1.1. INTRODUCTIONThe pancreas is retroperitoneal organ. The exocrine and endocrine parts of the a land play a vital role in the metabolism of carbohydrate, fat andprotein. 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 posteriorabdominal wall behind the peritoneum. It lies behind the stomach andseparated from it by the cavity of lesser sac. It crosses the trans pyloricplane.The pancreas is a mixed gland containing of both exocrine and endocrineparts. The exocrine portion of the gland produces enzymes that arecapable 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.

ShapeIt 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.

SituationIt occupies the posterior part of epigastrium and left hypochondrium.

SizeLength:12 -15 cm.Breadth:3 -4cm.Thickness:1.5 -2cm.Weight:80-90 gms

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

HeadIt 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.RelationsAnteriorTransverse 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.PosteriorInferior vena cava and both renal veinsRight sympathetic trunk, right psoas majors, bodies of li & 1^Right curs of diaphragm, right middle supra renal, renal and gonadalarteries.Celiac ganglionAzygos vein.Bile ductAbdominal aorta - behind the uncinate processUpper Border1st part of duodenumNeckIt connects the body with head. It is 2 cm. long. It presents anteriorand posterior surfaces and upper and lower bordersRelationsAnteriorCovered by peritoneum and is related to pyloric end of stomach PosteriorSuperior mesenteric vein and portal vein Upper border I * part of duodenum Lower borderRoot of transverse mesocolon BodyBody 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.

RelationAnterior Stomach separated by stomach surface bedInferior surface Duodeno jejuna! flexure Coils of jejunum Left colic flexure Posterior surfaceAbdominal aorta with the origin of superior mesenteric arteryLeft crus of diaphragmLeft psoas with sympathetic trunkLeft supra renal glandLeft kidney across its hilumLeft renal vessels and pelvis of left ureterLeft supra renal and gonadal veinsSplenic veins which separate the above mentioned structures frompancreasSuperior borderIt presents a conical projection called tuber omentaleThe coeliec artery veins above the tuber and hepatic artery to the left oftuber

Anterior borderIt gives the attachment of root of transverse mesocolonInferior borderSuperior mesenteric vessels under cover of right end of this bordgrTailIt 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 PANCREASPancreatic DuctThe exocrine pancreas deliveries its secretions via pancreatic ductsMain Pancreatic duct (Duct of Wirsung)It begins in the tail by the union of a number of smaller ducts. This ductcrosses left to right through midway between upper and lower marginsclose 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 toreach posterior medial wall of 2nd part of duodenum. The duct pierces theduodenal wall and meets bile duct to from ampulla of Vater. This opensinto the summit of major duodenal papilla about 8 to 10 cm distal topylorus.

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.Neuro Vascular Supply

Arterial supplyHead and neckVentral and dorsal anatomosis of superior and inferior pancreaticduodenal artery.Body ami tail\Pancreatic branches of splenic artery

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

Lymphatic drainageHead and neckVentral and dorsal groups of pancreatico duodenal lymph nodes.Body and tailPancreatico splenic lymph nodes.The lymphatics from these nodes terminate into the coeliac and superior mesenteric groups of pre aortic lymph nodes.Nerve SupplySympathetic derived from celiac and supper mesenteric plexuses. Parasympathetic supply is from both vagal nerves.1.3 DEVELOPMENT OF THE PANCREASThe 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 C- shaped, 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 thehead 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 atthe 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.

FIG 3 : DEVELOPMENT OF PANCREASMalformations 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. 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.

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.Endocrine pancreasThis 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 ofLangerhansHuman pancreas has one million islets.Islets are richly supplied by blood through dense capillary plexus andseparated 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 thistype. 8 or D cells: These secrete hormones gastin and somatostatinPP cells: These secrete pancreatic polypeptide,'r.Dl cells: These contains vasoactive intestinal polypeptide.The A cells are situated at the periphery and B cells are in the centre ofislets.The B cells are stained by aldehyde fimchin the alpha cells by acidfunchin . The D cells stain black with Silver salts (i.e. agyrophill).

FIG 4 : PANCREAS (SECTIONAL VIEW)

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 pancreasAt least 4 peptides with hormonal activity are secreted by the Islets of Langerhans of pancreas. They are: Insulin Glucagon Somatostatin Pancreatic polypeptideInsulin and glucagon have important function in the regulation ofintermediately metabolism of carbohydrates, proteins and tats.Somatostatin plays are important role in the regulation of islet cellsecretion.The function of pancreatic polypeptide is unsettled.

INSULIN StructureInsulin is a polypeptide hormone containing 2 chains of ammo acids linked by disulfide bridge.

Biosynthesis and secretionIt 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.

MetabolismThe half-life of insulin in the circulation is about 5 minutes.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 andkidneys.Effects of insulinThe 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 sensitivecells.Intermediate (minutes)Stimulation of protein synthesisInhibition of protein degradationActivation of glycogen synthesisInhibition of phosphorylase and gluconeogenic enzymesDelayed (hours)Increase in mRNA for lipogenic other enzymesConsequence of insulin deficiencyFar-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, weightloss 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 MetabolismDiminished protein synthesis and accelerated protein catabolism leads to negative nitrogen balance.

Fat MetabolismAcceleration of lipid catabolism and increased formation of ketonebodies 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 ofblood glucose directly on B cells of pancreas.Others are amino acids, intestinal hormomes (GIF, gastrin).Inhibitors of insulin secretion are- somatostratin, and adrenergicstimulators (non epinephrine, epinephrine) B blockers (propanalol).

GLUCAGONHuman glucagon is a linear polypeptide with molecular weight of 3485.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 GluconeogenesisLipolytic

Ketogenic

Factors effecting glucagon secretionStimulators of glucagon secretion are hypoglycemia. Other than this amino acids, exercise, infections, stress, gastrin etc. Same stimulators ofinsulin secretion like glucose and aminoacids increase secretion of glucagon.

SOMATOSTATINSomatostatin 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.>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 juicePancreatic 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 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.

Table 1 : Secretions of exocrine pancreas

EnzymesSubstrateCatalytic function or product.

TrypsinProteins polypeptidesCleaves peptide bonds

Chymotrypsins

Proteins PolypeptidesCleaves peptide bonds

ElastaseElastinCleaves bonds adjacent to aliphatic amino acids

Carboxypeptidase A and BProteins PolypeptidesCleaves carboxyl-terminal amino acids

ColipaseFat dropletsBinds to bile salt triglyceride water inter phase making anchor for lipase

Pancreatic lipaseTriglyceridesMonoglycerides and fatty acids

Cholesterol ester hydrolaseCholesterol estersCholesterol

Pancreatic a amylaseStarchTake salivary amylase

RibonucleaseRNANucleotides

DeoxyribonucleaseDNANucleotides

Phospholipase APhospholipidFatty acids

Regulation of secretionThe 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.

1.6 INVESTIGATIONS OF PANCREATICDISEASEA large number of laboratory tests investigations and imaging modalitiesare available for the diagnosis of pancreatic disease.The choice of examination depends upon the clinical presentation of thepatient.The investigations may be grouped as follows: Routine blood test Assessment exocrine function Assessment of endocrine function Visualisation of pancreas Tumour markers Cytology. Radio nuclideRoutine blood testsRoutine 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 blood urea.Exocrine functionSerum 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 functionSerum 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.

Visualisation of pancreasImaging 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 detect gallstones, pancreatic fluid collections,pancreatic tumours, and stones and calcifications in 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. 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 T2 weighted image eliminates signal from all tissues except stationary free water protons in pancreatic ducts. Arteriography with selective catheterisation is less frequently used.

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 divisumTumour markersCA19-9, 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.

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 ImagingThis is used to detect tumours of pancreatic islet cells .The radionuclideindium n labelled with octreotide, which is a somatostratin analogue hasa high affinity for these tumours.Somatostratin receptor scintigraphy may also be used to identify islet tumors.

1.7 CT SCAN OF PANCREASTECHNIQUE

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 parenchymaII. Enhance peripancreatic vessels for identification and assessment ofpatency.III. 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 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 retroperitoneum 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.

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 15The 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 .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.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 PANCREAS1.8 PATHO PHYSIOLOGY OF LESIONS PRESENTING AS PANCREATIC MASS

Normal Variants11Detailed 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} 17Acute pancreatitis is a disease characterised by abdominal pain and elevations in the levels of serum lipase and amylase.

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 pancreatitisAcute emphysematous pancreatitis

Path physiologyAcute 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: Proteolytic destruction of pancreatic substance Necroses of blood vessels and subsequent haemorrage Necrosis of ft by lipolytic enzymes Inflammatory reactionCause

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

IdiopathicSymptoms 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 complicationsPhlegmone (inflammatory mass) Peripancreatic effusion. Necrosis / pancreatic abscess. Non-pancreaticGastrointestinal ileus.Pancreatic ascites / pleural effusion.Bile duct obstruction.

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 EncephalopathyTable 2 : Diagnosis of acute pancreatitis

LAB IMAGING

Increased serum amylaseIncreased only 80-85% cases may be normal in pancreatitis due to hyper-lipidemia

X-ray

CXR: Lt sided pleural effusion, It basal pneumonitis, and High left dome of diaphragm.

Serum lipaseIncreased, as sensitive as amylase

Alanine aminotrasferase(ALT)3 fold increase in associated with gallstone.

Bones: Avascular necrosis, Lytic lesionsAbdomen: Shows duodenal ileus, sentinel loop, gas less abdomenColon cut-off sign, mottled shadows due to fat necrosis.Gall stoneUSG (low sensitivity due to localileus) Gall stone Pancreatic swelling, necrosis.Peripancreatic fluid collection,mass.ERCPDiagnosis of acute pancreatitis of occult cause.Removal of stone

SphincterotomyCT-Vide infraMRI- Not generally used. But oedema and fluid shows decreased signal intensity in Tl and increased signal intensity in T2 weighted image.

Criteria for assessing severity of acute pancreatitis

Several methods are used to predict the severity of acute pancreatitisapart 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.CausesVirtually any organism can infect the pancreas. They include gram-negative 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.

Other organisms like Echinococcus may also cause pancreatic abscess.

Tuberculosis of PancreasFew 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.Chronic pancreatitisThe 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 pancreaticadenocarcinoma.There can be diffuse or focal enlargement of pancreas and in later case itbecomes difficult to differentiate from pancreatic tumours.

Pathophysiology

Exact pathophysiology of chronic pancreatitis is unknown. Differentcauses have different mechanism of injury. Regardless of cause ultimateeffect is damage to'pancreatic acini, ducts nerves and islet cells.Gross pathologic specimens show that gland is hard and exhibits foci ofcalcification and folly developed pancreatic calculi.There are several patterns, chronic calcifying pancreatitis that occurs inalcoholics. There is atrophy of acini and increase in interlobular fibroustissue 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.CausesAlcohol Tropical pancreatitisFamilial pancreatitis

Cystic fibrosis.Idiopathic pancreatitis. Pancreatic duct obstruction Auto immune Recurrent acute pancreatitisClinical 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.MalahsorptionStratorrhoea 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 MelUtusPancreatic 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 sensitivityFUNCTIONSTRUCTURE

Secretin or secretin cholecystokinin testEndoscopic ultrasoundDirect visualisation of pancreatic duct, parenchyma, is more sensitive thanCTorMRCP

Fecal elastase

ERCP

Duct dilatation, stricture, irregular contour, filling of cavities or pseudocysts

Serum trypsin (reasonably accurate)MRIandMRCP

Sensitivity is still less than ERCP

Fecal fatComputed tomography Vide infra.

Blood glucose- too insensitiveUltrasonogram

Can demonstrate calculi calcifications markedly dilated ducts

-,.__-_.-_ 1

Cystic Lesions of PancreasCysts 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 cystsA 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 5cm in diameter.These cysts are lined by smooth glistening membrane that may onhistological section have total atrophy of lining epithelial cells or mayshow preservation of flattened pavement or low cuboidal epithelial cells.They are usually enclosed in a thin fibrous capsule and are filled with aclear to turbid mucoid or serious fluid.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 damageand 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 ofpancreatic duct, causing retention cysts containing inactivated enzymes.

Clinical featuresAsymptomatic.Abdominal mass.Presents with complications like haemorrhage or infection and mayrupture 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 maybe situated in pancreatic substance or adjacent to pancreas; especially intail area.Thick and fibrous walls line the cyst; there is no epithelial liningconnection or communication with surrounding ductal system.Cyst fluid may be serous or turbid. There may be marked inflammatoryreaction in the fibrous capsule.Often organising blood clots, old blood pigment precipitates of calciumand cholesterol crystals are also found.They are usually unilocular.

Location11These 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 wallcircumscribed outline.21CT 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, rarelyportal vein, ureters and colon Rupture.FatePseudocysts usually spontaneously resolve if < 6 cm in diameter, Symptomatic pseudocysts can be treated with surgical, endoscopic and percutaneous drainage.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 SignsCystic 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.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 StudiesThe 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 SignsCystic 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 thrombosis with formation of gastric varices or directtumour invasion is a less common presentation.

Diagnostic StudiesThe diagnosis usually is suggested is suggested by abdominal CT orultrasonographic detection of a large, cystic pancreatic mass. Thesestudies usually are obtained for evaluation of vague abdominalcomplaints.It may be difficult from these non-invasive imaging studies todifferentiate cystic pancreatic neoplasms from non-neoplastic pancreaticpseudo 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 chronicPancreatitis, or biliary tract disease makes pancreatic pseudocystsunlikely and cystic neoplasm of the pancreas more likely in patients whoare found to have an isolated cystic lesion of the gland. .Endoscopic- ultrasound is extremely useful in the evaluation of cysticlesions, often providing additional detail not seen by CT.It can clarify whether the lesion is a simple cyst (strongly suggestingpseudocyst) or a cystic mass. For cystic mass lesions, it can oftendistinguish serous cystic lesions (which are almost always benign) frommucinous cystic lesions (which have a high risk of malignancy).Serous ("microcystic") cystadenomas have characteristic honeycombappearance with central fibrosis or calcification.EUS can be used to sample cystic fluid, which can be examined forenzyme levels, viscosity, tumour marker levels, and cytology.Pancreatic pseudocysts have high amylase content. Serous cystadenomashave 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.TreatmentMost patients with either benign or malignant cystic neoplasms should be considered for surgical resection, even if the tumour is large or locally invasive.

Vascular malformations11'13Pancreas is surrounded by vascular structures and a number of vascularentities in this region may be mistaken for pathologic conditions of thepancreas.These abnormalities can related to inflammatory, atherosclerotic orneoplastic involvement of-the vessel.Most common vascular lesions is splenic artery aneurysms and pseudoaneurysms-these commonly occurs in women of child bearing age whotake contraceptive pills. Others are hepatic artery aneurysms, superior mesenteric artery

,!aneurysms, and celiac artery anemysms.These commonly contain calcifications and are mostly atherosclerotic inorigin.Cavernous transformation of portal veins needs special mention. Thisconsists of multiple venous collaterals in the area off portal vein, It isthought to be a congenital problem.

Tumours of the pancreasBenign tumorsFatty TumoursFatty tumours lipomatous pseudohypertrophy, lipomas are rare.AdenomasThese are benign solid tumours of both ductal and acinar origin. Overallincidence is rare.Malignant tumorsAdenocarcinomaincidence and aetiologyPancreatic 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 1st 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 Hippel-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.

GrossThe tumour has infiltrative margin. Carcinomas in body and tail due large head irregular tumours.Microscopic 17Most 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 VomitingMost 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 patientsmostly presents with large retroperitoneal mass and metastasis.Obstruction of distal common bile duct results in enlarged palpable nortender gall bladder and is called Courvoisier's sign.Laboratory findings:9Routine blood test:Anaemia, high ESRIncreased serum alkaline phosphates.Increased serum bilirabinRarely elevations of serum amylase

Tumour markers:A tumour marker is any substance the when measured in abnormalconcentration in body fluid or tissues indicate the presence of amalignancy and define its site of origin.CA 19-9 is mostly used 37 U/ml is the cut off value. Sensitivity is 81-85% and specificity 81-90%.Elevated carcinoembryonic antigen is present in 70% of patients.Others are a fetoprotein, RNase, Galactosyl transferase II (GT-II),oncofetal antigen.

RADIOLOGYX-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 involvethe distal duodenum. There is widening of C loop with mucosal abnormality. Gastric mucosal abnormality in the posterior wall.ERCP: Complete block of main pancreatic duct is the commonestabnormality. Pancreatic duct stricture is less common.Filling defects and irregular contrast filled cavities are also hallmark ofpancreatic 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.SiteLesions may occur any where in pancreas but most show tairly standarddistributionHead -60%Body-15% to 20%Tail -5%TreatmentPancreatic 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 In situ carcinoma

Stage-ITumour localized within pancreatic capsule

Stage-IIInvasion of s duodenum bile duct , or peri pancreatic tissue

State IIIInvolvement of lymph nodes.

Stage-IVTumor extends directly into stomach, spleen, colon or adjacent large vessels: distant metastases.

SURGERY The minority7 of patients with pancreatic neoplasms undergo curative surgical resection, primarily because less than 20% present with potentially curable disease.One third of the patients had neither resection nor surgical bypassbecause of locally advanced or metastatic disease, advanced age, ordebility.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 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.18ChemotherapyGemcitabine appears to be the most promising chemotherapeutic agent for the palliation of patients with non resectable pancreatic cancer.Radiation TherapyWhen 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 blockFor 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 tumoursStage I (resectable)

Good performance statusSurgery with adjubant chemoradiation

Stage II ( unresectable) Consider entry into experimental protocol to down stage tumour.

Clinical trials.

Chemoradiation

Gemcitabine

Stage-I

Poor performance status Gemcitabine based therapy

Supportive care

Stage-II & Stage III

Good performance status Clinical trials

Chemoradiation

Gemcitabine- based therapy

Stage IV

Good performance statusClinical trials

Gemcitabine based therapy

Stage II, III, IV

Poor performance statusGemcitabine-based therapy

Supportive care

Pancreatic islet-cell tumoursPancreatic 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 peptide-secreting 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 localor metastasic tumour growth.Clinical findingsMany of the patients with pancreatic islet-cell tumours present with signsand symptoms of excess hormone secretion. The most common tumourof islet-cell origin, namely the insulinoma.Insulinoma: usually is manifested by profound hypoglycaemia withdiaphoresis, confusion, and syncope.Gasinnonm: is the second most common tumour of islet-cells origin.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 neoplasiasyndrome type-1 (MEN-1).VIPomas : are associated with a syndrome of watery diarrhoea, hypokalemia, and achlorhydria.Ghtcagonomas : can present with diabetes, deep-vein thrombosis,depression, and dermatitis(necrolytic migratory erythema).Somatostatmomas: These are quite rare and may present with symptomsincluding 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)

TreatmentThe vas majority of pancreatic islet-cell neoplasm can be treated by segment resection of the gland or enucleating the tumour.PANCREATIC LYMPHOMAS9'11'13Pancreatic 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 findingsThe difference of pancreatic lymphoma form pancreatic adenocarcinoma is important preoperatively because the primary form oftherapy for lymphoma is chemotherapy rather thanresection. Ingeneral, patients with pancreatic iyraphoma present with signs andsymptoms identical to those with adenocarcinoma. However, patientswith pancreatic lymphoma have lower levels of serum bilirubin andalkaline phosphates thanwith comparably bulky pancreaticadenocarcinoma,

TreatmentWhen patients with pancreatic lymphoma are diagnosed preoperatively. chemotherapy can be initiated with cyclophosphamide, prednisone, and doxorubicin.Metastsis and adjacent tumoursMetastatic 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 MASSNormal variants 11As 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.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 planesComplications Phlegmon; mass like edema and inflammation, seen as ill-definedheterogeneous soft tissue and fluid densities (20-40 H) in and aroundthe 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 clearlyidentifiable fibrous capsule. Necrosis: liquefaction of portions of the gland identified by lack of contrast medium enhancement. 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 ANormal pancreas

Grade BFocal 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.

Grade CIntrinsic pancreatic abnormalities with haziness and streaky densities repreasenting inflammatory changes in peripancreatic fat.

Grade DSingle ill defined fluid collection with no capsule or wall .

Grade ETwo or more poorly defined fluid collections or presence of gas in or adjacent to pancreas.

Fig.5: Acute Pancreatitis

Fig.6: Pancreatic Pseudo cyst with thin capsule

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).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.

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 pancreatitisCT 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 surfacelobulation 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 carcinomaSigns of potential resectability:a.Isolated pancreatic mass with or without dilatation of thebile and pancreatic ducts,b.Combined bile-pancreatic duct dilatation without anidentifiable pancreatic mass (Pancreatic duct>5 mm inhead 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 ofdefinition of the vessel by perivascular fat. Deformity of vessel by adjacent tumor. Enlargement of collateral vessels Absence of vessel enhancemente.Metastasis to the liver -usually hypodense and poorlyenhancing.f.Ascites which is presumptive evidence of peritonealcarcinomatosis.

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.

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 overlong period.Functioning islet cell tumors:These tumors have bimodal distribution .31Cluster 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.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 andare usually between 2-6cm in size and 50% case may containcalcification.Somatosttinonias:33These 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 showedheterogeneous contrast enhancement.

Figure 13: Insulinoma;small enhancing massCystic tumours Microcystic adenoma:These tumours consists of honey comb network of innumerable cystsranging from millimetres up to few centimetres .CT shows a welldemarcated usually large tumour tumour (10 cm average),low densitymass with enhancing septations.A central scar may be present which calcifies in 20 % cases.

Figure 14: Microcystic adenomaMucinous cystic neoplasms:Mostly occurs in body and tail (75-95%) cases.CT shows cysts 6 or fewer 2cm or greater .They have thick wall andseptations with papillary projections.

Figure 15: Mucinous cyst adenomaMetastatic tumours11These can not be identified from primary tumours. However careful history taking and evidence of tumours helps to characterize these lesions.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 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.2.2 AIMS AND OBJECTIVESAims: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 inBangladesh.II. To differentiate the benign from malignant masses on the basis ofCT findings.III. To guide management planning.IV. To find out the accuracy and efficacy comparing clinical findingsand other diagnostic studies.2.3 MATERIALS & METHODSThis 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 ofRadiology and Imaging . Bangabandhu Sheik Mujib Medical University,CT scan was done by a helical CT scanner at 10 mm slice thicknessbefore and after administration of oral and intravenous contrast,For oral contrast 60ml iodinated contrast media diluted in 750 ml ofwater was given and for intravenous contrast 50ml of non ionic contrastmedia 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 hepalo-biliary 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

2.4 RESULTSThis 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 61-70 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.

AGE GROUPS36 (65.5%) patients in this study group were male and 19(34.5%) patients in this study group were female.

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 MassNumberPercentage

Inflammatory mass (Phlegmone)3 "5.46%

Necrosis of pancreas23.6%

Pancreatic abscess47.28%

Pancreatic pseudocyst1120%

Chronic focal pancreatitis23.6%

Tuberculosis11.8%

Pancreatic Carcinoma2341.8%

Metastastic lesions916.3%

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 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.5Among 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 massesAmong the inflammatory masses most patients belonged to the age group 31-40 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%) 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 GROUPSGraph 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.

AGE GROUPSGraph 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.

GROUPSGRAPH 6: Sex incidence of patients presenting with neoplastic and inflammatory pancreatic mass

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 FACTORPERCENT

Smoking38%

Gall stone disease20%

Diabetes14%

History of trauma09%

Other malignancy5.4%

Alcohol intake1.8%

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)COMPLAINTSPERCENTAGE

Pain80%

Nausea /Vomiting69%

Palpable abdominal mass47%

Abdominal distension38%

Weight lossFever.4% 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%.Table 2.4: Presenting complaints of Patients with neoplastic pancreatic mass (n=32)COMPLAINTSPERCENTAGE

Obstructive Jaundice82%.

Weight loss66%

Fever with Jandice63%

Pain-45%

Coagulation28%

Renal impairment29%

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 TESTPATIENTSPERCENTAGE

Raised serum amylase28.6%

Raised serum lipase421%

Ultrasound detectable lesions1982%

Ultrasound negative417%

GRAPH 7: Diagnosis of inflammatory mass by USG11 (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)MASSPATIENT NOPERCENT

Pancreatic pseudocyst1147%

Phlegmone417%

Pancreatic abscess313%

Necrosis28.6%

Chronic focal pancreatic28.6%

Pancreatic tuberculosis14.3%

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 15patients had raised CA19-9 or CEA.

Table 2.7: Distribution of investigations (n=35)INVESTIGATIONNo%

USG35100

CT35100

ERCP2571

Tumor marker1542

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 pancreaticcarcinoma. In one patient both were given as possible diagnosis.1 patient of pancreatic tuberculosis was also diagnosed as pancreaticcarcinoma. In case of the 3 remaining patients: 1 proved to be metastasisfrom cholangiocarcinoma, 2 periampullary carcinoma invading thepancreatic head.

Table 2.8: Comparison between CT and Biopsy findings in patientswith solid pancreatic mass (n=35)NUMBER OF PATIENTS%BIOPSYCT

2365%Ca pancreasCa pancreas

25.7%Chronic pancreatitis1 : Ca pancreas 1 :D/D chronic pancreatitis Ca pancreas

12.8%TB pancreasCA pancreas

617%Metastatic tumorMetastatic tumor

35.7%Metastatic tumorCa pancreas

112Over 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 in4(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.

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

Contour change23100

Hypodense mass2295

Isodense mass1-5

Hypodense after contrast23100

Calcification00

Necrosis522

Pancreatic duct dilatation1043

Biliary obstruction1669

Vascular involvement1356

Local organ involvement626

Ascitcs834

Lymph nodes939

Liver metastasis1043

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).STAGENUMBER%

Stage-I14.3

Stage- II313

Stage-Ill939

Stage-IV1043

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.

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 patients2.5 DISCUSSIONAbdominal 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 the 6th-7th decade No patient with neoplastic lesion in thisstudy 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 ~4fe decade. The youngest patient in this study group was a 12 year old boy; he presented with a post traumatic pseudocyst.iMost 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%,

These presenting complaints correlate well with the studies of Silverstein etal36 and ElmasN37.

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 al37 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.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.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 c