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Curs gastro 15

Gross anathomy
 The gallbladder is a small
pear-shaped organ that
stores and concentrates
bile.
 The gallbladder is
connected to the liver by
the hepatic duct.
 It is approximately 3 to 4
inches (7.6 to 10.2 cm)
long and about 1 inch
(2.5 cm) wide.
Function
 The function of the
gallbladder is to store
bile and concentrate.
 Bile is a digestive
liquid continually
secreted by the liver.
The bile emulsifies
fats and neutralizes
acids in partly
digested food.
 A muscular valve in the
common bile duct
opens and the bile
flows from the
gallbladder into the
cystic duct, along the
common bile duct and
into the duodenum.
Bile ducts diseases
 Congenital variations and malformations
 Gallstones
 Cholangiocarcinomas
 Primary sclerosing cholangitis
 Primary biliary cirrhosis
 Biliary atresia
LITIAZA BILIARĂ
 prezenţa calculilor în VB sau căi
 clinic sdr. dispeptic biliar sau colici biliare
 Epidemiologie
- incidenţa ↑cu vârsta
- 35% F, 20% B după 70 ani
- fact. ereditari predispozanţi, apoproteina E
- F >2B, multipare, anticoncepţionale
- obezitate, CH, DZ
- diete, post prelungit
Etiopatogenie
 factori favorizanţi în formarea calc. colest.
- suprassaturarea bilei în colesterol cu ↑acidului deoxicolic (litogen)
- ↓acidului chenodeoxicolic (antilitogen)
- nucleerea cristalelor de colesterol → calculi
- infecţiile bacteriene → rol minim
Morfopatologie
 calculi biliari de colesterol (80%)
– colesterol → cristale cu nucleu, Rx opaci 15%, mici, multipli,
faţetaţi; obezi, DZ, hep. cr.
 calculi pigmentari negri
- bilirubină, duri, Rx opaci 60%, mici, multipli, aspri, neregulaţi;
CH, hemoliză
 calculi bruni
- bilirubinat Ca → mici, friabili; obstrucţie biliară cronică
Classification

 cholesterol stones

 pigment stones
Cholesterol stones
 composed mainly of
cholesterol (more than 70%)
and can be subdivided into
pure cholesterol stones
(usually solitary) and mixed
stones which contain
cholesterol in a matrix of
calcium bilirubinate, calcium
phosphate and protein.
 Mixed stones are usually
multiple and faceted.
 Cholesterol gallstones account
for about 75% of the
gallstones in Europe and the
United States.
Bile pigment stones
 Brown pigment stones are soft
and friable and consist of calcium
bilirubinate, cholesterol and
calcium soaps.
 Pure pigment stones ('black
stones') are black, hard and brittle
and contain an insoluble black
pigment, calcium bilirubinate,
calcium carbonate and phosphate,
calcium salts of fatty acids and bile
acids.
 All pigment stones contain a large
amount of mucoprotein matrix (up
to 70%).

 Mai frecvent la cirotici


Morfopatologie
 peretele veziculei biliare

- leziuni tip acut catarale


flegmonoase
- cronice → VB scleroatrofică
LITIAZA BILIARĂ VEZICULARĂ
 timpul între formarea calculilor şi apariţia simptomelor = 12 ani
Clinic
 asimptomatică → dg. întâmplător → nu necesită tratament
 sindrom dispeptic biliar
- dureri hipocondru drept, balonări postprandiale
- gust amar, tulburări tranzit
- “migrenă biliară”
 colici biliare
- migrare calcul
- colecistită acută simptomatică (colică 15min- 24h)
- colecistită cronică → inflamaţie cronică
- disconfort abdominal, saţietate precoce
- intoleranţă grăsimi
- litiaza coledociană → eliminare duoden
→ pancreatită acută
→ colangită, abcese hepatice
Diagnostic diferenţial

 colică renală dreaptă


 apendicită acută
 cancer colon drept
 colon iritabil
 colici pancreatice → durere epigastru “ în bară”
 ulcer duodenal, ulcer gastric
 pleurezie diafragmatică dreaptă
 pneumonie dreaptă
 IM anterior, posterior → ecg
Paraclinic

 sânge → ↑colesterol, ↑bilirubină, ↑calciu


 Rx. pe gol → calculi radioopaci 20-30%
 colecistografie orală
 ecografie
- ieftin, rapid, disponibil
- imagine hiperreflectogenă, con umbră post.
 CT
Complicaţii
 Infecţioase
1. Colecistita acută
- obstrucţia cistic de calcul
- inflam. bilei apoi invazie bacteriană
- clinic - F>40 ani, obeză
- durere intensă epigastru, noaptea, iradiere
- poziţie antalgică, transpiraţii
- greţuri, vărsături, tahicardie, febră
- Murphy pozitiv → palpare VB destinsă, dureroasă

- paraclinic
- leucocitoză, neutrofilie
- echo →perete>5mm
2. Empiemul colecistic (abcesul colecistic)
 frecvent ERCP
 febră, frisoane, dureri, apărare musculară
3. Perforaţia colecistului
 peritonită acută biliară
 abces pericolecistic
 perforaţie cronică cu fistulă digestivă internă
4. Colecistită emfizematoasă
 streptococ, anaerobi, E.coli
5. Colecistita cronică litiazică
 meteorism, greaţă, vărsături
 dureri hipocondru drept
 echo → diagnostic
Complicaţiile mecanice
 Litiaza coledociană
– colangita acută → triada Charcot ICTER
DURERE
FEBRĂ, FRISON

 Colangita acută cu icter


- icter colestatic moderat
- scaune acolice, urini hipercrome
- dureri colicative → greţuri, vărsături
- febră, frisoane
- ↑ → GGT, FA, Bd, transaminaze, amilaze
- echo → coledoc>7mm, CBIH dilatate
Colangio RM

MRCP

Gallstones. Coloured
magnetic resonance
imaging
 Colangita acută supurativă
- febră
- icter Caracterizat prin 5 elemente IR + trombocitoză →CID
- durere (comitetul Reynold)

- hipotensiune
- confuzie

 Sindromul Mirrizi
- calcul inclavat în cistic sau istm colecist → comprimă coledoc
- hidrops vezicular
 Pancreatita acută biliară
- migrare calcul prin papila Vater → inclavat
- ↑amilaze + transaminaze, echo, ERCP
- sfincterotomie

 Complicaţii neoplazice
- cancerul veziculei biliare
Tratamentul litiazei biliare
 tratament medical –teoretic-

- ursofalk 6-8mg/kgc/zi → dizolvare 40-60%


- dizolvare directă calculi
cateter transcutan → metilterţ-butil eter
- litotripsie extracorporeală
undă de şoc → 20-25%
 tratament chirurgical

- laparoscopic
- colecistectomie
Colecistita acută
 dietă hidrică, antispastice

 antibiotice

- cefalosporină
- piperacilină (2g x 3-4/zi) + aminoglicozid (genta 3-5mg/kgc/zi)
 tratament chirurgical → colecistectomie
Colecistita cronică litiazică
 dietă săracă în grăsimi

 colecistectomie
Litiaza coledociană
 antibiotice
 extragere calcul endoscopic

Colangita acută supurată


 antibioterapie
 ERCP cu sfincterotomie şi extracţie calcul
sau
 drenaj biliar percutan
 chirurgical
Benign biliary strictures
 In about 95% of patients these are a consequence of
biliary tract surgery. The remainder are caused by
gallstones eroding the bile duct and, rarely, blunt injury to
the abdomen. Signs of biliary stricture may be
detected in the immediate postoperative period but
are often delayed.
 Liver function tests reveal a cholestatic pattern and blood
cultures may yield an organism. The precise delineation of
the stricture requires ERCP or PTC.
 Biliary stricture is not a benign condition; untreated
it will usually progress to biliary cirrhosis with portal
venous hypertension and liver failure.
Malignant biliary stricture
 This is most commonly due to adenocarcinoma
of the head of the pancreas but may also be
caused by adenocarcinomas of the bile ducts, of
the ampulla of Vater and rarely of the
gallbladder.
 Occasionally the cause is lymph node
enlargement at the porta hepatis due to
malignant metastases or lymphoma.
Symptoms
 The onset is insidious with deepening
jaundice, itching and weight loss.
 A dull nagging upper abdominal pain which
radiates to the back is common.
 In contrast to choledocholithiasis and benign
strictures, cholangitis is unusual.
Cholangiocarcinoma
 Cholangiocarcinoma is cancer
of biliary epithelium.
 It may arise from intrahepatic
or extrahepatic bile ducts.
 Sporadic cholangiocarcinoma
is quite uncommon, but
cholangiocarcinoma has a high
incidence in the presence of
certain benign conditions.
Pathophysiology
 More than 90% are adenocarcinomas and the remainder
are squamous cell tumors.
 The etiology of most bile duct cancers remains
undetermined.
 Long-standing inflammation, as with primary sclerosing
cholangitis (PSC) or chronic parasitic infection, has been
suggested to play a role by inducing hyperplasia, cellular
proliferation and, ultimately, malignant transformation.
 Intrahepatic cholangiocarcinoma may be associated with
chronic ulcerative colitis and chronic cholecystitis.
Classifications
 Clinically, intrahepatic and extrahepatic
cholangiocarcinomas are distinct entities
 Based on staging and treatment considerations:
upper and lower duct cholangiocarcinomas
 TNM system
Symptoms
 Jaundice is the most common manifestation of bile duct
cancer and, in general, is best detected in direct sunlight. The
obstruction and subsequent cholestasis tend to occur early if
the tumor is located in the common bile duct or common
hepatic duct. Jaundice often occurs later in perihilar or
intrahepatic tumors and is often a marker of advanced disease.
 Pruritus usually is preceded by jaundice, but itching may be
the initial symptom of cholangiocarcinoma. Pruritus may be
related to circulating bile acids.
 Weight loss is a variable finding and may be present in one
third of patients at the time of diagnosis.
 Abdominal pain is relatively common in advanced disease
and often is described as a dull ache in the right upper
quadrant.
Signs
 If the cholangiocarcinoma is located distal to the
cystic duct takeoff, the patient may have a
palpable gallbladder, which commonly is known
as Courvoisier sign.
 An abdominal mass or palpable
lymphadenopathy is uncommon, but
hepatomegaly may be noted in as many as 25%
of patients.
Differential diagnosis
 Bile duct strictures
 Cholecystitis
 Bile duct tumors
 Choledochal cysts
 Biliary disease
 Choledocholithiasis
 Biliary obstruction
 Cholelithiasis
 Cholangitis
 Cholangiohepatitis
Laboratory findings
 Laboratory tests suggest extrahepatic biliary
obstruction.
 Characteristically, the bilirubin rises over several
weeks to a level of 20 mg/dL if the jaundice is
unrelieved and the direct reacting fraction accounts for
more than 50% of the total bilirubin.
 Marked elevation of serum alkaline phosphatase and
GGT levels and mild elevation of transaminase levels are
also usual.
 CA 19-9 & CEA
 Cholangiocarcinoma does not produce alpha-fetoprotein.
Imaging studies
 In general, ultrasonography or computed
tomography (CT) is performed initially,
followed by a type of cholangiography.
Ultrasound
 May demonstrate biliary duct dilatation and
larger hilar lesions
 Small lesions and distal cholangiocarcinomas are
difficult to visualize.
 Patients with underlying primary sclerosing
cholangitis (PSC) may have limited ductal
dilatation secondary to ductal fibrosis.
 Doppler ultrasound may show vascular
encasement or thrombosis.
65-year-old woman with hepatic steatosis and cholangiocarcinoma. Peritumoral sparing
of fatty infiltration surrounds cholangiocarcinoma. Transverse sonogram shows increased
liver echogenicity suggestive of hepatic steatosis and slightly hypoechoic mass in right hepatic
lobe. Mass is surrounded by wedge-shaped hypoechoic areas (arrowheads). Capsular retraction
adjacent to mass (arrows) is evident.
CT
 CT resembles ultrasound in that it may
demonstrate ductal dilatation and large mass
lesions.
 CT also has the capability to evaluate for
pathologic intra-abdominal lymphadenopathy.
 Helical CT scans are accurate in diagnosing the
level of biliary obstruction.
 Three-dimensional and multiphase CT images
may improve CT yield.
Magnetic resonance imaging
 MRI demonstrates hepatic parenchyma
 MR cholangiography enables imaging of bile
ducts and, in combination with MR
angiography, permits staging (excluding vascular
involvement). Hepatic involvement can also be
detected.
 This technique likely will replace angiography
for vascular evaluation.
On the left a hypovascular mass with irregular enhancement in the late arterial and late portal
venous phase. This is a sign of malignancy.
On the delayed images a relative dense structure is seen centrally, which looses its contrast
slower compared to normal liver.
This means that this tumor is mainly composed of fibrous tissue.
The fibrous tissue has also retracted the liver capsule.
These imaging findings are very suggestive of a cholangiocarcinoma.
Positron emission tomography
 PET has shown promise in diagnosing underlying
PSC.
 Small lesions (ie, <1 cm) have been demonstrated.
 PET is accurate for detecting nodular carcinomas,
but the sensitivity diminishes for infiltrating lesions.
 PET should be interpreted with caution in patients
with PSC and stents in place.
 PET/CT has been shown to be valuable in
detecting unsuspected distant metastases
Endoscopic ultrasonography
 EUS enables both bile duct visualization and
nodal evaluation.
 This technique also has the capability to aspirate
for cytologic studies.
 EUS-guided fine-needle aspiration results may
be positive when other diagnostic tests are
inconclusive.
 Intraductal EUS allows direct ultrasonographic
evaluation of the lesion.
Cholangiography

 MR cholangiography

 endoscopic retrograde cholangiopancreatography


(ERCP)

 percutaneous transhepatic cholangiography (PTC)


Angiography
 Evaluation of vascular involvement is important if
considering surgical treatment.
 Arteriography demonstrating extensive encasement
of the hepatic arteries or portal vein precludes
curative resection.
 Combining the findings on cholangiography with
those on arteriography has been found to have a
greater accuracy in predicting unresectability.
 An occasional patient has compression of vascular
structures rather than true malignant invasion.
Hilar cholangiocarcinoma (Klatskin tumor)”
Procedures
 ERCP demonstrates the site of obstruction by direct
retrograde dye injection and excludes ampullary pathology by
endoscopic evaluation.
 Brush cytology, biopsy, needle aspiration, and shave biopsies via
ERCP can provide material for histologic studies.
 Palliative stenting to relieve biliary obstruction can be performed at
the time of evaluation.
 PTC may allow access to proximal lesions with obstruction of
both right and left hepatic ducts. Material for cytologic studies
may be obtained and drainage performed.
 Other methods to obtain tissue include CT- or ultrasound-
guided needle aspiration, if a mass lesion is present and
EUS fine-needle aspiration.
TNM classification system
 T - Primary tumor
 TX - Primary tumor cannot be assessed
 T0 - No evidence of primary tumor
 TIS - Carcinoma in situ
 T1a - Tumor invades mucosa
 T1b - Tumor invades muscularis
 T2 - Tumor invades perimuscular connective tissue
 T3 - Tumor invades liver, gallbladder, duodenum, stomach, pancreas, or colon
 N - Regional lymph nodes
 NX - Regional lymph nodes cannot be assessed
 N0 - No metastases in regional lymph nodes
 N1 - Metastases in cystic duct or pericholedochal or hilar lymph nodes of
hepatoduodenal ligament
 N2 - Metastases in peripancreatic (head only), periduodenal, posterior
pancreatoduodenal, periportal, celiac, or superior mesenteric regional lymph nodes
 M - Metastasis
 MX - Presence of metastases cannot be assessed
 M0 - No distant metastases
 M1 - Distant metastases (includes lymph node metastases beyond N2)
TNM groupings by stage
 Stage 0 - TIS N0 M0
 Stage I - T1 N0 M0
 Stage II - T2 N0 M0
 Stage III - T1-2 N1-2 M0
 Stage IVa - T3 N0-2 M0
 Stage IVb - T1-3 N0-2 M1
Prognosis
 Patients with perihilar tumors that are completely resected may achieve
long-term survival. Prognosis is poorest for patients with
intrahepatic tumors.
 Patients with distal extrahepatic tumors may have the best hope
for survival if tumors are excised completely; tumors at this site are the
most likely to be resectable. These patients may experience a 5-year
survival rate as high as 40%. The median survival duration in
patients who undergo resection and postoperative chemoradiation may
be as high as 17-27.5 months.
 An intermediate prognosis (ie, median survival duration of 7-17 mo) is
achieved for patients who are unable to undergo resection but can
tolerate adjuvant chemoradiation or possibly photodynamic therapy.
 The poorest prognosis is for the patient with unresectable
disease, with or without overt metastatic disease, who can
tolerate only palliative stent placement.
Sclerosing cholangitis
 Sclerosing cholangitis is the description applied
to multiple strictures and bead-like dilatations of
the intrahepatic and extrahepatic biliary tree.

 Primary sclerosing cholangitis


Primary sclerosing cholangitis
(i) absence of gallstones
(ii) absence of previous biliary surgery
(iii) sufficiently long follow-up to exclude
carcinoma of the bile duct

 affects males more than females (2:1) and about


70% of patients have ulcerative colitis
Clinical findings
 The usual clinical presentation is cholestatic
jaundice and cholangitis.
 A significant proportion of patients are
asymptomatic or present with cirrhosis and
portal venous hypertension.
Laboratory
 Serum biochemistry shows cholestatic liver function
tests.
 A raised serum alkaline phosphatase is almost
invariable.
 Consequently the diagnosis should be considered in
patients with cirrhosis whose liver function tests show
cholestatic features.
 The IgM concentration is commonly elevated.
 Liver biopsy may be helpful and usually indicates
large bile duct obstruction
Investigations
 MRCP
 Cholangiography with ERCP or PTC
 Laparotomy should not be performed

 It may be confused with primary biliary cirrhosis,


but the serum mitochondrial antibody is always
negative in primary sclerosing cholangitis.
Prognosis and complications

 The prognosis is variable, but most patients


eventually develop cirrhosis and liver failure.

 Bile duct adenocarcinoma is a late


complication.
Primary biliary cirrhosis
 is a chronic and progressive cholestatic disease
of the liver
 etiology is unknown, although it is presumed to
be autoimmune in nature.
 The major pathology of this disease is a
destruction of the small-to-medium bile ducts,
which leads to progressive cholestasis and often
end-stage liver disease.
Causes
 unknown etiology, but various factors have been
implicated as the causes of this illness.

 Genetic factors: First-degree relatives have a 570- to


1000-fold increased chance of developing primary biliary
cirrhosis..

 Infection with organisms of the family


Enterobacteriaceae: Cross-reactivity between antigens
on the bacterial wall and the mitochondria has been
postulated. Patients with primary biliary cirrhosis present
with an increased incidence of gram-negative urinary
tract infections.
25% are incidentally diagnosed during a routine blood
evaluation.
 Fatigue (65%)
 Fatigue is the first reported symptom. It can cause disability in
some patients and has been associated with depression and
obsessive-compulsive behavior. The etiology is unknown;
however, a sleep abnormality, particularly excessive daytime
somnolence, has been identified in a significant proportion of
patients
 Pruritus (55%)
 10% of patients experience severe pruritus.
 The cause of this symptom is not known.
 Pruritus appears unrelated to the deposition of bile acids in the
skin.
 Right upper quadrant discomfort occurs in 8-17% of
patients.
In the early stages, examination findings are normal.
As the disease advances, excoriations of the skin, xanthelasmata,
or findings of cirrhosis may be present.
 Hepatomegaly (25%)
 Hyperpigmentation (25%)
 Splenomegaly (15%)
 Jaundice (10%)
 Xanthelasmata (10%) - In late stages of the disease
 Sicca syndrome (50-75%) - Xerophthalmia (ie, dry eyes),
xerostomia (ie, dry mouth)
 Kayser-Fleischer rings (extremely rare)
 Stigmata of advanced liver disease (ie, cirrhosis), such as
spider nevi, palmar erythema, ascites, temporal and proximal
muscle wasting, and peripheral edema
Differential diagnosis
 Autoimmune hepatitis
 Biliary obstruction
 Graft versus Host disease
 Primary sclerosing cholangitis
 Sarcoidosis
 Drug-induced hepatotoxicity
 Idiopathic adulthood ductopenia
Laboratory
 elevation of ALT and AST, significant elevations of the
alkaline phosphatase (ALP), γ -glutamyl transpeptidase
(GGTP) and immunoglobulin levels (mainly
immunoglobulin M [IgM])
 an elevated bilirubin level, a prolonged prothrombin time, and a
decreased albumin level can be found. The increased bilirubin
level is an ominous sign of disease progression.
 Lipid levels and cholesterol levels may be increased, with an
increased high-density lipoprotein (HDL) fraction.
 An increased erythrocyte sedimentation rate is another finding.
 Thrombocytopenia is indicative of portal hypertension.
 Elevated levels of ceruloplasmin, bile acids and serum
hyaluronate
 The hallmark of this disease is the presence of
antimitochondrial antibodies (AMAs) in the sera.
Imaging Studies
 abdominal ultrasonography
 computed tomography (CT) scanning
 magnetic resonance imaging (MRI)
 The diagnosis of primary biliary cirrhosis should be
established or confirmed by performing a
percutaneous or laparoscopic liver biopsy. This
procedure also provides additional information
about the stage of the disease and the patient's
prognosis.
 In the late stages of the disease (ie, cirrhosis), an
upper endoscopy study should be performed.
MR images of a patient with primary biliary
cirrhosis
Histologic findings
 Characterized by chronic, nonsuppurative, destructive
cholangitis of the small interlobular bile ducts with a
diameter of 40-80 mm.
 Early lesions signal damage of the basement membrane
of the bile ducts and reactive hyperplasia of the
epithelial lining.
 Lymphocytic and plasma cell infiltration, with
eosinophilic condensation in the portal tracts, is
another feature.
 Epithelioid aggregates or granulomas may be found
around the bile ducts.
 Fibrosis and cirrhosis develop later.
Granulomatous cholangitis in primary
biliary cirrhosis (PBC). Detail from a
portal tract with dense lymphoplasmacytic
infiltrate and lymphoid aggregate (left).
The interlobular bile duct (center) shows a
focal rupture of its cholangiocytic lining,
at the site of an adjacent epithelioid
granuloma. (H&E)

Micrograph of primary biliary cirrhosis


showing bile duct inflammation and injury.
Cancers of the biliary tract

 Cholangiocarcinoma (cancers arising from the


bile duct epithelium)
 Ampulla of Vater cancer
 Gallbladder cancer

 All subtypes of biliary tract cancers are rare and


have an overall poor prognosis. They are also
difficult to diagnose.
Gallbladder cancer
 Gallbladder cancer is the
fifth most common GI
cancer in the United
States and the most
common hepatobiliary
cancer.
Histologic findings
 Adenocarcinoma is the primary histologic finding in
80-85% of gallbladder carcinomas.
 Additional rare histologic types of gallbladder cancer
exist. These include squamous cell cancer,
sarcomas, carcinoid, lymphoma and melanoma.

 Poorly differentiated tumors associated with a


poorer prognosis than the typically less infiltrative,
better differentiated tumors with metaplasia.
Etiology
 genetic characteristics
 gallstone disease
 bile composition
 calcification of the gallbladder wall
 anomalous junction of the biliary and pancreatic ducts
 congenital biliary cysts
 some infections
 environmental carcinogens
 drugs
Pathology
 There is a progression from dysplasia to carcinoma in
situ to invasive cancer in the gallbladder epithelium
that appears to take about 15 years.
 Premalignant lesions are associated with gallbladder
cancer and it is thought that chronic inflammation
may play a role in development of premalignant
lesions.
 Two types of metaplasia, intestinal and squamous,
have been found in patients with gallbladder cancer.
Clinical presentation
 Signs and symptoms of gallbladder cancer are
nonspecific. This explains the delay in diagnosis in
most patients with gallbladder cancer.
 In TNM stage I and II symptoms often mimic
those of cholelithiasis and cholecystitis.
 In early stages, the cause of symptoms may be the
associated cholelithiasis.
 Pain is the most common initial complaint; it may be
dull and aching, colicky, sharp, constant or
intermittent, and it may or may not radiate to the back.
 Other symptoms include nausea, vomiting and
anorexia.
Clinical presentation
 In later TNM stages, weight loss, jaundice,
hepatomegaly, a palpable mass or ascites may
develop.
 Jaundice develops in 30% to 60% of patients and is
a poor prognostic sign because it is caused by
extension of the tumor beyond the gallbladder, with
obstruction of the extrahepatic bile ducts; 85% of
patients with jaundice have unresectable tumors.
 The patients may also have obstruction of the
duodenum or colon. Malignant cholecystoenteric
fistula may be the first indication of gallbladder
cancer.
Laboratory
 Laboratory findings are not diagnostic but are
related to abnormalities associated with bile duct
obstruction.
 Patients frequently have increased alkaline
phosphatase and bilirubin levels.
 Blood levels of CEA or CA 19-9, another tumor
marker, may also be elevated.
Investigations
 Cholecystography (ERCP, PTC)
 Ultrasonography
 CT scanning
 MRI
 EUS
 Angiography
 Chest X-ray
ULTRASONOGRAPHY SUGGESTIVE, BUT NOT
DIAGNOSTIC

 thickening of the wall


 a mass projecting into the lumen
 calcification of the gallbladder
 multiple masses or a fixed mass in the gallbladder
 a mass extending into the liver
 an extracholecystic mass
 A report of mucosal thickening should also be
viewed with suspicion.
CT

 CT scanning may help in


the diagnosis but is of
limited help in staging
the disease except in
estimating the extent of
hepatic invasion
MRI
TNM system - Primary tumor
 Category T
 TX - Primary tumor cannot be assessed
 T0 - No evidence of primary tumor
 Tis - Carcinoma in situ
 T1 - Tumor invades lamina propria or muscle layer
 T1a - Tumor invades lamina propria
 T1b - Tumor invades muscle layer
 T2 - Tumor invades perimuscular connective tissue; no extension beyond serosa or into liver
 T3 - Tumor perforates the serosa (visceral peritoneum) and/or directly invades the liver and/or one
other adjacent organ or structure, such as the stomach, duodenum, colon, pancreas, omentum, or
extrahepatic bile ducts
 T4 - Tumor invades main portal vein or hepatic artery or invades multiple extrahepatic organs or
structures
 Regional lymph node
 Category N
 NX - Regional lymph nodes cannot be assessed
 N0 - No metastases in regional lymph nodes
 N1 - Metastases in regional lymph nodes
 Distant metastases
 Category M
 MX - Presence of metastases cannot be assessed
 M0 - No distant metastases
 M1 - Distant metastases
TNM groupings by stage
 Stage 0- Tis N0 M0
 Stage IA - T1 N0 M0
 Stage IB - T2 N0 M0
 Stage IIA - T3 N0 M0
 Stage IIB - T1-3 N1 M0
 Stage III - T4 any N M0
 Stage IV - Any T any N M1
Prognosis
 Survival at 5 years is correlated with stage of
disease at presentation.
 Only 10-20% of patients present with localized
disease.
 The median survival for advanced disease is
short (2-4 mo).