9Hepatolithiasis

HepatolithiasisÕπÿæß»å μ—ÈßÕ√ÿ≥ —πμ‘

Àπ૬‚√§∑“߇¥‘πÕ“À“√ ‚√ß欓∫“≈√“¡“∏‘∫¥’

Review Article

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

§”®”°—¥§«“¡¢Õß‚√§

¿“«– hepatolithiasis (HL) §◊Õ°“√æ∫π‘Ë« (stones, mud and/or sludge)

„π intrahepatic bile ducts „πμ”·Àπàß∑’ËÕ¬Ÿà‡Àπ◊ÕμàÕ common hepatic duct1

 “¡“√∂·∫à߉¥â‡ªìπ primary ·≈– secondary HL ‚¥¬ primary HL §◊Õ °“√¡’

π‘Ë«∑’ˇ°‘¥¢÷Èπ‡Õß„π intrahepatic duct  à«π secondary HL ‡°‘¥®“° retrograde

migration ¢Õßπ‘Ë«®“° extrahepatic bile duct ·≈– gallbladder

 ”À√—∫ primary HL ‡√“¬—ß·∫àß™π‘¥¢Õßπ‘Ë«μ“¡Õߧåª√–°Õ∫ÕÕ°‰¥â‡ªìπ

3 ™π‘¥ §◊Õ calcium bilirubinate stones, cholesterol stones ·≈– mixed

stones2-4

Syndrome of çrecurrent pyogenic cholangitis (RPC)é §◊Õ °≈ÿà¡Õ“°“√

∑’Ë¡’°“√μ‘¥‡™◊ÈÕ·∫§∑’‡√’¬´È”Ê „π∑“߇¥‘ππÈ”¥’ ´÷Ëß¡’≈—°…≥–®”‡æ“–§◊Õ¡’§«“¡ —¡æ—π∏å

°—∫ primary HL

Digby5 ‰¥â√“¬ß“π°≈ÿà¡Õ“°“√π’ȧ√—Èß·√°„πªï 1930 ·μà‡√‘Ë¡¡’°“√„™â§”

«‘π‘®©—¬«à“ recurrent pyogenic cholangitis §√—Èß·√°‚¥¬ Cook6 πÕ°®“°π’È ¬—ß

¡’™◊ËÕ‡√’¬°Õ◊ËπÊ ‡™àπ oriental cholangiohepatitis7, oriental cholangitis8, Hong

Kong disease9 ·≈– biliary obstruction syndrome of the Chinese10

®“°√“¬ß“π∑’˺à“π¡“æ∫«à“ºŸâªÉ«¬ RPC ®–æ∫π‘Ë«„π∑“߇¥‘ππÈ”¥’√à«¡¥â«¬

√âÕ¬≈– 75-80  à«π∑’ˇÀ≈◊Õ∑’ˉ¡àæ∫π‘Ë«√à«¡¥â«¬ Õ“®¡’ “‡Àμÿ®“°°“√μ‘¥‡™◊ÈÕ´È”Ê „π

∑“߇¥‘ππÈ”¥’ À√◊Õ®“°§«“¡º‘¥ª°μ‘Õ◊ËπÊ ¢Õß∑àÕ∑“߇¥‘ππÈ”¥’

10 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“߇¥‘πÕ“À“√·Ààߪ√–‡∑»‰∑¬, ¡°√“§¡-‡¡…“¬π 2557

¿“«–∑’Ë·∫§∑’‡√’¬‡¢â“ Ÿà°√–· ‡≈◊Õ¥™—Ë«§√“«∑“ß portal vein Õ“®‡ªìπ°≈‰°

∑’Ë∑”„Àâ·∫§∑’‡√’¬‡¢â“ Ÿà∑àÕ∑“߇¥‘ππÈ”¥’ ´÷Ëß𔉪 Ÿà°“√μ‘¥‡™◊ÈÕ·≈–°“√‡°‘¥π‘Ë«„π∑“ß

‡¥‘ππÈ”¥’μ“¡¡“ ®π°√–∑—Ë߇ªìπ«ß®√‰ª‡√◊ËÕ¬Ê  ”À√—∫‡™◊ÈÕ∑’Ëæ∫∫àÕ¬‡¡◊ËՇ擖‡™◊ÈÕ®“°

πÈ”¥’ ‰¥â·°à Escherichia coli, Klebsiella pneumoniae, Pseudomonas

aeruginosa ·≈– Proteus spp.  à«π anaerobes æ∫‰¥â‰¡à∫àÕ¬π—°

≈—°…≥–¢Õß∑àÕ∑“߇¥‘ππÈ”¥’º‘¥ª°μ‘∑’Ëæ∫‰¥â„π RPC ‰¥â·°à °“√¢¬“¬¢Õß

extrahepatic ·≈– intrahepatic duct √à«¡°—∫ focal stricture „π intrahepatic

biliary tree ≈—°…≥–∑“ß欓∏‘«‘∑¬“∑’˺π—ߢÕß∑àÕ∑“߇¥‘ππÈ”¥’®–æ∫«à“¡’ fibrosis

·≈–¡’ inflammatory cell infiltration ‚¥¬®ÿ¥∑’Ë¡—°æ∫欓∏‘ ¿“æ∫àÕ¬∑’Ë ÿ¥§◊Õ left

hepatic duct ‚¥¬‡©æ“–∑’Ë left lateral segment  “‡Àμÿ∑’Ëæ∫∫àÕ¬∑’Ëμ”·Àπàßπ’È

¬—߉¡à∑√“∫·πà™—¥ ·μàÕ“®Õ∏‘∫“¬®“°¡ÿ¡∑’ËÀ—°ßÕ¡“°°«à“‡¡◊ËÕ‡∑’¬∫°—∫ right hepatic

duct ®÷ßÕ“®∑”„Àâ¡’‚Õ°“ ‡°‘¥°“√μ’∫¢Õß∑àÕ∑“߇¥‘ππÈ”¥’·≈–¡’°“√§â“ߢÕßπÈ”¥’‰¥â

¡“°°«à“ π‘Ë«„π∑“߇¥‘ππÈ”¥’∑’Ëæ∫®–¡’®”π«π¡“° ¢π“¥·μ°μà“ß°—π  à«π¡“°‡ªìπ

calcium bilirubinate À√◊Õ brown pigment stones ·≈–®–æ∫ hypertrophy of

the papilla of the sphincter of Oddi ®“°°“√À≈ÿ¥ºà“π¢Õßπ‘Ë«´È”Ê

√–∫“¥«‘∑¬“

¿“«– hepatolithiasis æ∫‰¥â∫àÕ¬„π·∂∫‡Õ‡™’¬μ–«—πÕÕ°·≈–‡Õ‡™’¬μ–«—π

ÕÕ°‡©’¬ß„μâ11-18 ‚¥¬¡’√“¬ß“πÕÿ∫—μ‘°“√≥å°“√‡°‘¥¿“«–π’È√âÕ¬≈– 4-52 „π·∂∫‡Õ‡™’¬

μ–«—πÕÕ° ·μàæ∫‡æ’¬ß√âÕ¬≈– 0.6-1.3 „π·∂∫μ–«—πμ°19 Õ¬à“߉√°Áμ“¡ ªí®®ÿ∫—π

æ∫„πª√–‡∑»·∂∫μ–«—πμ°æ∫Õÿ∫—μ‘°“√≥å¢Õß‚√§π’È Ÿß¢÷Èπ®“°°“√Õæ¬æ¢Õߪ√–™“°√

·≈–„π∑“ß°≈—∫°—π°Áæ∫¿“«–π’È≈¥≈ß„πª√–‡∑»·∂∫μ–«—πÕÕ° ´÷ËßÕ“®‡π◊ËÕߥ⫬°“√

¡’¿“«–‚¿™π“°“√·≈–§«“¡‡ªìπÕ¬Ÿà∑’Ë¥’¢÷Èπ √«¡∑—Èß°“√√—∫‡Õ“«—≤π∏√√¡°“√∫√‘‚¿§

Õ“À“√·∫∫™“«μ–«—πμ°‡¢â“¡“

‡§¬¡’√“¬ß“π™à«ßÕ“¬ÿ∑’Ëæ∫¿“«–π’ȉ¥â∫àÕ¬§◊Õ 20-40 ªï20 ·μஓ°¢âÕ¡Ÿ≈≈à“ ÿ¥

æ∫«à“Õ“¬ÿ‡©≈’ˬ¢ÕߺŸâªÉ«¬‡¡◊ËÕ‡√‘Ë¡¡’¿“«–π’ÈÕ¬Ÿà∑’Ë 50-60 ªï21 ¿“«–π’Èæ∫„π‡æ»™“¬·≈–

À≠‘߇∑à“Ê °—π21,22 ‚¥¬‡©æ“–„π°≈ÿà¡∑’ˇ»√…∞“π– —ß§¡‰¡à¥’·≈–¡’°“√∫√‘‚¿§Õ“À“√

11Hepatolithiasis

∑’Ë¡’§“√å‚∫‰Œ‡¥√μ Ÿß·μà‚ª√μ’π·≈–‰¢¡—πμË”23

 “‡Àμÿ

¬—߉¡à “¡“√∂√–∫ÿ “‡Àμÿ∑’Ë·πà™—¥‰¥â ·μஓ°°“√∑’Ëæ∫¡“°„πª√–™“°√°≈ÿà¡∑’Ë

‡»√…∞“π– —ß§¡‰¡à¥’ ®÷ߧ‘¥«à“ªí®®—¬∑“ß ‘Ëß·«¥≈âÕ¡πà“®–‡ªìπªí®®—¬À≈—°Õ¬à“ßÀπ÷Ëß

 ”À√—∫ “‡Àμÿ∑’Ë¡’°“√°≈à“«∂÷ß·≈–æÕ¡’À≈—°∞“πª√“°Ø ‰¥â·°à

1. Parasitic infection

°“√μ‘¥‡™◊ÈÕ欓∏‘„π∑“߇¥‘ππÈ”¥’∑”„À⇰‘¥°“√∑”≈“¬¢Õ߇´≈≈凬◊ËÕ∫ÿ∑“߇¥‘π

πÈ”¥’ °“√Õÿ¥μ—π¢Õß∑àÕ∑“߇¥‘ππÈ”¥’ ·≈–Õ“®‡ªìπ®ÿ¥‡√‘Ë¡μâπ¢Õß¿“«–π’È24 ‚¥¬æ¬“∏‘

∑’ˇªì𠓇Àμÿ ‰¥â·°à Clonorchis sinensis, Opisthorchis species, Fasciola he-

patica ·≈– Ascaris lumbricoides Õ¬à“߉√°Áμ“¡ ºŸâªÉ«¬ RPC π—Èπ®– “¡“√∂μ√«®

æ∫°“√μ‘¥‡™◊ÈÕ欓∏‘¥—ß°≈à“«‰¥â‡æ’¬ß√âÕ¬≈– 20-4524-26 ‡∑à“π—Èπ ́ ÷ËßÕ“®‡π◊ËÕߥ⫬§«“¡

‰«¢ÕßÀâÕߪؑ∫—μ‘°“√„π°“√μ√«® ·≈–„π¢≥–∑’Ë¡’°“√¥”‡π‘π‚√§π—Èπ°“√μ‘¥‡™◊ÈÕ

欓∏‘Õ“®®–À“¬‰ª·≈⫉¥â À≈—°∞“π∑’Ë π—∫ πÿπ«à“欓∏‘‡À≈à“π’ȇªì𠓇Àμÿ §◊Õ ¡’°“√

»÷°…“∂÷ßÕߧåª√–°Õ∫¢Õßπ‘Ë«„π∑“߇¥‘ππÈ”¥’„πºŸâªÉ«¬ RPC æ∫ ova ¢Õß欓∏‘

‡À≈à“π’ȇªìπ nidus ¢Õßπ‘Ë«27,28

2. Bacterial infection

æ∫«à“ pigment stone „πºŸâªÉ«¬ RPC Õ“®‡°‘¥®“°°“√∑’Ë bacterial glu-

curonidase ‡ª≈’ˬπ bilirubin glucuronide „À⇪ìπ unconjugated bilirubin

´÷Ëß®–‰ª®—∫°—∫ calcium ‡ªìπ complex ∑’ˉ¡à≈–≈“¬πÈ” ‡°‘¥‡ªìππ‘Ë«¢÷Èπ„π∑“߇¥‘ππÈ”¥’

·≈–‡¡◊ËÕπ‘Ë«‡°‘¥¢÷Èπ·≈â«°Á®–‡ªìπ‡Àμÿ„À⇰‘¥«ß®√¢Õß°“√Õÿ¥μ—π¢Õß∑àÕ∑“߇¥‘ππÈ”¥’

¿“«–πÈ”¥’§—Ëß °“√μ‘¥‡™◊ÈÕ·∫∫´È”Ê ·≈–𔉪 Ÿà°“√‡°‘¥π‘Ë«‰ª‰¥âÕ’°‡√◊ËÕ¬Ê

¡’¢âÕ¡Ÿ≈∑“ß°“√«‘®—¬æ∫«à“°“√√—∫ª√–∑“πÕ“À“√∑’Ë‚ª√μ’πμË”¢Õß™“«

‡Õ‡™’¬ àߺ≈„Àâ¡’°“√≈¥≈ߢÕß glucuro-1,4-lactone ´÷Ëß∑”Àπâ“∑’ˬ—∫¬—Èß β-glucu-

ronidase29

12 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“߇¥‘πÕ“À“√·Ààߪ√–‡∑»‰∑¬, ¡°√“§¡-‡¡…“¬π 2557

3. Bile stasis

¿“«–∑àÕ∑“߇¥‘ππÈ”¥’μ’∫∑’ˇ°‘¥μ“¡¡“®“°°√–∫«π°“√Õ—°‡ ∫·≈–°“√´àÕ¡

·´¡À≈“¬Ê §√—Èß °ÁÕ“®‡ªìπÕ’°ªí®®—¬Àπ÷Ëß∑’Ë𔉪 Ÿà°“√μ‘¥‡™◊ÈÕ´È”Ê ·≈–π‘Ë«„π∑“߇¥‘π

πÈ”¥’

Õ“°“√∑“ߧ≈‘π‘°

 à«π„À≠ຟâªÉ«¬¡—°¡“¥â«¬ recurrent cholangitis ‚¥¬¡’Õ“°“√‰¢â μ—«μ“

‡À≈◊Õß ·≈–‡®Á∫™“¬‚§√ߢ«“ (Charcotûs triad) „π∫“ß°√≥’Õ“®¡’¿“«–§«“¡¥—π

‚≈À‘μμË” ·≈–´÷¡À√◊Õ —∫ π√à«¡¥â«¬ (Reynoldsû pentad)

ºŸâªÉ«¬√âÕ¬≈– 15-30 ‰¥â√—∫°“√«‘π‘®©—¬¿“«–π’Èμ—Èß·μà¡’Õ“°“√§√—Èß·√°

ºŸâªÉ«¬ ŸßÕ“¬ÿÕ“®¡’ atypical presentation ‡™àπ ‰¡à‰¥â¡’‰¢âÀ√◊ÕÕ“°“√ª«¥∑âÕß∑’Ë™—¥‡®π

πÕ°®“°π’È ¬—ßÕ“®¡“¥â«¬¿“«–·∑√°´âÕπÕ◊ËπÊ ®“°π‘Ë«„π∑“߇¥‘ππÈ”¥’ ‡™àπ biliary

colic, acute pancreatitis, obstructive jaundice ·≈–∑’Ëæ∫‰¥âπâÕ¬°«à“§◊Õ ¡“

¥â«¬ hepatomegaly ·≈– abnormal liver biochemistry19,21

 ”À√—∫¿“«–·∑√°´âÕπÕ◊ËπÊ ‡™àπ bile duct perforation, bile peritoni-

tis, secondary biliary cirrhosis, thrombophlebitis ·≈– thrombosis ¢Õß

portal vein À√◊Õ hepatic vein μ≈Õ¥®π pulmonary thromboembolism „π

ªí®®ÿ∫—πæ∫‰¥âπâÕ¬≈ß¡“° ‡π◊ËÕß®“°°“√«‘π‘®©—¬·≈–°“√√—°…“∑’ˇ√Á«¢÷Èπ3,19,21 °“√¡’∑“ß

‡¥‘ππÈ”¥’Õÿ¥μ—π‡√◊ÈÕ√—ßπÕ°®“°∑”„Àâ¡’μ—«μ“‡À≈◊Õß·≈–§—π·≈â« Õ“®π”‰ª Ÿà°“√‡°‘¥Ωï

„πμ—∫ (liver abscess) ·≈–°“√ΩÉÕμ—«¢Õ߇π◊ÈÕμ—∫ (liver atrophy) ‰¥â ‚¥¬Õ“®

‡À≈◊Õ‡æ’¬ß fibrous tissue ·≈– dilated duct ´÷Ëß¡—°‡ªìπ∑’Ë left lobe ·≈– left

lateral segment ®π°√–∑—Ëß„π∑’Ë ÿ¥Õ“®‡°‘¥¿“«– secondary biliary cirrhosis

(æ∫‰¥â√âÕ¬≈– 7) ·≈– cholangiocarcinoma μ“¡¡“‰¥â21,22,30,31 ºŸâªÉ«¬∑’ËÕ“°“√

∑“ߧ≈‘π‘°·¬à≈ß ‡™àπ ¡’Õ“°“√‡À≈◊Õß¡“°¢÷Èπ πÈ”Àπ—°≈¥ À√◊Õ¡’À≈—°∞“π¢Õß

cholestasis ¡“°¢÷È𠇙àπ ¡’°“√‡æ‘Ë¡¢÷Èπ¢Õß alkaline phosphatase ‚¥¬À“‡Àμÿ

Õ◊ËπÕ∏‘∫“¬‰¡à‰¥â ·æ∑¬å§«√ ß —¬ cholangiocarcinoma ‚¥¬μ”·ÀπàߢÕß¡–‡√Áß

¡—°Õ¬Ÿà∫√‘‡«≥ atrophic left lobe ¢Õßμ—∫

13Hepatolithiasis

Õÿ∫—μ‘°“√≥å¢Õß cholangiocarcinoma „πºŸâªÉ«¬°≈ÿà¡π’ÈÕ¬Ÿà∑’Ë√âÕ¬≈– 5-10

‚¥¬μ—«‡≈¢·μ°μà“ß°—π‰ª„π·μà≈–√“¬ß“π34-35 ·≈–¡—°æ∫¢≥–Õ“¬ÿ 50 ªï À√◊Õ 10-

30 ªïÀ≈—ß®“°‡√‘Ë¡¡’ recurrent cholangitis ·≈–æ∫„π‡æ»À≠‘ß¡“°°«à“™“¬‡æ’¬ß

‡≈Á°πâÕ¬

·¡â«à“®– “¡“√∂°”®—¥ hepatolithiasis ÕÕ°‰ª‰¥âÀ¡¥·≈â« °Á¬—ß¡’‚Õ°“ 

‡°‘¥ cholangiocarcinoma ‰¥â ∑—Èßπ’ÈÕ“®‡π◊ËÕß®“°¬—ß¡’¿“«–πÈ”¥’§—Ëß °“√μ‘¥‡™◊ÈÕ

·∫§∑’‡√’¬´È”Ê ·≈–°“√μ‘¥‡™◊ÈÕ欓∏‘ Clonorchis sinensis ∑’ˇªìπªí®®—¬„π°“√‡°‘¥

¡–‡√ÁßÕ¬Ÿà36,37  ”À√—∫ª√–‚¬™πå¢Õß°“√μ√«®§—¥°√ÕßÀ“ cholangiocarcinoma „π

¿“«–π’Ȭ—߉¡à™—¥‡®π

°“√«‘π‘®©—¬

Õ“»—¬ª√–«—μ‘ °“√μ√«®√à“ß°“¬ ·≈–º≈‡≈◊Õ¥∑’˺‘¥ª°μ‘ ‡™àπ leukocytosis,

abnormal liver chemistry ∑’Ë¡’°“√‡æ‘Ë¡¢÷Èπ¢Õß serum alkaline phosphatase

·≈– bilirubin À√◊Õ„π∫“ß°√≥’Õ“®¡’°“√‡æ‘Ë¡¢÷Èπ¢Õß serum transaminase ‰¥â

μ≈Õ¥®π°“√ àßμ√«®¿“æ«‘π‘®©—¬∑’ˇ¢â“‰¥â°—∫¿“«–π’È ‰¥â·°à ultrasound, CT scan,

MRI, MRCP, ERCP ·≈– percutaneous transhepatic cholangiography (PTC)

‚¥¬∑’Ë ERCP ·≈– PTC ®–¡’ª√–‚¬™πå„π·ßà¢Õß°“√√—°…“¥â«¬

ºŸâªÉ«¬ hepatolithiasis ¡’≈—°…≥–∑“ߧ≈‘π‘°∫“ߪ√–°“√∑’˧≈⓬§≈÷ß°—∫

primary sclerosing cholangitis ·μà¡’§«“¡·μ°μà“ß°—πÀ≈“¬ª√–°“√ ¥—ß √ÿª„π

μ“√“ß∑’Ë 1

°“√«‘π‘®©—¬‚¥¬¿“æ∑“ß√—ß ’

‚¥¬∑—Ë«‰ª¿“æ∑“ß√—ß ’¡’∫∑∫“∑ ”§—≠„π°“√«‘π‘®©—¬¿“«– RPC μ≈Õ¥®π

™à«¬ª√–‡¡‘πμ”·Àπàß ·≈–§«“¡√ÿπ·√ߢÕß欓∏‘ ¿“æ ‚¥¬‡§√◊ËÕß¡◊Õ∑’Ë¡’∫∑∫“∑¥—ß

°≈à“« ‰¥â·°à ultrasound, computed tomography (CT) scan, contrast cho-

langiography ·≈– magnetic resonance cholangiopancreatography (MRCP)

 ”À√—∫ plain radiography of the abdomen ¡—°‰¡à™à«¬„π°“√«‘π‘®©—¬

14 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“߇¥‘πÕ“À“√·Ààߪ√–‡∑»‰∑¬, ¡°√“§¡-‡¡…“¬π 2557

μ“√“ß∑’Ë 1 §«“¡·μ°μà“ߢÕß≈—°…≥–∑“ߧ≈‘π‘°√–À«à“ß primary sclerosing cholangitis ·≈– hepatolithiasis

Primary Sclerosing Cholangitis Hepatolithiasis

Ethnic group

AgeGenderPresenting symp-toms and signs

Laboratory investi-gations

Radiologic findings

Associated dis-eases

Typical cl inicalcourse

Microscopic find-ings

(From SEMINARS IN LIVER DISEASE/VOLUME 31, NUMBER 1 2011)

æ∫∫àÕ¬„π¬ÿ‚√ª·≈–Õ‡¡√‘°“

æ∫¡“°™à«ßÕ“¬ÿ 25-40 ªï™“¬ : À≠‘ß 2-3 : 1Fatigue, vague upper abdominal pain,intermittent jaundiceCholangitis less common

Raised serum ALP, GGTBilirubin raised as disease progresses

Typically ùûbeadedû appearance involv-ingboth intra- and extrahepatic bile ducts,strictures, diverticulaIdiopathic inflammatory bowel disease,including ulcerative colitis and CrohnûsdiseaseProgressive, overall 12 to 18 years fromdiagnosis to death or transplantationMay be complicated by cholangiocar-cinomaLymphoplasmacytic infiltrates aroundlarge intrahepatic ducts,+/-acute inflam-matoryinfiltratesOnion-skin type of periductal fibrosisaround medium-sized to large bile ductsObliteration of bile ducts that are re-placed by fibrous whorls; extensive ductlossPortal tract inflammation+/-interfacehepatitis, ductular reaction, and chroniccholestasis

æ∫∫àÕ¬„π‡Õ‡™’¬μ–«—πÕÕ° ·≈–‡Õ‡™’¬μ–«—πÕÕ°‡©’¬ß„μâæ∫¡“°™à«ßÕ“¬ÿ 50-60 ªïæ∫„𙓬·≈–À≠‘ßæÕÊ°—πEpigastric pain, backache, fever,jaundiceA significant proportion asymptom-aticDuring attacks, raised ALP, bilirubinand ALT levelsWBC may also be raisedDilatation of first and second divisionsof intrahepatic ducts, abrupt nonvi-sualization of peripheral divisions;calculi, pneumobilia, lobar atrophyParasitic infestation, including Clonor-chiasis and Ascariasis

Recurrent attacks of cholangitis, maydie of sepsisMay be complicated by cholangiocar-cinomaBilirubinate stones, fibrous thicken-ing of ectatic large ducts, with lym-phoplasmacytic infiltration,+/-suppu-rative cholangitisPeriductal lamellar fibrosis of septaland small interlobular ductsSmall bile ducts may show duct at-rophy, fibrous obliteration, and ductlossHyperplasia of peribiliary glands

15Hepatolithiasis

‡π◊ËÕß®“°π‘Ë«„π∑“߇¥‘ππÈ”¥’ à«ππâÕ¬‡∑à“π—Èπ∑’ˇªìπ radiopaque

Ultrasonography

‡ªìπ¿“æ«‘π‘®©—¬·√°∑’˙૬„π°“√«‘π‘®©—¬ºŸâªÉ«¬∑’Ë¡’Õ“°“√ ·≈–Õ“°“√· ¥ß

¢Õß°“√μ‘¥‡™◊ÈÕ„πμ—∫·≈–∑“߇¥‘ππÈ”¥’ ª√–‚¬™πå §◊Õ À“‰¥âßà“¬ ª≈Õ¥¿—¬ ·≈–

 “¡“√∂μ√«®¢â“ß‡μ’¬ß‰¥â ·μà°Á¡’¢âÕ®”°—¥§◊Õ ‡ªìπ°“√μ√«®∑’˺≈≈—æ∏å¢÷Èπ°—∫§«“¡

™”π“≠¢ÕߺŸâμ√«®

„π¿“«– RPC °“√μ√«® ultrasonography ®–æ∫∑àÕ∑“߇¥‘ππÈ”¥’¢¬“¬

·≈–π‘Ë«∑’ËÕ“®æ∫ posterior acoustic shadow „π∑àÕ∑“߇¥‘ππÈ”¥’π—Èπ ‚¥¬Õ“®æ∫

§«“¡º‘¥ª°μ‘¢Õß∑àÕ∑“߇¥‘ππÈ”¥’∑—Èß„π·≈–πÕ°μ—∫ °“√μ√«®æ∫π‘Ë«„π¿“«–π’È¢÷Èπ

°—∫¢π“¥ shadowing characteristics ≈—°…≥– echogenicity ·≈–μ”·ÀπàߢÕß

π‘Ë«

°“√»÷°…“¢Õß Lim „πºŸâªÉ«¬ 48 √“¬ æ∫«à“ ultrasound μ√«®æ∫π‘Ë«„π

∑“߇¥‘ππÈ”¥’‰¥â√âÕ¬≈– 9838 ‚¥¬æ∫≈—°…≥– echogenic with shadowing √âÕ¬

≈– 77 without shadowing √âÕ¬≈– 13 ·≈– mixed pattern √âÕ¬≈– 10  ”À√—∫

echogenic stones π—È𮔇ªìπμâÕß·¬°°—∫¿“«– pneumobilia ¥â«¬ ∫“ߧ√—Èßæ∫

≈—°…≥– prominent periportal echogenicity Õ—π‡π◊ËÕß¡“®“° pericholangitis

·≈– periportal fibrous thickening ‰¥â√âÕ¬≈– 3039 ≈—°…≥–Õ◊ËπÊ ∑’ˬ—ß “¡“√∂

æ∫‰¥â®“° ultrasound ‰¥â·°à gallstones, liver abscesses, biloma ·≈–

cholangiocarcinoma

¢âÕ®”°—¥¢Õß ultrasound ¬—ßæ∫„π°“√μ√«®ºŸâªÉ«¬∑’ËÕâ«π´÷Ëßμ—∫«“ßμ—«Õ¬Ÿà

„πμ”·Àπàß Ÿß À√◊Õ„πºŸâªÉ«¬∑’Ë¡’≈¡„π∑“߇¥‘πÕ“À“√¡“° À√◊Õ¡’·º≈ºà“μ—¥ºπ—ßÀπâ“

∑âÕß¡“°„π∫√‘‡«≥∑’Ë®–μ√«® ·≈–¿“«– extensive pneumobilia ¬—ßÕ“®√∫°«π

°“√μ√«®‰¥â

CT scan

πÕ°®“°°“√«‘π‘®©—¬¿“«– RPC ‰¥âÕ¬à“ߥ’·≈â« CT scan ¬—ß “¡“√∂„Àâ¢âÕ¡Ÿ≈

¢Õß¿“«–·∑√°´âÕπ‰¥â ‡™àπ liver abscess, liver cirrhosis, biloma, bile duct

rupture with peritonitis, cholangiocarcinoma ·≈– pancreatitis

16 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“߇¥‘πÕ“À“√·Ààߪ√–‡∑»‰∑¬, ¡°√“§¡-‡¡…“¬π 2557

æ∫«à“√âÕ¬≈– 90 ¢Õß pigmented stones „π¿“«– RPC ¡’≈—°…≥–

hyperdensity ‡¡◊ËÕ‡∑’¬∫°—∫ non-contrasted liver parenchyma

®“°°“√»÷°…“‚¥¬ Chan „πºŸâªÉ«¬ RPC 50 √“¬ æ∫«à“∑ÿ°√“¬¡’ intrahe-

patic duct dilatation ®“°°“√μ√«®‚¥¬ CT scan40  à«π≈—°…≥–Õ◊ËπÊ ∑’Ëæ∫πâÕ¬

≈߉ªμ“¡≈”¥—∫ ‰¥â·°à intrahepatic calculi, common duct dilatation,

pneumobilia, segmental atrophy, common duct calculi, strictures ·≈–

splenomegaly

®“°°“√»÷°…“¢Õß Kim æ∫«à“ cholangicarcinoma ∑’ˇ°‘¥„π RPC π—Èπ

¡—°æ∫„πμ—∫ à«π∑’Ë atrophy ·≈–¡’ portal vein narrowing À√◊Õ obliteration

‚¥¬„π°“√»÷°…“π—Èπæ∫Õÿ∫—μ‘°“√≥å¢Õß peripheral cholangiocarcinoma √âÕ¬≈–

88 „π hepatic atrophy ·≈–√âÕ¬≈– 83 „π∫√‘‡«≥∑’Ë¡’ portal vein narrowing

À√◊Õ obliteration41

Contrast cholangiography

‡ªìπ°“√μ√«®∑’Ë ”§—≠„π°“√ª√–‡¡‘πºŸâªÉ«¬°àÕπ°“√ºà“μ—¥ ‚¥¬Õ“®„™â«‘∏’ per-

cutaneous transhepatic cholangiography, endoscopic retrograde

cholangiopancreatography (ERCP), operative cholangiography À√◊Õ T-

tube cholangiography

≈—°…≥–∑’Ë®”‡æ“–¢Õß¿“«–π’È®“° cholangiography §◊Õ decreased ar-

borization of intrahepatic ducts, distortion of branching pattern, central

dilatation of ducts with rapid tapering at the periphery (the arrowhead

sign) (¿“æ∑’Ë 1), complete non-opacification of bile ducts (missing duct

sign) (¿“æ∑’Ë 2) ·≈– dilatation of the common bile duct ‚¥¬¿“æ√«¡¢Õß∑àÕ

∑“߇¥‘ππÈ”¥’¥—ß°≈à“« Õ“®‡√’¬°‡ªìπ pruned-tree appearance

‡¡◊ËÕ‡ª√’¬∫‡∑’¬∫°—∫ MRCP æ∫«à“ contrast cholangiography

 “¡“√∂ª√–‡¡‘π peripheral À√◊Õ smaller ducts ‰¥â¥’°«à“ ·μà¡’¢âÕ®”°—¥§◊Õ Õ“®

‰¡à “¡“√∂· ¥ß∑àÕ∑“߇¥‘ππÈ”¥’∑’˺‘¥ª°μ‘∫“ßμ”·Àπà߉¥â À“°¡’∑àÕ∑“߇¥‘ππÈ”¥’μ’∫

¡“°À√◊Õμ—π μ≈Õ¥®π‰¡à “¡“√∂· ¥ß∂÷ß欓∏‘ ¿“æπÕ°∑àÕ∑“߇¥‘ππÈ”¥’‰¥â À“°

17Hepatolithiasis

¿“æ∑’Ë 1 T-tube cholangiography · ¥ß≈—°…≥– typical rapid tapering of the peripheral ducts

(arrowhead sign) (From SEMINARS IN LIVER DISEASE/VOLUME 31, NUMBER

1 2011)

¿“æ∑’Ë 2 ERCP · ¥ß≈—°…≥– non-opacification „π right intrahepatic bile ducts ∑’Ë∫àß∂÷ß°“√Õÿ¥

μ—π®“°°“√μ’∫¢Õß∑àÕ∑“߇¥‘ππÈ”¥’ (missing duct sign) (From SEMINARS IN LIVER

DISEASE/VOLUME 31, NUMBER 1 2011)

18 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“߇¥‘πÕ“À“√·Ààߪ√–‡∑»‰∑¬, ¡°√“§¡-‡¡…“¬π 2557

欓∏‘ ¿“æπ—Èπ‰¡à‰¥â¡’º≈μàÕ∑àÕ∑“߇¥‘ππÈ”¥’

MRCP

„™â‡∑§π‘§ heavily T2-weighted imaging sequences ∑”„Àâ —≠≠“≥

¢Õß fluid-filled structures ‡™àπ ∑àÕ∑“߇¥‘ππÈ”¥’·≈–∑àÕ¢Õßμ—∫ÕàÕπ ‡æ‘Ë¡™—¥¢÷Èπ

‡¡◊ËÕ‡∑’¬∫°—∫ background ¢âÕ¥’¢Õß MRCP ‡¡◊ËÕ‡∑’¬∫°—∫ contrast cholangiog-

raphy §◊Õ “¡“√∂ª√–‡¡‘π ∑àÕ∑“߇¥‘ππÈ”¥’μ’∫À√◊Õμ—𠉥â·≈–°“√„™â‡∑§π‘§ thin-

slice, less heavily T2-weighted images  “¡“√∂ª√–‡¡‘ππ‘Ë«¢π“¥‡≈Á°Ê ‰¥â

≈—°…≥–Õ◊ËπÊ ∑’Ë “¡“√∂μ√«®æ∫®“° MRI ‰¥â·°à thickening of the bile

duct wall, segmental atrophy, biloma, abscesses, cirrhotic changes ·≈–

cholangiocarcinoma

°“√«‘π‘®©—¬·¬°‚√§®“°¿“æ∑“ß√—ß ’

Dilated duct

√Ÿª·∫∫¢Õß∑àÕ∑“߇¥‘ππÈ”¥’∑’Ë¢¬“¬μ—«„π¿“«– RPC μà“ß®“°°“√Õÿ¥μ—π¢Õß

∑“߇¥‘ππÈ”¥’®“°‡ÀμÿÕ◊Ëπ (´÷Ëß®–æ∫≈—°…≥– diffusely dilated ducts with smooth

and gradual change of caliber of bile ducts) §◊Õ¿“«– RPC ®–æ∫≈—°…≥–

rapid tapering of the peripheral ducts ·≈–æ∫πâÕ¬¡“°∑’Ë®–¡’欓∏‘ ¿“æ∑ÿ°

 à«π¢Õßμ—∫

 ”À√—∫¿“«– sclerosing cholangitis ®–æ∫ focal ·≈– discontinuous

¢Õß bile duct dilatation ∫“ߧ√—Èß¡’≈—°…≥– beaded appearance ·≈– serpigi-

nous course ·≈–æ∫ thickening of the bile ducts

 à«π„π Caroli’s disease ∑’Ë¡—°æ∫„πºŸâªÉ«¬Õ“¬ÿπâÕ¬ ®–æ∫ segmental

dilatation ·≈– dilated saccules ¢Õß intrahepatic ducts

Filling defects or lesions in ducts

¿“«– pneumobilia ®–æ∫≈—°…≥– air bubbles ‡ªìπ round À√◊Õ co-

lumnar shape °√–®“¬Õ¬Ÿà„π à«π∑’ˇªìπ nondependent ´÷ËßÕ“®‡ªìπªí≠À“„π

¿“æ«‘π‘®©—¬®“° ultrasound ∑’Ë¡’≈—°…≥– echogenic ·≈– MRI ∑’Ë¡’≈—°…≥– sig-

19Hepatolithiasis

nal void ·μà CT scan  “¡“√∂·¬°¿“«–π’ȉ¥â¥’ central cholangiocarcinoma

®–æ∫‡ªìπ filling defect „π dilated duct ‚¥¬¡—°®–‡ªìπ immotile irregular

À√◊Õ eccentric mural thickening

πÕ°®“°π’Ȭ—ßæ∫Õÿ∫—μ‘°“√≥å intraductal papillary neoplasm ‡æ‘Ë¡¢÷Èπ„π

RPC42 ´÷ËßÕ“®„Àâ≈—°…≥–§≈⓬π‘Ë«„π∑“߇¥‘ππÈ”¥’‰¥â °“√ àßμ√«® CT scan ·≈–

MRI ®–™à«¬·¬°¿“«–π’È ·≈–°“√ àÕß°≈âÕßμ√«®∑“߇¥‘πÕ“À“√ à«πμâπÕ“®æ∫ mu-

cus ∫√‘‡«≥ ampulla À√◊Õ duodenum

Mass within or adjacent to liver parenchyma

æ∫ focal hepatic abscesses ‰¥â√âÕ¬≈– 20 ¢ÕߺŸâªÉ«¬ RPC ‚¥¬¡’≈—°…≥–

uni- À√◊Õ multi-loculated collection with rim and septal enhancement

Õ“®æ∫ biloma ´÷Ëß¡’≈—°…≥–‡ªìπ unilocular collection without enhancing

wall

πÕ°®“°π’ȺŸâªÉ«¬ RPC ¬—ßæ∫Õÿ∫—μ‘°“√≥å¢Õß peripheral cholangiocar-

cinoma ∑’ˇªìπ hypovascular tumor ¡’≈—°…≥– delayed enhancement ·≈–

retraction of liver margin ·≈–¬—ßæ∫ hepatocellular carcinoma ‡æ‘Ë¡¢÷Èπ

¥â«¬

Yoon ‰¥â·π–π”„Àâ√«¡ inflammatory pseudotumor ‰«â„π°“√«‘π‘®©—¬

·¬°‚√§¢Õß°âÕπ„πμ—∫„πºŸâªÉ«¬ RPC ‰«â¥â«¬43 ´÷Ëß®–æ∫≈—°…≥– central hypo-

attenuating areas with iso/hyperattenuating thickened periphery À√◊Õ

multi-septate appearance with hyper-attenuating internal septa and

periphery

μ“√“ß∑’Ë 2 Tsunoda Classification for severity of intrahepatic disease

I No marked dilatation or strictures of intrahepatic ducts

II Diffuse dilatation of intrahepatic ducts without strictures

III Unilateral solitary or multiple cystic dilatation of intrahepatic ducts with strictures

IV Bilateral solitary or multiple cystic dilatation of intrahepatic ducts with strictures

20 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“߇¥‘πÕ“À“√·Ààߪ√–‡∑»‰∑¬, ¡°√“§¡-‡¡…“¬π 2557

°“√ª√–‡¡‘𧫓¡√ÿπ·√ߢÕß‚√§

¡’°“√„™â Tsunoda Classification (μ“√“ß∑’Ë 2) „π°“√· ¥ß§«“¡√ÿπ·√ß

¢Õß¿“«–π’È

°“√√—°…“

‡ªÑ“À¡“¬À≈—° §◊Õ °“√√—°…“∑“߇¥‘ππÈ”¥’Õ—°‡ ∫‡©’¬∫æ≈—π ·≈–¬—∫¬—Èß°“√

¥”‡π‘π‚√§Õ—π®–𔉪 Ÿà°“√‡°‘¥¿“«– biliary cirrhosis „π∑’Ë ÿ¥44-46

Endoscopic approach

∂÷ß·¡â«à“ ERCP ®–¡’ª√–‚¬™πå„π°“√ª√–‡¡‘𰓬«‘¿“§¢Õß∑“߇¥‘ππÈ”¥’„π

¿“«–π’È ·μà∫∑∫“∑„π°“√√—°…“ hepatolithiasis ¬—ߧߡ’®”°—¥ ‡π◊ËÕß®“°°“√¡’ bile

duct strictures, peripheral stone impaction À√◊Õ ductal angulation47,48

®“°°“√»÷°…“·∫∫¬âÕπÀ≈—ߢÕß Tanaka49 „π°“√√—°…“ºŸâªÉ«¬ hepa-

tolithiasis 57 √“¬ ¥â«¬°“√∑” sphincterotomy ·≈–π”π‘Ë«„π common bile duct

ÕÕ° æ∫«à“ “¡“√∂π”π‘Ë«„π intrahepatic duct ÕÕ°‰¥âÀ¡¥ 18 √“¬ ·≈–π”ÕÕ°

‰¥â∫“ß à«π 36 √“¬ ‚¥¬ 3 √“¬„π°≈ÿà¡∑’ˬ—ߧߡ’π‘Ë«§â“ß„π™à«ß·√°π—Èπ π‘Ë« “¡“√∂

À≈ÿ¥ÕÕ°¡“‰¥â‡Õß®πÀ¡¥„π‡«≈“μàÕ¡“ ·≈–®“°°“√μ‘¥μ“¡‰ªπ“π 66-183 ‡¥◊Õπ

(§à“¡—∏¬∞“π 114 ‡¥◊Õπ) æ∫«à“ºŸâªÉ«¬√“¬∑’ˬ—ß¡’π‘Ë«§â“ßÕ¬Ÿà¡’¿“«–·∑√°´âÕπμ“¡¡“ ‰¥â·°à

cholangitis 7 √“¬ (‡ ’¬™’«‘μ 2 √“¬) liver abscess 3 √“¬ (‡ ’¬™’«‘μ 1 √“¬)

‡¡◊ËÕ‡∑’¬∫°—∫°≈ÿà¡∑’ˉ¡à¡’π‘Ë«‡À≈◊Õ§â“ßÕ¬Ÿà´÷Ë߉¡àæ∫¿“«–·∑√°´âÕπ¥—ß°≈à“«‡≈¬

Percutaneous approach

¡’°“√æ—≤π“«‘∏’ percutaneous transhepatic drainage ·≈– dilation

procedures ‚¥¬ “¡“√∂«“ß catheters „π intrahepatic duct ·≈–¢¬“¬

¢π“¥∑àÕ∑“߇¥‘ππÈ”¥’‡ªìπ 18 Fr º≈≈—æ∏å¢Õß percutaneous transhepatic

cholangioscopy (PTCS) „π°“√°”®—¥π‘Ë«ÕÕ°®πÀ¡¥·≈–‚Õ°“ „π°“√¡’π‘Ë«°≈—∫

21Hepatolithiasis

¡“‡ªìπ´È”π—Èπ‡∑’¬∫‡∑à“°—∫°“√ºà“μ—¥ Õ¬à“߉√°Áμ“¡‚Õ°“  ”‡√Á®®–≈¥≈ßÀ“°ºŸâª«¬¡’

∑àÕ∑“߇¥‘ππÈ”¥’μ’∫¡“°

®“°°“√»÷°…“·∫∫¬âÕπÀ≈—ߢÕß Huang50 „πºŸâªÉ«¬ hepatolithiasis 245

√“¬∑’Ë√—∫°“√√—°…“¥â«¬ PTCS lithotomy ·≈–μ‘¥μ“¡‰ª 1-22 ªï æ∫«à“  “¡“√∂

°”®—¥π‘Ë«ÕÕ°‰¥âÀ¡¥ 209 √“¬ (85.3%) ‚¥¬¡—°®–‡À≈◊Õπ‘Ë«§â“ßÀ“°‡ªìπºŸâªÉ«¬∑’Ë¡’

∑àÕ∑“߇¥‘ππÈ”¥’μ’∫ (29/118, 24.6% ‡∑’¬∫°—∫ 7/127, 5.5%; p=0.002) æ∫¿“«–

·∑√°´âÕπ√ÿπ·√ß 4 √“¬ (1.6%) ‰¥â·°à liver laceration 2 √“¬ intra-abdominal

abscess 1 √“¬ ·≈– disruption of the percutaneous transhepatic biliary

drainage fistula 1 √“¬ Õ—μ√“°“√‡ªìπ´È”¢Õß hepatolithiasis ·≈–/À√◊Õcholan-

gitis Õ¬Ÿà∑’Ë√âÕ¬≈– 63.2 ‚¥¬Õ—μ√“°“√‡ªìπ´È”¢Õßπ‘Ë«π—Èπ‰¡à —¡æ—π∏å°—∫¿“«–∑àÕ∑“ß

‡¥‘ππÈ”¥’μ’∫ (51/89, 56.2% ‡∑’¬∫°—∫ 53/120, 44.4%; p=0.08) ·μà√–¬–‡«≈“„π

°“√‡ªìππ‘Ë«´È”¢ÕߺŸâªÉ«¬∑’Ë¡’¿“«–∑àÕπÈ”¥’μ’∫®– —Èπ°«à“¢ÕߺŸâªÉ«¬∑’ˉ¡à¡’∑àÕπÈ”¥’μ’∫

Õ¬à“ß¡’π—¬ ”§—≠ (11 ªï ‡∑’¬∫°—∫ 18 ªï; p=0.007) Õ—μ√“°“√‡ªìπ´È”®– Ÿß°«à“„πºŸâ

ªÉ«¬∑’Ë¡’¿“«–∑àÕ∑“߇¥‘ππÈ”¥’¢¬“¬ (20/34, 58.8% ‡∑’¬∫°—∫ 33/86, 38.4%; p=0.042)

·≈–°“√‡°‘¥ recurrent cholangitis À√◊Õ°“√‡°‘¥ cholangiocarcinoma „π°≈ÿà¡

∑’Ë¡’π‘Ë«°≈—∫‡ªìπ´È”·≈–‰¡à “¡“√∂°”®—¥ÕÕ°‰¥âÀ¡¥®– Ÿß°«à“„π°≈ÿà¡∑’ˉ¡à¡’π‘Ë«´È”

Õ¬à“ß¡’π—¬ ”§—≠∑“ß ∂‘μ‘ (44.3%, 27/61 ‡∑’¬∫°—∫ 16.2%, 24/148; p<0.001 ·≈–

6.6%, 4/61 ‡∑’¬∫°—∫ 0.7%, 1/148; p=0.026)

Lee51 μ‘¥μ“¡ºŸâªÉ«¬ 92 √“¬∑’ˉ¥â√—∫°“√√—°…“¥â«¬ PTCS æ∫«à“ “¡“√∂

°”®—¥π‘Ë«ÕÕ°‰¥âÀ¡¥ 74 √“¬ (80%) ‚¥¬Õ—μ√“°“√°”®—¥π‘Ë«‰¥â®–πâÕ¬°«à“Õ¬à“ß¡’π—¬

 ”§—≠„π°≈ÿà¡∑’Ë¡’∑àÕ∑“߇¥‘ππÈ”¥’„πμ—∫μ’∫Õ¬à“ß√ÿπ·√߇¡◊ËÕ‡∑’¬∫°—∫°≈ÿà¡∑’ˉ¡à¡’∑àÕ

∑“߇¥‘ππÈ”¥’μ’∫ (14/24, 58% ‡∑’¬∫°—∫ 16/16, 100%, p<0.01) À√◊Õ‡∑’¬∫°—∫°≈ÿà¡

∑’Ë¡’∑àÕ∑“߇¥‘ππÈ”¥’„πμ—∫μ’∫‡≈Á°πâÕ¬∂÷ߪ“π°≈“ß (14/24, 58% ‡∑’¬∫°—∫ 44/52, 85%,

p<0.05) ºŸâª«¬∑’Ë¡’∑àÕ∑“߇¥‘ππÈ”¥’„πμ—∫μ’∫Õ¬à“ß√ÿπ·√߬—ßæ∫Õ—μ√“°“√‡°‘¥π‘Ë«´È”

¡“°°«à“°≈ÿà¡∑’ˉ¡à¡’∑àÕ∑“߇¥‘ππÈ”¥’μ’∫À√◊Õμ’∫‡æ’¬ß‡≈Á°πâÕ¬ (100% ‡∑’¬∫°—∫ 28%,

p<0.01) ·≈–®“°°“√»÷°…“π’ÈÀ“°·∫àߧ«“¡√ÿπ·√ߢÕß‚√§μ“¡ Tsunoda classifi-

cation æ∫«à“„πºŸâªÉ«¬ type I, II ¡’ºŸâªÉ«¬°≈—∫‡ªìππ‘Ë«´È” 2 √“¬ (12%) ∑’Ë 28 ·≈– 32

22 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“߇¥‘πÕ“À“√·Ààߪ√–‡∑»‰∑¬, ¡°√“§¡-‡¡…“¬π 2557

‡¥◊ÕπÀ≈—ß°“√°”®—¥π‘Ë«ÕÕ°®πÀ¡¥  à«πºŸâªÉ«¬ type III, IV ¡’Õ—μ√“°“√‡ªìππ‘Ë«´È”

√âÕ¬≈– 50 ∑’Ë 60 ‡¥◊Õπ

¢âÕ∫àß™’È¢Õß°“√ºà“μ—¥

À“°æ¬“∏‘ ¿“æ¢Õß hepatolithiasis π—Èπ®”°—¥„π à«π„¥ à«πÀπ÷ËߢÕßμ—∫

«‘∏’°“√√—°…“Àπ÷Ëß∑’Ëπ‘¬¡§◊Õ°“√ºà“μ—¥μ—∫ à«π∑’Ë¡’欓∏‘ ¿“æÕÕ°‰ªæ√âÕ¡°—∫π‘Ë«·≈–

∑àÕ∑“߇¥‘ππÈ”¥’∑’˺‘¥ª°μ‘„π∫√‘‡«≥π—Èπ

®“°°“√»÷°…“·∫∫¬âÕπÀ≈—ߢÕß Jan „πºŸâªÉ«¬∑—ÈßÀ¡¥ 614 √“¬ ‚¥¬¡’

°“√μ‘¥μ“¡ºŸâªÉ«¬ 427 √“¬π“π 4-10 ªï ´÷Ë߇ªìπ°≈ÿà¡∑’ˉ¥â√—∫°“√ºà“μ—¥ 380 √“¬

·≈–√—°…“¥â«¬ PTCS 47 √“¬ æ∫«à“ ¡’Õ—μ√“°“√‡°‘¥π‘Ë«´È”√âÕ¬≈– 29.6 (105/355)

¡’°“√ºà“μ—¥´È”√âÕ¬≈– 18.7 (80/427) ¡’¿“«– secondary biliary cirrhosis √âÕ¬≈–

6.8 (29/427) ‡°‘¥ cholangiocarcinoma √âÕ¬≈– 2.8 (12/427) ·≈–‡ ’¬™’«‘μ

√âÕ¬≈– 10.3 (44/427) ºŸâªÉ«¬∑’ˉ¥â√—∫°“√ºà“μ—¥μ—∫ à«π∑’Ë¡’欓∏‘ ¿“æÕÕ°¡’

§ÿ≥¿“æ™’«‘μ∑’Ë¥’°«à“ §◊Õ ‰¡à¡’Õ“°“√ ¡’Õ—μ√“°“√°≈—∫‡ªìπ´È”¢Õßπ‘Ë«πâÕ¬°«à“ (√âÕ¬≈–

9.5) ¡’Õÿ∫—μ‘°“√≥å¢Õß secondary biliary cirrhosis πâÕ¬°«à“ (√âÕ¬≈– 2.1) ·≈–

‰¡àæ∫ cholangiocarcinoma ‡¡◊ËÕ‡∑’¬∫°—∫°≈ÿà¡∑’ˉ¡à‰¥â√—∫°“√ºà“μ—¥ (p<0.01)

À“°æ¬“∏‘ ¿“æ®”°—¥‡©æ“–μ—∫°≈’∫´â“¬ ‚¥¬∑—Ë«‰ª°“√√—°…“∑’Ë·π–π”§◊Õ

°“√ºà“μ—¥μ—∫ à«ππ—ÈπÕÕ°53,54 ·μà®–‰¡à·π–π”°“√√—°…“«‘∏’π’È„πºŸâªÉ«¬∑’Ë¡’§«“¡´—∫´âÕπ

¢Õß欓∏‘ ¿“æ ‡™àπ ¡’π‘Ë«Õÿ¥μ—πÕ¬Ÿà„πμ—∫∑—Èß 2 °≈’∫ À√◊Õ¡’ªí®®—¬‡ ’ˬßÕ◊ËπÊ μàÕ°“√

ºà“μ—¥

Tsunoda ‰¥â‡ πÕ·π«∑“ß°“√√—°…“‚¥¬°“√ºà“μ—¥μ“¡§«“¡√ÿπ·√ߢÕß‚√§

(Tsunoda classification)55 ´÷Ë߉¥â√«∫√«¡¢âÕ¡Ÿ≈ºŸâªÉ«¬ 119 √“¬∑’ˉ¥â√—∫°“√√—°…“

‚¥¬°“√ºà“μ—¥„π‚√ß欓∫“≈¡À“«‘∑¬“≈—¬π“ß“´“°‘√–À«à“ßªï §.». 1969-1984 æ∫

«à“ºŸâªÉ«¬ type I, II ®–‰¥â√—∫°“√√—°…“‚¥¬ choledocholithotomy À√◊Õ

choledochojejunostomy  à«πºŸâªÉ«¬ type III ®–‰¥â√—∫°“√√—°…“‚¥¬°“√ºà“μ—¥

μ—∫ÕÕ°∫“ß à«π ·≈– ºŸâªÉ«¬ type IV ®–‰¥â√—∫°“√√—°…“‚¥¬°“√ºà“μ—¥μ—∫ÕÕ°∫“ß

 à«π√à«¡°—∫ bilioenteric anastomosis √«¡‰ª∂÷ß extended hepatico-

23Hepatolithiasis

‡Õ° “√Õâ“ßÕ‘ß

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°“√‡ ’¬™’«‘μ„π™à«ß·√°°Á¡—°®–æ∫„π type IV ‡™àπ‡¥’¬«°—π ºŸâªÉ«¬‡°◊Õ∫∑ÿ°√“¬®–

¬—߇À≈◊Õπ‘Ë«Õ¬Ÿà À≈—ß®“°μ‘¥μ“¡ºŸâªÉ«¬„π√–¬–¬“«‡ªìπ®”π«π 88 √“¬ æ∫«à“ ºŸâªÉ«¬

Õ“°“√¥’¢÷Èπ√âÕ¬≈– 100 „π type I, √âÕ¬≈– 87 „π type II, √âÕ¬≈– 83 „π type III,

·≈–√âÕ¬≈– 84 „π type IV

24 ®ÿ≈ “√ ¡“§¡·æ∑¬å√–∫∫∑“߇¥‘πÕ“À“√·Ààߪ√–‡∑»‰∑¬, ¡°√“§¡-‡¡…“¬π 2557

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25Hepatolithiasis

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27Hepatolithiasis

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