Imaging Approach to Imaging Approach to Pancreas tumoursPancreas tumours

Ryno vd BergDept Radiology

Kimberley hospital13/4/2012

Pancreas:Pancreas: Retroperiteal organ, except for tail

in splenorenal lig at L1 level Head(uncinate process), neck,

body & tail. Size decreases with age; rough

guide: Head≤3.5cm & Rest ≤2.5cm. Pancreatic duct 1-3mm.

Bloodsupply from splenic, R gastro-omental & Sup mesenteric aa.

Drainage to portal system.

Endocrine part (2%):Langerhans islets: α-,β-,δ- & PP-cellsIslets clustered together crossed by network of capillaries

Exocrine part:Acinar cells producing & secreting digestive enzymesAlkaline juice secreted by ductal cellsSecreted into duodenum for digestion with bile

Imaging classification:Imaging classification:Solid lesions

MalignantBenign

Cystic lesionsUnilocular simpleSmall cysticSeptated

Solid with cystic components

Solid Pancreas lesions:Solid Pancreas lesions:

Malignant:1.AdenoCA*2.Neuroendocrine*3.Solid Pseudopapillary*4.Panceaticoblastoma5.Lymphoma6.Mets to Pancreas*7.Very rare:

Epthelial: Acinar cell, Giant cell & Colloid CAMesenchymal: Granular cell CA, Fibrous histiocytoma, Juvenile hemangioendothelioma, Fibroma, Inflam Myoblastic tumor & Sarcoma*Mixed: Squamous cell & Mixed endo-exocrine tumors

Benign:1.Focal Pancreatitis2.Fatty infiltration/replacement3.Intrapancreatic accessory spleen4.Pancreas lobulation/Cong anomalies5.Miscellaneous:

Pancreatic SarcoidosisCastleman’s Disease

*May have cystic degeneration

Malignant & Potentially Malignant Malignant & Potentially Malignant Solid Pancreas tumoursSolid Pancreas tumours

Pancreatic AdenocarcinomaPancreatic Adenocarcinoma

85-95% of all Pancreatic malignancies Age 60-80y, Males(2:1) Head – 60-70%, Body – 10-20%, Tail- 5-10% Poor prognosis (5-y survival < 5%) Non-resectable in 75% on presentation Surgery only cure (5-y survival 20%) Need appropriate pt selection to prevent

unnecessary surgery

CT:Hypovascular with low attenuation best seen in arterial phasePorto-venous phase to detect mets & evaluate surrounding veins10% Isodense, look for secondary signs (Abn pancreas shape, ductal obstruction, vascular

invasion)Mets commonly to liver, lymphnodes, peritoneum & lung

Isodense mass in head causing abrupt distal narrowing & dilatation of CBD

Double duct sign

MRI:Fibrotic nature – Low on T1 & T2Often thin peritumour ring of increased enhancementSuperior to CT for detecting small tumours & MetsAccuracy for detecting & staging of AdenoCA 90-100%

Endoscopic US:Role in detecting small tumours (2-3mm) and help clarify equivocal CT & MR findingsIll-defined, heterogenous hypoechoic mass98% sensitivity in detecting adenoCA However operator dependent & narrow field of view for assessing local invasion

PET:Increased uptake & retention of FDGSensitivity 85-100%, Specificity 84-93%Biggest impact ability to detect small metastasesFalse negatives: Mucinous tumours, Necrotic tumours, Peritoneal mets < 1cm & hyperglyceamiaFalse positives: Inflammatory tissue

Resectible:1. No mets2. No abutment, distortion, tumour

thrombus or encasement of SMV/PV3. Clear fat planes around CA, SMA & HA

Borderline resectable:1. Abutment or encasement of SMV/PV

(No impingement/ narrowing of lumen)2. Short segment occlusion from tumour

thrombus/ encasement, but allowing safe resection & reconstruction

3. Encasement of Gastroduodenal a up to HA (only short segment encasement/ abutment of HA & no involvement of CA)

4. <180° Abutment of SMA circumference

Not resectable:1.Mets2.Lymphnode mets beyond the field of resection3.>180° Encasement of SMA4.Unreconstructable occlusion of SMV/PV5.Aortic invasion/ encasement

National Comprehensive Cancer Network- Radiographics, July 2011

Criteria for defining the respectability of Pancreatic AdenoCA

Pancreatic Neuroendocrine tumours Pancreatic Neuroendocrine tumours Previously Islet cell tumours1-5% of all Pancreas tumours, Age 51-57y, Equal both gendersMostly sporadic, but may be associated with MEN type 1, Von Hippel-Lindau,

Neurofibromatosis type 1 & Tuberous SclerosisClassified into Functioning & Non-functioningFurther histologically:- Well differentiated benign features- Well differentiated uncertain- Well differentiated carcinoma- Poorly differentiated carcinoma

Insulinoma:• Most common NET (60-75%)• 10% Malignant• M:F = 2:3 Age: 40-60 yr• Associated with MEN I in 10%• No predilection for any part of the pancreas• Mostly <2cm• Classically hypervascular • Surgical resection is curative• Localization of tumour prior to surgery:

– Endoscopic US / intra-operative US– Angiography – Intra-Arterial Calcium Stimulation with Hepatic Venous Sampling

• Catheterize – Superior mesenteric artery (SMA)– Gastroduodenal artery (GDA)– Splenic artery (SpA)

• Twofold rise in insulin levels following calcium gluconate injection in SMA or GDA = tumour is located in the pancreatic head or uncinate process

• Twofold rise after injection into the SpA suggests caudal location

Gastrinoma:• 2nd most common NET• 80% in patients < 20yr M>F• Associated with MEN I in 50-60%• 50-60% malignant • Tumour size does not appear to be associated with biological behaviour or clinical

course• Lymph node or liver metasteses present in 70-80% of cases at diagnosis• Zollinger –Ellison syndrome: Hypersecretion of gastrin leading to Acid secretion with

peptic ulceration & diarrhoea• Average tumour size 3,5cm (up to 15cm)• Tend to be less vascular than insulinoma• More often multiple compared to insulinoma• Associated metasteses• Associated gastric wall thickening, indicating peptic ulcer disease and gastric

hyperplasia due to effects of gastrin can be helpful in diagnosis

Non-Functioning NET:• 3rd most common• Histological from alpha or beta cells• Mean age 57 yrs• Symptoms due to mass effect (present like adenocarcinoma)• Predominantly in pancreatic head• 90% malignant at presentation• Imaging

– Large in size 3- 25cm– Large, well-defined masses with moderate to strong enhancement– No invasion of adjacent vessel– Associated with cystic degeneration and calcifications– More easily detected by mass effect compared to functioning tumors

Glucagonoma:• Uncommon tumour• Middle age M<F• Associated with MEN• Secrete excessive amounts of glucagon and cause a syndrome characterized by

dermatitis, stomatitis, weight loss, and anaemia(fatigue) • ( 4D syndrome = dermatosis, diarrhoea, depression, dvt )• Increased glucagon leads to glucose intolerance (DM) and cachexia (catabolic

effects)• Third of patients with glucagonoma syndrome have secondary thromboembolic

phenomena– This feature is unique among the different NET

Predominantly in pancreas body & tail Large tumour (>5cm in 70%) with solid and necrotic elements Hypervascular in 90 % 60-80% malignant transformation 60% liver metasteses at presentation

VIPoma:• Excretes Vasoactive Intestinal Peptide

– Acting directly on cyclic AMP within epithelial cells in bowel– Relaxes vascular smooth muscle + causes electrolyte secretion

• WDDH syndrome:– Watery diarrhoea + hypokalaemia + hypochlorhydria – “pancreatic cholera” / Verner-Morrison syndrome

• >50% malignant transformation

Somatostatinoma:• May be associated with NF1• symptoms reflect the general inhibitory action of somatostatin on global

gastroenteropancreatic function– often have history findings consistent with diabetes mellitus, which is probably

secondary to the inhibitory action of somatostatin on insulin and glucagon release– Inhibition of the action of cholecystokinin by somatostatin causes relative biliary

stasis and the formation of gallbladder calculi– diarrhea and/or steatorrhea, both of which are likely to be caused by the inhibition

of pancreatic enzyme and bicarbonate secretion Predominantly in

◦ Pancreas head◦ Duodenum at ampulla of Vater

Tumour size 0,6-20cm ( avg >4cm ) >50% chance of malignant transformation 60% liver/lymph node metasteses at presentation

Imaging approach to NETImaging approach to NETCT:Most distinctive feature: rich blood supply – enhancing more rapid + intense than

surrounding tissue in arterial phaseHomogenous enhancement of tumours < 2cm & more heterogenous for larger tumours

which can be ring-likePorto-venous phase show no typical patternMetastases often follow same enhancement pattern as primarySensitivity 94%

MR:Generally have longer T1&T2 relaxation than other tumours and normal pancreasLow on T1 and intermediate to high on T2Sensitivity 85-94%

Endoscopic US:Sensitivity 94%, but combined with CT up to 100%Also useful in detecting duodenal gastrinomas & used in u/s guided FNA

SPECT/CT:Radiolabeled Octreotide (Somatostatin analog) taken up by most NET, except insulinomasSensitivity 90% Specificity 80%, however helpful in detecting mets

PET:Role in detecting poorly differentiated NET, which have a high proliferative rate (High FDG

uptake), compared to well differentiated NET with low proliferation rates

Differentiating NET from AdenoCA:

AdenoCA NET

Enhancement Hypovascular Hypervascular

Calcifications Only 2% 20%

Vascular involvement Encasement Infiltration & tumour thrombus

Ductal involvement Often Uncommon

Central necrosis/Cystic deg Less More often

Insulinoma:

Insulinoma: Solid mass with hypervascular periphery

Splenic arteriogram showing tumour in pancreatic tail

Gastrinoma: heterogeneous mass in the head of the pancreas with cystic degeneration and shell-like dense calcification. (b) Wall of the gastric antrum is hypertrophied

Solid Pseudopapillary tumourSolid Pseudopapillary tumourSolid cystic papillary epithelial-, Papillary cystic-, Solid and cystic-/ Franz tumour1-2% of Pancreas tumoursAge range 10-74y (mostly young adults), female predominance (9:1), African & AsianLow malignant potential with excellent prognosis post resectionMets uncommon (7-9%): Liver, omentum, peritoneumTypically large (mean 9cm), slow-growing, well encapsulated massCommon in pancreas tail & tend to displace rather than invade

CT:Hypodense pseudocapsule (compressed

pancreas tissue & fibrosis)Peripheral heterogenous enhancement

during arterial phase followed by progressive non-uniform enhancement (generally less than surrounding pancreas)

10-20% fluid-fluid or fluid-debris level30% Peripheral calcifications

MR:Capsule low T1&T2Internal haemorrhage & cystic

degeneration due to fragile vascular network of tumour

Subacute bleeding (high on T1), Chronic bleed (Low on T1+T2)

Main differential to consider:Solid Pseudopapillary Cystic NET

Age of presentation Young adults Rarely <30y

MR T1 Haemorrhage may show as high Low

Enhancement Heterogeneous & less enhancement than surrounding tissue

More vascular with diffuse / rimlike hyperenhancement

Well encapsulated solid tumour, low on T1 & interm-high on T2

PancreatoblastomaPancreatoblastoma0.2% of all pancreas tumours, but the most common in children (mean age 5y)Male predominance (1.3:2.7), Asian (>50% of all cases)Raised α-FP in 25-33%Slow growing & usually manifest as asymptomatic large mass (mean 10cm)Adrenocorticotropic hormone secretion have been documented (Cushing’s / Inapp ADH)Due to large size often not possible to identify organ of origin and generally require biopsy to

diagnoseRarely cause bile/ duodenal obstruction due to soft gelatinous consistencyMetastases: Liver, lymphnodes, lung, bone, mediastinum, peritoneum & omentum

US:Heterogeneous mass with hypoechoic cystic spaces (necrosis) and hyperechoic internal

septaeOccasionally only hypoechoic solid massCT:Generally multiloculated heterogeneous mass with enhancing septaeCalcifications if present rimlike or clusteredMild contrast enhancementMR:Low-interm T1 & High T2

US: Large heterogenous mass with cystic spaces encasing CA & displacing the Portal vein

CT: Solid mass with cystic components displacing the Portal confluence & stomach anteriorly

Pancreatoblastoma in 5y old:

Pancreatic LymphomaPancreatic LymphomaMost commonly B-cell type of Non-Hodgkin lymphomaPrimary: <2% of Extranodal lymphomas & 0.5% of Pancreatic tumoursSecondary: In 30% of widespread NH LymphomasAge 35-75y, ImmunocompramisedTwo morphological patterns:

1.Focal well circimscribed: 80% in headMean size 8cmCT: Uniform hypodenseMR: Low T1, Interm T2 Faint contrast enhancement

2.Diffuse form: CT: Infiltrative with enlargement & poorly defined of pancreas

MR: Low T1 + T2Homogeneous contrast enhancement

Important to distinguish from AdenoCa, because better prognosis & Chemo as 1st line treatment:

Mild pancreatic duct dilatation & CBD dilatation more common Enlarged lymphnodes below the level of the renal vein Invasive – infiltrates retroperitoneum, surrounding organs & GIT Vascular invasion less common Calcifications & necrosis not feature

Primary Pancreas Lymphoma:Pt 10y post renal transplantFocal hypodense tumour in head

Secondary Pancreas Lymphoma:Local invasion of pancreas tail from lymphomatous infiltration of the spleenAlso extensive retroperitoneal lymphadenopathy

Metastases to the PancreasMetastases to the Pancreas2-5% of Pancreatic neoplasmsMostly from: Renal cell CA, Lung CA, Breast CA, Colorectal CA & MelanomaUS:Hyper- / hypoechoicCT:Hypo-/IsodenseMR:Low T1 & high on T2Follow enhancement pattern of primary>1.5cm mostly peripheral enhancement with central necrotic area & smaller lesions mostly

homogeneous enhancementRenal cell CA hypervascular, need to differentiate from NETRest mostly hypovascular, need to diff from AdenCAPast medical history very important

Mets from Renal cell CAAsymptomatic pt had nephrectomy 20y agoHypervascular tumour with cystic-necrotic degeneration & intratumour vessels

Benign solid Pancreatic massesBenign solid Pancreatic masses

Focal PancreatitisFocal PancreatitisChronic pancreatitis:Focal inflammatory mass, often in headAccount for 5-10% of pancreatectomies for presumed malignancyDifficault to distinguish from AdenoCA, even histologically

Shared features Favour focal Pancreatitis

Favour AdenoCA

US: Hypoechoic Duct penetrating sign: Non dilated/ smooth tapering duct through mass

Abrupt interruption of dilated pancreas duct

CT: Hypodense Non-abrupt gradual narrowing of ducts

Upstream pancreas atrophy

MR: Low T1&T2 Calcifications High ratio of duct diameter to gland diameter

Double duct sign Modest atrophyDuctal stricturesInfiltration of adjacent fatArterial encasementPeripancreatic venous obstruction

Focal chronic pancreatitisFocally enlarged head with irregular contour & internal calcificationsRemained stable over 3y after follow up imaging

Autoimmune Pancreatitis: (AIP)

25% of focal pancreatitsMay occur alone or with other autoimmune disorders; most patients have increased IgG

and antinuclear antibody levelsUS: focal hypoechoic, diffuse enlargement (“sausage”)/ normalCT: diffuse enlargement , loss of normal surface indentations, tail retracted from splenic

hilum, capsule-like rim enhancement, peripancreatic adenopathy, no calcification or vascular encasement

MRCP/ERCP: diffuse irregular narrowing of pancreatic duct(often >3cm long), CBD stricture

Diffusely enlarged pancreas with hypodense capsule-like rim

Groove pancreatitis:Uncommon form of focal pancreatitis

involving pancreaticoduodenal grooveTwo forms: 1. Segmental – Involves head

with scar tissue in the groove

2. Pure – Affects the groove, but spares the head

May manifest as duodenal or biliary obstruction

CT: Sheetlike hypodense fibrotic scar tissue in groove, delayed contrast enhancement

MR: Low on T1, Interm-high on T2Associated with smooth stricture of

pancreatic part of CBD & Wall thickening + cystic dysplasia of duodenum

Fatty infiltration-replacementFatty infiltration-replacementCommon finding in elderly & obese, but usually diffuseAlso associated with chronic pancreatitis & Cystic fibrosisHas predilection for anterior part of head, sparing posterior part & uncinate processUS:Fat – Hyperechoic & spared areas hypoechoicCT:If macroscopic will show negative HU on uncontrasted scan (contrast spread between fat increasing

attenuation)Absence of mass effectMR:Modality of choiceMacroscopic fat easily detected on fat-sat sequencesMicroscopic fat detected with chemical shift imaging

Dual phase T1 weighted GRE series: Areas show high on the in-phase & signal loss on opposed-phase sequence

Hypoechoic area of fatty sparing in hyperechoic fatty pancreas

Intrapancreatic accesory spleenIntrapancreatic accesory spleenFailed fusion of splenic anlage in dorsal mesogastriumTypically 1-3cm, well-defined ovoid mass in tailUS:Homogeneous, mildly echogenic.May show posterior acoustic enhancementVascular hilum sometimes seen with dopplerCT:Greater enhancement similar to spleen with same tigroid patternMR:Lower on T1, Higher on T2Need to diff from other vascular lesions:

Superparamagnetic iron-oxide MR: Phagocytosed by reticuloendothelial cells, leading to decreased signal on post-contrast series

Scintography:Splenic tissue traps 90% 99m-Tc Heat damaged RBC

Well-defined oval mass with same intensity as spleen

Same enhancement pattern

SPECT/CT with 99m-TC HDRBC

Congenital anomaliesCongenital anomaliesPancreatic lobulation:

Bifid pancreas tail:Tuber omentale:Focal prominence of anterior pancreatic surface left of sup mesenteric vessels

Very rare solid massesVery rare solid massesSarcoidosis:Idiopathic systemic granulomatous disorderPancreatic involvement very rare, only 19 biopsy-proven cases in literatureSolitary/ multiple masses, may reach 6-7cmPeripancreatic lymphnode enlargentUS: HypoechoicCT: Hypodense & non-enhancingMR: Low T1, High T2 & HypoenhancingHistory & other findings

Castleman Disease:Rare angiofollicular lymphnode hyperplasiaOnly 10 cases of pancreatic involvement documentedCT: Solid, well-encapsulated mass with strong enhancement (may be ringlike)May have calcifications & cystic changes

Cystic pancreatic lesionsCystic pancreatic lesionsBenign:

Serous cystadenomaCystic teratoma

Inflammatory:Pseudocyst, Abscess, Echinococcus

True epithelial cysts:Von Hippel-LindauAdult PCKDCystic fibrosis

Rare:LymphangiomaHemangiomaParaganglioma

Malignant/ Potentially malignant:Mucinous cystic neoplasmIntraductal papillary mucinous

neoplasm (IPMN)Solid with cystic degeneration:

AdenoCaSolid pseudopapillary tumourNeuroendocrine tumoursMetsSarcomaCystic teratoma

Morphological classificationMorphological classification

Pseudocyst, IPMN, Serous cystadenoma, Epithelial cysts

Serous Cystadenoma

Mucinous cyst adenoma,IPMN

Mucinous cystic neoplasmIPMNAdenoCaSolid pseudopapillary tumourNeuroendocrine tumoursMetsSarcomaCystic teratoma

Inflammatory cystsInflammatory cystsPseudocyst:No epithelial lining, but fibrous wall surrounding pancreatic fluid, cellular debris & bloodMost common cystic massComplication of acute or chronic pancreatitis or pancreatic traumaUS:Usually well defined, smooth-walled anechoic cystMay be multilocular with internal septations with internal echoes or fluid-fluid levels if

heamorrhage or infectedCT:Usually well defined round thin/thick walled fluid collection with mild rim enhancement

Pancreas abscess

Haemorrhagic pseudocyst

Echinococcus cyst:Rare, liver & lung involvement much more commonUni-/multilocularPeripheral enhancement Peripheral calcifications my be present

True epithelial cystsTrue epithelial cystsUssually multiple small simple cysts

PCKD with cyst in pancreas Von Hippel-Lindau disease

Benign cystic lesionsBenign cystic lesionsSerous cystadenoma (Microcystic adenoma)Glycogen containing hypervascular tumourFemale predominance (4.5:1), Mean age 60yUsually micro-/polycystic pattern (from 2mm up to 2cm) May appear solid (due to vascularity & honeycomb appearance) with multiple

surrounding cystsEnhancing septa & cyst wall30% show central scar, which may calcify

Serous cystadenoma:Echogenicity due to interaction between multiple tiny cysts

T2 weighted image sowing multiple cysts with fibrous central scar

Macrocystic serous cystadenoma:RareDifficult to distinguish from Mucinous cystic neoplasmUsually more lobular outline & less peripheral enhancement

Cystic teratoma:Very rareWell defined mostly cystic & solid components

Well defined cystic mass with thick walls & septations. Areas of fat

Malignant & Potentially malignantMalignant & Potentially malignantMucinous cystic neoplasms:Includes Mucinous cystadenoma & CystadenocarcinomaFemale predominence, Average age 60y70-90% occur in body & tailUsually hypovascular thick-walled multilocular (occasionally unilocular) with a few

compartments (>2cm)Septations usually very thin walledOccasionally peripheral calcifications (↑ chance of malignancy)Contain mucin, sometimes debris/ haemorrhageCT show enhancement of wall & septationsMR show the content with variable signal intensity probably due to proteinaceous fluid/

blood

VS

Multilocular serous cystadenoma

Endoscopic US: Septated cyst

Peripheral calcifications

Intraductal papillary mucinous neoplasms (IPMN):Potentially malignantCharacterized by papillary proliferation of pancreatic ductal epithelium & production of

mucin3 Types:

Main duct (70% chance of malignancy)Branch duct (20% chance of malignancy)Mixed

More common in older menCT:Cystic dilatation of a main or a side branch duct that contains thick mucoid secretionsMural nodules within a cyst/ duct is highly suggestive of malignancy

ERCP: Diffusely or segmentally dilated pancreatic duct without stricturing Side branches may also be dilated Filing defects may be seen due to mucus or mural nodules The papilla resembles a "fish-mouth," frequently with mucus extruding from the orifice Able to do cytology by aspiration of the duct contents or brushings & therapeutic drainagePancreatoscopy also possibleMRCP:Less invasiveMore sensitive than ERCP for differentiating mural nodules from mucin (mucin has same signal intensity as pancreatic fluid)

Cysts with solid componentsCysts with solid componentsAdenoCaSolid pseudopapillary tumourNeuroendocrine tumoursMetsSarcoma

Hypoattenuating AdenoCA with cystic degeneration

Necrotic NET (63 y old pt presenting with diarrhoea)

Necrotic pancreatic sarcoma mimics mucinous cystic neoplasm in this 58-year-old man with left upper quadrant pain. Liver mets.

Solid Pseudopapillary tumour: 16-year-old girl who presented with mid epigastric pain.

Summerize:Summerize:Solid lesions: Malignant:

◦ AdenoCA: Hypovasc, Encasement, Ductal involvement◦ NET: Assoc sympt, Hypervasc, Calcif, Infiltrative, Often cystic changes◦ Solid pseudopapil: Young adult, Fibrous pseudocapsule, Cystic◦ Pancreatoblastoma: Child, Large heterogenous◦ Lymphoma: Immunity, Other LN, Invasive, Not calcify/necrosis◦ Mets

Benign:◦ Pancreatitis◦ Fatty changes◦ Acces spleen◦ Congenital

Cystic lesions Unilocular: Inflamm (Pseudo/Abscess), Epithelial (assoc syndromes) Small cystic: Serous cystadenoma (Vascular, Central calcif) Septated: Mucinous cystic (Body+tail, Few compartments, Periph calcif,

Content variable)IPMN (Duct dilat with mucin, Mural nodules)

Mixed solid & Cystic:AdenoCa, Solid pseudopapillary tumour, Neuroendocrine tumours, Mets, Sarcoma

Final points:Final points:

Important to distinguish between benign /malignant lesions & respectability Multimodality imaging approach often helpful Proper clinical history & associated findings Helpful to divide lesions into:

◦ Solid◦ Cystic◦ Solid with cystic component

References:References: Multimodality imaging of neoplastic and non-neoplastic solid lesions of the

pancreas, Low G, et al, Radiographics, July 2011 Cystic pancreatic lesions: A simple imaging-based classification sytem for

guiding management, Dushyant VS, et al, Radiographics, Nov 2005 Cystic masses of the pancreas, Pablo RR, et al, Radiographics, July 1992 Imaging diagnosis of cystic pancreatic lesions: Pseudocyst vs Non-

pseudocyst, Young HK, et al, Radiographics, May 2005 Solid pseudopapillary tumour of the pancreas, Coleman KM,

Radiographics, Nov 2003 Clinical manifestations, diagnosis, and staging of exocrine pancreatic

cancer, Castillo CF, et al, Review Feb 2012, Uptodate New Diagnostic Imaging Modalities for Pancreatic Disease, Piraka C,

Scheiman JM, Current Opinion Gastroenterology, 2011;27(5):475-480 Primer of Diagnostic Imaging, Weissleder, et al, 4th ed, 2007