1.1.

INTRODUCTION
The pancreas is retroperitoneal organ. The exocrine and endocrine parts of the
a land play a vital role in the metabolism of carbohydrate, fat and
protein. Pancreatic masses can result from both inflammatory and neoplastic
conditions, Sometimes, congenital anomalies or normal variations may look
like mass, The surrounding structures like duodenum, blood vessels, and
retroperitoneal lymph nodes may also mimic pancreatic mass. Pancreas may
also be the site of metastatic deposits. So it is vital for the radiologist to have
a thorough knowledge about the pancreas and to be able to differentiate
normal from pathology.
Aim of this dissertation is to discuss the role of CT in the evaluation of
pancreatic mass. Pancreatic lesions are not uncommon in Bangladesh. High
risk factors for pancreatic disease like: gallstone, diabetes, smoking, tropical
calcifying pancreatitis even alcohol consumption are quite prevalent.
Pancreatic lesions; both inflammatory and neoplastic, can be fatal for the
patient .Acute pancreatitis and its sequels like abscess, pseudo aneurysms
can be life threatening. CT scan can be used in addition to clinical assessment
for proper management planning and to identify patients who may benefit
from surgical intervention. Chonic pancreatitis results in chronic disability
and may also present as a mass, One has to always remember that
tuberculosis of the pancreas may also cause a mass which may be diagnosed
as a fatal condition carcinoma of pancreas.

1.2 ANATOMY OF PANCREAS

Gross anatomy
The pancreas is a

soft lobulated organ that lies in the posterior

abdominal wall behind the peritoneum. It lies behind the stomach and
separated from it by the cavity of lesser sac. It crosses the trans pyloric
plane.
The pancreas is a mixed gland containing of both exocrine and endocrine
parts. The exocrine portion of the gland produces enzymes that are
capable of hydrolyzing proteins, fats and carbohydrate.
The endocrine portion of the gland produces hormones insulin, glucagon,
somatostatin which play key role is carbohydrate, protein
and fat metabolism.

Shape
It resembles a retort shaped flask; the bowl of the retort representing head
of pancreas.

Pancreatic carcinoma is a iaial disease. The rate of 5 years survival even in

western countries is dismal; the exact incidence of pancreatic carcinoma
in Bangladesh is unknown. Bui there is close association of pancreatic
carcinoma with diabetes and tropical calcifying pancreatitis, and these
conditions are quite common in this country. Most patient ol carcinoma
pancreas is diagnosed too late. However some palliative procedure may be
done to improve the quality of life of the patient; CT can play a vital role in
staging of pancreatic carcinoma and management planning,
There are many modalities which can be used to investigate the pancreas,
Plain X ray and contrast examinations have a limited role. Pancreas is a
difficult organ to evaluate by ultrasound; because great deal of operator skill
is needed. Moreover the quality of the scanner, patient's built and
preparation is also important. It can thus be used for screening purposes
only. Endoscopic retrograde eholangio-panereaiography (ERCP) is
considered gold standard in the imaging of pancreas. However newer and
more non invasive methods like CT. muitisliee CT, MRL MRCP and
endoscpic ultrasound are increasingly replacing the need for diagnostic
ERCP. CT scan is a quick and non invasive way to assess the pancreas. It
offers a global view the abdomen and proved to have high sensitivity and
specificity and accuracy.
Cases of pancreatic masses of different pathology reported for CT scan to
BSMMU, DMCH and BIRDEM Hospital from a period of January to June
2003.This small series is a small step in evaluating pancreatic mass by CT
and hopefully this work will stimulate more intensive study in future with
lager study group and create awareness amongst the patients.

Situation
It occupies the posterior part of epigastrium and left hypochondrium.

Size
Length

12 -15 cm.

Breadth

3 -4cm.

Thickness

1.5 -2cm.

Weight

80-90 gms

Parts
From right to left the pancreas presents - Head, neck, body and tail.

Head
It is right most part of pancreas. It lies at the level of L1 and L2 vertebrae
which is lower than body. Head is contained within the C loop of
duodenum. Part of the head that extends to left behind the superior
mesenteric vessels is called uncinate process.

Relations

Anterior
Transverse colon on upper part (non peritoneal)
Lower part is covered by peritoneum and is related to coils of jejunum.
Uncinate process is related to superior mesenteric vessel.
Posterior
Inferior vena cava and both renal veins
Right sympathetic trunk, right psoas majors, bodies of LI & 1^
Right curs of diaphragm, right middle supra renal, renal and gonadal
arteries.
Celiac ganglion
Azygos vein.
Bile duct
Abdominal aorta - behind the uncinate process
Upper Border
1st part of duodenum
Neck

It connects the body with head. It is 2 cm. long. It presents anterior

and posterior surfaces and upper and lower borders

Relations
Anterior
Covered by peritoneum and is related to pyloric end of stomach
Posterior
Superior mesenteric vein and portal vein
Upper border I * part of duodenum Lower
border
Root of transverse mesocolon

Body
Body is prismoid in appearance. It extends from the front of the aorta to the
front of the left kidney. It has 3 surfaces and 3 borders.

Relation
Anterior
Stomach separated by stomach surface bed

Inferior surface Duodeno

jejuna! flexure Coils of
jejunum
Left colic flexure
Posterior surface
Abdominal aorta with the origin of superior mesenteric artery
Left crus of diaphragm
Left psoas with sympathetic trunk
Left supra renal gland
Left kidney across its hilum
Left renal vessels and pelvis of left ureter
Left supra renal and gonadal veins
Splenic veins which separate the above mentioned structures from
pancreas
Superior border
It presents a conical projection called tuber omentale
The coeliec artery veins above the tuber and hepatic artery to the left of
tuber

Anterior border
It gives the attachment of root of transverse mesocolon
Inferior border
Superior mesenteric vessels under cover of right end of this bordgr

Tail
It is the narrow left end of the gland, contained in lieno-renal ligament. It is
lies above the head of pancreas opposite the lower border of T12.

FIG 1 : PANCREAS IN SITU

FIG 2 : POSTERIOR RELATION OF PANCREAS

10

Pancreatic Duct
The exocrine pancreas deliveries its secretions via pancreatic ducts
Main Pancreatic duct (Duct of Wirsung)

It begins in the tail by the union of a number of smaller ducts. This duct
crosses left to right through midway between upper and lower margins
close to the posterior surface.
It receives a number of smaller ducts at regular angles and resembles
"Herring bone". At the neck the duct turns downwards to the right to
reach posterior medial wall of 2nd part of duodenum. The duct pierces the
duodenal wall and meets bile duct to from ampulla of Vater. This opens
into the summit of major duodenal papilla about 8 to 10 cm distal to
pylorus.

Accessory Duct

(Duct of Santorin^

It receives, the secretions from uncinate process. This duct passes

upwards and to the right of main pancreatic duct. It opens at the summit of
minor duodenal papilla 2 cm above and ventral to the major papilla.

11

Neuro Vascular Supply

Arterial supply

Head and neck

Ventral and dorsal anatomosis of superior and inferior pancreatic
duodenal artery.

Body ami tail

Pancreatic branches of splenic artery

Venous drainage
The venous drainage corresponds to arterial supply and drain into superior
mesenteric, splenic and portal veins.

Lymphatic drainage
Head and neck
Ventral and dorsal groups of pancreatico duodenal lymph nodes.

Body and tail

Pancreatico splenic lymph nodes.

12

The lymphatics from these nodes terminate into the coeliac and superior
mesenteric groups of pre aortic lymph nodes.

Nerve Supply
Sympathetic derived from celiac and supper mesenteric plexuses.
Parasympathetic supply is from both vagal nerves.

13

1.3 DEVELOPMENT OF THE PANCREAS

The pancreas develops from dorsal and ventral pancreatic buds of
endodermal cells that arise from the caudal part of the foregut which is
developing into the proximal part of the duodenum.
The larger dorsal bud appears first and grows rapidly into the dorsal
mesentery. The ventral bud develops near the entry of the bile duct into the
duodenum.
When the duodenum rotates to the right (clockwise) and becomes Cshaped, the ventral pancreatic bud is carried dorsally with the bile duct,
inferior and posterior to the dorsal pancreatic bud. It then fuses with the
dorsal bud.

Most of the pancreas is derived from the dorsal bud.

The ventral bud forms the uncinate process and the interior part of the
head of the pancreas. As the pancreatic buds fuse, the ducts anastomose.
The main pancreatic duct forms from the duct of the ventral bud and the
distal part of the duct of the dorsal bud. The proximal part of the duct of the
dorsal bud often persists as an accessory pancreatic duct and opens at

14

the summit of the minor duodenal papilla, located about 2cm cranial to the
main duct. The two ducts often communicate with each other. In about 9 per
cent of people the pancreatic duct systems fail to fuse and the original
double ducts persist.

Histogenesis of the pancreas

The pancreatic parenchyma is derived from endoderm, which forms a
network of tubules. Early in the fetal period, acini begin to develop from cell
clusters around the end of these tubules, or primitive ducts.
The islets of Langerhans develop from groups of cells that separate from the
tubules and soon come to lie between the acini.
Insulin secretion begins at about 20 weeks. The connective tissue
covering and the septa of the pancreas develop from the surrounding
splanchnic mesenchyme.

15

FIG 3 : DEVELOPMENT OF PANCREAS

16

Malformations of the pancreas

Heterotopic, or accessory, pancreatic tissue is most often located in the

wall of the stomach or duodenum, or in a Meckel's diverticulum.

Annular Pancreas

It is a rare malformation that warrants description because it may cause

duodenal obstruction and presents as like a mass. The annular portion of
the pancreas consists of a thin flat band of pancreatic tissue surrounding
the second part of the duodenum. An annular pancreas may cause
obstruction of the duodenum shortly after birth or any time in life.
Males are affected much more frequently than females. Although other
explanations have been offered, this abnormality probably results from the
growth of a bifid ventral pancreatic bud around the duodenum. The
portions of the ventral bud then fuse with the dorsal bud, forming a
pancreatic ring.

17

1.4. HISTOLOGY OF PANCREAS

The pancreas is a mixed gland, which is partly endocrine, partly

exocrine, the main bulk of the gland being exocrine. it is a compound
recimose gland devoid of any fibrous capsule It consists of numerous
lobules separated by inter lobular septa.

The Exocrine Part

The main bulk of the gland -about 98% is exocrine. Main function is to
secrete different digestive enzymes. This part of the pancreas is
composed of a serous compound tubo alveolar
gland. Lobules of pancreas contain ultimate ramifications of main
pancreatic duct ending in numerous alveoli.
The secretory elements are tall columnar cells. Their lumen is small.
The lining cells appear triangular in section and have spherical nuclei
situated basally.
In haematoxylin and eosin stained preparations the cystoplasm of cells are
basophilic containing numerous secretory (zymogen) granules.

18

These granules are eosinophillic.

The secretory cells secrete two types of secretions.

Watery rich in bicarbonate secretion stimulated by hormone secretion.

Other containing numerous enzymes (tryposinogen, lipase, amylase

chymotyposiongen) The secretion is stimulated by the hormone
pancreozymin and nasal stimulation.

The enzymes are synthesized in the rough endoplasmic retinaculum from

where they pass to the Golgi complex where they are surrounded by
membranes and released in the cytoplasm as secretion granules. The
granules move to the luminal surface of cells where secretions are poured by
exocytosis.
The addition to the secretory cells, the alveoli of .the exocrine pancreas
contain centro acinar cells that are located near the centre of acinus .
These cells belong to the intercalated duct.
Secretions produced by alveoli are excreted into intercalated ducts. From
this the secretions pass to larger ducts and finally into the main and
accessory (when present) pancreatic duct and finally to the duodenum. Large
ducts are lined by columnar epithelium.

The terminal portion of the pancreatic duct is surrounded by the

sphincter. Similar sphincter is also present in the accessory pancreatic duct.
19

Endocrine pancreas
This consists of numerous rounded collections of cells, which are
embedded, in the exocrme part. These collections measure 76x175 urn.
They are scattered throughout the gland most numerous in the tail than body
and head.
These collections of cells are. called pancreatic islets or islets of
Langerhans
Human pancreas has one million islets.
Islets are richly supplied by blood through dense capillary plexus and
separated from surrounding alveoli by a thin lager of reticular tissue.

Islets contain four types of cells:

A cells (a cells): Secretes glucagon . They form 20% of islet cells.

B cells ( p cells ) : Secretes insulin .80% are of cells are of this

type.

8 or D cells: These secrete hormones gastin and somatostatin

PP cells: These secrete pancreatic polypeptide

,'r.

Dl cells: These contains vasoactive intestinal polypeptide.

20

The A cells are situated at the periphery and B cells are in the centre of
islets.

The B cells are stained by aldehyde fimchin the alpha cells by acid
funchin . The D cells stain black with Silver salts (i.e. agyrophill).

FIG 4 : PANCREAS (SECTIONAL VIEW)

21

1.5 PHYSIOLOGY OF PANCREAS

The pancreas is a gland that is partly endocrine partly exocrine, main bulk
of the gland is exocrine. The exocrine pancreas secretes enzymes that play
important role in the digestion of carbohydrates, proteins and fats. After
digestion and absorption through the gut, these products are carried to the
liver through the portal vein. The endocrine part produces two important
hormones, insulin and glucagon. These hormones influences the
metabolism of carbohydrates, proteins and fats ,
The function of exocrine and endocrine pancreas is thus linked.

Endocrine function of pancreas

At least 4 peptides with hormonal activity are secreted by the Islets of
Langerhans of pancreas. They are:
Insulin
Glucagon
Somatostatin
Pancreatic polypeptide

22

Insulin and glucagon have important function in the regulation of

intermediately metabolism of carbohydrates, proteins and tats.
Somatostatin plays are important role in the regulation of islet cell
secretion.
The function of pancreatic polypeptide is unsettled.

INSULIN

Structure

Insulin is a polypeptide hormone containing 2 chains of ammo acids

linked by disulfide bridge.

Biosynthesis and secretion

It is synthesized in the endoplasmic reticulum of B cells. From there it is
transported to Golgi apparatus, where it packed in membrane bound
granules. These granules are expelled to the exterior of cell all by
exocytosis.

Metabolism
The half-life of insulin in the circulation is about 5 minutes.

23

Insulin binds to insulin receptors and is internalized.

It is destroyed in the endosomes formed by the endocyotic process.
The principal enzyme involved is insulin protease.
Insulin receptors are found in many cells of the body including classic
"insulin sensitive" cells.
80% of the secreted insulin is normally degraded in the liver and
kidneys.

Effects of insulin
The net effect of the hormone is storage of carbohydrate, protein and fat.
Insulin is therefore, called "hormone of abundance".

Principal actions of insulin rapid (seconds)

Increase transport of glucose, amino acids and K+ into insulin sensitive
cells.

Intermediate (minutes)
Stimulation of protein synthesis
Inhibition of protein degradation
Activation of glycogen synthesis
Inhibition of phosphorylase and gluconeogenic enzymes

24

Delayed (hours)
Increase in mRNA for lipogenic other enzymes

Consequence of insulin deficiency

Far-reaching physiologic effects of insulin are high lightered by a
consideration of extensive and serious consequence of insulin deficiency.

Carbohydrate metabolism
*
DIABETES MELLITUS characterized by polyurea, polydypsia, weight
loss in spite of polyphagia , hyperglycemia ,glycosuria, ketosis, acidosis and
coma. This results from reduced entry of glucose into peripheral tissues and
increased liberation of glucose from liver into the circulation.

Protein Metabolism
Diminished protein synthesis and accelerated protein
catabolism leads to negative nitrogen balance.

25

Fat Metabolism
Acceleration of lipid catabolism and increased formation of ketone
bodies decreased synthesis of fatty acids and triglycerides resulting in the
elevation of plasma free fatty acids ,ketosis, acidosis .

Regulation of Secretion

Average amount of insulin secreted per day in a normal human is 40U

(287 mmol).
The major control of insulin secretion is exerted by feedback effect of
blood glucose directly on B cells of pancreas.
Others are amino acids, intestinal hormomes (GIF, gastrin).
Inhibitors of insulin secretion are- somatostratin, and adrenergic
stimulators (non epinephrine, epinephrine) B blockers (propanalol).

GLUCAGON
Human glucagon is a linear polypeptide with molecular weight of 3485.

26

Biosynthesis and secretion

It is synthesized by a cells of pancreatic islets. Glucagon is

also found in gastrointestinal tact mucosa.

Metabolism

Glucagon has a half-life in the circulation of 5-10 minutes. Many tissues

particularly liver degrade it.

Action
Glycogenolysis
Gluconeogenesis
Lipolytic
Ketogenic

Factors effecting glucagon secretion

Stimulators of glucagon secretion are hypoglycemia. Other than this
amino acids, exercise, infections, stress, gastrin etc. Same stimulators of
insulin secretion like glucose and aminoacids increase secretion of
glucagon.
27

SOMATOSTATIN
Somatostatin 14 and somatostatin 28 are found in d cells of pancreatic
islets. Both forms inhibit the secretion of insulin, glucagon and
pancreatic poly peptide and may act locally in paracrine fashion
Somatostatin in excess amounts may produce hyperglycemia and inhibit the
function of CCK.
The secretion of somatostatin is increased by same factors which
increase the secretion of insulin like glucose, amino acids and CCK

PANCREATIC POLYPEPTIDE

Is a linear peptide containing 36 amino acids.

F cells of Islet of Langerhans secrete it.
The secretion of polypeptide is under cholinergic control, plasma levels fall
after the administration of atropine. Increased secretion is also due to
lasting, high protein containing diet, exercise, and acute
hypoglycemia.
>

28

Its secretion is decreased by somtostatin and intravenous glucose.

The exact physiological function of pancreatic poly peptide is not
known.

Exocrine function of pancreas

Pancreatic juice contains enzymes that are of major importance in

digestion.
The secretion is control by in a part by reflex mechanism and in part by the
gastrointestinal hormones secretin and CCK.

Composition of pancreatic juice

Pancreatic juice is alkaline and has high HCo3 content. About 1500 ml of
pancreatic juice is secreted each daily.

Along with bile and intestinal juice, pancreatic juice neutralizes the
gastric juice. The powerful protein splitting pancreatic juice is secreted as a
inactive pro enzyme. Trypsinogen is converted to active enzyme trypsin by
29

bush border enzyme enterokinase , when pancreatic juice enters

duodenum.
Trypsin converts chymotripsinogen into chymotrypsin and other proactive
enzyme into active enzymes.
Trypsin also activates typsinogen; therefore it is an autocatalytic chain
reaction.
Pancreas contains trypsin inhibitors this neutralizes small amount of
trypsin released in the pancreas normally and stops the chain reaction.
Another enzyme activated by trypsin is phospholipase A2. This enzyme splits
fatty acids off lecithin forming lipolecithin. This can damage cell membrane
and in acute pancreatitis, this enzyme is activated in pancreatic duct
causing formation of lipolecithin

which causes disruption of pancreatic

tissue and necrosis of fat. Small amount of pancreatic and amylase

normally leaks into the circulation. But in acute pancreatitis this increases
markedly.

30

Table 1 : Secretions of exocrine pancreas

Enzymes

Substrate

Catalytic

function

or

product.
Trypsin

Proteins

Cleaves peptide bonds

polypeptides
Chymotrypsins

Proteins

Cleaves peptide bonds

Polypeptides
Elastase

Elastin

Cleaves bonds adjacent to

aliphatic amino acids

Carboxypeptidase A Proteins

Cleaves

carboxyl-terminal

and B

Polypeptides

amino acids

Colipase

Fat droplets

Binds to bile salt triglyceride

water inter phase making
anchor for lipase

Pancreatic lipase

Triglycerides

Monoglycerides and fatty

acids

Cholesterol

ester Cholesterol

hydrolase

Cholesterol

esters

Pancreatic a amylase Starch

Take salivary amylase

Ribonuclease

RNA

Nucleotides

Deoxyribonuclease

DNA

Nucleotides

Phospholipase A

Phospholipid

Fatty acids

31

Regulation of secretion

The secretion of pancreatic juice is under hormonal control.

Hormones like secretin ,CCK, acetylcholine increases pancreatic
secretion Vagally mediated of reflex secretion of pancreatic juice in
response to sight and smell of food is also said to occur.

32

1.6 INVESTIGATIONS OF PANCREATIC

DISEASE

A large number of laboratory tests investigations and imaging modalities

are available for the diagnosis of pancreatic disease.
The choice of examination depends upon the clinical presentation of the
patient.
The investigations may be grouped as follows:
Routine blood test
Assessment exocrine function
Assessment of endocrine function
Visualisation of pancreas
Tumour markers
Cytology.

Radio nuclide

Routine blood tests

Routine blood tests may show anaemia, elevation of erythrocyte
sedimentation rate, elevation of bilirubin, transaminase, and alkaline
phosphatase. Acute pancreatitis is associated with low calcium, high
33

blood urea.

Exocrine function
Serum amylase- Useful in acute disease not in chronic Serum lipase- Raised
in acute disease Duodenal enzymes after hormone stimulation with CCK
and secretin and food (Lundh meal)

Helpful in diagnosis of chronic

pancreatitis. ^
PABA test - may be used in pancreatic insufficiency. Fat excretion Faecal
fat intimation and breath test which estimates expired

14

Co2 following

oral ingestion of labelled fatty acids are used to demonstrate pancreatic

disease as a cause of steatorhoea.

Exocrine function
Serum levels of insulin, glucagons , pancreatic polypeptide, gastrin and
vaso active intestinal peptide-Jhese are only indicated if hormone
secreting tumour is suspected . Plasma pancreatic polypeptide is raised in
all endocrine tumours.
Glucose tolerance test- most commonly used test for assessment of the
deficiency of insulin and glucose tolerance.

34

Visualisation of pancreas
Imaging of pancreas is become increasingly more accurate.

Abdominal X-ray: To detect calcification especially in chronic

pancreatitis, rarely haematomas,

Barium meal: Rarely used now but can demonstrate several

pancreatic pathology like: pancreatic pseudocyst, annular pancreas,
and pancreatic tumour.

Conventional ultrasound: Widely used, inexpensive and easy to

perform.

It

can

collections,pancreatic
in

detect
tumours,

gallstones,
and

stones

pancreatic
and

fluid

calcifications

chronic pancreatitis. However obesity or excessive bowel gas

may hamper visualization.

Ultrasound depends greatly on operator's skill and knowledge.

Endoscopic ultrasound:BQ$t technique for detecting small

pancreatic tumour and small stones in CBD.

Helical CT: CT with dynamic enhancement enables pancreas to

be completely visualised in 30 seconds of breath hold and
extremely useful in pancreatic disease. Detailes of CT examination
of pancreatic mass lesions are given vide infra.

35

 Multi slice C7:The multislice scanners have the ability

to demonstrate the anatomy of pancreas in exquisite detail
.Smallest vessel can be visualised, even tiny ones entering
parenchyma itself.
It is most likely that multislice CT will eventually replace
diagnostic ERCP .The most subtle change of density or margin of
structures can be identified.. More over multiplanner reconstruction
is possible.
MRI: This has the advantage over CT in that in does not
involve ionising radiation and has multi planer ability. But the
scan time is prolonged. CT and MRI have been found to be
equally sensitive in visualization of pancreas.
Magnetic resonance chalangiopancreatography (MRCP)
This is a very non-invasive way to visualise the pancreatic duct and may
challenge diagnostic ERCP. Heavily T 2 weighted image eliminates signal
from all tissues except stationary free water protons in pancreatic ducts.

Arteriography with selective catheterisation is less frequently used.

36

ERCP: (Endoscopic retrograde cholangiopancreatography):

ERCP is considered as gold standard for the visualisation of pancreatic

duct. Through MRCP may replace diagnostic role of ERCP the future.
It is used to detect suspected pancreatic disease in where USG or CT
is normal or technically unsatisfactory.
It is used to delineate the exact ductal anatomy prior to surgery
Assessment of complications of acute pancreatitis
Intervention : gall stone

dissimpaction

in acute

pancreatitis,pancreatic stone extraction, balloon dilatation of

minor papilla in pancreatic divisum

Tumour markers
CA19-9, a sialylated Lewis antigen associated with circulating mucins is the
most widely used marker for pancreatic malignancy. Most commonly used
cut off level is 37u/ml. This is most commonly elevated in pancreatic
adenocarcinoma other malignancies like bile duct stomach; colon cancers
may show elevated level. Minor elevations may occur in benign conditions
like acute and chronic pancreatitis.

37

Other tumour markers of pancreatic malignancy are carcinoembryonic

antigen (CEA), and a fetoprotien, RNase, gataclosyl transferase (GIII)
oncofetal antigen, CA 50, CA 242.

Cytology
It is the principal mode of diagnosis of pancreatic cancer. Fine needle
aspiration (FNA) can be done using CT or ultrasound guidance. During
ERCP pancreatic ductal bushing or biopsy sample can also be obtained.

Radionuclide Imaging
This is used to detect tumours of pancreatic islet cells .The radionuclide
indium n labelled with octreotide, which is a somatostratin analogue has
a high affinity for these tumours.

Somatostratin receptor scintigraphy may also be used to identify islet

tumors.

38

1.7 CT SCAN OF PANCREAS

TECHNIQUE

Complete filling of the stomach and duodenal loop with contrast medium is
necessary for high quality CT .Eight to sixteen ounces of oral contrast is
given immediately before scanning. Glucagon 0.1 mg by intravenous
injection may be given to stop peristalsis in the duodenum and aid with
bowel opacification. Intravenous contrast agent (150mL) given rapidly by
mechanical injector is needed to:
I.

Enhance the normal pancreatic parenchyma

I.

Enhance peripancreatic vessels for identification and assessment of

patency.

II. Enhance the liver parenchyma to detect involvement by pancreatic

disease.
Scanning is best performed with helical technique using 5-mm
collimation and a pitch of 1. Reconstruction is performed at 3- to 5-mm
intervals. Conventional CT is performed using contiguous 5-to 10mm

39

thick slices. Detection of functioning islet cell tumours requires dynamic

helical scanning with rapid contrast agent infusion.

CT ANATOMY10'11'13 Location

The pancreas is located in the anterior pararenal space of retro

peritoneum just anterior to the perirenal (Gerota's) facia and posterior to
parietal peritoneum.
The uncinate process is situated behind the superior mesentric vein and
artery.
The gross anatomic relationship with stomach duodenum and colon are
fairly constant.
The head of pancreas is medial and posterior to the bulb of duodenum bound
laterally by the second and inferiorly by the 3rd part of duodenum.
The neck lies anterior to the superior mesenteric artery. The tail and body of
pancreas lies immediately posterior to the fundus and antrum of the
stomach.
The pancreas is separated from the stomach by lesser sac or omental bursa
this can only be visualised if the sac fills with fluid.

40

The tail of the pancreas of the pancreas is adjacent to the hilum of the
spleen and just anterior to left adrenal gland and upper pole of left
kidney.
The main and accessory pancreatic duct is well visualised in CT.

The common bile duct travels in the free margin of lesion omentum with
portal rein and hepatic artery and is visualised as a low density
structure.
Vascular anatomy around the pancreas can be demonstrated well with
spiral CT. However vascular detail visible in multi slice scanner is
spectacular. Apart from the main vessels like splenic, hepatic, superior
mesenteric branches like gastro duodenal, pancreaticodudenal and
transverse pancreatic arteries are well depicted. Normally calcification
occurs in splenic artery and this should not be confused with pancreatic
calcifications.

Dimensions 15
The size of normal pancreas may be measured in different ways the most
widely accepted anterior posterior measurements are head 23(3) mm; neck 19(2.5 )mm; body 20(3) and tail 15(2.5)mm .

41

The pancreatic size measured by Ultrasonography is smaller than CT

because of better visualisation of splenic vein artery.
However the size of pancreas decrease with age but the ratio of head to body
remains constant.
Mean craniocaudal dimensions of pancreas are 5.9 cm (range 7.2 -7.8cm) for
men and for women 6.2 cm(range 4.8-7.6cm)16

Density

The density of pancreas is normally same as soft tissue between 30-50H

units. Normal gland enhance after contrast administrations. In the normal
gland variable amount of fat tissue may be present interposed along the
margin of the gland or within gland or the entire pancreas may be replaced
by fat.

Normal Variants11

There may be variation in the normal shape of pancreas which may

sometimes create confusion. In general the head is larger than the body or tail
and the neck is the portion of pancreas.

42

In Dumbbell shaped pancreas there is a large head and tail but the neck is
narrow. The tail may be slightly bulbous, angulated or cross way around the
left kidney.
The head generally lies below the tail however, head tail may be horizontal
and in some cases tip of the tail be below spleen or higher than normal
position.

FIG 5 : CT ANATOMY OF PANCREAS

43

1.8

PATHO

PHYSIOLOGY

OF

LESIONS

PRESENTING AS PANCREATIC MASS

Normal Variants11
Detailed knowledge about different normal variants is necessary before
interpretation of pancreatic CT; otherwise these can be confused with
mass in USG, CT or MRI. Most common anomalies that mimic
pancreatic neoplasm are:
Annular pancreas
Pancreatic divisum: secondary changes resulting from recurrent

pancreatitis may cause focal enlargement. Prominent fitsion anomaly:

Prominent head of pancreas at the junction point between head and neck
may cause change in the contour of the gland and mimic a mass. Details
of different normal variants are given in previous section.

Acute pancreatitis 9} 17
Acute pancreatitis is a disease characterised by abdominal pain and
elevations in the levels of serum lipase and amylase.

44

The essential feature of acute pancreatitis is the elaboration of an

inflammatory reaction, which results in oedema of the pancreas and
extensive local and systemic effects.
Peripancreatic fluid collections and inflammatory phlegmone may
present as a diffuse mass around the pancreas.
Acute pancreatitis is of two types:
Acute oedematous pancreatitis
Acute emphysematous pancreatitis

Path physiology
Acute pancreatitis is believed to begin as autodigestive process within the
gland as a result of premature activation of zymogens within the
secretary cells, duct systems or interstitial space.-This results in acinar all
damage, necrosis, oedema and inflammation.
In addition, impaired microcirculation, oxidative stress, release of
cytokines like interleukin, tumour necrosis factors, platelet activating
factor results. All these factors contribute to both pancreatic and extra
pancreatic complications.
Histologically four basic alterations occur:

45

 Proteolytic destruction of pancreatic substance

Necroses of blood vessels and subsequent haemorrage
Necrosis of ft by lipolytic enzymes
Inflammatory reaction

Cause
Gallstones:

This results in acute

pancreatitis when a stone from

gallbladder is impacted in the duodenal papilla. This causes a sudden

increase in the pressure of pancreatic duct resulting in a "secretory block"
of digestive enzymes at the level of acinar cells along with reflux of bile
from bile duct.
Chronic excessive alcohol use
Drugs (azothioprine, salicylates, sulphonamides)
Infections (ascariasis, mumps, coxsakie virus, tuberculosis)
Blunt or penetrating abdominal trauma
Surgery
ERCP
Pancreatic ampullary tumour.
Toxins (organophosphate, scorpion venom)
Cystic fibrosis
Hereditary disease
46

 Idiopathic
Symptoms and signs

Abdominal pain is the cardinal manifestation of acute pancreatitis and

present in 95% cases
Fever, tachycardia, hypertension tachypnea.
Nausea, vomiting abdominal distension
Shock.

Complications

Pancreatic complications
Phlegmone (inflammatory mass)
Peripancreatic effusion.
Necrosis / pancreatic abscess.
Non-pancreatic
Gastrointestinal ileus.

Pancreatic ascites / pleural effusion.

Bile duct obstruction.
47

Systemic complications of acute pancreatitis

Hypovolumia
Hypo tension and shock.
Oliguria and renal failure
ARDS (acute respiratory distress syndrome)
Vascular thrombosis, DIG
Hypocalcaemia, hyperglyeaemia, metabolic acidosis
Peripheral fat necrosis
Encephalopathy

Table 2

: Diagnosis of acute pancreatitis

LAB

IMAGING

Increased serum amylase

X-ray

Increased only 80-85% cases may CXR: Lt sided pleural effusion, It

be normal in pancreatitis due to basal pneumonitis, and High left
hyper-lipidemia

dome of diaphragm.

Serum lipase

Bones: Avascular necrosis, Lytic

Increased, as sensitive as

lesions

amylase

Abdomen: Shows duodenal

48

ileus, sentinel loop, gas less

Alanine

abdomen

aminotrasferase(ALT)

Colon cut-off sign, mottled

3 fold increase in associated with

shadows due to fat necrosis.

gallstone.

Gall stone
USG (low sensitivity due to
localileus) Gall stone Pancreatic
swelling, necrosis.
Peripancreatic

fluid collection,

mass.

ERCP
Diagnosis of acute pancreatitis
of occult cause.
Removal of stone
Sphincterotomy
CT-Vide infra
MRI- Not generally used.
But oedema and fluid shows
decreased signal intensity in Tl and
increased signal intensity in T2
weighted image.

49

Criteria for assessing severity of acute pancreatitis

Several methods are used to predict the severity of acute pancreatitis
apart from lab findings. CT findings

play a vital role in scoring of by

these methods.
Commonly used methods are:

Radson criteria. Modified Glasgow

(Imrie) Criteria and Acute Physiologic and Chronic Health Evaluation

(APACHE) II criteria.
Dynamic CT looks for non-enhancing pancreatic tissue following
intravenous contrast administration.

Pancreatic abscess
Pancreatic abscess are severe life threatening problem.
Causes

Virtually any organism can infect the pancreas. They include gramnegative and gram-positive organisms and also Candida albicans. The
organism may reach the pancreas as a result of haematogenous spread,
lymphatic spread, gastrointestinal perforations or fistula or response to
some type of iatrogenic procedure like ERCP.

50

Other organisms like Echinococcus may also cause pancreatic abscess.

Tuberculosis of Pancreas
Few cases of tuberculosis of pancreas, presenting as pancreatic mass has been
reported by some authors .This should always come as a differential diagnosis,
especially in areas where tuberculosis is common, like Bangladesh. Both
Mycobacterium tuberculosis mdAfycobacterium bovis may infect the pancreas.
Mycobacterium avium-intmcellulare is important cause of tuberculosis in
elderly women and in immune suppressed patients. Common manifestations of
tuberculosis of pancreas are:
Clinically and radio logically presents as pancreatic carcinoma "
Pancreatic abscess refractory to antibiotic therapy
Unexplained obstructive jaundice
Portal hypertension.
Organisms may reach the pancreas by ingestion, swallowing of expectorated
mycobacterium during active pulmonary disease, or haematogenous spread from
the primary site of infection.

51

Chronic pancreatitis

The 1983 Cambridge symposium classified chronic pancreatitis as a continuing

inflammatory disease of the pancreas characterised by irreversible
morphological change typically causing pain and or a permanent loss of
exocrine and endocrine function.
Chronic pancreatitis is associated with increased risk of pancreatic
adenocarcinoma.
There can be diffuse or focal enlargement of pancreas and in later case it
becomes difficult to differentiate from pancreatic tumours.

Pathophysiology
Exact pathophysiology of chronic pancreatitis is unknown. Different
causes have different mechanism of injury. Regardless of cause ultimate
effect is damage to'pancreatic acini, ducts nerves and islet cells.
Gross pathologic specimens show that gland is hard and exhibits foci of
calcification and folly developed pancreatic calculi.
There are several patterns, chronic calcifying pancreatitis that occurs in
alcoholics. There is atrophy of acini and increase in interlobular fibrous

52

tissue and chronic inflammatory infiltrate around interlobular and intra lobar
ducts are dilated with protein plugs in their lumina. Pseudo cyst formation is
common.
In Chronic obstructive pancreatitis, which is most often associated with
cholilithiasis protein plugs, stones calcifications are rare.

Causes
Alcohol
Tropical pancreatitis
Familial pancreatitis
Cystic fibrosis.
Idiopathic pancreatitis.
Pancreatic duct obstruction
Auto immune
Recurrent acute pancreatitis

Clinical findings Pain

Chronic pain, usually varying in severity, pattern, quality and frequency. Pain is
dull constant located in epigastrium and made worse by eating or supine
position.

53

Malahsorption
Stratorrhoea occurs late in chronic pancreatitis only when the secretory
capacity is reduced to less than 10% of normal. Patient presents with
weight loss, osteopenia and deficiency of vitamin D and A,

Diabetes MelUtus
Pancreatic islets are more resistant to damage than acinar and ductal cells
and diabetes occurs less frequently than steatorrhoea. It occurs in 30% of
patients with chronic pancreatitis.

Table 3: Diagnostic tests of chronic pancreatic listed in order or

decreasing sensitivity
FUNCTION
Secretin or secretin cholecystokinin

STRUCTURE
Endoscopic ultrasound

test

Direct visualisation of pancreatic

Fecal elastase

duct,
ERCPparenchyma, is more sensitive
Duct dilatation, stricture, irregular

Serum

trypsin

(reasonably

accurate)
Fecal
fat
Blood glucose- too insensitive

contour, filling of cavities or

MRIandMRCP
pseudocysts
Sensitivity is still less than ERCP
Computed tomography
Vide infra.
Ultrasonogram
Can
demonstrate

calculi

calcifications markedly dilated ducts

54

Cystic Lesions of Pancreas

Cysts are infrequent findings in the pancreas but are of considerable
clinical importance as they may present as abdominal masses that are
suspected of being malignant. Cysts can be classified as true cysts (25%) and
pseudocysts(75%)
True cysts can be congenital and acquired; like retention cysts, dermoid
cysts, and malignant cysts.

Congenital cysts
A congenital cyst results from anomalous development of pancreatic ducts.
Congenital cystic disease of pancreas, liver kidney not infrequently
coexists. These cysts are usually multiple but may occur singly. These cysts
do not generally communicate with the pancreatic ducts.

Their size range from microscopic lesions to larger spaces up to 3 to 5

cm in diameter.
These cysts are lined by smooth glistening membrane that may on
histological section have total atrophy of lining epithelial cells or may
show preservation of flattened

pavement or low cuboidal epithelial cells.

They are usually enclosed in a thin fibrous capsule and are filled with a
clear to turbid mucoid or serious fluid.

55

Von Hippel Lindau disease is a rare entity presenting with cysts in

pancreas, liver and kidney.

Pancreatic pseudo cysts:

Pseudo cysts are rounded collections of fluid surrounded by a visible capsule;
this term is applied to collection of fluid that arises from loculation of
inflammatory process, necrosis or haemorrhages.

Causes:
Pseudo pancreatic cysts can occur as a consequence of acute and chronic
pancreatitis.
It can also follow traumatic injury to the abdomen with direct damage
and hemorrhage in the pancreas.
Acute pancreatitis or trauma precedes the clinical discovery of a pseudo
cyst in nine often cases.
In case of pseudo cyst occurring in the setting of acute pancreatitis,
there is usually

ductal

disruption and necrosis with escape

of

pancreatic juice containing activated enzymes . It takes at least 6 weeks of

pancreatic fluid collection to mature into pseudocyst.
A pseudocyst complicating chronic pancreatitis is due to obstruction of
pancreatic duct, causing retention cysts containing inactivated enzymes.

56

Clinical features
Asymptomatic.
Abdominal mass.
Presents with complications like haemorrhage or infection and may
rupture causing generalised peritonitis.
Pseudocysts in chronic pancreatitis present as worsening of chronic pain,
wasting syndrome or remain asymptomatic.

Pathophysiology:
These cysts are usually solitary and most measures 5-10 cm. They may
be situated in pancreatic substance or adjacent to pancreas; especially in
tail area.
Thick and fibrous walls line the cyst; there is no epithelial lining
connection or communication with surrounding ductal system.
Cyst fluid may be serous or turbid. There may be marked inflammatory
reaction in the fibrous capsule.
Often organising blood clots, old blood pigment precipitates of calcium
and cholesterol crystals are also found.
They are usually unilocular.

57

Location11
These are typically located in the pancreas of immediate peri pancreatic region.
Omental bursa is the second most common location. It may extend beneath
the capsule of the liver, posterior mediastinum. These can also occur in the
spleen, liver, and kidney.

Diagnosis:
USG shows these sono lucent areas with relatively smooth wall
circumscribed outline.21
CT findings are discussed later.

Complication9'18
Haemorrhage from small vessels in the capsule
Infection by gram negative organism

Obstruction of surrounding organs like bile duct duodenum, rarely

portal vein, ureters and colon

Rupture.

Fate
Pseudocysts usually spontaneously resolve if < 6 cm in diameter, Symptomatic
pseudocysts can be treated with surgical, endoscopic and percutaneous
drainage.

58

Cystic Neoplasms.
Pancreatic carcinomas other than adenocarcinoma of pancreatic ductal origin
and islet-cell tumors are uncommon, representing only 5% of pancreatic
cancers.
Special mention is made of cyst adenomas and eystadenocarcinomas because
they are often mistaken for benign pancreatic pseudo cysts and because they
have a much more favourable natural history than non-cystic pancreatic
adenocarcinoma.
Clinical findings
Symptom and Signs

Cystic neoplasms are most commonly found in the body or tail of the pancreas
of young to middle aged adults, especially women. The tumours remain
asymptomatic until they become quite large, when they may present with
symptoms caused by local tumour growth like compression of adjacent
abdominal structures.
These include abdominal pain, a palpable mass, weight loss, nausea, and
vomiting. Obstruction of the common bile duct resulting in jaundice.

59

purities and cholangitis are less common than with non-cystic

adenocarcinoma. Similarly, upper gastrointestinal tract bleeding caused by
splenic vein thrombosis with formation of gastric varices or direct tumour
invasion is a less common presentation.

Diagnostic Studies
The diagnosis usually is suggested is suggested by abdominal CT or
ultrasonographic detection of a large, cystic pancreatic mass. These Studies
usually are obtained for evaluation of vague abdominal complaints. It may
be difficult from these non-invasive imaging studies to differentiate cystic
pancreatic neoplasms from non-neoplastic pseudocysts.

Symptoms and Signs

Cystic neoplasms are most commonly found in the body or tail of the pancreas
of young to middle aged adults, especially women. The tumours remain
asymptomatic until they become quite large, when they may present with
symptoms caused by local tumour growth with compression of adjacent
abdominal structures.
These include abdominal pain, a palpable mass, weight loss, nausea, and
vomiting. Obstruction of the common bile duct resulting in jaundice, pruritus,
and cholangitis is less common than with non-cystic adenocarcinoma.
Similarly, upper gastrointestinal tract bleeding caused by splenic vein

60

thrombosis

with

formation

of

gastric

varices

or

direct

tumour invasion is a less common presentation.

Diagnostic Studies

The diagnosis usually is suggested is suggested by abdominal CT or

ultrasonographic detection of a large, cystic pancreatic mass. These
studies usually are obtained for evaluation of vague abdominal
complaints.
It may be difficult from these non-invasive imaging studies to
differentiate cystic pancreatic neoplasms from non-neoplastic pancreatic
pseudo cysts.
It is extremely important to consider the diagnosis of cystic neoplasms of the

pancreas in patients who'present with isolated cystic lesions who do not have
risk factors for pancreatic pseudocysts.
The absence of trauma, alcoholism, a history of acute or chronic
Pancreatitis, or biliary tract disease makes pancreatic pseudocysts
unlikely and cystic neoplasm of the pancreas more likely in patients who
are found to have an isolated cystic lesion of the gland. .
Endoscopic- ultrasound is extremely useful in the evaluation of cystic
lesions, often providing additional detail not seen by CT.
It can clarify whether the lesion is a simple cyst (strongly suggesting
pseudocyst) or a cystic mass. For cystic mass lesions, it can often
61

distinguish serous cystic lesions (which are almost always benign) from
mucinous cystic lesions (which have a high risk of malignancy).
Serous ("microcystic") cystadenomas have characteristic honeycomb
appearance with central fibrosis or calcification.
EUS can be used to sample cystic fluid, which can be examined for
enzyme levels, viscosity, tumour marker levels, and cytology.
Pancreatic pseudocysts have high amylase content. Serous cystadenomas
have a clear serous fluid, a low amylase content and low CEA level.

Mucinous have a fluid that is viscous, contains mucin, and has a low amylase
level.
Malignant cystadenocarcinomas may have a high CEA level and positive
cytology.

Treatment
Most patients with either benign or malignant cystic neoplasms should be
considered for surgical resection, even if the tumour is large or locally invasive.

Vascular malformations11'13
Pancreas is surrounded by vascular structures and a number of vascular
entities in this region may be mistaken for pathologic conditions of the
62

pancreas.
These abnormalities can related to inflammatory, atherosclerotic or
neoplastic involvement of-the vessel.
Most common vascular lesions is splenic artery aneurysms and pseudo
aneurysms-these commonly occurs in women of child bearing age who
take contraceptive pills.

Others are hepatic artery aneurysms, superior mesenteric artery

,

aneurysms, and celiac artery anemysms.

These commonly contain calcifications and are mostly atherosclerotic in
origin.
Cavernous transformation of portal veins needs special mention. This
consists of multiple venous collaterals in the area off portal vein, It is
thought to be a congenital problem.

Tumours of the pancreas

63

Benign tumors

Fatty Tumours
Fatty tumours lipomatous pseudohypertrophy, lipomas are rare.

Adenomas
These are benign solid tumours of both ductal and acinar origin. Overall
incidence is rare.

Malignant tumors
Adenocarcinoma
incidence and aetiology

Pancreatic cancers are highly fatal malignancy. About 29,200 patients with
pancreatic neoplasm are diagnosed annually in United States. The annual
estimated incidence in US is 10 per 100.000 person over the age of 50. Certain
ethnic groups like blacks, Polynesians and native New Zealanders have increase
incidence. Mean age of onset is T^-S* decade. Genetic predisposition is a great
risk for the development of pancreatic cancer and 10% patient will have 1 st
degree or 2nd relatives with pancreatic cancer.
A very small percentage of cases of pancreatic cancer arise in familial and
hereditary chronic pancreatitis, as an autosomal dominant condition. There is
increased incidence of pancreatic cancer in certain cancer syndromes like
Puetz-Jeghers syndrome, hereditary non polyposis colon cancer. Von Hippel64

Lindau syndrome and ataxia telangiactasia.

Risk factors are alcohol consumption, gallstones, and diabetes mellitus high
intake of animal tat use of high-refilled flour, certain environmental agents like
petroleum products and wood pulps.
Most significant environmental risk factor is cigarette smoking which studies
show increased relative risk of 1.5 to 5.5 fold.
Patients with chronic pancreatitis appear to have a 4% risk of developing
pancreatic cancer in 20 years.

Pathophysioiogy:
Pancreatic adenocarcinomas are believed to originate from ductal cells in which
a series of genetic mutations have occurred in proto-oncogenes and tumour
suppressor genes.
Mutations of K- ras oncogene are believed to be an early event in tumour
development and present in 90% of tumours. This is associated with loss of
function of several tumour suppressor genes (pi6. p53. APc and DPc4) and this is
formed in 40%-60% of tumours.
The detection of K-ras mutations is used in clinical research setting to
diagnose pancreatic cancer.

Gross

65

The tumour has infiltrative margin. Carcinomas in body and tail due large
head irregular tumours.
Microscopic 17

Most show well differentiation glandular pattern which may be mucin or non
mucin secreting. The glands are atypical, irregular, small and bizzre lined by
anaplastic cuboidal to neither columnar epithelial cells. 10% may have
adenosquanous pattern. Giant cell formation is the hallmark of extreme
atypia. 8% arise in cysts are called cyst adenomas. Rarely carcinomas arise in
children and arise from acinar cells and are called acinar cell carcinomas.
These carcinomas arise in children.
Essential clinical symptoms
*

Trousseau's sign: migratory thrombophebitis associated with

adenocarcinoma

* Vague dull mid epigastric abdominal discomfort

* Weight loss,
* Anorexia
*

Dysgensi

* Diarrhoea
* Jaundice
* Weakness
* Vomiting

66

Most patients present late in course of disease. Early in course of disease there
are only a few signs and symptoms to suggest the diagnosis. Patient mostly
presents with vague pain, anorexia, dysgeusia, diarrhoea, weakness and
vomiting .50% patients develop jaundice mostly due to bulky tumours
involving the head of the gland, which encase distal part of common bile
ducts. On occasion tumour may be small and involve the ampulla. However
30-40% tumours develop in the tail region. These patients
mostly presents with large retroperitoneal mass and metastasis.
Obstruction of distal common bile duct results in enlarged palpable nor
tender gall bladder and is called Courvoisier's sign.
Laboratory findings:9

Routine blood test:

Anaemia, high ESR

Increased serum alkaline phosphates.
Increased serum bilirabin
Rarely elevations of serum amylase

Tumour markers:

67

A tumour marker is any substance the when measured in abnormal

concentration in body fluid or tissues indicate the presence of a
malignancy and define its site of origin.
CA 19-9 is mostly used 37 U/ml is the cut off value. Sensitivity is 8185% and specificity 81-90%.
Elevated carcinoembryonic

antigen is present in 70% of patients.

Others are a fetoprotein, RNase, Galactosyl transferase II (GT-II),onco

fetal antigen.
RADIOLOGY
X-ray: Adenocarcinomas do not calcify.
Barium Meal: Large pancreatic masses displace the stomach superiorly and
anteriorly with widening of retro gastric space. Lesions in the head affect the
pyloric antrum or duodenal loop. Lesions in the body involve

the distal duodenum. There is widening of C loop with mucosal

68

abnormality. Gastric mucosal abnormality in the posterior wall.

ERCP: Complete block of main pancreatic duct is the commonest
abnormality. Pancreatic duct stricture is less common.
Filling defects and irregular contrast filled cavities are also hallmark of
pancreatic cancer.

Ultrasound: Usually presents as echopoor mass,

MRI/MRCP:

Early

detection

of

pancreatic

carcinoma

remains

problematic .These appear as areas of low intensity in Tl weighted fat

suppressed image .On T2 the lesion is iso to hypointense.

Site
Lesions may occur any where in pancreas but most show tairly standard
distribution
Head -60%
Body-15% to 20%
Tail -5%

Treatment

69

Pancreatic adenocarcinoma can be cured only by surgical excision.

Unfortunately, a potentially curative surgical resection is possible in less than
20% of patients at the time of diagnosis. The importance of preoperative
staging cannot be overstated. Patients with tumour associated with vascular
invasion (e.g., superior mesenteric artery),
peripancreatic or distal nodal involvement or distant metastases have a median
survival of less than 1 year, which is not improved with surgical resection. This
staging system is not commonly used for management decisions, and criteria for
resection vary from institution to institution. Therapeutic approaches for
pancreatic adenocarcinoma are outlined.
Table 4: Staging of carcinoma of exocrine pancreas.
Stage -0
Stage-I
Stage-II
State III
Stage-IV

In situ carcinoma
Tumour localized within pancreatic capsule
Invasion of s duodenum bile duct , or peri pancreatic tissue
Involvement of lymph nodes.
Tumor extends directly into stomach, spleen, colon or
adjacent large vessels: distant metastases.

SURGERY
The minority7 of patients with pancreatic neoplasms undergo curative surgical
70

resection, primarily because less than 20% present with potentially curable
disease.
One third of the patients had neither resection nor surgical bypass
because of locally advanced or metastatic disease, advanced age, or
debility.
For patients with confirmed carcinoma of the head of the pancreas, the Whipple
resection (pancreaticoduodenectomy) is the procedure of choice. This
involves resection of the pancreas to mid -body, the duodenum, the common
bile duct, and the gallbladder, followed by anatomosis of a limb of jejunum to
the stomach, proximal bile duct and stomach,
'The mortality rare from this operation is less than 5% in patients with
experienced surgeons. The main source of morbidity and mortality from the
Whipple procedure arise from the pancreaticojejunostomy, through which
anastomotic leaks and haemorrhage, Despite its technical difficulty' and
associated morbidity. Whipple resection provides the only real hope of cure for
patients with carcinoma of the head of the pancreas.

Even when core is not achieved, it may provide a long period of palliation
with improved quality of life, particularly among good risk patients who have
small periampiillary neoplasm. Despite improved rates of operative mortality and
71

morbidity, the 5-year survival remains only 20% for the selected subset of
patients who undergo potential curative surgical resection of tumour.
En bloc resection of the entire pancreas, duodenum, spleen, and greater
omentum with subtotal gastectomy has been suggested by some investigators
to have advantages over the Whipple procedure for patient with carcinoma of
the head of the pancreas.18
Chemotherapy
Gemcitabine appears to be the most promising chemotherapeutic agent for the
palliation of patients with non resectable pancreatic cancer.
Radiation Therapy
When used alone, external beam radiation therapy gives very
disappointing results, with median survivals of only 6-12 months. Moreover,
radiation can produce substantial injury to adjacent organs, such as the spinal
cord, liver, and duodenum, although improvements in radiation equipment
and delivery techniques have decreased the

occurrence of these

complications. The use of external beam radiation therapy combined with

chemotherapy is widely used as an adjuvant therapy following surgical
resection of pancreatic adenocarcinoma.

Celiac Plexus block

72

For many patients, extensive retroperitoneal tumour infiltration produces

disabling, intractable pain, Celiac plexus block can help patients who do
not respond to standard narcotics of radiation therapy.

Table-5: Different treatment options of pancreatic tumours

Stage I (resectable)

Surgery with adjubant chemoradiation

Good performance status

Stage II ( unresectable)

Consider entry into experimental protocol to

down stage tumour.
Clinical trials.
Chemoradiation

Stage-I

Gemcitabine
Gemcitabine based therapy

Poor performance status

Supportive care

Stage-II & Stage III

Clinical trials

Good performance status

Chemoradiation

Stage IV

Gemcitabine- based therapy

Clinical trials

Good performance status

Stage II, III, IV

Gemcitabine based therapy

Gemcitabine-based therapy

Poor performance status

Supportive care

Pancreatic islet-cell tumours

73

Pancreatic islet-cell tumours constitute about 2% of all pancreatic neoplasms.

Up to half of these tumours are "functional" and secrete one or more
biologically active peptides, which result in the development of clinical
symptoms. Five clinical types of tumours have been described; instilinoma,
gastrinoma, glticagonoma. somatostatinoma, and vasoactive intestinal peptidesecreting tumours (VlPoma). Occasionally these tumours will secrete more
than one peptide, A significant proportion of the tumours are not associated with
hormone overproduction ("nonfunctional") and are diagnosed on the basis of
symptoms caused by local
or metastasic tumour growth.

Clinical findings
Many of the patients with pancreatic islet-cell tumours present with signs
and symptoms of excess hormone secretion. The most common tumour
of islet-cell origin, namely the insulinoma.
Insulinoma: usually is manifested by profound hypoglycaemia with
diaphoresis, confusion, and syncope.
Gasinnonm: is the second most common tumour of islet-cells origin.

74

Classically, these tumours present with peptic ulcer disease. Other

common symptoms include diarrhoea and esophagitis. About one third of
gasrinomas are associated with multiple endocrine neoplasia
syndrome type-1 (MEN-1).
VIPomas : are associated with a syndrome of watery diarrhoea,
hypokalemia, and achlorhydria.
Ghtcagonomas : can present with
depression,

and

diabetes, deep-vein thrombosis,

dermatitis(necrolytic

migratory

erythema).

Somatostatmomas: These are quite rare and may present with symptoms
including cholelithiasis, weight loss, abdominal pain, diabetes.
steatorrhea, and diarrhea.

Hormonally inactive islet-cell tumours of the pancreatic head may present

with jaundice, purities, or abdominal pain. Islet tumours commonly
metastasise to the liver, where they may cause hepatic enlargement pain, or
jaundice.

Diagnostic studies
In most patients, elevated serum hormone levels (insulin, gastrin,
vasoactive intestinal peptide, glucagons)
75

Treatment
The vas majority of pancreatic islet-cell neoplasm can be treated by segment
resection of the gland or enucleating the tumour.
PANCREATIC LYMPHOMAS9'11'13

Pancreatic lymphomas are infrequent,, probably representing 1-3% of all

pancreatic neoplasms. An increase in pancreatic lymphomas is now being
seen among patients with AIDS. These latter patients have B cell non-Hodgkin's
lymphomas arising primarily in the pancreas, wall of the duodenum, or even
common bile duct.
Clinical findings
The difference of pancreatic lymphoma form pancreatic adenocarcinoma is
important

preoperatively

because

the

therapy for lymphoma is chemotherapy rather than

primary

form

of

resection. In

general, patients with pancreatic iyraphoma present with signs and

symptoms identical to those with adenocarcinoma. However, patients
with pancreatic lymphoma have lower levels of serum bilirubin and
alkaline phosphates than

with comparably bulky pancreatic

adenocarcinoma,

Treatment
When patients with pancreatic lymphoma are diagnosed preoperatively.
chemotherapy can be initiated with cyclophosphamide, prednisone, and
76

doxorubicin.

Metastsis and adjacent tumours

Metastatic tumors of the pancreas are not uncommon. Commoo tumours with
metastasizes to pancreas are breast lung, ovary, colon, gallbladder, as well as
hepatoma, melanoma. Gastric, kidney, colon, and tumours duodenum may
spread to pancreas,

CT APPEARANCES OF DIFFERENT
PANCREATIC MASS
Normal variants 11
As mentioned earlier prominent fusion anomalies, annular pancreas may be
mistaken for pancreatic mass.
Contrast enhanced CT plays a vital role in identifying these lesions. Normal
pancreatic tissue will enhance in proportion to rest of the gland. All pancreatic
malignancies are hypo vascular and do not enhance,

Acute Pancreatitis
The diagnosis of pancreatitis is made clinically.
CT may be normal in mild cases.
77

The role of CT is to document the presence and severity of complication,

CT findings are:
Pancreatic changes

Focal or diffuse enlargement of the pancreas

Decrease in density due to edema

Blurring of the margins of the gland due to in inflammation

Peripancreatic changes
Stranding densities in fat and blurring of fat planes
Thickening of retroperitoneal facial planes

Complications

* Phlegmon; mass like edema and inflammation, seen as ill-defined

heterogeneous soft tissue and fluid densities (20-40 H) in and around
the pancreas,

* Fluid collection: non encapsulated homogeneous collections of fluid with

water density (10-20 H) in the pancreatic bed, the retro peritoneum, and
often widespread throughout the abdomen.

* Pseudo cyst; well-defmed round or oval fluid collection with clearly

identifiable fibrous capsule.

* Necrosis: liquefaction of portions of the gland identified by lack of

contrast medium enhancement.
78

* Abscess: bacterial growth within necrotic tissues seen as a loculated fluid

collection; it may contain gas, and percutaneous aspiration is usually
needed to confirm the diagnosis,

* Hemorrhage: due to erosion of blood vessels or bowel and seen as high

attenuating fluid in retroperitoneuni or peritoneal cavity,

* Pseudo aneurysm: due to encapsulation of arterial hemorrhage with

continued communication with eroded artery.

* Thrombosis of splenic vein or other peripancreatic vessel.

* Pancreatic -ascites: leakage of pancreatic juice into the peritoneal cavitv
with high amvlase level in fluid.

Table 4: CT classification of severity of acute pancreatitis

Grade A
Grade B

Grade C

Grade D
Grade E

Normal pancreas
Focal or diffuse enlargement with
contour irregularity , parenchymal ,
inhomogeneours . Attenuation
dilatation of pancreatic duct. And
foci of small fluid collections within
the gland without peripancreatic
inflammation.
Intrinsic pancreatic abnormalities
with haziness and streaky densities
repreasenting inflammatory changes
in peripancreatic fat.
Single ill defined fluid collection
with no capsule or wall .
Two or more poorly defined fluid
collections or presence of gas in or
adjacent to pancreas.

79

Fig.5: Acute Pancreatitis

Fig.6: Pancreatic Pseudo cyst with thin capsule

80

Fig. 7: A 53 year-old male with pancreatic necrosis. Contrast-enhanced CT

shows no enhancement of the parenchyma in the pancreatic body and tail
arrow).

Fig. 8: CECT abdomen showing a large pseudoaneurysm of the splenic

artery (black arrow).

81

Chronic Pancreatitis :
* Dilatation of the pancreatic duct often in a beaded
*

Decrease in visible pancreatic tissue due to parenchyma.atrophy

* Calcifications, varying from tiny stippled to course.

* Fluid collections, both irttra pancreatic and extra pancreatic
*

Focal enlargement of the pancreas due to benign inflammation and

fibrosis.

* Dilatation of the biliary duct due to fibrosis or mass in the pancreatic head
* Fasical thickening and stranding in the peripancreatic fat.

82

Figure 9: CT: Dilated and irregular Wirsung duct (black arrow) and
pseudocyst in the head of the pancreas (arrowhead).

Figure 10: Mass due to chronic pancreatitis

83

CT Signs of Pancreatic Carcinoma

Hypodense mass that enhances minimally compared with
normal pancreatic parenchyma, due to hypo-vascularity.

Focal enlargement of the pancreas with loss of surface

lobulation

Blunting of the normally tapered uncinate process

Dilated pancreatic duct and/or common bile duct
Atrophy of the pancreas proximal to the tumor
Signs of pancreatitis proximal to the tumor

Figure 11:potentially resectable pancreatic carcinoma

84

Signs of potential resectability:

a. Isolated pancreatic mass with or without dilatation of the

bile and pancreatic ducts,
b. Combined

bile-pancreatic

duct

dilatation

without

an

identifiable pancreatic mass (Pancreatic duct>5 mm in

head or >3 mm in tail; common bile duct >9 mm)
Signs of unresectability:
a. Extension of tumor beyond the margins of the pancreas.
b. Tumor

tissue

invasion

of

adjacent

organs

(spleen,

stomach, duodenum)
c. Enlarged regional lymph nodes (>1.5 cm)
d. Involvement of celiac axis, superior mesenteric vessels,
portal and veins. Signs include:
Thickening of vessel wall
Soft

tissue

obscuring

normally

sharp

definition

of

definition of the vessel by perivascular fat.

Deformity of vessel by adjacent tumor.
Enlargement of collateral vessels
Absence of vessel enhancement

85

e. Metastasis to the liver -usually hypodense and poorly

enhancing.
f. Ascites which is presumptive evidence of peritoneal
carcinomatosis.

Figure 12. Computed tomography images depicting spectrum of localized

pancreatic cancer. Black arrows point to low density tumors; white arrows
point to superior mesenteric vein (SMA) and show the relationship of
tumor to vessel. A: Resectable tumor with clear fat plane around the
SMA. B: Borderline resectable pancreatic cancer with tumor abutting
about half of the SMA circumference. C: Locally advanced, unresectable
disease with completed encasement of the SMA.

86

Islet cell tumors:

None functioning islet cell tumors have three specific CT findings.
Tumors are typically large
They contain calcification
Show enhancement after contrast administration.
The tumor may be homogenous or heterogeneous in density.
These tumors grow slowly and show minimal change in size over
long period.

Functioning islet cell tumors:

These tumors have bimodal distribution .31
Cluster 1: This includes gastrinomas, somatostatinomas, and pancreatic poly
peptide -secreting tumours. These are located to the right of superior
mesenteric artery in 75 % of the case.
Cluster 2: These include insulinomas and glucagonomas.75% case they occur to
the left of superior mesenteric artery.

87

Insulinoma:
Large amount of contrast with mechanical injector is needed to demonstrate
this hyper vascular tumour .Characteristically these tumours are isodense in
non contrast scans and show intense contrast enhancement. The
enhancement may be uniform or target like.

Glucagonoma:
These tumours are hvpodense to the parenchyma in contrast scans and
are usually between 2-6cm in size and 50% case may contain
calcification.
Somatosttinonias:33
These are rare tumours and may be quite large .CT findings are non specific,
they present as soft tissue mass and only 8 cases has been reported. No
mention has been made of vascularity or calcification.

lipoma
Only one case has been reported. Tumour was large (5x7cm) and showed
heterogeneous contrast enhancement.

88

Figure 13: Insulinoma;small enhancing mass

Cystic tumours
Microcystic adenoma:
These tumours consists of honey comb network of innumerable cysts
ranging from millimetres up to few centimetres .CT shows a well
demarcated usually large tumour tumour (10 cm average),low density
mass with enhancing septations.
A central scar may be present which calcifies in 20 % cases.

89

Figure 14: Microcystic adenoma

Mucinous cystic neoplasms:

Mostly occurs in body and tail (75-95%) cases.
CT shows cysts 6 or fewer 2cm or greater .They have thick wall and
septations with papillary projections.

90

Figure 15: Mucinous cyst adenoma

Metastatic tumours11
These can not be identified from primary tumours. However careful history
taking and evidence of tumours helps to characterize these lesions.

91

2.1 Introduction:
Many modalities are currently being used to image the pancreas .None has the
advantage that CT has-it can provide information about the nature of the
pancreatic lesion; whether it is solid or cystic, the size of the lesion, the
location of the lesion and the status of the local structures, Most important is that
CT scan is quick and non invasive and provides a global view of the abdomen
and can guide management planning.
Though CT scanning is a costly examination - in the long run it has proved
time and again that it can provide more accurate information than other non
invasive methods like ultrasound. X-ray and contrast examinations. Role of
diagnostic ERCP is reducing ever}' day as newer and more non invasive
techniques are becoming available.
The main criteria of diagnosis of pancreatic mass are: changes in morphology
of the gland, density of the lesion, presence or absence of calcification and fat as
well as the contrast enhancement characteristics. Involvement of surrounding
structures, lymph.node status, metastasis to liver and ascites are hallmarks of
92

malignant lesion,
The staging of malignant tumours can guide management planning and clearly
divide the patients into two groups: those who will not benefit from the
surgery and those who will benefit from surgery. Though most malignant
tumours are not surgically curable; a great number of patients will benefit from
palliative procedures. CT is also invaluable in follow up of patients after
surgery.

In case of inflammatory lesions; like abscess or pseudo cyst CT can accurately

measure the size of the lesion and thus guide management planning.
Improvements of CT scanner technology had resulted in new generations of
multi-slice scanners where pancreas can be viewed in exquisite detail. High
standard of professional skill has consolidated the role of CT scan in the
diagnosis and subsequent management of pancreatic mass in our country.

93

2.2 AIMS AND OBJECTIVES

Aims:
The aim of this study is to show the accuracy and sensitivity of CT in
demonstration of pancreatic mass, differentiating benign and malignant lesions
and guide management planning.

Objectives:
The objectives were:
I.

To analyze various types of pancreatic masses

prevalent in

Bangladesh.
II.

To differentiate the benign from malignant masses on the basis of

CT findings.

III.

To guide management planning.

IV.

To find out the accuracy and efficacy comparing clinical findings

and other diagnostic studies.

94

2.3 MATERIALS & METHODS

This study represents a prospective study of 55 cases of pancreatic mass, These
patients were selected from Bangabandhu Sheikh Mujib Medical University,
Dhaka Medical College Hospital and Bangladesh Institute of Research and
Rehabilitation in Diabetic Endocrine and Metabolic Disorders; from a period
covering January 2003-June 2003,
Patients were clinically evaluated by a detailed history and a through clinical
examination. All data were meticulously recorded (Appendix-II), Routine blood
examination like ESR, complete blood picture, serum bilirubin , serum
amino transferase, serum amylase, serum lipase were done in respective
institutions.
Serum tumor markers (CA 19-9) were done only in clinically suspected cases.
Ultrasonogram of

all the patients were done in the department of

Radiology and Imaging . Bangabandhu Sheik Mujib Medical University,

CT scan was done by a helical CT scanner at 10 mm slice thickness
95

before and after administration of oral and intravenous contrast,

For oral contrast

60ml iodinated contrast media diluted in 750 ml of

water was given and for intravenous contrast 50ml of non ionic contrast
media like iopamiro 370mg was given by rapid injection.
In necessary cases images were obtained at 2mm slice thickness.
All patients were also clinically reviewed by a gastroenterologists and hepalobiliary pancreatic surgeon. ERCP was done in relevant cases in BSMMU and
BIRDEM Hospital. CT guided and endoscopic biopsy specimens were taken in
appropriate cases.
Exploratory laparotomy was done in a few numbers of the patients having
primary pancreatic neoplasm, even when the imaging labeled some of them to
be inoperable for palliative purpose. During this procedure biopsy specimens
were also obtained.
CT scan findings were evaluated according to the format in appendix-Ill

96

2.4 RESULTS
This study included 55 patients presenting with pancreatic mass. The age of
patient ranged from 12-85 years.
The commonest age group was 51-60 years and 20(36.37%) patients were in
these age groups. The next common age groups were 41-50 years and 11(20%)
patients were in this age group. 8 (14.55%) patients were in the age group of 6170 years, 4(7.28%) were in the age group 21-30yrs and 2 (3.64%) each in age
groups ll-20yrs and 71-80yrs and 1(1.8%) was in the age group 81-90 yrs.

97

AGE GROUPS

36 (65.5%) patients in this study group were male and 19(34.5%) patients in
this study group were female.

98

GRAPH 2: Sex distribution of the study. [n=55]

Different types of pancreatic masses were diagnosed by CT scan. The

distribution of different pancreatic masses are shown in Table 2.1
Table 2.1: Distribution of different pancreatic masses (n=55)
Pancreatic Mass

Number

Percentage

Inflammatory mass (Phlegmone)

3"

5.46%

Necrosis of pancreas

3.6%

Pancreatic abscess

7.28%

Pancreatic pseudocyst

11

20%

Chronic focal pancreatitis

3.6%

Tuberculosis

1.8%

Pancreatic Carcinoma

23

41.8%

Metastastic lesions

16.3%

The commonest pancreatic mass found in CT images was pancreatic carcinoma.

23(41.8%) patients were diagnosed with pancreatic neoplasm. Next
common presentation was pancreatic pseudocyst, 11(20%) patients presented
with this lesion. Secondary deposits in the pancreas were present in 9(16.3%)
patients. 4(7.28%) patients presented with pancreatic abscess, 2(3.6%) with
99

necrosis of pancreas and 3(5.4%)

patients presented with inflammatory mass or phlegmone.
Chronic focal pancreatitis presenting as a pancreatic mass was present in 2
(3.6%) patients and 1(1.8%) patient was diagnosed as pancreatic tuberculosis.

Among the 55 patients presenting with pancreatic masses, inflammatory mass

was present in 23 (41.3%) and neoplastic 32(58.18%). Primary neoplastic mass
was 23 (41.8%) and secondary deposits were 9( 16.3%).

Graph 3: Distribution of inflammatory and neoplastic masses

Among the inflammatory masses most patients belonged to the age group 3140 years. 7(30.4%) patient were in this age group. 6 (26.1%) patients were in the
age group 41-50 years. Next common age group was 21-30 years and 4(17.4%)
100

patients were in this age group.4 (17.4%) patients were also in the age group
51-60 years. 2 (8.70%) patients were in the age group 11-20 years.

AGE GROUPS
Graph 4: Age Distribution of Inflammatory mass

In case of malignant lesions of pancreas, no patients presented with malignant

lesions of pancreas below 40 years.
4(12.5%) patients were in the age groups 40-50 years. 18(56.25%) patients
belonged to the age groups 50-60 years and 6 (18.75%) patients in age groups
60-70 years and 4(12.5%) patients above 71-80 years. And 1(3.1%) patient was
above 80yrs.

101

AGE GROUPS
Graph 5: Relative age incidence of neoplastic lesions of pancreas

Among the 23 patients with inflammatory lesions 14(60.86%) were male and
9(39.13%) female.
Among the 32 patients with neoplastic lesion of pancreas 10 (31%) was female
and 22(68.75%) were male.

GROUPS
GRAPH 6: Sex incidence of patients presenting with neoplastic
and inflammatory pancreatic mass
102

21 (38%) patients had positive history of smoking, 11(20%) patients had

gallstone diease.8 (14,5%) patients were diabetic and 5( 9%) patients had
history of trauma and 3(5.4 %) patients abdominal CT was to in the staging
of other malignancy and 1(1.8%) patient had history of alcohol intake.

Table 2,2: Distribution of different causative factors of pancreatic

mass(n=55)
CAUSATIVE FACTOR
Smoking
Gall stone disease
Diabetes
History of trauma

PERCENT
38%
20%
14%
09%

Other malignancy

5.4%

Alcohol intake

1.8%

103

The common presenting complaints of the patients with inflammatory

pancreatic mass were pain 80%, vomiting 69% abdominal mass 47%
abdominal distension 38%, weight loss 4% and fever 5%.

Table 2.3: The complaints of patients with inflammatory pancreatic mass

(n=23)
COMPLAINTS

PERCENTAGE

Pain

80%

Nausea /Vomiting

69%

Palpable abdominal mass

47%

Abdominal distension

38%

Weight loss

4%

Fever

5%

Presenting complaints of patients with primary or secondary neoplastic

pancreatic lesion were: Obstructive jaundice 82%, weight loss 66%, cholangitis
63%, pain 45%, renal impairment 29%, coagulation disorder 28%, and
incidental finding in the diagnostic workup of other malignancy 3%.

104

Table 2.4: Presenting complaints of Patients with neoplastic

pancreatic mass (n=32)

COMPLAINTS

PERCENTAGE

Obstructive Jaundice

82%

Weight loss

66%

Fever with Jandice

Pain

63%
-45%

Coagulation

28%

Renal impairment

29%

Incidental finding in staging of other malignancy

.3%

Serum amylase was raised in 2(8.6%) patients and lipase 4 (21%)

patients .Ultrasound could detect the lesion in 19(82%) patients but did not
yield satisfactory result in 4 (17%) patients.

Table 2.5: Investigations findings of inflammatory pancreatic lesions

(n=23)
DIAGNOSTIC TEST

PATIENTS

PERCENTAGE

Raised serum amylase

8.6%

Raised serum lipase

21%

Ultrasound detectable lesions

19

82%

Ultrasound negative

17%

105

GRAPH 7: Diagnosis of inflammatory mass by USG

11 (47%) patients presented with pancreatic pseudocyst.4(17%) patients

presented with inflammatory mass (phlegmone). 3(13%) patients with
pancreatic abcess, 2 (8.6%) patients presented with pancreatic necrosis and
2(8.6%) with chronic focal pancreatitis and 1 (4.3%) presented with
tuberculosis of pancreas.
Table 2.6: Distribution of inflammatory mass.(n=23)
MASS

PATIENT NO

PERCENT

11

47%

Phlegmone

17%

Pancreatic abscess

13%

Necrosis

8.6%

Chronic focal pancreatic

8.6%

Pancreatic tuberculosis

4.3%

Pancreatic pseudocyst

106

In this study there were 35 cases of solid pancreatic mass. Most of the solid
pancreatic masses were situated in the head; 24(68%) patients presented with
mass in the head of pancreas and in 4 (11%) patients mass was located both head
and body and in 4( 11% ) patients mass arose from body and in 3(8 %) patients
in tail.

GRAPH 8: Distribution of solid pancreatic mass (n-35)

USG and CT were done in all 35 patients. 25 patients had ERCP and 15
patients had raised CA19-9 or CEA.

Table 2.7: Distribution of investigations (n=35)

INVESTIGATION

No

USG

35

100

CT

35

100

ERCP

25

71

Tumor marker

15

42
107

Solid masses involving the pancreas were 35 in number. Among these CT

diagnosed 23 cases as pancreatic carcinoma and 6 as metastasic tumor
due to the presence of tumor in other organs like: lung, kidney andGB.
One patient with chronic focal pancreatitis was labeled as pancreatic
carcinoma. In one patient both were given as possible diagnosis.
1 patient of pancreatic tuberculosis was also diagnosed as pancreatic

carcinoma. In case of the 3 remaining patients: 1 proved to be metastasis

from cholangiocarcinoma, 2 periampullary carcinoma invading the
pancreatic head.

Table 2.8: Comparison between CT and Biopsy findings in patients

with solid pancreatic mass (n=35)

NUMBER OF

BIOPSY

CT

23
PATIENTS

65%

Ca pancreas

Ca pancreas

5.7%

Chronic pancreatitis

1 : Ca pancreas
1 :D/D chronic

2.8%

TB pancreas

pancreatitis
CA pancreasCa

17%

Metastatic tumor

Metastatic tumor

5.7%

Metastatic tumor

Ca pancreas
112

108

Over all accuracy in detection of the tumors was 100 % however the accuracy
of diagnosis of nature of solid pancreatic mass this series was 82%.
In case of masses due to primary pancreatic carcinoma; all produced detectable
change in the contour of pancreas.
22 (95%) masses were hypo dense to the rest of the pancreas. 1(5%)
mass was isodense to pancreas.
All the masses; 23 (100%) were hypodense to pancreas after contrast.
Calcification was present none of the masses. 5(22%) masses showed necrosis
or cystic degeneration.
Associated dilatation of pancreatic duct was present in 10(43 %) of the cases.
Biliary duct dilation was present in 16(69%) cases.
Vascular involvement was present in 13 (56%).
Celiac axis was involved in 4(17%) patients, Superior mesenteric vein was
involved in 3(13%) patients, Portal vein in 2 (8%) patients and splenic vein
in 2 (8%) and in 2 (8%) patients there was more than one vessel
involvement.
The following pattern of local organ involvement was observed: Stomach
in 1(4%), kidney in 1(4%) patient, retroperitoneal fat in

4(17%),
Lymph nodes were detectable in 9(39%) patients; ascites was present in 8(34%)
patients and metastasis in the liver in 10(43%) patients.

109

Table 2.9: Distribution of CT Findings (n=23) in primary pancreatic

tumors
CT FINDING

NO

PERCENT %

Contour change

23

100

Hypodense mass

22

95

Isodense mass

Hypodense after contrast

23

100

Calcification

Necrosis

22

Pancreatic duct dilatation

10

43

Biliary obstruction

16

69

Vascular involvement

13

56

Local organ involvement

26

Ascitcs

34

Lymph nodes

39

Liver metastasis

10

43

110

Only 19(4.3%) patient presented with stage I lesion which was resected, 3
(13%) patients stage II lesions, 9 (39%) patients had stage III lesions and
the 10(43%) patients had stage IV lesions.
Table 2. 10: Staging of primary pancreatic neoplasm (n= 23).

STAGE

NUMBER

Stage-I

4.3

Stage- II

13

Stage-Ill

39

Stage-IV

10

43

In only one case the tumor was resectable.

Surgery was done in 2 cases of stage II tumors; in one case of these,
there was evidence of peritoneal spread. So the CT staging was not
accurate. 1 received chemotherapy. ERCP was done in 1 case.
In 9 patients with stage III tumors; ERCP was done in 7 cases but failed in
2 cases. 4 cases received chemotherapy also. In 3 cases chemical
splanchniactomy was done. Two cases could not be followed up after
diagnosis.
In case of 3 stage IV tumor, chemical splanchniectomy was done and in 3
cases, in 4 cases palliative ERCP was done. ERCP failed in two cases.

111

Only supportive care was done in 3 cases. In 2patients no follow up was

possible after diagnosis.

GRAPH 9: Distribution of different treatments offered to patients

112

2.5 DISCUSSION
Abdominal CT is becoming increasingly important imaging modality used for
diagnosis of masses of the pancreas. It has the advantage of being quick, non
invasive and having high accuracy.
Helical CT scanning was done to evaluated 55 patients presenting with
pancreatic mass in BSMMU, DMCH and BIRDEM hospital. 10 mm slice
thickness was generally used; however 2 mm slices were taken wherever
applicable. Oral and intravenous contrast was given to all patients. This
study was carried out over a period of 6 months commencing from January
2003.

The patients were form different age groups having different regions and
occupation.
The age of the patient ranged from 12-85 yrs.
Highest number of patients 20(36.37%) were in the age group 51-60yrs,
followed by 11 (20%) patients in 41-50 years. 8(14.55%) patients were in the
age group of 61-70yrs.4 (7.28%) patients were in age group 21-30 years and
2(3.64%) patients each in age groups of 11-20 years and 71-SOyears .1 (1.8%)
patient was over 80 years of age.
32(58%) patients presented with primary or metastatic tumor .18 (56%) of
them were in the age group of 5^-6^ decade. Followed by 6(18.5%) patients in
113

the 6th-7th decade No patient with neoplastic lesion in this

study was below 40 years of age. Pancreatic carcinoma occurs in earlier age
group in our country than in western world.
According to the study of Gordis et al

35

' pancreatic carcinoma is more

prevalent in 6th -7fe decade in USA.

Patients presenting with inflammatory masses were mostly in 3 ~4 fe decade.
The youngest patient in this study group was a 12 year old boy; he presented
with a post traumatic pseudocyst.
i
Most of the patient in this study was male.
Percentage of male and female patients presenting with inflammatory mass
was 60% and 39% and neoplastic mass was 68%-31%. Pancreatic tumours
are more common in male. Gordis et al 3" also found that pancreatic
carcinoma was more common in male than female. However in case of
metastatic tumor the sex incidence in this study were equal.
In this study 23 (41%) patients presented with inflammatory mass and 32
(58%)

with

neoplastic

mass,

which

included

both

primary

adenocarcinoma and metastatic lesion.

38% patients in this study were smokers. History of trauma was present in
9% of patients. Gallbladder stone in 20% patients. 1(1.8%) patient give
positive history of alcohol abuse.
In case of inflammatory masses of pancreas; history was short. Presenting
complaints were; vomiting / nausea 69%, pain 80% cases, abdominal mass
47%, abdominal distension 38%, weight loss 4% and fever 5%,

114

These presenting complaints correlate well with the studies of Silverstein etal 36
and ElmasN 37 .
Overall raised serum amylase and lipase was present in 2(8.6%) and 4(17%) of
cases respectively. This correlates with one finding of Elmas et al

37

, who

concluded that serum lipase is a serum better maker than amylase in patients
presenting after 3 days of symptom.
The

distributions

of

the

inflammatory

masses

were

11 (47%)

pseudocysts, in 4 (17%) cases of phlegmone, 3 (17%) cases abscess, 2 (8.6%)

cases of necrosis.2 (8.6%) focal pancreatitis and 1 (4.3%) tuberculosis.
Ferucci et al40 also reported cases where focal pancreatitis was mistaken for
pancreatic carcinoma. Ali et al,39 in their study also found chonic focal
pancreatitis in 15% of patients suspected of having pancreatic carcinoma.
Pancreatic tuberculosis is rare but not perhaps in our country. In the study of
Ali et al,39 5 cases mimicking carcinoma head of pancreas was reported.
Gottfried et al41 also reported one case of isolated tuberculosis of pancreas
mimicking carcinoma head of pancreas. Lankisch42 reported one case of painless
acute pancreatitis mimicking pancreatic carcinoma.

Ultrasound could diagnose 19 (82%) of the 23 inflammatory masses, in

4( (17%) cases the lesions could not be identified due to gas and 1 cases USG
missed diagnosis . This finding correlate well with the finding of Elmas et al 37
who found the accuracy of 85% at USG. But in a study of 45 patients, Jeffery38
found the accuracy of ultrasound to be 78 % in acute cases.

115

Most common presenting complaints of patients neoplastie masses was

Jaundice. 82% patients presented with jaundice. Other complaints were fever
with jaundice in 63%, renal impairment 29%, weight loss 66% and pain 45%,
coagulation disorders 28% and as incidental finding in the diagnostic work up
of other malignancy 3 %. In a study done of 60 patients with mass in the head of
pancreas by Ali et al,39 84% patient presented with jaundice and 63% with
Cholangitis.
In our study 35 patients were diagnosed by CT of having solid pancreatic mass.
We did not find any cystic tumors.

In our study 24(68 %) of solid masses are situated in the head.4 (11%) tumors
were situated in both head and body, 4(11%) were situated in the body and 3
(8%) in the tail. Ultrasound detected 31 of the 35 solid pancreatic masses and
accuracy was 91%. The accuracy rate of ultrasound in our study group is
higher compared to the study of Pantti

4?

and colleges whose accuracy was

88%.We missed 2 tumors in tail region and one tumor in head measuring 4.5cm
by ultrasound. In 15 patients serum markers were done and positive .ERCP was
done in 25 patients mostly for stenling purposes and in 5 cases for diagnostic
reasons. In our study almost all tumors presented with change of contour. This

is possibly due to the fact patients present late in our country and most
tumors are large at presentation. In a study of 72 masses by Muranaka et al43
and most tumors between 4-6 cm.

116

22 (95%) masses were hypo dense to the rest of the pancreas.

1(5%) mass was isodense to pancreas. Ariyama et al44' also reported few cases of
isodense pancreatic mass .All the masses; 23 (100%) were hypodense to
pancreas after contrast. Calcification was present none of the masses. In fact
calcification is very rare in adenocarcinoma of pancreas and its presence
suggests other rare pancreatic tumor, especially nonsecreting islet cell tumor,
Niederu et al 45.5(22%) masses showed necrosis or cystic degeneration.
Associated dilatation of pancreatic duct was present in 10(43 %) of the cases.
Biliary duct dilation was present in 16(69%) cases. Ward el al 46 also concluded
that pancreatic duct dilatation is a common finding in head masses .Vascular
involvement was present in 13 (56%).
Celiac axis was involved in 4(17%) patients, Superior mesenteric vein was
involved in 3(13%) patients, Portal vein in 2 (8%) patients, splenic vein in 2
(8%) and in 2 (8%) patients there was more than one vessel involvement.
The following pattern of local organ involvement was observed:
Stomach in 1(4%), kidney in 1(4%) patient, retroperitoneal fat in 4(17%).
Lymph nodes measuring >1.5 cm were detectable in 9(39%) patients; Ascites
was present in 8(34%) patients and metastasis in the liver in 12(48%) patients.

Only 1 (4.3%) patient presented with stage I lesion which was resected, 3 (13%)
117

patients stage II lesions, 9 (39%) patients had stage III lesions and the 10 (43%)
patients had stage IV lesions.
Surgery was done in 2 cases of stage II tumors; in one case of these,
there was evidence of peritoneal spread. So the CT staging was not
accurate.
Castillo el al 48 also reported that 20-30% of cases peritoneal metastasis
may be present without any imaging and their presence is documented by
peritoneal washing during laparoscopy. ERCP was done in lease.
In 9 stage III tumors; ERCP was done in 7 cases but failed in 2 cases. Two
cases could not be followed. 4cases received chemotherapy also. Chemical
splanchniectomy was done and in 3 cases. 2 cases could not be followed up
after diagnosis.diagnosis.
In case of 3 stage IV tumor, chemical splanchniectomy was done, in 4 cases
palliative ERCP was done. But ERCP failed 2 cases. Two cases could not be
followed. 3 cases were managed with supportive care.
Over all accuracy in detection of the tumors was 100 % however the accuracy
of diagnosis of nature of solid pancreatic mass this series was 82%.
In a series of Pantti 47and colleagues the accuracy of CT was 96% and efficiency
97% and Specificity was 96.9% cases.

Freeny

48

and colleagues found the accuracy of CT 97-98% for detecting

118

pancreatic carcinoma .All these studies were done on primary neoplasms of

pancreas and both these studies included small tumors measuring < 2cm.
Common tumors which had metastatic deposit to pancreas were: Gall bladder
mass in 4 cases, 2 cases of Cholangiocarcinoma, one case of bronchogenic
carcinoma one renal mass and one periampulary lesion.Anderson49 and
Lee et al50 also found that metastasis to pancreas from Gall Bladder mass was
most common.
i

Though only one of the patients presented with a potentially curable tumor,
this reflects that pancreatic tumors are detected late in our country due to the
lack of awareness and unavailability diagnostic facilities.
In the western world 20% of respectable tumors are .detected, Wolfman et al51
and Hyoty et al52.
However a variety of palliative procedures are being offered to the patients
to improve the quality of life.
CT Imaging scan play a vital role in guiding the management of these patients.

119

2.6 SUMMARY
CT

scanning

is

increasingly

replacing

the

invasive

diagnostic

examinations like ERCP for imaging of the pancreas. Specialists like

gastroenterologist and hepatobiliary and pancreatic surgeons are relying on CT
scan more and more to evaluate patients with pancreatic mass lesions and
guide management planning.
The aim of this study show the role and accuracy of CT scan in
demonstrating the diverse causes of pancreatic mass and subsequently directing
management planning.
A prospective study 55 cases were evaluated in BSMMU, BIRDEM
HOSPITAL and DMCH for CT scanning. Helical CT scan was performed
at 10mm slice thickness before and after oral and intravenous contrast. 2mm
slice thickness was used whenever needed. Axial images of the abdomen were
taken.
The age of the patient varied between 12 to 85 years. Maximum number of
patients 20 (36.37%) were in the age group of 51-60yrs. Incase of
inflammatory mass, common age group was 31-40 years and neoplastic mass
common age group was 51-60 yrs. 65.5% of the total study group was male and
34.5% were female.
Different types of pancreatic masses were diagnosed in this study, 58% of the
120

masses were inflammatory and 41% were neoplastic.

The distribution of the mass was: inflammatory phlegmone in 3 (5.4%) cases,
necrotic mass in 2(3.6%), abscess in 4(7.28%) cases, pseudocyst in 11(20%)
cases, chronic focal pancreatitis in 2(1.8%)cases, pancreatic carcinoma
23(41%)cases and metastatic lesion in 9(16%) cases.
38% of the patients were smokers and 20% patients had gall stone disease,
14% were diabetic. 9% had history of trauma.
Commonest complaints of inflammatory mass was pain in 80%, nausea
vomiting 69% cases and palpable mass 47%. Commonest complains of
neoplastic mass was obstructive jaundice 82% cases and cholangitis in 63%
cases.
Ultrasound could detect and characterize 19(82%) of the inflammatory masses
and 31(91%) of the neoplastic masses.
Of the 35 solid masses suspected of being primary or metastatic lesions to the
pancreas most were situated in the head; 22(68%).
23(65%) patients were diagnosed as carcinoma pancreas and 6 (17%) patients
as metastatic tumor by both by CT and biopsy. 1(2.8%) case of pancreatic
tuberculosis and 1 case of chronic focal pancreatitis and 3(5.7%) cases of
metastatic tumor was diagnosed as carcinoma pancreas in CT. In one case
chorinic focal pancreatitis and carcinoma were offered as differencial diagnosis.

121

Common tumors with metastasis to pancreas were GB tumor and

Cholangiocarcinoma.
Overall accuracy of detection was 100% but specificity was 82%.
All the solid masses produced contour changes and were hypo dense after
contrast. Only 1 mass was iso-dense before contrast. 5(22%) showed
necrosis, and 10(43%) were associated with pancreatic duct dilatation 16(69%)
with bile duct dilatation. Vascular involvement was seen in 13(56%) of the
masses. Most advanced masses showed retroperitoneal involvement 4(17%),
local organ involvement was also present, stomach in 1(4%) case, kidney in
l(4%)case, lymph nodes in 9(39%) cases and liver metastasis in 10(43%) case
and ascites in 8(34%) case.
1(4.3%) patient was in Stage I lesion, 3 (13%) in stage II lesion and 9(39%) in
Stage III lesion and 10 (43%) in stage IV lesion.
Surgery was possible in 4 cases and in one case CT could not detect peritoneal
metastasis.
In other cases ERCP, chemotherapy, chemical splanchniectomy and only
supportive care was taken 3 cases and 4 patients could not be followed up
after diagnosis.

122

2.7 CONCLUSION
CT scanning is playing an increasingly dominating role in the diagnosis of
pancreatic masses. The advantage of CT is that it is quick, accurate, non
invasive, vital for staging and important also for management for both neoplastic
and non-neoplastic lesions of the pancreas. It offers a global view of abdomen,
which cannot be accessed by other modalities like endoscopic ultrasound. ERCP
is increasingly used in cases where intervention is contemplated. Ultrasound is a
good modality for screening purposes but has many limitations. MRI and MRCP
has found to de as accurate as CT in detecting pancreatic mass, Sheridan53 '
however in accessing resectability MRI is better. But new generation of
multislice CT Scanners offer an exquisite detailed view of pancreas and CT will
eventually become indispensable in imaging and management of pancreatic
disease.
Though both benign and malignant masses of pancreas cause considerable
morbidity and mortality. However many different forms of treatment and
palliative procedures are being offered to the patients.CT is invaluable part of the
clinical management.CT scanners are becoming available in different parts of our
country .So training of the radiologist is essential. More extensive study on
involving larger number of patients and longer period will enable us to incidence

123

of not only common lesions but rare and functional tumors as well.

BIBLIOGRAPHY
1.

Me Minn R M H ed 1990. Last's Anatomy 9th ed. Edinburgh: Churchill

Livingstone, pp 351-355.

2.

Datta Ka 1995. Essentials of Human Anatomy. Calcutta: Current Book

International. Vol 2 pp 272-278.

3.

Snell RS 1997. Clinical Anatomy for Medical Students 3rd ed. Boston:
Little Brown pp.249-250
i

A.

Moore K L 1982. The Developing Human 3rd ed. Philadelphia: WB Saunders

Company, pp 234-235

5.

Singh Inderbir 1987. Textbook of Human Histology. New Delhi:

Jaypee. pp 226-227.

6.

Junqueria C L, Carrreiro J, Kelly R 0 (eds) 1995. Basic Histology 8 th

ed. London: Appleton with Lange. pp 303-306.

7.

Ganong W F 1995. Review of Medical Physiology. 16th ed. Norwalk:

Appleton and Lange. pp 302-322, 428-432.

8.

Kumar P, Clarke M 2000. Clinical Medicine 4th ed. Edinburgh: W B

Saunders. pp 900-903, 959-989

9.

Friedman Scott L, Me Qua id R K, Grendell J H (eds) 2003. Current

Diagnosis and Treatment in Gastroenterology 2nd ed. New York: Me
Graw Hill, pp 489-495, 496-509, 509-520.

124

10.

Murfitt J, Whitehouse W R 2003. In: Sutton D ed. Text Book of

Radiology and Imaging 7th ed. London: Elsevier Science Ltd. pp 787824.

11.

Haaga J R, Lanzieri C F, Gilkeson R C (eds) 2003.CT and MR Imaging

of the Whole Body 4th ed. St Luis: Mosby. Vol 2 pp 1395-1486.

12.

Frenny P 1998.In: Grainger R G, Allison D (eds). Textbook of Radiology

3rd ed. New York: Churchill Livingstone. Vol 2 pp1269-95.

13.

Webb R, Brant W E, Helms C A (eds) 1998. Fundamentals of Body CT

2nd ed pp 223-235.

14.

Levitt R G, Geisse GG, Sagel S 1998: Complementary use of

ultrasound and compted tomography in studies of the pancreas and
kidneys. Radiology 126:149.

15.

Kreel L, Sandin B 1973: Changes in the pancreatic morphology with

age. Gut 14:952.

16.

Kolmann S F, Swensen T, Vatn M H, Larsen S 1982: Computed

tomography and Ultrasound of normal pancreas. Act. Radiol [Diagn]
(Stockh) 23:443.

17.

Ramzi S, Rotran RS, Kumer V, Collins T (eds)1999. Robbins

Pathological Basis of Disease 6th ed. Philadelphia: WB Sanders
Company, pp 981-1010.

18.

Das K

1982.Clinical methods of Surgery 12 th ed. Calcutta: J P

Brothers, pp 300-302
19.

Karne S, Gorelick FS 1999: Etiopathogenesis of Acute pancreatitis.

125

Surgical Cliniques of North America 79(4): 699-707.

20.

McKay CJ, Imrie C W 1999: Staging of acute Pancreatitis; is it important.

Surgical Cliniques of North America 79(4): 733-741.

21.

Fried M A 1998.Me Grahan J P, Goldberg B B. Diagnostic Ultrasound a

Logical Approach. Philadelphia: Lippincott- Raven, pp 761-785.

22.

Federle M P, Jeffrey R B, Crass RA, Van Dalen V 1981: Computed

tomography of pancreatic abscesses. AJR 136:879.

23.

Hurley J F, Vargish T 1987: Early Diagnosis and outcome of

Pancreatic Abscesses in Pancreatitis. Am Surg 53:29-33.

24.

Kitai I C, Harid A C, Mategna J A 1987. Tuberculosis of pancreas

mimicking pancreatic carcinoma: A case report.

Cent Afr J Med

33:19-22
25.

Haddard F S, Ghossain A, Sawaya E, et al 1987. Abdominal

Tuberculosis. Dis Colon Rectum 30:724-35.

26.

De Miguel F, Belfran J, Saba S JA, et al, 1985: Tuberculous

Pancreatic abscess. Br J Surg 72:438.
27.Mathieu D, Vasile N, Dibie C et al, 1985 : Portal Cavernoma :Dynamic CT features and
transient differences in hepatic attenuation. Radiology 154:743-748

28.

Muranaka T, Teshima K, Honda H et al, 1989: Computed tomography

of pancreatic metastasis from distant sources. Acute Radiology 30:
615-619, 1989

29.

Balthaza E L, Ramon G T C, Naidich D et al 1985 : Acute Pancreatic

Prognostic value of CT. Radiology, 156: 767-72

30.

Eelkema E A, Stephans D H, Word E M et al, 1984: CT features of

nonfunctioning Istel cell tumor AJR 143: 943.
126

31.

Yulbilla A L, Hajan S I 1995: Islet cell tumors of pancreas. Arch Palhol

99: 204-207,

32.

Breatnach E S, Han S Y et al 1985: CT evaluation of glucagonomas J

Comput Assist Tomogr 9: 25.

33.

Robert L Jr. Dunnick N R , Foster W I, Jret et al 1984:

Somatostatinoma of endocrine Pancreas: CT Findings. J Comput
Assist Radiology 8: 1015

34.

Tham R T , Falke T H M et al 1989: CT and M R imaging of advanced

Zollinger - Elison syndrome. J Compt Assist Tomogr 13: 821-828

35.

Gordis L, Gold E B 1986. Epidemiology and Etiology of pancreatic

cancer. In: Colman V W L ed. The exocrine pancreas-.biology,
pathophysiology and disease. New York: Raven pp 621-36.

36.

Silverstein W. Iskoff M B, Hill C, Me Barkin J 1981: Diagnostic

Imaging of acute pancreatitis: prospective study using CT and
sonography AJRVol 137 pp 497-502.

37.

Elmas N 2001: Role of diagnostic radiology in pancreatitis. Eur J

Radiolo38*2):120-32

38.

Jeffrey R B 1989. Sonography in acute pancreatic: Radiol Clin North

Am: Vol27pp5-17.

39.

Ali M et al, 2003: Evaluation & management of clinically labeled

carcinoma of head of - a prospective study of 60 patients. Bang Med
res. Coun. Bull 29(9).

40.

Ferruci J R, et al 1979: Computed body tomography in chronic

pancreatitis .Radiology 130:175.
127

41.

Gottfried F, Spengler U et al, 1995: tuberculosis of pancreas

masquerading as a pancreatic mass. Am J od Gastroenterol Vol 90
(12)2227-22230.

42.

Lankinch P G et al 1994: Painless acute pancreatitis mimicking

pancreatic carcinoma. Pancreas Vol 10(4) 413-414.

43.

Muranaka T, Barkin K 1995: Computed tomography of pancreatic

mass: study of 72 cases. Radiology 50: 456-471

44.

Ariyama J et al, 1980: Critical comparison of the methods of

examination for the diagnosis of pancreatic carcinoma. ROFA 133:6

45.

Niederau C, Grendell J H. Diagnosis of pancreatic carcinoma Imaging

techniques and tumor markers. Pancreas 7(1) ; 66-86 1992

46.

Ward E, et al 1983: Computed tomographic characteristics of

pancreatic carcinoma analysis of 100 cases. Radiographics 3:547.

47.

Pentti A et al, 1992: A prospective study of the value of Imaging,

serum markers and their combination in the diagnosis of pancreatic
carcinoma in symptomatic patients. Anticancer Research 12:2309-

48.

Freeny P C et al, 2001: Pancreatic Carcinoma imaging update. DigDis19(1):37-4.

49.

Anderson G 2000: GallBladder Mass: imaging update. Anticancer

research 21:45-9.
x

50.

Lee S I, Glen R, Robin E 1999: Obstructive jaundice a study of 100

cases. Radiol Clin North Am: Vol 22 pp 45-49

51.

Wolfman N T et al, 1985: Pancreatic carcinoma Computed tomography

sonography and Pathologic findings. Radiology 170:171-77.
128

52.

Hoyoty M K 1991: Computed tomography is important in assessing

resectability in pancreatic carcinoma even after ultrasonography.
Ann Chir Gyneacol 8 (3)259-62.

53.

Sheridan M B, Ward J, et al 1999: Dynamic contrast enhanced MR

imaging and dual-phase helical CT in the preoperative assessment of
suspected pancreatic cancer: a comparative study with receiver
operating characteristic analysis. AJR 173(3): 583-90.

129

APPENDIX II

DATA COLLECTION SHEET

1.

Particulars of the patient:

Name:
Age:
Sex:
Occupation:
Address:

2.

History
Chief complaints:
H/O present illness:
H/0 past illness:

3.

General examinations:
Appearance
Anemia
Jaundice
Pulse
BP
Heart
130

Lung
4.

Local examination:
Liver palpable/Not palpable
GB
Lump
Skin change

5.

Lab investigation results:

6.

Provisional diagnosis:

7.

USG evaluation:

8.

ERCP findings if available

9.

Biopsy results:

10.

Operative finding in surgical cases:

11.

Final diagnosis:

131