'Pan' Modality Imaging of the Pancreas and Pathologies.

Transcription

1 'Pan' Modality Imaging of the Pancreas and Pathologies. Poster No.: C-2650 Congress: ECR 2013 Type: Educational Exhibit Authors: R. P. Patel, S. Barrett, J. Coyle, A. Buckley, W. C. Yee, A Harris ; Vancouver, BC/CA, Dublin/IE, Cork/IE, CA Keywords: Pathology, Diagnostic procedure, PET-CT, MR, CT, Pancreas DOI: /ecr2013/C-2650 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 69

2 Learning objectives Lesions of the pancreas encompass a heterogeneous group of processes which include benign and malignant entities. The exhibit aims to illustrate a wide spectrum of US, ERCP, CT and MRI so that lesions can be morphologically differentiated. Page 2 of 69

3 Background Pancreatic pathologies are encountered in the course of routine radiology practice due to escalating imaging volumes and greater diagnostic capabilities of contemporary imaging techniques or during routine pancreatic disease work up. Accurate and timely imaging and diagnosis is essential to guide clinical management and help determine patient prognosis. Lesions may require surgery, follow up imaging or may be clinically insignificant and require no further action. Advances in imaging techniques allow pancreatic lesions to be characterized on the basis of morphologic, hemodynamic and metabolic findings which is helpful in equivocal or complex cases. Page 3 of 69

4 Imaging findings OR Procedure details The exhibit will include a multimodality review pancreatic pathological processes and examples of each. Congenital A wide spectrum of anomalies of the pancreas and the pancreatic ductal system are commonly encountered at radiologic evaluation. These anomalies may simulate various neoplastic, inflammatory and posttraumatic conditions and should be part of the differential diagnosis for a variety of abnormalities found at diagnostic imaging. Annular Pancreas Fig 1, 2 Annular pancreas is a rare congenital anomaly in which incomplete rotation of the ventral anlage leads to a segment of the pancreas encircling the second part of the duodenum. It has a prevalence of 1 in 2,000 persons and occurs either as an isolated finding or with other congenital abnormalities. May present in childhood or as adult. Narrowed and stretched descending duodenum. Circumferential mass around 2nd portion of duodenum; easily identified on CT, MR. Enhances like rest of pancreas. Symptoms of duodenal obstruction and/or pancreatitis. Pancreatic divisum Fig 3, 4 The most common congenital anomaly of the pancreatic ductal system, being reported in 4%-10% of the population. Ventral and dorsal pancreatic ducts fail to fuse. The ventral duct (duct of Wirsung) drains only the ventral pancreatic anlage, whereas the majority of the gland empties into the minor papilla through the dorsal duct (duct of Santorini). Clinically, most cases are asymptomatic but may contribute to pancreatitis or recurrent episodes. Trauma Fig 5,6 Page 4 of 69

5 Pancreatic trauma is either blunt or penetrating; 3-12% of all abdominal injuries. Lacerations usually accompany midline compression injury against the vertebral column and may involve other solid organs. Presentation: History of trauma, upper abdominal pain, post prandial vomiting Clinically: Raised serum amylase/lipase, leukocytosis. Complications include: Recurrent pseudoaneurysm, fistula, abscess. pancreatitis, pseudocyst, hemorrhage, CT: accurate in detecting extrapancreatic fluid collections, pancreatic lacerations/fractures. Emergency ERCP: Investigate pancreatic injuries when CT positive and status of PD uncertain hours delayed scans may uncover findings not present earlier. Inflammation Autoimmune pancreatitis (AIP) Fig 7-9 A multisystem disease process classified into two subtypes; lymphoplasmocytic sclerosing pancreatitis (LPSP) and idiopathic duct centric pancreatitis (IDCP). Asian Consensus diagnostic criteria for AIP (Otsuki 2008): - Pancreatic parenchymal imaging reveals diffuse/segmental/focal gland enlargement, occasionally with a mass and/or rim of hypoattenuation. - Pancreaticobiliary duct imaging reveals diffuse/segmental/focal duct narrowing, often with stenosis of the bile duct. And either of the following - Elevated serum IgG or IgG4 concentration and detection of antibodies, or Page 5 of 69

6 - Lymphoplasmocytic infiltration of pancreatic tissue with abundant IgG4-postive plasma cells, Or (optional criterion) - Response to steroid therapy : due to dramatic positive response to steroids in AIP an optional criterion was included. This stated that diagnostic trials of steroid therapy could be conducted in those patients fulfilling criterion 1 alone and negative work up for pancreaticobiliary cancer. Acute pancreatitis Fig 10,11. Acute inflammatory process of the pancreas with variable involvement of other local tissues and remote organ systems. It is associated with elevated pancreatic enzyme levels in blood and/or urine. Imaging: CT: focal or diffuse pancreatic enlargement, inhomogenous enhancement and necrotic foci, peripancreatic fluid collections and obliteration of fat planes. Chronic pancreatitis Fig The end result of a continuous, prolonged, inflammatory and fibrosing process that affects the pancreas. This results in irreversible morphologic changes and permanent endocrine and exocrine pancreatic dysfunction. Imaging: Atrophy of gland, dilated main duct, intraductal calculi, thickening of peripancreatic fascia. Fibroinflammatory mass; clinical and imaging features overlap with cancer and there is an increased risk of adenocarcinoma in chronic pancreatitis (x20). Biopsy not always helpful. Look for: Pancreatic calcification (chronic pancreatitis). Smoothly tapering duct: benign. 'double duct sign' (stricture of distal CBD and pancreatic duct). Page 6 of 69

7 vascular complications; splenic vein thrombosis and its sequelae and pseudoaneurysms of gastroduodenal or other arteries. Pancreatic pseudocyst Fig 16,17 A complication of pancreatitis in 10-20% patients. An acute pancreatic fluid can transition into a pseudocyst after 4-6 weeks. Increased amylase and lipase activity within the cyst due to communication with the pancreatic ductal system (70% cases). Imaging: CT or MR; well circumscribed, round or oval peripancreatic fluid collection of homogenously low attenuation surrounded by a well defined enhancing wall (capsule consisting of fibrous or granulation tissue). No enhancement of pseudocyst contents. Gas within pseudocyst = infection or communication with gut wall. Pseudoaneurysm can be caused by or simulate a pseudocyst. Pancreatic necrosis: (parenchymal necrosis, peripancreatic necrosis, or both) Fig 18, 19 Enlarged pancreas, indistinct borders, lack of or no parenchymal enhancement(<30hu). Peripancreatic necrosis; most often around body and tail of pancreas, anterior pararenal space, lesser sac. Parenchymal and peripancreatic necrosis most common (75-80% of patients with acute necrotizing pancreatitis. Associated necrotic collections which contain non liquefied material; Acute non encapsulated necrotic collections (<4 weeks ) after acute episode of pancreatitis or walled off necrosis and encapsulated (>4 weeks). Pancreatic abscess Fig 20 Infections that contain non liquefied material are more likely to become infected. Imaging; gas pockets suspended within well circumscribed round, oval or irregular fluid collections with enhancing walls/rind of inflammatory tissue. Definitive proof by FNA (+ve for gas forming organisms). Benign neoplasm Pancreatic lipoma Fig 21 Mesenchymal tumors exceedingly rare (1%). Page 7 of 69

8 Imaging: CT; homogenous distribution of fat density with no central or peripheral contrast enhancement, Housefield units of -80 to -120 and a sharp demarcation with no evidence of intra- and extra-pancreatic adjacent structures infiltration. Serous cystic neoplasm (Formerly called serous cystadenoma) Fig Usually benign (<3% probability of degeneration). Mainly women, peak age 65, 10% of cystic tumors. Imaging; Microcystic; body/tail, no connection with pancreatic duct, numerous microcysts cluster around central scar (calcification up to 30%), lobulated shape, radiate fibrous scar with delayed enhancement. Spongelike: Increasing size of cysts along periphery. Honeycomb like; Cysts of equal size in periphery and center. Oligocystic mainly pancreatic head unilocular or macrocystic (thin walls no unlike MCN, no central scar or calcification). Malignant neoplasm Mucinous cystic neoplasm (MCN) (formerly mucinous cystadenoma) Fig Exclusively women ( cyst comprises subepithelial ovarian stroma), premenopausal (peak age 47), 8% of cystic tumors premalignant, Male: female 1:9. Lab data; Increased CEA, increased cyst fluid levels of ca 19-9, mucinous cyst content. Imaging; Singular or lobulated tumor 3-23cm; Unilocular or multilocular cysts, body/ tail pancreas, no connection with pancreatic duct, singular cysts in small numbers (greater in size than in SCN), 'cyst in cyst', enhancement of cyst wall and septae (<2mm thick), +/- hemorrhagic cyst content. Suspicion of malignancy; solid mural nodules, thick enhancing septations, cyst size >6cm, peripheral 'eggshell' calcification. Page 8 of 69

9 Intraductal papillary mucinous neoplasm (IPMN) Fig Mucinous transformation of the pancreatic ductal epithelium. Men>women 3:2, peak age 60-70, 24% of cystic tumors, premalignant. Main pancreatic duct, sidebranch or mixed type. Main duct type Mainly body, tail, also head, connection with pancreatic duct, macrocystic, diffuse or segmental duct dilatation with cyst formation. Suspicion of malignancy: duct dilatation >1cm, enhancing mural tumor nodules, calcifications, cyst size >3cm, extrapancreatic extension. Branch duct type Mainly uncinate process, multifocality in 30%, connection with pancreatic duct. Macrocystic or unilocular, bulbous dilated minor ducts, cysts clustered or bundled together like clover leaves. Mixed type Neuroendocrine tumor (NET) Fig Functioning or non functioning 1-5% all pancreatic tumors, equal gender distribution, 51-57yrs. Sporadic, association with MEN 1, Von Hippel Lindau syndrome, neurofibromatosis type 1, tuberous sclerosis. Imaging: CECT; Functioning (85%); small, +/-calcification (20%), mostly hypervascular in arterial phase and portal venous phase; solid iso, hypo or hyper, Solid or ring enhancement (insulinoma). Non functioning; larger and complex, cystic or necrotic areas +/- calcifcation, can be hypervascular, early tumor thrombus invasion of portal vein, hypervascular ring metastases common. MRI: Page 9 of 69

10 Longer T1 and T2 relaxation times, therefore most are T1 hypo intense and T2 hyperintense. T1 fat sat; Homogenous avid arterial enhancement <2cm size, heterogeneous for larger tumors. Portal venous phase; hyper, iso, hypoenhancing. Hypervascular ring metastases are common. Higher sensitivity (up to 100%) with combined endoscopic USS and triple phase CECT. SPECT/CT; better attenuation correction and increased specificity. FDG/PET; role in poorly differentiated octretide negative NETs (high uptake due to high proliferative rate of tumor cells) Pancreatic adenocarcinoma Fig 48, % of all pancreatic malignancies. Malignancy that arises from ductal epithelium of exocrine pancreas. Male: Female 2:1 CT or MR imaging; 60-70% pancreatic head, Irregular, heterogeneous, poorly enhancing mass with abrupt obstruction of pancreatic ± common bile duct ("double duct" sign). 10% isodense/isointense and primary tumor not visualized. Calcification rare (<2%). 10% cystic/necrotic degeneration. T1/T2 hypointense, hypovascular +/- thin peripheral rim enhancement. Parenchymal atrophy and ductal dilation upstream from tumor, contiguous vascular ± organ invasion, mesenteric vascular invasion (SMV 'tear drop sign'), Involvement = encasement of > 1/2 circumference of vessel, narrowing, or occlusion. Peritoneal and liver metastases common. Endoscopic USS high resolution imaging method for small tumors ( cm). FDG/PET avid tumor. Pancreatic lymphoma Fig 50 Most commonly B-cell NHL. Secondary lymphoma - most common, 30% NHL pts with widespread disease, usually direct spread from peripancreatic lymph nodes. Primary rare, <2% extranodal disease, more common in immunocompromised patients. Page 10 of 69

11 Imaging: Two morphological patterns. Focal well circumscribed vs. diffuse form. Features to help distinguish from adenocarcinoma +/-peripancreatic and other lymph node enlargement ( below renal veins). +/- encasement of peripancreatic vessels. Less likely to cause MPD dilatation (CBD dilatation >MPD ). Invasive tumor growth that does not respect anatomical boundaries, infiltrates retroperitoneal or upper abdominal organs and GI tract. Focal type Pancreatic head (80% cases). CT; uniform low attenuation. MR; T1 hypo, T2 intermediate, faint contrast enhancement. Diffuse type Enlargement of pancreas with infiltrating tumor ± peripancreatic fat involvement; may simulate acute pancreatitis. CT; Homogenous soft tissue mass, little enhancement. MR; T1 and T2 hypointensity, homogenous contrast enhancement. Pancreatic plasmacytoma Fig 51, cases in the literature. An extramedullary neoplastic proliferation of plasma cells outside the confines of the osseous system. Typically presents as a solitary plasmacytoma of the paranasal and pharyngeal soft tissues (80%) or a secondary manifestation of systemic disease/ multiple myeloma. Involvement of GI tract 10% cases. Imaging: CT; Focal multilobulated solid hypodense mass with homogenous post contrast enhancement, or rarely diffuse enlargement (+/- biliary duct dilatation). Solid and pseudopapillary tumor (SPT) Fig 53, 54, % all pancreatic tumors, 9:1 female predilection, average age 25yrs Large ~9cm, slow growing, well encapsulated mass, cystic or hemorrhagic foci, calcification (30%), head>tail, metastases uncommon (7-10% cases). Displaces rather than invades surrounding structures. Imaging: Page 11 of 69

12 Peripheral heterogeneous enhancement arterial phase, progressive non uniform enhancement thereafter, enhancement usually less than normal pancreas CT; Well defined heterogeneous large mass +/- calcification (5-10%), low density areas within, thick enhancing capsule (solid component). MR; T1 large demarcated mass with mixed hypo and hyperintensity (hemorrhagic areas), low intensity fibrotic capsule. Page 12 of 69

13 Images for this section: Fig. 1: Annular pancreas. Axial contrast enhanced CT (CECT) shows the pancreas (arrow) encircling the descending portion of the duodenum. Page 13 of 69

14 Fig. 2: Annular pancreas. Coronal CECT shows the pancreas (arrow) encircling the descending portion of the duodenum. Page 14 of 69

15 Fig. 3: Pancreatic divisum. Axial CECT in a patient with acute recurrent pancreatitis and pancreatic divisum shows a dilated duct of Santorini (arrow). Page 15 of 69

16 Fig. 4: Axial T2 MR shows drainage of the pancreas through the duct of Santorini (arrow). Page 16 of 69

17 Fig. 5: Axial CECT 12 hours after blunt trauma reveals a fracture plane (arrow) across the pancreatic body, retropancreatic fluid, fluid in the peri-renal spaces and lesser sac. Page 17 of 69

18 Fig. 6: Axial T2 fat sat MR, hyperintense enlarged pancreatic gland with irregular contour, hyperintense transection plane along body (arrow), intra and retroperitoneal fluid. Page 18 of 69

19 Fig. 7: AIP. CECT, diffuse infiltration and enlargement of the pancreas with loss of normal fatty lobulation. Note the peripancreatic hypodense 'halo' or capsule with relatively little spread into the adjacent tissues (arrow) Page 19 of 69

20 Fig. 8: AIP. Diffuse sausage like enlargement of the pancreas with loss of fatty lobulation. Stricture of distal pancreatic segment common bile duct and biliary dilatation (short arrow). Note the inflammtory aortic aneurysm (long arrow) related to IgG4 related sclerosis disease. Page 20 of 69

21 Fig. 9: AIP. IgG4 related sclerosing cholangitis. ERCP depicts stenosis and irregularity in the intrapancreatic segment of common bile duct and subsequent upstream biliary dilatation and obstructive jaundice. Page 21 of 69

22 Fig. 10: Acute pancreatitis axial CECT, pancreatic enlargement and heterogeneous enhancement, peripancreatic stranding and edema. Page 22 of 69

23 Fig. 11: Acute pancreatitis coronal CECT, pancreatic enlargement, heterogeneous enhancement, extensive inflammatory infiltration of the mesentery and mild wall thickening of the 2nd part of the duodenum (arrow). Page 23 of 69

24 Fig. 12: Chronic pancreatitis. Abdominal radiograph showing cluster of small irregular calcifications along the pancreatic gland (arrow). Page 24 of 69

25 Fig. 13: Chronic pancreatitis. Transverse greyscale USS image showing dilated main pancreatic duct and echogenic foci (arrow) with posterior acoustic shadowing (calcifications). Page 25 of 69

26 Fig. 14: Chronic pancreatitis. Axial CECT showing diffuse pancreatic atrophy and extensive parenchymal and intraductal calcification (arrow). Page 26 of 69

27 Fig. 15: Focal chronic pancreatitis. Axial CECT of fibroinflammatory mass in the pancreatic head (arrow), parenchymal calcification and associated biliary tree dilatation. Page 27 of 69

28 Fig. 16: Pancreatic pseudocyst. Axial CECT sows homogenous hypodense cyst with encapsulated enhancing wall (arrow). Note the pancreatic duct stent. Page 28 of 69

29 Fig. 17: Coronal CECT large pancreatic pseudocyst (long arrow) that displaces the stomach and causes massive thickening of the gastric wall (short arrow). Page 29 of 69

30 Fig. 18: Acute necrotizing pancreatitis axial CECT after 5 weeks. Walled off necrosis anterior to pancreas extending along Gerota's fascia, note heterogeneous content with debris (arrow). Page 30 of 69

31 Fig. 19: Necrotizing pancreatitis. Coronal CECT shows extent of walled off necrosis with enhancing rim and non liquefied material/debris (arrow). Areas of pancreatic and peripancreatic fat necrosis. Page 31 of 69

32 Fig. 20: Pancreatic abscess/infected walled off necrosis. Axial CECT shows gas and fluid within a well-encapsulated spherical mass (arrow) in the pancreatic bed. Page 32 of 69

33 Fig. 21: Incidental finding of a benign, homogenous, non enhancing fat attenuation pancreatic c body lipoma on CECT (arrow). Page 33 of 69

34 Fig. 22: USS grayscale of serous cystic (microcystic) neoplasm (arrow). Echogenic solid appearing mass with anechoic cystic areas, small cysts display interfaces. Page 34 of 69

35 Fig. 23: Lobulated, 'honeycomb' like microcystic serous cystic neoplasm (SCN) in the pancreatic body (arrow) axial CECT. Note the mild capsular enhancement. Page 35 of 69

36 Fig. 24: Pancreatic body SCN. Axial fat sat T1 post contrast delayed venous phase MR, note the enhancing fibrotic septa (arrow). Page 36 of 69

37 Fig. 25: Axial fat sat T2 MR shows a lobulated microcystic SCN in the pancreatic body. Note the lack of mass effect and duct dilatation in the distal pancreas. Page 37 of 69

38 Fig. 26: Coronal T2 MRCP demonstrates a lobulated microcystic SCN in the pancreatic body (arrow). Note the lack of mass effect and duct dilatation in the distal pancreas. Page 38 of 69

39 Fig. 27: Axial non contrast CT showing 'spongelike' microcystic SCN in pancreatic head, small calcifications in a central scar (arrow) and septa. Page 39 of 69

40 Fig. 28: T2 Axial MR of microcystc SCN, 'spongelike' microcystic T2 hyperintensities and central T2 hypointensity from calcification and scarring (arrow). Page 40 of 69

41 Fig. 29: USS grayscale MCN shows multiloculated cystic mass with echogenic internal septae, cyst contents are a mixture of anechoic and echogenic with debris (arrow). Page 41 of 69

42 Fig. 30: MCN axial CECT Large unilocular cyst with wall enhancement. Page 42 of 69

43 Fig. 31: MCN coronal T2. Predominantly T2 hyperintense with hypointense thick cyst wall (arrow), internal septa and solid debris. Page 43 of 69

44 Fig. 32: MCN axial T1 fat suppressed. Variable cyst signal intensity, fluid like material hypointense, hyperintense proteinaceous and hemorrhagic material. Page 44 of 69

45 Fig. 33: MCN contrast enhanced portal venous phase axial T1 fat suppressed. Enhancement of internal septations and cyst wall. Page 45 of 69

46 Fig. 34: MCN. Coronal CECT. Multilocular cyst with 'cyst in cyst' appearances and thin enhancing internal septations (arrow). Page 46 of 69

47 Fig. 35: MCN axial CECT shows multilocular 'cyst in cyst' appearance. Higher cystic attenuation values as shown reflective of mucin content within. Page 47 of 69

48 Fig. 36: Side branch IPMN coronal CECT, with enhancing mural papillary nodule (arrow). Note the subsequent common bile duct dilatation. Page 48 of 69

49 Fig. 37: Lobulated side branch IPMN (arrow) which communicates with main pancreatic duct, coronal MRCP. Page 49 of 69

50 Fig. 38: Side branch IPMN, with enhancing mural nodule (arrow), axial T1 fat sat CE MR. Page 50 of 69

51 Fig. 39: Main duct IPMN with gross dilatation of the main pancreatic duct and broad opening into the duodenum (arrow) coronal CECT. Page 51 of 69

52 Fig. 40: Main duct IPMN coronal T2 MR. Gross cystic dilatation of the main pancreatic duct. Note the bulging ampulla (arrow), another characteristic feature of IPMN. Page 52 of 69

53 Fig. 41: Main duct IPMN axial T2 MR. Upstream diffuse pancreatic duct dilatation (arrow). Page 53 of 69

54 Fig. 42: IPMN Mixed type coronal MRCP. Main pancreatic duct is diffusely dilated and mulitilobulated side branch IPMN (arrow) along pancreatic body. Smaller side branch IPMN's along distal body and tail. Page 54 of 69

55 Fig. 43: NET axial arterial CECT shows 2cm hypervascular tumor in pancreatic tail (arrow). Resected and confirmed as Islet cell tumor. Page 55 of 69

56 Fig. 44: NET coronal portal venous phase CECT iso/hyperdense pancreatic tail tumor (arrow). Page 56 of 69

57 Fig. 45: NET axial T1 fat sat axial MR shows well defined homogenously hypointense pancreatic head tumor (arrow). Page 57 of 69

58 Fig. 46: NET axial contrast enhanced arterial phase T1 fat sat MR, arterially enhancing pancreatic head tumor. Page 58 of 69

59 Fig. 47: NET coronal contrast enhanced portal venous T1 fat sat MR shows hypointense pancreatic head mass. Note the upstream pancreatic duct dilatation. Page 59 of 69

60 Fig. 48: Pancreatic adenocarcinoma axial T1 fat sat MR shows hypointense tumor in the tail (arrow) and involvement of adjacent peri-pancreatic fat. Note the normal T1 hyperintense pancreatic gland. Page 60 of 69

61 Fig. 49: Pancreatic adenocarcinoma axial post contrast portal venous phase T1 fat sat MR shows hypovascular enhancing tumor with thin peripheral enhancing rim (arrow) which may help establish disease focality. Page 61 of 69

62 Fig. 50: Burkitt's lymphoma of the pancreas axial CECT. Infiltrating homogenously enhancing pancreatic gland enlargement, encased mesenteric vasculature, infiltration of fat planes and infra renal vein lymphadenopathy (arrow). Page 62 of 69

63 Fig. 51: Pancreatic plasmacytoma axial CECT shows diffuse homogenous contrast enhancement and gland enlargement. Note the splenic vein encasement and ascites. Page 63 of 69

64 Fig. 52: Pancreatic plasmacytoma coronal CECT shows extensive glandular enlargement and ascites. The patient had multiple lytic lesions throughout the bony skeleton and multiple myeloma. Page 64 of 69

65 Fig. 53: SPT coronal CECT well encapsulated heterogeneous mass in the pancreatic head (arrow). Page 65 of 69

66 Fig. 54: SPT coronal T2 MR shows heterogenously hyperintense well encapsulated mass with a thick hypointense capsule (arrow). Page 66 of 69

67 Fig. 55: SPT axial post contrast arterial phase T1 fat sat MR shows peripheral and non uniform enhancement pattern. Page 67 of 69

68 Conclusion Solid lesions of the pancreas have a broad spectrum of neoplastic and non neoplastic causes. A multimodality approach combines the strengths of individual imaging modalities and has a synergistic effect of improving diagnostic yield. Key radiological features allow confident lesion characterization and differentiation from other disease entities. Page 68 of 69

69 References 1) Multimodality Imaging of Pancreatic and Biliary Congenital Anomalies. RadioGraphics 2006;26: Mortele # KJ et al. 2) The Revised Atlanta classification for acute pancreatitis: Its importance for the radiologist and its effect on treatment. Radiology March 2012; 262: Ruedi F et al. 3) Autoimmune pancreatitis. AN illustrated guide to diagnosis. Clinical Radiology Nov 2012;1-11 R.D Procter et al. 4) Diagnosis and management of cystic pancreatic neoplasms. Clinical Radiology Feb 2012; B Buerke et al. 5) Cystic lesions of the pancreas AJR 2011; 196:W668-W677 Khan A et al. 6) Multimodality imaging of neoplastic and non neoplastic solid lesions of the pancreas. Radiographics2011;31: Low G et al. 7) Extramedullary plasmacytoma of the pancreas and jejunum. Clinical Imaging2009; P Gupta et al. Page 69 of 69