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LIVER & BILLARY APPARATUS
Presented by: Dr. Isha Jaiswal
Moderator: Dr. Rohini Khurana
Date: 23 July 2014
Liver-Introduction
• Also called ‘hepar’.
• Largest gland in the body.
• 2nd largest gland of the body
• Weighs about 1600 gm in
males,1300 gm in females.
• Occupies the right hypochondrium,
epigastrium & left hypochondrium.
• Most part of the liver is covered by
ribs & costal cartilages.
Lobes of Liver
• Liver is divided into right & left lobes by falciform ligament .
• Ligaments
 Coronary ligament
 Triangular ligament
 Ligament of treitz
 falciform ligament
Visceral relations :impression of neighbouring
viscera
Peritoneal relations of the Liver
The Lesser omentum
• Encloses the portal triad (bile duct, hepatic artery and portal vein )
• Passes from the liver to lesser curvature of the stomach + 2 cm of duodenum
• Thick free edge -- hepatoduodenal ligament
• Sheet like remainder – hepatogastric ligament
Couinaud’s segments
Arterial supply is by portal vein &
hepatic artery.
Venous drainage is by hepatic veins
which drain into inferior vena cava.
Blood supply
• Nerve Supply
Parasympatheticsupply is by the preganglionicfibers of the vagus nerve.
Sympathetic innervation is by the postganglionic fibers from the coeliac
plexus.
• Lymphatic Drainage
Lymphatics from upper surface drain into nodes in the posterior
mediastinum.
Lymphatics from lower surface drain into hepatic nodes and celiac nodes.
Biliary Apparatus :
It collects bile from the liver ,stores in the gallbladder&
transmits to 2nd part of duodenum
• Gall bladder.
• Cystic duct.
• Right and left hepatic ducts which unite to form
Common Hepatic Duct.
• Common Bile duct formed by the union of cystic duct
and common hepatic duct.
Gall Bladder
• Pear shaped organ
• Reservoir of bile
• Situated in gb fossa
• Fundus
• Body
• Neck
• Infundibulum
• Cystic duct
Parts of Gall Bladder
Calot triangle
 The triangle is bounded by the
cystic duct, the common hepatic
duct, and the inferior border of
the liver.
 Important structures including:
the cystic artery, the right
hepatic artery, and the cystic
duct lymph node.
GALL BLADDER
Blood Supply
• Arterial supply is by cystic artery, a branch of the right hepatic artery.
• Venous drainage is into the portal vein.
Nerve Supply
• Parasympatheticsupply is by pre-ganglionic fibers from the vagus nerve.
• Sympathetic innervation is by post-ganglionic fibers from the coeliac
plexus.
Lymphatic Drainage
• Lymphatics drain into cystic nodes, hepatic nodes and coeliac nodes
RADIOLOGICAL ANATOMY
ABDOMINAL AORTA & IVC
PORTAL VEIN
HEPATIC ARTERY
SPLENIC VEIN
SUPERIOR MESENTRIC ARTERY
Percutaneous (through the skin) Transhepatic (through the liver)
Cholangiogram.
In this procedure, a thin needle is inserted through the skin and into the bile
ducts. A dye is injected through the needle so that a contrast image will show
up on X-rays
PER CUTANEOUS TRANSHEPATIC
CHOLANGIOGRAPHY
Edoscopic Retrograde Cholangiopancreatography (ERCP).
endoscopic procedure that involves the use of fiberoptic endoscopes
ERCP
This radiograph taken during an ERCP procedure demonstrates the hepatic ducts;
common hepatic duct, cystic duct, and common bile duct are demonstrated. Note
the spiral appearance of the cystic duct due which is the valve of Heister. The
pancreatic ducts and ampulla of Vater are not demonstrated
Hepatobilliary malignancies
• Hepatocellular
carcinoma
• Gallbladder carcinoma
• Bile duct cancer
• Hepatocellular cancer is the fifth most
common cancer in the world and the
third most common cause of cancer
mortality
• Male to female:3:1
• Geographical variation: more common
in sub Saharan Africa, South Korea
,China & less in US ,UK
• however the incidence is increasing due
to greater prevalence of HCV infection
VIRAL:
with persistent HBV & HCV infection, the risk of HCC
increases by a factor of 100.
CHEMICALS & TOXINS:
Chemical injuryinducedby
• Ethanol,
• aflatoxin
• Fungi: Aspergillus flavus & parasiticus
CHRONIC LIVER DISEASES
• Chirrhosis (70-90%)
• hemochromatosis,
• Wilson's disease,
• hereditary tyrosinemia
RISK FACTORS
Pathogenesis:
integration of viral dna with host dna
activation of protooncogenes
alterd expression of tumor supressor gene
Hepatocellular carcinoma
• Mean age: 6th -7th decade
• M:F= 3:1
• Prevention: HBV vaccination, disposable syringes, blood
screening, universal precaution of health care worker,
timely treatment of HCV with interferon
• Surveillance: as per AASLD
in high risk pt only
AFP & ultrasonography at 6 month interval
• Diagnosed as per AASLD criteria: AFP levels of more than
200ng/ml with a dominant liver nodule more than 2 cm in a
chirrhotic pt on a dynamic imaging technique with typical
enhancement pattern oh HCC
• In general a chronic hepatitis or chirrhotic pt with any
dominant solid nodule that is not clearly a hemangioma
should be considered HCC unless proven otherwise
• Histological diagnosis reserved for pt planned for non
surgical therapy.
• tumor seeding from FNAC & biopsy 1.6-5%
Spread of HCC
• Local spread
• Intrahepatic metastasis
• Hematogenous: portal vein & hepatic vein are
invaded in 20-90%of HCC depending on
size(dynamic ct required)
• Lymphatic spread least common
• Lung is the most common site of distant
metastasis
Role of AFP
• Valuable diagnostic marker
• Normal value less thn 20 ng/ml
• Tested by radioimmuno assay
• Elevated in 80-90% cases
• Level corelates with tumor size
• May be elevated in chronic hepaptitis and chirrhosis
• Level above 250ng/ml are more sugestive of HCC
• AFP along with CEA used to diffrentiaie HCC from liver
secondaries
• Other tm marker: DCP(des gamma carboxy prothrombin) or PIVKA
(protein induced by vit k def. or antagonist) raised in 91 %)
Clinical presentation
• asymptomatic
• Patients with symptoms usually
suffer from chronic hepatitis and
liver cirrhosis.
• Clinical symptoms include
general fatigue, nausea
low grade fever,
 poor appetite,
wt. loss,
abdominal distension ,pain
jaundice,
Bleeding manifestations
CLINICAL HISTORY
• history of hepatitis, jaundice, blood transfusion, use of intravenous
drugs, or exposure to aflatoxins, alcohol abuse
EXAMINATION
• may reveal clubbing cynosis, jaundice, flapping tremors, skin
pigmentation, anemia
• hepatomegaly splenomegaly, dilated abdominal veins, palmar
erythema, leg oedema, ascitis abdominal bruit
• Paraneoplastic: hypoglycemia, polycythemia ,hypercalcemia
,hypercholestrolemia, carcinoid syndrome,porphyria,etc
Advanced disease may manifest with symptoms of hepatic
failure
HEPATOCELLULAR CARCINOMA
ON CT SCAN
HCC ON MRI this man was referred for liver
transplantation for a solitary 5 cm liver nodule on cect (yellow)
but mri s/o multiple lesion on delayed images
Billiary tract cancer
• They are highly lethal because most are locally advanced at
presentation.
• Gallbladder cancer (m.c) 2/3rd
• bile duct cancer 1/3rd
• surgery is the treatment of choice and is associated with long term
survival For unresectable tumours, the purpose of treatment is to
palliate symptoms such as obstructive jaundice, biliary tract infection,
pain, and ascites.
Gall bladder cancer
• it is the fifth most common cancer of the gastrointestinal tract
• Most common billiary tract cancer
• Gallbladder carcinoma is associated with stones in over 90% of patients
• Poor prognosis, highly malignant, rapidly disseminating difficult to
diagnose preop.
• Age: 6 th to 7 th decade
• ratio of females to males is 3:1
• In India high incidence in north and central india less in south
• M.c HPE: adeno ca
• Location:
 fundus (60%),
 body (30%),
 neck (10%)
• Disorder of gallbladder:
– Cholelithiasis in 64-98%
• Gallbladder carcinoma occurs in only 1% of all patients with gallstones!
– Porcelaingallbladder(in 4-60%): prophylectic cholecystectomy indicated
– Chronic cholecystitis
– Gallbladderpolyp: a polyp >2 cm is likely malignant!
– Chronic typhoid carriers
• Disorder of bile ducts:
– Primary sclerosing cholangitis
– Congenital biliary anomalies:cystic dilatationof biliary tree, choledochal cyst,
anomalous junction of pancreaticobiliary ducts, low insertion of cystic duct
• Inflammatory bowel disease (predominantly ulcerative colitis, less common in Crohn disease)
• Familialpolyposis coli
• exposure to carcinogens (azotoluene, nitrosamines)
Gallbladder Carcinoma: risk factors
SPREAD OF GB CANCER
• Routes of spread:
 local invasion: liver seg 4 & 5, duodenum ,transverse colon porta hepatis.
Lymphatic: pericholedochal, cystic, sup pancreaticodudnal, retropancreatic
celiac ,paraaortic L.N
Hematogenous via hepatic and portal veins to liver ,lung
Perineural in wall of gall bladder
Transperitoneal spread to omentum ,peritoneum leading to ascitis
Intraductal spread in papillary varity
Clinical features of CA GALLBLADDER
• Asymptomatic at early stage except tm located at
neck of gall bladder
• advanced diseases at presentation
• Early CA GB incidental finding on cholecystectomy
• Clinical features:  abd. pain., dyspepsia,
anorexia,nausea vomiting.wt
loss .
 jaundice pallor
 ascitis
 hemetemesis,malena
• Diagnosis is by USG and CT
• Dynamic CT angiography is advised if surgery is planned
• ERCP & PTC may be used to evaluate billiary tree if usg does not show site
of billiary obstruction
• Histological diagnosis can be attempted USG guidedbiopsy/FNAC from
liver mets.
• Gb biopsy is usually not advisable in view of billiary peritonitis (5%)
however FNAC can be attempted (88.5% accuracy)
• Radical cholecystectomy is TOC
 Cholecystectomy
 +resection of liver (wedge & anatomic seg 4 & 5)
 +portal lymphadenectomy from hilum of liver, pancreas, duodenum celiac
axis
 Invasion of hepatic artery and portal vein are considered criteria of
unresectibility
Gallbladder CarcinomaGallbladder Carcinoma
Direct invasion of the liver by gallbladder cancer in a 66-year-old
woman
Bile Duct Carcinoma:
 Rare tumor and about two third are located at the hepatic duct bifurcation
 Very common in endemic areas of developing countries such as northeast
Thailand
 Mean age of presentation:60-65 years
 M:F=1.3:1
 95% are adenocarcinoma
 term cholangiocarcinoma describes cancers arising from the
epithelial cells of the bile ducts, which include intrahepatic,
perihilar, and extrahepatic biliary tree.. But is more commonly used
for peripheral intrahepatic tm
 Anatomical division:
*intrahepatic ;
*perihilar (Klatskin tumors)
*proximal extrahepatic
*distal extrahepatic
49
Risk factors for bile duct cancer
Hepatolithiasis :2-10%
Choledochal cyst
Polycystic liver
Parasitic infection: Liver fluke: Clonorchis sinensis and Opisthorchis viverinni
Primary sclerosing cholangitis (PSC)
Ulcerative colitis
 Biliary cirrhosis
HCV infection
Nitrosamine exposure
PATHOGENESIS: long standing inflammation &
chronic injury to billiary epithelium
Bile Duct Cancer
Intrahepatic CCs: develop in the
smaller bile duct branches inside the
liver
Extrahepatic CCs: originate in the bile
duct along the hepato-duodenal
ligament
Hilar CCs: develop at the hilum
Classification of bileduct cancer is important for
undurstanding of pathogenesis, diagnosis, and
management
Intrahepatic biliary duct cancers manifest similar as liver cancers with minimal
dilation of billiary radicals &non obstructive jaundice
Extra hepatic biliary cancers (more than 50% in upper 1/3rd) .
Result in Dilation of intra & extra hepatic bile duct till level of obstruction
manifest as obstructive jaundice
for tumors in upper and mid 1/3rd PTC is use
to observe the biliary tree.
In lesion arising in distal 1/3rd or non dilated
intrahepatic radicals ERCP is useful
for diagnosis
Spread of bile duct cancer
• Local spread: longitudinally along bile duct or adjacent vascular
structure(hepatic artery ,portal vein) and in liver
• Lymphatic: cystic, pericholedochal. peri pancreatic, celiac ,superior
mesentric nodes.
• Hematogenous spread: mc to liver
53
Sign and Symptom
The most common presenting symptoms of obstruction of the bile
duct
include
 painless jaundice,
clay-colored stool,
 tea-colored urine,
pruritus.
 abdominal pain,
fever,
general malaise,
abdominal distention,
anorexia,
and weight loss
Criteria of unresectibility:
 extensive b/l intrahepatic spread on cholangiography
 Involvement of main trunk or both branches of portal
vein or hepatic artery
 Involvement of 1 branch of portal vein with opp branch of
hepatic artery
 Combined vascular involvement on 1 side with extensive
cholangiographic involvement on other side
Cholangiocarcinoma with IHBRD
Klatskin Tumor: Axial CT of the abdomen with
intravenous contrast reveals an enhancing mass near
the gallbladder neck (yellow arrow). This is
compatible with a Klatskin tumor (hilar
cholangiocarcinoma)
Intrahepatic Biliary Dilatation: Axial CT
of the abdomen at a more superior level
reveals significant intrahepatic biliary
dilatation (yellow arrows)
Small hilar cholangiocarcinoma (Arrowhead) producing obstruction of the right
posteral sectoral duct (Short arrow). Right anterior sectoral duct (long arrow) and
left hepatic duct. (A) Thick oblique coronal MRCP. (B) Axial portal phase CT (C)
Longitudinal US. (D) Transverse color Doppler US (Open arrow, normal left portal
vein).
CT- abdomen- intra & extra-hepatic bile duct dilatation to the
level of the hepatic hilium. Suggestion of 2cm mass at hilium
cholangiocarcinoma-(Klatskin tumour)
CHOLANGIOCARCINOMA
Comparison of radiographic images showing
cholangiocarcinoma; A, computed tomography (CT)
image; B, cholangiogram (ERCP) image. Arrows designate the
tumor.

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Liver & billary apparatus

  • 1. LIVER & BILLARY APPARATUS Presented by: Dr. Isha Jaiswal Moderator: Dr. Rohini Khurana Date: 23 July 2014
  • 2. Liver-Introduction • Also called ‘hepar’. • Largest gland in the body. • 2nd largest gland of the body • Weighs about 1600 gm in males,1300 gm in females. • Occupies the right hypochondrium, epigastrium & left hypochondrium. • Most part of the liver is covered by ribs & costal cartilages.
  • 3. Lobes of Liver • Liver is divided into right & left lobes by falciform ligament . • Ligaments  Coronary ligament  Triangular ligament  Ligament of treitz  falciform ligament
  • 4. Visceral relations :impression of neighbouring viscera
  • 5. Peritoneal relations of the Liver The Lesser omentum • Encloses the portal triad (bile duct, hepatic artery and portal vein ) • Passes from the liver to lesser curvature of the stomach + 2 cm of duodenum • Thick free edge -- hepatoduodenal ligament • Sheet like remainder – hepatogastric ligament
  • 7. Arterial supply is by portal vein & hepatic artery. Venous drainage is by hepatic veins which drain into inferior vena cava. Blood supply
  • 8. • Nerve Supply Parasympatheticsupply is by the preganglionicfibers of the vagus nerve. Sympathetic innervation is by the postganglionic fibers from the coeliac plexus. • Lymphatic Drainage Lymphatics from upper surface drain into nodes in the posterior mediastinum. Lymphatics from lower surface drain into hepatic nodes and celiac nodes.
  • 9. Biliary Apparatus : It collects bile from the liver ,stores in the gallbladder& transmits to 2nd part of duodenum • Gall bladder. • Cystic duct. • Right and left hepatic ducts which unite to form Common Hepatic Duct. • Common Bile duct formed by the union of cystic duct and common hepatic duct.
  • 10.
  • 11. Gall Bladder • Pear shaped organ • Reservoir of bile • Situated in gb fossa • Fundus • Body • Neck • Infundibulum • Cystic duct Parts of Gall Bladder
  • 12. Calot triangle  The triangle is bounded by the cystic duct, the common hepatic duct, and the inferior border of the liver.  Important structures including: the cystic artery, the right hepatic artery, and the cystic duct lymph node.
  • 13. GALL BLADDER Blood Supply • Arterial supply is by cystic artery, a branch of the right hepatic artery. • Venous drainage is into the portal vein. Nerve Supply • Parasympatheticsupply is by pre-ganglionic fibers from the vagus nerve. • Sympathetic innervation is by post-ganglionic fibers from the coeliac plexus. Lymphatic Drainage • Lymphatics drain into cystic nodes, hepatic nodes and coeliac nodes
  • 15.
  • 16.
  • 22. Percutaneous (through the skin) Transhepatic (through the liver) Cholangiogram. In this procedure, a thin needle is inserted through the skin and into the bile ducts. A dye is injected through the needle so that a contrast image will show up on X-rays
  • 24. Edoscopic Retrograde Cholangiopancreatography (ERCP). endoscopic procedure that involves the use of fiberoptic endoscopes
  • 25. ERCP This radiograph taken during an ERCP procedure demonstrates the hepatic ducts; common hepatic duct, cystic duct, and common bile duct are demonstrated. Note the spiral appearance of the cystic duct due which is the valve of Heister. The pancreatic ducts and ampulla of Vater are not demonstrated
  • 26. Hepatobilliary malignancies • Hepatocellular carcinoma • Gallbladder carcinoma • Bile duct cancer
  • 27. • Hepatocellular cancer is the fifth most common cancer in the world and the third most common cause of cancer mortality • Male to female:3:1 • Geographical variation: more common in sub Saharan Africa, South Korea ,China & less in US ,UK • however the incidence is increasing due to greater prevalence of HCV infection
  • 28. VIRAL: with persistent HBV & HCV infection, the risk of HCC increases by a factor of 100. CHEMICALS & TOXINS: Chemical injuryinducedby • Ethanol, • aflatoxin • Fungi: Aspergillus flavus & parasiticus CHRONIC LIVER DISEASES • Chirrhosis (70-90%) • hemochromatosis, • Wilson's disease, • hereditary tyrosinemia RISK FACTORS
  • 29. Pathogenesis: integration of viral dna with host dna activation of protooncogenes alterd expression of tumor supressor gene
  • 30. Hepatocellular carcinoma • Mean age: 6th -7th decade • M:F= 3:1 • Prevention: HBV vaccination, disposable syringes, blood screening, universal precaution of health care worker, timely treatment of HCV with interferon • Surveillance: as per AASLD in high risk pt only AFP & ultrasonography at 6 month interval
  • 31. • Diagnosed as per AASLD criteria: AFP levels of more than 200ng/ml with a dominant liver nodule more than 2 cm in a chirrhotic pt on a dynamic imaging technique with typical enhancement pattern oh HCC • In general a chronic hepatitis or chirrhotic pt with any dominant solid nodule that is not clearly a hemangioma should be considered HCC unless proven otherwise • Histological diagnosis reserved for pt planned for non surgical therapy. • tumor seeding from FNAC & biopsy 1.6-5%
  • 32. Spread of HCC • Local spread • Intrahepatic metastasis • Hematogenous: portal vein & hepatic vein are invaded in 20-90%of HCC depending on size(dynamic ct required) • Lymphatic spread least common • Lung is the most common site of distant metastasis
  • 33. Role of AFP • Valuable diagnostic marker • Normal value less thn 20 ng/ml • Tested by radioimmuno assay • Elevated in 80-90% cases • Level corelates with tumor size • May be elevated in chronic hepaptitis and chirrhosis • Level above 250ng/ml are more sugestive of HCC • AFP along with CEA used to diffrentiaie HCC from liver secondaries • Other tm marker: DCP(des gamma carboxy prothrombin) or PIVKA (protein induced by vit k def. or antagonist) raised in 91 %)
  • 34. Clinical presentation • asymptomatic • Patients with symptoms usually suffer from chronic hepatitis and liver cirrhosis. • Clinical symptoms include general fatigue, nausea low grade fever,  poor appetite, wt. loss, abdominal distension ,pain jaundice, Bleeding manifestations
  • 35. CLINICAL HISTORY • history of hepatitis, jaundice, blood transfusion, use of intravenous drugs, or exposure to aflatoxins, alcohol abuse EXAMINATION • may reveal clubbing cynosis, jaundice, flapping tremors, skin pigmentation, anemia • hepatomegaly splenomegaly, dilated abdominal veins, palmar erythema, leg oedema, ascitis abdominal bruit • Paraneoplastic: hypoglycemia, polycythemia ,hypercalcemia ,hypercholestrolemia, carcinoid syndrome,porphyria,etc
  • 36. Advanced disease may manifest with symptoms of hepatic failure
  • 38. HCC ON MRI this man was referred for liver transplantation for a solitary 5 cm liver nodule on cect (yellow) but mri s/o multiple lesion on delayed images
  • 39.
  • 40. Billiary tract cancer • They are highly lethal because most are locally advanced at presentation. • Gallbladder cancer (m.c) 2/3rd • bile duct cancer 1/3rd • surgery is the treatment of choice and is associated with long term survival For unresectable tumours, the purpose of treatment is to palliate symptoms such as obstructive jaundice, biliary tract infection, pain, and ascites.
  • 41. Gall bladder cancer • it is the fifth most common cancer of the gastrointestinal tract • Most common billiary tract cancer • Gallbladder carcinoma is associated with stones in over 90% of patients • Poor prognosis, highly malignant, rapidly disseminating difficult to diagnose preop. • Age: 6 th to 7 th decade • ratio of females to males is 3:1 • In India high incidence in north and central india less in south • M.c HPE: adeno ca • Location:  fundus (60%),  body (30%),  neck (10%)
  • 42. • Disorder of gallbladder: – Cholelithiasis in 64-98% • Gallbladder carcinoma occurs in only 1% of all patients with gallstones! – Porcelaingallbladder(in 4-60%): prophylectic cholecystectomy indicated – Chronic cholecystitis – Gallbladderpolyp: a polyp >2 cm is likely malignant! – Chronic typhoid carriers • Disorder of bile ducts: – Primary sclerosing cholangitis – Congenital biliary anomalies:cystic dilatationof biliary tree, choledochal cyst, anomalous junction of pancreaticobiliary ducts, low insertion of cystic duct • Inflammatory bowel disease (predominantly ulcerative colitis, less common in Crohn disease) • Familialpolyposis coli • exposure to carcinogens (azotoluene, nitrosamines) Gallbladder Carcinoma: risk factors
  • 43. SPREAD OF GB CANCER • Routes of spread:  local invasion: liver seg 4 & 5, duodenum ,transverse colon porta hepatis. Lymphatic: pericholedochal, cystic, sup pancreaticodudnal, retropancreatic celiac ,paraaortic L.N Hematogenous via hepatic and portal veins to liver ,lung Perineural in wall of gall bladder Transperitoneal spread to omentum ,peritoneum leading to ascitis Intraductal spread in papillary varity
  • 44. Clinical features of CA GALLBLADDER • Asymptomatic at early stage except tm located at neck of gall bladder • advanced diseases at presentation • Early CA GB incidental finding on cholecystectomy • Clinical features:  abd. pain., dyspepsia, anorexia,nausea vomiting.wt loss .  jaundice pallor  ascitis  hemetemesis,malena
  • 45. • Diagnosis is by USG and CT • Dynamic CT angiography is advised if surgery is planned • ERCP & PTC may be used to evaluate billiary tree if usg does not show site of billiary obstruction • Histological diagnosis can be attempted USG guidedbiopsy/FNAC from liver mets. • Gb biopsy is usually not advisable in view of billiary peritonitis (5%) however FNAC can be attempted (88.5% accuracy) • Radical cholecystectomy is TOC  Cholecystectomy  +resection of liver (wedge & anatomic seg 4 & 5)  +portal lymphadenectomy from hilum of liver, pancreas, duodenum celiac axis  Invasion of hepatic artery and portal vein are considered criteria of unresectibility
  • 47. Direct invasion of the liver by gallbladder cancer in a 66-year-old woman
  • 48. Bile Duct Carcinoma:  Rare tumor and about two third are located at the hepatic duct bifurcation  Very common in endemic areas of developing countries such as northeast Thailand  Mean age of presentation:60-65 years  M:F=1.3:1  95% are adenocarcinoma  term cholangiocarcinoma describes cancers arising from the epithelial cells of the bile ducts, which include intrahepatic, perihilar, and extrahepatic biliary tree.. But is more commonly used for peripheral intrahepatic tm  Anatomical division: *intrahepatic ; *perihilar (Klatskin tumors) *proximal extrahepatic *distal extrahepatic
  • 49. 49 Risk factors for bile duct cancer Hepatolithiasis :2-10% Choledochal cyst Polycystic liver Parasitic infection: Liver fluke: Clonorchis sinensis and Opisthorchis viverinni Primary sclerosing cholangitis (PSC) Ulcerative colitis  Biliary cirrhosis HCV infection Nitrosamine exposure PATHOGENESIS: long standing inflammation & chronic injury to billiary epithelium
  • 50. Bile Duct Cancer Intrahepatic CCs: develop in the smaller bile duct branches inside the liver Extrahepatic CCs: originate in the bile duct along the hepato-duodenal ligament Hilar CCs: develop at the hilum Classification of bileduct cancer is important for undurstanding of pathogenesis, diagnosis, and management
  • 51. Intrahepatic biliary duct cancers manifest similar as liver cancers with minimal dilation of billiary radicals &non obstructive jaundice Extra hepatic biliary cancers (more than 50% in upper 1/3rd) . Result in Dilation of intra & extra hepatic bile duct till level of obstruction manifest as obstructive jaundice for tumors in upper and mid 1/3rd PTC is use to observe the biliary tree. In lesion arising in distal 1/3rd or non dilated intrahepatic radicals ERCP is useful for diagnosis
  • 52. Spread of bile duct cancer • Local spread: longitudinally along bile duct or adjacent vascular structure(hepatic artery ,portal vein) and in liver • Lymphatic: cystic, pericholedochal. peri pancreatic, celiac ,superior mesentric nodes. • Hematogenous spread: mc to liver
  • 53. 53 Sign and Symptom The most common presenting symptoms of obstruction of the bile duct include  painless jaundice, clay-colored stool,  tea-colored urine, pruritus.  abdominal pain, fever, general malaise, abdominal distention, anorexia, and weight loss
  • 54. Criteria of unresectibility:  extensive b/l intrahepatic spread on cholangiography  Involvement of main trunk or both branches of portal vein or hepatic artery  Involvement of 1 branch of portal vein with opp branch of hepatic artery  Combined vascular involvement on 1 side with extensive cholangiographic involvement on other side
  • 55. Cholangiocarcinoma with IHBRD Klatskin Tumor: Axial CT of the abdomen with intravenous contrast reveals an enhancing mass near the gallbladder neck (yellow arrow). This is compatible with a Klatskin tumor (hilar cholangiocarcinoma) Intrahepatic Biliary Dilatation: Axial CT of the abdomen at a more superior level reveals significant intrahepatic biliary dilatation (yellow arrows)
  • 56. Small hilar cholangiocarcinoma (Arrowhead) producing obstruction of the right posteral sectoral duct (Short arrow). Right anterior sectoral duct (long arrow) and left hepatic duct. (A) Thick oblique coronal MRCP. (B) Axial portal phase CT (C) Longitudinal US. (D) Transverse color Doppler US (Open arrow, normal left portal vein).
  • 57. CT- abdomen- intra & extra-hepatic bile duct dilatation to the level of the hepatic hilium. Suggestion of 2cm mass at hilium cholangiocarcinoma-(Klatskin tumour)
  • 58. CHOLANGIOCARCINOMA Comparison of radiographic images showing cholangiocarcinoma; A, computed tomography (CT) image; B, cholangiogram (ERCP) image. Arrows designate the tumor.