Õß¡–‡√ßÁ ¡“°πÕâ ¬‡æ¬’ ß„¥ ‡æÕ◊Ë „À°â “√√“¬ß“π¡§’ «“¡ ¡∫√Ÿ ≥å ®ß÷ ¢Õ𔇠πÕÀ«— ¢Õâ ∑§’Ë «√ª√“°Ø
„π√“¬ß“π ”À√—∫°“√µ√«®ª√–‡¡‘π‡«≈“®–√“¬ß“π°“√«‘π‘®©—¬¢Õß hepatocellular carcinoma ·≈–
cholangiocarcinoma Õ¬“à ߉√°µÁ “¡  ”À√—∫™È‘π‡πÕÈ◊ ∑Ë’‰¥âπâÕ¬ ‡™πà °“√‡®“–¥«â ¬‡¢Á¡ À√◊Õºà“µ¥— ™‘Èπ‡π◊ÕÈ
‡≈°Á Ê ®– “¡“√∂√“¬ß“π‰¥â‡©æ“–∫“ßÀ«— ¢âÕ ‰¥·â °à ™◊ËÕ‚√§¡–‡√Áß ™π¥‘ ¬àÕ¬ (∂“â ¡)’ ‡°√¥ ·≈– ¿“«–
¢Õ߇π◊ÕÈ µ∫— ∑µ’Ë ‘¥¡“°∫— ‡πÈÕ◊ ßÕ° ‡ªìπµâπ

À«— ¢Õâ ¢Õß°“√√“¬ß“π (1)

À—«¢Õâ √“¬ß“π¢Õß°“√«‘π‘®©¬— ¡–‡√ßÁ µ—∫ª∞¡¿¡Ÿ ®‘ “°™π‘È ‡πÕ◊È ª√–°Õ∫¥â«¬
1. Histological types
2. Tumor Grade
3. Size of tumor
4. Extent and location of tumor
5. Status of lymphovascular and perineural invasion
6. Margins of excision
7. Lymph node status
8. Condition of surrounding liver parenchyma

Histological types
1. Hepatocellular carcinoma ·∫ßà ÕÕ°‡ªπì classic type ·≈– variants(2) ¥—ßπÈ’

1.1 Hepatocellular carcinoma, classic type
1.2 Hepatocellular carcinoma with fatty change
1.3 Hepatocellular carcinoma, clear cell type
1.4 Hepatocellular carcinoma, small cell type
1.5 Hepatocellular carcinoma, undifferentiated type
1.6 Hepatocellular carcinoma, spindle cell type
1.7 Hepatocellular carcinoma, giant cell type
1.8 Fibrolamellar hepatocellular carcinoma
1.9 Hepatocellular carcinoma with biliary differentiation
1.10 Combined hepatocellular-cholangiocarcinoma

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2. Cholangiocarcinoma ·∫ßà ÕÕ°‡ªìπ classic type ·≈– variants (3) ¥—ßπ’È
2.1 Cholangiocarcinoma, classic type
2.2 Adenosquamous carcinoma
2.3 Squamous cell carcinoma
2.4 Mucinous carcinoma
2.5 Mucinous cystadenocarcinoma
2.6 Sarcomatoid cholangicarcinoma
2.7 Clear cell variant
2.8 Signet ring cell carcinoma

Tumor Grade

1. Hepatocellular carcinoma „À„â ™â Edmondson and Steiner grading system ´ßË÷ 𬑠“¡(1)
¥—ßπ’È

Grade I : Reserved for those areas in Grade-II hepatocellular carcinoma where
the difference between the tumor cells and hyperplastic liver cells is so minor that
a diagnosis of carcinoma rests upon the demonstration of more aggressive growths
in other parts of the neoplasm.

Grade II : Cells show marked resemblance to normal hepatic cells. Nuclei are
larger and more hyperchromatic than normal cells. Cytoplasm is abundant and
acidophilic. Cell borders are distinct. Acini are frequent and variable in size.
Lumina are often filled with bile or protein precipitate.

Grade III: Nuclei are larger and more hyperchromatic than Grade II cells.
The nuclei occupy a relatively greater proportion of the cell (high N/C ratio).
Cytoplasm is granular and acidophilic, but less so than Grade II tumors. Acini are
less frequent and not as often filled with bile or protein precipitate. More single
cell growth in vascular channels is seen than in Grade II.

Grade IV: Nuclei are intensely hyperchromatic. Nuclei occupy a high percentage
of the cell. Cytoplasm is variable in amount, often scanty. Cytoplasm contains
fewer granules. The growth pattern is medullary in character, trabeculae difficult
to find, and cell masses seem to lie loosely without cohesion in vascular channels.
Only rare acini are seen. Spindle cell areas have been seen in some tumors.
Short plump cell forms, resembling çoat cellécarcinoma of the lung seen in some.

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2. Cholangiocarcinoma „Àâ„™â grading system ∑’‡Ë  πÕ¢“â ß≈à“ßπÈ’ (3) °“√µ√«®∑“ß欓 ‘∏«‘∑¬“
Papillary adenocarcinoma
Well-differentiated adenocarcinoma
Moderately differentiated adenocarcinoma
Poorly differentiated adenocarcinoma

● ‡Àµÿº≈∑Ë’·¬° papillary adenocarcinoma Õ¬àŸ„π°≈ÿࡵà“ßÀ“° ‡π◊ËÕß®“°¡’ biliary
papillary neoplasm of the liver(4), intraductal papillary neoplasia of the liver(5)
·≈– intraductal growth pattern ¢Õß intrahepatic cholangiocarcinoma ∑Ë’¡’惵°‘ √√¡
§≈⓬ non-invasive form À√◊Õ microinvasive form ¥—ßπÈ—π °≈ÿà¡ papillary
adenocarcinoma ∂â“°“√°√–®“¬¢Õ߇´≈≈å¡–‡√Á߉ªµ“¡∑àÕ‰¡à¡“° ·≈– “¡“√∂
ºà“µ—¥‡πÈÕ◊ ßÕ°ÕÕ°‰¥Àâ ¡¥ ®–¡’欓°√≥‚å √§∑Ë’¥’¡“°

● °“√·∫àß well, moderately ·≈– poorly differentiated adenocarcinoma Õ“®æ®‘ “√≥“
Õπÿ‚≈¡µ“¡ tumor grade ∑Ë’‡ πÕ‰«â(1) ‚¥¬¥Ÿ —¥ à«π¢Õ߇π◊ÈÕ‡¬Ë◊Õ¡–‡√Áß∑Ë’¡’‡´≈≈å®—¥
‡√¬’ ßµ«— ‡ªìπµàÕ¡À√Õ◊ ∑àÕ ¥ß— πÈ’ „Àâ well-differentiated adenocarcinoma µÕâ ß¡’°“√®¥—
‡√¬’ ߇ªπì µÕà ¡À√Õ◊ ∑Õà ¡“°°«“à √Õâ ¬≈– 95, „Àâ moderately differentiated adenocarcinoma
µâÕß¡’°“√®—¥‡√’¬ß‡ªìπµàÕ¡À√◊Õ∑àÕ√–À«à“ß√âÕ¬≈– 50-95, „Àâ poorly differentiated
adenocarcinoma ·≈– undifferentiated adenocarcinoma ‡¡Õ◊Ë ¡’°“√®¥— °≈¡àÿ ‡ªìπµÕà ¡
À√◊Õ∑àÕπÕâ ¬°«“à √Õâ ¬≈– 50 ·≈– 5 µ“¡≈”¥—∫

Size of tumor
«—¥¢π“¥¢Õß°Õâ 𠇪ìπ ____ ´¡ x____ ´¡ x ____ ´¡
„Àâ√“¬ß“π¢π“¥¢Õß°Õâ π∑Ë’„À≠à∑’ Ë ¥ÿ °√≥∑’ ¡Ë’ –‡√Áß¡’À≈“¬°Õâ π

Extent and location of tumor (1)
„À‡â ≈◊Õ°√“¬°“√¢“â ß≈à“ßπ’È
✦ The tumor is solitary and confined to right/left lobe of the liver
✦ Satellite tumor nodules are present, but the tumor is confined to right/left lobe
of the liver
✦ The tumor is multifocal, but confined to right/left lobe of the liver
✦ The tumor is multifocal with tumor nodules present within both lobes of the liver
✦ The tumor invades the following extrahepatic structure (s): (portal vein,
gallbladder, visceral peritoneum etc. Major portal or hepatic veins are defined
as right/left/middle hepatic vein)

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Status of lymphovascular and perineural invasion
„Àâ√“¬ß“π«“à æ∫¡’À√Õ◊ ‰¡¡à ’ vascular invasion, lymphatic invasion, perineural invasion

°√≥¡’ ’ vascular invasion ∂“â  “¡“√∂√–∫‡ÿ  âπ‡≈Õ◊ ¥∑Ë∂’ °Ÿ ≈°ÿ ≈“¡‰¥â „Àâ√“¬ß“π¥â«¬ ‡™πà involvement of
right/left portal vein; involvement of right/left/middle hepatic vein; involvement of branches of the
portal vein; ·≈– tumor thrombi in small vessels (1) ‡ªπì µπâ

Margins of excision (1)
„À‡â ≈◊Õ°√“¬°“√¢â“ß≈à“ßπ’È
✦ No tumor identified at margins
✦ The parenchymal resection, distal bile duct, and vascular margins are free
of tumor
✦ The tumor is ________ cm from the parenchymal resection margin
✦ The tumor is ________ cm from the distal bile duct margin
✦ The hepatic capsule is free of tumor
✦ The tumor is present beneath the hepatic capsule but not on the surface
✦ Tumor is present at/on the :
distal bile duct margin
parenchymal resection margin
hepatic capsule surface
other___________________________________________________

Lymph node status
°≈à¡ÿ ¢ÕßµÕà ¡π”È ‡À≈Õ◊ ß∑¡’Ë ’§«“¡ ”§≠— ‰¥â·°à
1. Hilar lymph nodes; 2.Celiac lymph nodes; ·≈– 3. Periaortic-pericaval lymph

nodes °“√√“¬ß“π„Àâ∫Õ°®”π«πµàÕ¡π”È ‡À≈◊Õß∑’˵√«®æ∫ ·≈–®”π«πµàÕ¡∑’˺≈∫«° °√≥’À≈—ßπ’È
„À√â –∫¥ÿ ⫬ ∂“â æ∫¡’ extranodal extension into perinodal adipose tissue (1)

Condition of surrounding liver parenchyma (1)
§«√√“¬ß“π ¿“æ¢Õ߇πÈ◊Õ‡¬Ë◊Õµ—∫∑’ËÕ¬àŸπÕ°°âÕπ‡π◊ÈÕ¡–‡√Áß «à“¡’°“√‡ª≈Ë’¬π·ª≈ßµà“ßÊ

πÀ’È √Õ◊ ‰¡à
✦ Cirrhosis
✦ Chronic Hepatitis (specify type and activity-mild/moderate/severe)
✦ Steatosis
✦ Dysplastic Nodule (s), (specify grade-high/low grade)
✦ Large cell change (large cell dysplasia) in surrounding liver parenchyma
✦ Small cell change (small cell dysplasia) in surrounding liver parenchyma
✦ Macroregenerative Nodule
✦ Other____________________________________________

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References °“√µ√«®∑“ß欓 ‘∏«‘∑¬“

1. Dabbs DJ, Geisinger KR, Ruggiero F, Raab SS, Nalesnik M, Silverman JF. Recommendations
for the reporting of tissues removed as part of the surgical treatment of malignant liver
tumors. Hum Pathol 2004;35:1315-23.

2. Wee A, Sampatanukul P. In: Fine Needle Aspiration Cytology of The Liver: Diagnostic
algorithms, a Southeast Asian Perspective. Bangkok : Year Book Publisher 2004; p.49-85.

3. Sripa B, Pairojkul C. Pathology of cholangiocarcinoma. In: Vatanasapt V, Sripa B eds.
Liver Cancer in Thailand: epidemiology, diagnosis and control. Khon Kaen : Siriphan Press
2000; p.65-99.

4. Nakanuma Y, Sasaki M, Ishikawa A, Tsui W, Chen TC, Huang SF. Biliary papillary
neoplasm of the liver. Histol Histopathol 2002; 17:851-61.

5. Chen TC, Nakanuma Y, Zen Y, Chen MF, Jan YY, Yeh TS, Chiu CT, Kuo TT, Kamiya J,
Oda K, Hamaguchi M, Ohno Y, Hsieh LL, Nimura Y. Intraductal papillary neoplasia of
the liver associated with hepatolithiasis. Hepatology 2001;34:651-8.

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∫∑∫“∑√—ß «’ ‘π‘®©—¬·≈–
√ß—  √’ à«¡√—°…“°—∫¡–‡√Áßµ∫—

·≈–¡–‡√Áß∑Õà πÈ”¥’

√“™«‘∑¬“≈—¬√ß—  ·’ æ∑¬å

§≥–º®âŸ ¥— ∑”

1. »“ µ√“®“√¬§å ≈π‘ °‘ ‡°¬’ √µ§‘ ≥ÿ 𓬷æ∑¬ å “‚√®πå «√√≥惰…å
2. 𓬷æ∑¬å ÿ‡¡∏ √‘π √ÿ ߧ«ß»å
3. ·æ∑¬Àå ≠‘ß®“¡√’ ‡™ÈÕ◊ ‡æ™√‚ ¿≥
4. ·æ∑¬åÀ≠ß‘ ‡Õ¡Õ√ ‰¡â‡√¬’ ß
5. 𓬷æ∑¬åÕ≈ß°√≥å ‡°¬’ √µ¥‘ ‘≈°√∞—

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∫∑∫“∑√ß—  «’ π‘ ‘®©—¬·≈–√—ß ’√«à ¡√°— …“°—∫ —√ß ’ ‘«π‘® —©¬·≈–√—ß ’ √à«¡ —√°…“
¡–‡√ßÁ µ∫— ·≈–¡–‡√Áß∑àÕπÈ”¥’

𓬷æ∑¬åÕ≈ß°√≥å ‡°¬’ √µ¥‘ ‘≈°√—∞

Imaging of Hepatocellular carcinoma

Imaging of Regenerative Nodules
ªí®®ÿ∫—π‡√“¬—߉¡à “¡“√∂µ√«®æ∫ regenerating nodule ‰¥â∑È—ßÀ¡¥‚¥¬‡©æ“–‡¡Ë◊Õ°âÕπ¡’¢π“¥‡≈Á°
regenerating nodule ‡ªπì proliferative hepatocytes ∑¡’Ë ≈’ °— …≥– tissue ·≈– imaging ‡À¡◊Õπnormal
liver ¬°‡«âπ«à“¡’ fibrous tissue ≈Õâ ¡√Õ∫Õ¬Ÿà
‡√“¡—°®– “¡“√∂ —߇°µÿ‡ÀÁπ regenerating nodule ‰¥â‡¡◊ËÕ¡’ metal or fat deposit ∑”„Àâ density or
signal intensity ‡ª≈¬’Ë π‰ª, ‡¡ÕË◊ nodule ¡¢’ 𓥄À≠à, ·≈–‡¡◊ËÕ fibrotic tissue √Õ∫Ê nodule ‡¥à𙥗
‡™àπ„πºªŸâ É«¬ advanced cirrhosis.

In ultrasound study regenerating nodule æ∫¡≈’ —°…≥– hypoechoic nodules surrounded by thin
hyperechoic septa
In CT, cirrhotic nodules æ∫¡’≈°— …≥– small hyperdense nodules on unenhanced CT scans
In MRI, 30 to 40% æ∫¡’≈—°…≥– hypointense on T2-weighted spin echo images, best seen on
pulse sequences using fast low-angle shots ≈—°…≥–∑“ß pathology æ∫«à“ hypointensity ∑ˇ’ ÀÁπ
‡ªπì º≈®“° hemosiderin deposits √à«¡°∫— hyperintense fibrous septa √Õ∫Ê nodule.

„πºŸªâ «É ¬ advanced cirrhosis ®–¡’≈°— …≥– contracted liver contour ·≈– nodularity surface Õ“®¡’
large fibrotic scar ‡ÀÁπ‡ªìπ hypodense band on CT, ‡√’¬°«à“ confluent hepatic fibrosis.

Imaging of Dysplastic Nodules
Dysplastic nodules ¡’≈—°…≥– hyperintense on T1-weighted, hypointense on T2-weighted images
™«à ¬·¬°®“° regenerating nodule ·≈– HCC ‰¥§â Õà π¢“â ß™¥— ‡®π ·µ„à π∫“ß√“¬°ÕÁ “®æ∫¡’ variable signal
intensity ∑”„À≡ࠓ¡“√∂·¬° dysplastic nodule °∫— early HCCs ‰¥â

CT arteriography and CT arterial portography æ∫«à“ dysplastic nodule ®–¡’ blood supply
 «à π„À≠¡à “®“° portal vein ¢≥–∑’Ë HCC nodule ®–¡’ blood supply  «à π„À≠¡à “®“° hepatic artery
¥ß— πÈπ— ∂Ⓡ√“‡ÀπÁ ≈°— …≥– hyperdense enhancing lesions „π™à«ß arterial phase CT °®Á –™«à ¬„À‡â √“·¬°
early HCCs ®“° dysplastic nodule ‰¥â¥’¢Èπ÷ ·¡«â à“„π reports ∫“ß©∫∫— ®–æ∫«à“ dysplastic nodules
 “¡“√∂ enhance homogeneously „π arterial phase ‰¥°â µÁ “¡

Imaging of Hepatocellular Cancer
Imaging findings ¢Õß HCCs base on morphology, histology, and tumor vascularity ‡√“Õ“®
classified morphology of HCCs ‰¥‡â ªìπ 3 types: nodular, massive, diffuse
prevalence ¢π÷È °∫— stage of the disease, presence or absence of cirrhosis, etiologic factors

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Computed tomography Findings
Unenhanced CT ‰¡à sensitive æÕ„π°“√ detect small HCCs, ‡æ√“– density ¢Õß tumor nodules
Õ“® uniform ·≈–‰¡ à “¡“√∂·¬°®“° surrounding hepatic parenchyma ‰¥â ®”‡ªπì µâÕß„™â intravenous
contrast enhancement technique ‡æÕË◊ ™«à ¬·¬° lesion HCC nodule  «à π¡“°‡ªπì hypervascular nodule
‰¥â blood supplies  «à π„À≠®à “° hepatic artery, °“√ scanning liver „π™à«ß early phase ®–‡ÀÁπ tumor
nodule ‰¥â™—¥‡®π∑Ë’ ÿ¥ „π advanced HCCs, patterns of tumor growth ®– spread beyond the
capsule; growth of tumors in the portal and hepatic veins, multiple satellite nodules

Magnetic Resonance Imaging Findings
≈—°…≥– HCC „π unenhanced MRI ¢÷Èπ°∫— morphology ¢Õß tumor ‡™àπ fibrous capsule, mosaic
patterns and the inhomogeneity ¢Õß tumor ®“° hemorrhage ·≈– necrosis
Capsule ®–¡’≈—°…≥– low signal intensity on T1-and T2-weighted images, ‡ÀÁπ‰¥â™—¥°«à“
„π T1-weighted images

Septum and nodules-in-nodule appearances, areas of tumor necrosis and hemorrhage ‡ÀÁπ‰¥â¥’
∑ßÈ— „π T1-and T2-weighted images ‚¥¬‡©æ“– lesions „À≠à°«à“ 3 cm.
Fatty metamorphosis æ∫‰¥∫â àÕ¬ ¡≈’ °— …≥– high signal intensity on T1-weighted images
Signal ¢Õß nodule correlate °—∫ª√¡‘ “≥¢Õß metal deposits in tumor and cellular differentiation

Signal intensity ¢Õß tumor nodules on T1-weighted images varies ®“° hypointense to isointense
to hyperintense ‡ª√¬’ ∫‡∑¬’ ∫°—∫ surrounding parenchyma.
Hyperintensity on Tl-weighted images ‡°¥‘ ®“° fatty metamorphosis ·≈– high copper content.
Tumor nodule  «à π¡“°®– hyperintense on T2-weighted images, correlates °∫— prominent clear
cell type
Tumors ∑’Ë¡’ high signal intensity on T1-weighted ·≈– low signal intensity on T2-weighted images
¡·’ π«‚πâ¡∑®Ë’ –¡’ better cellular differentiation

‡™πà ‡¥¬’ «°∫— „π contrast-enhanced CT, °“√„™â dynamic fast-scanning MRI technique after rapid
intravenous contrast administration ¡§’ «“¡ ”§—≠„π°“√™«à ¬ detecting tumor nodules
´÷Ë߇ÀÁπ‰¥¥â ’„π early phase of intravenous contrast enhancement

Screening Strategies
Goal of screening §◊Õ early detection in high-risk patients, ‡æ√“–°“√√—°…“µ“à ßÊ®– “¡“√∂∑”‰¥â
À√◊Õ‰¥âº≈∑πË’ à“æÕ„®„π°≈à¡ÿ early HCCs
§«“¡ “¡“√∂„π°“√ detect dysplastic nodules ·≈–°“√µ¥‘ µ“¡°“√‡ª≈ˬ’ π·ª≈ߢÕß lesion ‰ª‡ªìπ
early HCCs ‡ªìπ‡ª“Ñ  ”§—≠ ”À√—∫ screening program. °“√ screening ∑Ë’¥µ’ Õâ ß simple, safe, ·≈–
cost-effective

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imaging studies  à«π¡“° specific  ”À√∫— advanced disease, ·µà‰¡à sensitive „π°“√ detect early —√ß ’ ‘«π‘® —©¬·≈–√—ß ’ √à«¡ —√°…“
HCCs À√◊Õ·¬° dysplastic nodule °∫— HCCs

Sensitivity ¢Õß ultrasonography „π°“√ detect small lesion ¢π÷È °∫— ºµŸâ √«®Õ¬“à ß¡“° ·µ‡à ªπì °“√µ√«®∑Ë’
cost-effective ·≈– practical ª√–¡“≥ 70% ¢Õß HCCs ∑‡’Ë ≈Á°°«à“ 2 cm  “¡“√∂ detected ‰¥â‚¥¬
ultrasonography

CT ·≈– MRI ®”°—¥¥â«¬√“§“·≈– variability of techniques, ∑”„À≡à practical  ”À√—∫ screening
program

Screening approach ∑’ˉ¥â√∫— °“√¬Õ¡√∫— ‚¥¬∑—Ë«‰ª ”À√∫— high-risk patients §◊Õ°“√ check serum
α-fetoprotein ∑ÿ° 6 ‡¥◊Õπ√«à ¡°∫— °“√µ√«® ultrasonography of liver ∑°ÿ 6 ‡¥◊Õπ

Imaging Strategies for Diagnosis and Staging
 Ëß‘  ”§—≠ ”À√—∫ imaging goals „π°“√ diagnosis and staging §Õ◊ °“√«π‘ ‘®©—¬∑Ë’∂°Ÿ µÕâ ß ·≈–∫Õ°‰¥«â à“
§π„¥‡ªìπ candidates for surgery

Imaging studies should be designed to answer the following questions:
1. Is the tumor confined to a single lobe or region that makes it resectable?
2. Does the tumor invade the portal or hepatic vein?
3. Are there smaller lesions in other lobes or segments?
4. Is there evidence of liver cirrhosis or portal hypertension?
5. Are there lymph node metastases?
6. Are there any other metastases?

Treatment Decision and Planning
Surgery ‡ªìπ treatment of choice that offers the best potential for cure, ¢âÕ¡Ÿ≈®“°ºŸªâ É«¬ liver
transplantation ·≈– liver surgery ™«È’ à“ stage I disease ¡’ 5-year survival rate 70 to 75%.
5-year survival rates for stages II, III, ·≈– IVA ≈¥≈߇ªπì 60, 40, ·≈– 10%
„πºŸâª«É ¬∑’‰Ë ¡ à “¡“√∂ºà“µ¥— ‰¥â, cirrhosis À√◊Õ poor liver function reserve, °“√∑” chemoembolization
À√Õ◊ percutaneous tumor ablation ‡ªπì ∑“߇≈◊Õ°∑Ë¥’ ’ ‚¥¬‡©æ“– tumors ∑Ë’‡≈°Á °«“à 5 cm.

Chemoembolization of the Liver
Degree of tumor necrosis ¢π÷È °∫— area of complete staining of the tumor by iodized oil ºªŸâ É«¬ 85
∂ß÷ 90% æ∫¡’ significant decrease level of serum α-fetoprotein ·≈– “¡“√∂‡æ¡Ë‘ survival rates ‰¥â
The 3-year survival rates~55 to 78%, and the 4-year survival rate~67% „π≠’˪ÿÉπ
Median survival times ¢ÕߺŸâªÉ«¬„π¬‚ÿ √ª·≈–Õ‡¡√°‘ “ Õ¬√àŸ –À«“à ß 7-11 ‡¥◊Õπ

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Chemotherapeutic agents „π TOCE/TACE ¡’„™°â —πÕ¬àŸÀ≈“¬™π‘¥
Most common sole agent chemotherapeutic drug §Õ◊ doxorubicin,
Combination ¢Õß cisplatin, doxorubicin ·≈– mitomycin C À√◊Õ 5-Fluorouracil ‡ªìπ most common
combination drug regimen
¡√’ “¬ß“π∫“ß©∫∫— ∫ßà ™È’«à“ cisplatin effective °«“à doxorubicin as a single agent against HCC

Ethiodized oil (Ethiodol; Savage Laboratories, Melville, NY) „™‡â ªπì suspension medium  ”À√∫—
chemotherapeutic agents ‡æ√“–¡§’ ÿ≥ ¡∫µ— ∑‘ Ë®’ –‰ª®∫— tumor cell (HCC) ‰¥â¥’ ‡ªπì key ingredient
¢Õß chemoembolization ‡æ√“–‡ªπì ∑—ßÈ drug-carrying, tumor-seeking ·≈– embolic agent

Van Beers and colleagues, retrospective analysis of chemoembolization „πºªŸâ É«¬ HCCs 54 √“¬
æ∫«“à ºªâŸ «É ¬∑’¡Ë ’ oil retention „π tumor ¡“°°«à“ 50% ¡’ survival rates ‡æ¡‘Ë ¢È÷π (1-year and 2-year
survival rates of 82 and 65% versus 27 and 0%).
πÕ°®“°πÈπ— ¬—ß —߇°µæÿ ∫«à“ ºâŸª«É ¬∑Ë¡’ ’ poor oil retention ¡°— ‡ªπì infiltrative, hypovascular, ·≈– more
advanced, ¢≥–∑’Ë lesions ∑Ë’¡’ oil retention ¡“°°«à“ 50% ¡°— ‡ªπì nodular and hypervascular
¡’ embolic agents ∑„Ë’ ™„â π chemoembolization Õ¬ÀàŸ ≈“¬™π¥‘ ‡™πà gelatin sponge powder and pledgets
(Gelfoam; Upjohn, Kalamazoo, MI) À√Õ◊ polyvinyl alcohol.

Gelatine sponges cause ‡ªπì temporary vascular occlusion, ¡’ recanalization ¢Õß vessel ‰¥„â π
ª√–¡“≥ 2  ª— ¥“Àå
Polyvinyl alcohol particles ‡ªìπ permanent arterial occlusion

¡§’ «“¡·µ°µ“à ß„π«∏‘ ’°“√„Àâ embolic agents
∫“ß center „™â mixing °π— ∑ßÈ— À¡¥√–À«à“ß particles, chemotherapeutic drugs ·≈– oil
∫“ß center ®–„Àⵓ¡À≈—ß chemotherapy drug and/or oil mixture

¡’°“√»°÷ …“∑’Ë™’È«à“ injectable volumes of chemotherapy ·≈– long-term arterial patency „π°≈àÿ¡∑’Ë
embolized tumor-feeding vessel À≈ß— °“√„Àâ entire dose of chemotherapy π—πÈ ¥’°«“à
´Ë÷ß¡’º≈¥µ’ Õà chemoembolization ‡æ√“– “¡“√∂∑” TOCE ´”È ‰¥Õâ °’ À≈“¬Ê§√ȗ߉¥â
long-term arterial patency Õ“®∂Õ◊ ‡ªπì key element to the success of TOCE

„πºŸâªÉ«¬∑’Ë¡’ multiple tumors in one lobe,  “¡“√∂∑’Ë®–∑” less selective approach for catheter
placement ‰¥â ¢≥–∑ºË’ ªâŸ «É ¬∑’Ë¡’ single lesion §«√ superselective „À‰â ¥¡â “°∑ Ë’ ÿ¥‡æÕ◊Ë preserve normal
liver parenchyma

Follow-up
Goals of imaging À≈ß— surgery, chemoembolization À√Õ◊ tumor ablation §Õ◊ °“√ detect new or
metastatic lesions À√Õ◊ recurrent disease.
CT À√◊Õ MRI with dynamic intravenous contrast enhancement ‡ªìπ commonly used technique

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Cancer of the Bile Duck —√ß ’ ‘«π‘® —©¬·≈–√—ß ’ √à«¡ —√°…“
Cholangiocarcinoma ‡ªìπ malignant tumors ∑’‡Ë °¥‘ ®“° epithelial lining of mucosa of bile duct ·≈–
gallbladder ‡ªìπ adenocarcinomas
Cholangiocarcinoma Õ“® classified ÕÕ°‡ªπì intrahepatic type ‡°‘¥®“° small bile ducts „π hepatic
parenchyma, extrahepatic type ‡°‘¥®“° extrahepatic bile duct

Incidence of cholangiocarcinoma ‡æ‘Ë¡¢÷Èπµ“¡Õ“¬ÿ ™“¬°—∫À≠ß‘ ‰¡à·µ°µà“ß°π—
Common risk factors §Õ◊ chronic inflammation ¢Õß bile duct, ‚¥¬‡©æ“–°≈¡àÿ bile duct stones
·≈– liver fluke infestation (I.e., Clonorchissinensis in East Asia and Opisthorchis viverrini in Southeast
Asia ); primary sclerosing cholangitis, ºâŸªÉ«¬ ulcerative colitis; nitrosamine compounds in food;
choledochal cyst ·≈– Thorotrast use

Intrahepatic cholangiocarcinoma ¡°— ¡“¥«â ¬ hepatic mass ·≈–¡°— ¡¢’ 𓥄À≠‡à æ√“–‰¡¡à Õ’ “°“√ highly
infiltrative, ~50% of tumors contain areas of fiborsis, tumor necrosis, mucin production ∫√‘‡«≥
active tumor growth ¡—°æ∫∑Ë’¢Õ∫ tumor

Patterns of tumor growth ¢Õß extrahepatic cholangiocarcinoma Õ“® classified ‡ªìπ papillary,
nodular, diffuse type

Extrahepatic type ¬—ß “¡“√∂·∫ßà µ“¡ location of tumor ‡ªπì hilar type, tumor located in the hepatic
duct proximal to the insertion of the cystic duct; mid-common bile duct type, tumor located distal
to the cystic duct junction ; and the distal common bile duct type, tumor near the ampulla

Papillary tumor grows into the lumen of the bile duct, æ∫¡“°°«à“™π¥‘ Õπ◊Ë Ê (70 to 80%) æ∫∑’Ë
∫√‘‡«≥ distal bile duct
Nodular form ¡—°æ∫‡ªπì fibrotic mass infiltrates surrounding tissue,~70% æ∫∑’Ë confluence of right
and left hepatic duct ∫√‡‘ «≥ hilar fissure.
Diffuse or infiltrative form grows in the duct wall, ≈°— …≥– diffusely thickened wall §≈⓬ sclerosing
cholangitis

Local tissue invastion, lymph node metastasis, perivascular and perineural invasion ‡ªìπ common
patterns of tumor progression ∑”„Àâ¡—°‰¡à “¡“√∂ºà“µ—¥‰¥â πÕ°®“° incidental finding µÈ—ß·µà√–¬–
·√°À√Õ◊ ¡’Õ“°“√‡√Á«®“° obstructive jaundice

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Imaging of Intrahepatic Cholangiocarcinoma
Intrahepatic cholangiocarcinoma æ∫πâÕ¬„πª√–‡∑»∑“ßµ–«—πµ° ¡’ imaging characteristics §≈⓬
metastatic tumors ®“° primary adenocarcinomas Õ◊πË Ê‰¥â

„π ultrasonography, æ∫«à“ echogenicity ¢Õß mass πÈπ— ¡’ variable ¡“°, ·µ¡à ’ tendency ∑’Ë®–‡ªπì
hyperechoic lesion ·≈–¡°— æ∫¡’ homogeneous internal architecture ¡“°°«“à ∑®’Ë –‡ªπì heterogeneous
internal architecture ¢÷Èπ°∫— ª√‘¡“≥ fibrous tissue, mucin ·≈– calcification

„π CT, tumor ¡’∑Èß— ≈—°…≥– well defined À√◊Õ infiltrative, ‰¡æà ∫ fibrous capsule ‡À¡◊Õπ HCC
Contrast study ®–æ∫¡’ rapid enhancement ∑∫’Ë √‡‘ «≥¢Õ∫‰¥â ‡æ√“–‡ªπì ∫√‡‘ «≥∑¡’Ë ’ active tumor growth
·≈–®– isodense or hypodense „π portal phase.
Central area ¢Õß tumor ´÷Ëß¡’ fibrous tissue, ¡—°®–‰¡à enhance „π early phase ·µ®à – enhance
„π delayed phase scanning ª√–¡“≥ 4 ∂÷ß 20 π“∑’ ¬°‡«âπ„πæ«°∑¡Ë’ ’ central necrosis À√◊Õ produce
mucin

„π MRI scans, tumor ®–æ∫¡’ signal intensities §≈⓬ metastatic tumors ®“° primary adenocarci-
nomas ÕË◊πʧ◊Õ hypointense on T1-weighted ·≈– hyperintense on T2-weighted images.
Post contrast dynamic MR images ¡’À≈°— °“√‡À¡◊Õπ„π CT

Imaging of Carcinoma of Extrahepatic Bile Duct
Cholangiocarcinoma ∑Ë’ extrahepatic bile duct æ∫¡’À≈“¬ patterns ¢π“¥ tumor ¡—°¢πÈ÷ °∫— location
·≈– level of bile duct obstruction
Tumor ∑’Ë right À√◊Õ left hepatic duct ¡·’ π«‚πâ¡∑Ë®’ –¡¢’ 𓥄À≠à°«à“ infiltrate hepatic parenchyma
√Õ∫Ê
Intrahepatic duct dilation ·≈– atrophy ¢Õß hepatic parenchyma ‡ªπì signs ∑’Ë™«à ¬ suggest origin
¢Õß tumor
Tumor ∑’Ë common hepatic duct ·≈– common bile duct ¡—°æ∫µ—Èß·µà¢π“¥‡≈Á° ‡æ√“–®–¡“æ∫
·æ∑¬å‡√Á«®“°Õ“°“√¢Õß obstructive jaundice

Ultrasonography ·≈– magnetic resonance cholangiopancreatography (MRCP) ¡’ª√–‚¬™π„å π°“√
screen À“ “‡Àµÿ¢Õß bile duct obstruction ‡æ√“–‡ªìπ primary non invasive techniques
ultrasonography ¡’ cost-effectiveness ∑¥Ë’ ’ µ√«®À“ stone ‰¥â¥’ ·µà¡°— limited ¥«â ¬¢π“¥ body ·≈–
lesions ∑∫’ √‘‡«≥ distal half ¢Õß common bile duct

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Positive results ¢Õß ultrasonography for lesion detection and staging range from 21 to 87%. —√ß ’ ‘«π‘® —©¬·≈–√—ß ’ √à«¡ —√°…“
MRCP ‡ªπì excellent non invasive technique ∑’®Ë – demonstrate anatomic information ¢Õß bile duct
„πºŸªâ «É ¬ obstructive jaundice ·µà°“√µ√«®¬ß— ¡’√“§“ Ÿß·≈–∑”‰¥â„π∫“ß center ‡∑“à πÈπ—
Helical CT scanning with 3-5 mm slice thickness ®“° left hilar fissure ∂ß÷ head pancreas „π™«à ß
arterial ·≈– portal venous phases ™à«¬∫Õ° relation ¢Õß tumors ·≈– arteries/veins ¢“â ߇§¬’ ߉¥â¥’
Enhancement ¢Õß tumor ¡’ variable ¡“° ¢π÷È °—∫ tumor type
Small papillary tumors À√◊Õ tumors with neuroendocrine differentiation ¡—°‡ªìπ hypervascular
tumor ·≈–‡ÀÁπ‰¥¥â „’ π arterial phase
¢≥–∑’Ë nodular type ´ßË÷ ¡’ fibrous/scirrhous tissue ®–‡ÀπÁ ‰¥â™—¥¢÷πÈ „π portal phase
Imaging ¡’ limited use „π infiltrate/diffuse type of tumor ®–æ∫¡’≈—°…≥– diffuse thickening ¢Õß bile
duct ·≈–¡’ multiple foci of tumor ‰¥â

109

«“à ß

110

¿“§ºπ«°

111

¿“§ºπ«°

µ“√“ß∑Ë’ 1 Childûs classification

Points assigned to laboratory values and and signs*

Parameters 12 3

Laboratory value <2 mg per dL 2 to 3 mg per dL >3 mg per dL
Total serum (34 µmol per L) (34 to 51 µmol per L) <2.8 g per dL
2.8 to 3 g per dL >2.20
bilirubin level >3.5 g per dL (28 to 35 g per L)
Serum albumin (35 g per L) 1.71 to 2.20 Poorly controlled
Poorly controlled
level <1.70
International
None Controlled medically
Normalized Ratio None Controlled medically
Signs
Ascites
Encephalopathy

*--------------Based on total points, a patient with cirrhosis is assigned to one of three classes:
Child class A = 5 to 6 points; Child class B = 7 to 9 points; Child class C = 10 to 15 points.

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Performance status

µ“√“ß∑Ë’ 2 Karnofsky index

100% Perfectlywell
90% Minor symptoms-can live a normal life.
80 % Normal activity with some effort
70% Unable to carry on normal activity but able to care for oneself
60% Requires occasional help with personal needs
50% Disabled
40% The patient needs nursing assistance and medical care, but is not hospitalised
30% Severely disabled, in hospital
20% Very sick, active support needed
10% Moribund
0% Death

µ“√“ß∑’Ë 3 Eastern Cooperative Oncology Group (ECOG) performance status

Grade ECOG
0 Fully active, able to carry on all pre-disease performance without restriction
1 Restricted in physically strenuous activity but ambulatory and able to carry out work of

a light or sedentary nature, e.g., light house work, office work
2 Ambulatory and capable of all selfcare but unable to carry out any work activities.

Up and about more than 50% of waking hours
3 Capable of only limited selfcare, confined to bed or chair more than 50% of waking hours
4 Completely disabled. Cannot carry on any selfcare. Totally confined to bed or chair
5 Dead

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