LIVER & BILLARY APPARATUS

Presented by: Dr. Isha JaiswalModerator: 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 LiverThe 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 Parasympathetic supply is by the preganglionic fibers of the vagus nerve.Sympathetic innervation is by the postganglionic fibers from the coeliac plexus.

• Lymphatic DrainageLymphatics 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.

Ampula of Vater

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 BLADDERBlood Supply• Arterial supply is by cystic artery, a branch of the right

hepatic artery. • Venous drainage is into the portal vein.

Nerve Supply• Parasympathetic supply 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 injury induced by• Ethanol, • aflatoxin• Fungi: Aspergillus flavus &

parasiticusCHRONIC LIVER DISEASES• Chirrhosis (70-90%) • hemochromatosis,• Wilson's disease, • hereditary tyrosinemia

RISK FACTORS

Pathogenesis:

integration of viral dna with host dna

activation of protooncogenesalterd 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!

– Porcelain gallbladder (in 4-60%): prophylectic cholecystectomy indicated

– Chronic cholecystitis– Gallbladder polyp: a polyp >2 cm is likely malignant!– Chronic typhoid carriers

• Disorder of bile ducts:– Primary sclerosing cholangitis– Congenital biliary anomalies: cystic dilatation of 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)

• Familial polyposis 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 bladderTransperitoneal spread to omentum ,peritoneum

leading to ascitisIntraductal 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

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Risk factors for bile duct cancer

Hepatolithiasis :2-10%Choledochal cyst

Polycystic liverParasitic infection: Liver fluke:

Clonorchis sinensis and Opisthorchis viverinni

Primary sclerosing cholangitis (PSC)Ulcerative colitis Biliary cirrhosisHCV infectionNitrosamine 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

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Sign and SymptomThe 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.