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"Gall Bladder Malignancy "
By Prof. O. P. Sharma
History of gall bladder pathology, commonest being calculus
is possibly as old as the history of mankind. However, recognition
of gall bladder pathology is credited to Greek physician "Alexander
Trallianus" (525-605). Andreas Vesalius (1514-1516) reported accurate
description of human gall stone. First elective cholecystosonography
for hydrops gall bladder was performed by John S. Bobbs on 15th July 1867.
Roetntgen-ray skiagram of abdomen revealed presence of gall stone (A. Buxbaum 1898).
First cholecystogram was performed in 1924 by Evarts Graham & Warren-Cole.
First ultrasound of gall bladder was performed by Hubiltz in 1972 and mentioned
that cholecystosonogram is most useful in cases of nonfunctioning gall bladder
either due to infective or neoplastic disease.
Gall bladder disease is said to occur in female with "5" characteristics – Fat,
Forty, Female, fertile & flatulence which is not true at present time. Menu et
al (1990) had observed 65-95% female incidence with gall bladder stone or inflammatory
disease. Surveillance of gall bladder is being recommended for increased risk of carcinoma
because of new therapentic methods of treating stone – i.e. lithotripsy or stone dissolution
and gall bladder is not removed (So et al 1990).
Gall Bladder Carcinoma :
Cancer gall bladder is 5th most common malignancy of Gastrointestinal tract,
responsible for nearly 7000 deaths / annum in united state. In India, northern
part is exhibiting much more incidence of carcinoma gall bladder than southern
India. Incidental finding of 1-3% of carcinoma have been observed in cholecystectomy
specimen; on autopsy 5-7.4% incidence have been reported.
Risk Factors :
Gall Stone 65-95%
Chronic Cholecystitis 40-50%
Porcelain GB 22%
Age Factor : 6-7th decade of life. Our experience shows it's occurrence at 30 years of life.
Sex Incidence : 3-5 times more common in female.
Clinical Features : Early diagnosis is difficult because most patients present
with non specific findings of right upper quadrant pain, malaise, weight loss, jaundice,
anorexia & vomiting. These can be easily confused with symptomatic acute or chronic cholecystitis.
At the time of diagnosis, most of patients are unresectable because of direct extension
into adjacent organ, lymphnodes or distant organ metastasis.
Imaging Tools :Ultrasound is most common, cost effective, non-radiation technique,
non-invasive, performed as an out door patient and 95% specificity.
(1) Focal or Irregular wall thickening (normal wall thickness 3mm) Diffuse wall
thickening is suggestive of chronic / acute cholecystitis, adenomatosis, inadequate
distension, hepatitis, hypoproteinemia etc.
(2) Intramural polypoidal lesion > 2 cm arising from wall of the gall bladder
(3) Presence of calculus blended with mass but producing acoustic shadowing (75%).
(4) Hyperechoic / mixed echogenic mass lesion in the lumen of gall bladder occupying either
fundus, neck or whole of the gall bladder.
(5) When the mass replaces the lumen of gall bladder, it is difficult to
differentiate primary hepatic pathology or gall bladder disease particularly in
cases where calculus is not accompanied.
(6) Contiguous spread to adjacent liver surface or to lymphnode at portahepatis
or distant metastasis – liver and involvement of peritoneum produces ascites.
(7) Either affected gall bladder having mass with / without stone itself is so
large that it can cause compression to common hepatic duct or common bile duct or
the mass can infiltrate into the lymphnode at porta hepatis through lymphatic, results in
obstructive jaundice and produce dilated intrahepatic biliary channel in fashion so described
as 'parallel channel sign' or 'double barrel duct sign'.
(8) Malignant ascites can be differentiated from other types of ascites particularly
tubercular ascites as the previous one is having clear fluid without any internal debris or septa.
(9) Polypoidal growth don not present acoustic adowing and is difficult to be different
iated from cholestrol polyp, adenoma or adherent stone.
(10) Tumefactive sludge or blood clot can simulate polypoid carcinoma hence examination
in multiple projections help to differentiate as the sludge moves (one should be patience with
patience and devote some time for examination).
(11) Color Doppler examination revealed pulsatile vascular flow in the mass or vascular
pattern seen surrounding the mass itself like basket appearance.
CT Scan :- It is inferior to ultrasound in depicting mucosal irregularity, mural
thickening and cholelithiasis but superior for evaluation of thickness of gall bladder
wall which is obscured by stone or mural calcification on ultrasound.
On CT – Wall thickening, stone, mass in GB fossa, oedema in pericholecystic
fat, thickening of hepatoduodenal ligament etc.
MRI Scan :- Gall bladder is visualized in interlobar fissure on T2
weighted pulse sequences. T2 weighted pulse sequence with long echo delays routinely
to show gall bladder bile with high signal intensity similar to other fluid such as
gastric content and CSF. Appearance of gall bladder bile varies on T1WI depending upon
function of gall bladder and bile concentration. Unconcentrated bile has a water content
of approx 95% and shows a low signal intensity on T1WI consistent with long T1 of water.
With resorption of water content falls to approx 84% & T1 relaxation time decreases,
therefore appearance of bile on T1WI varies from hypointense to hyperintense than liver.
Failure of gall bladder to concentrate bile is a feature of disease & long T1 bile in fasting
subjects is a sign of acute, suppurative & haemorrhagic cholecystisis & impaired liver function
can lead to reduced gall bladder bile concentration. Gall bladder function is established by
imaging the patient both in fasting & non fasting states. Concentration of bile in fasting
state is determined by increasing signal intensity on T1WI would indicate normal function.
Regular concentric ring in a thickened gallbladder wall raises the possibility of malignancy.
The mass is seen on T2WI as thickening of a portion of gall bladder wall, hypointense relative
to very long T2 gallbladder bile. Early concentration of mass on Gadolinium enhanced MR correlates
with depth of growth. However a wall enhancement is greatest in acute cholecystitis which may be
accompanied by pericholecystic hepatic enhancement.
Survival Rate – 5year survival rate is < 5% (Furukawa et al 1997).
Metastasis
(1) 84-89% metastasis to liver with medial segment of left lobe & anterior segment of
right lobe. Involved area is hypodense in comparison to surrounding liver panenehyma
on contrast enhanced CT. Irregular boundary with normal liver panchyma suggest invasion.
(2) Porta hepatis, peripancereatic, celiac axis, foramen of winslow & superior pancreatic
duodenal lymphnodes are involved.
(3) Peritoneum
(4) Distant metastasis
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A case of Ca GB showing dilated intrahepatic biliary channels
A case of Ca GB showing fundal mass, thickened wall, L.N. at porta hepatis; causing obstruction of CBD.
Polypoidal growth in the lumen of GB blended with calculi.
CDFI shows peripheral vascularity in the mass of GB and zoomed view shows internal pulsatile vascularity.
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