Transcript Imaging Approach to Pancreas tumours - Learning

Imaging Approach to
Pancreas tumours
Ryno vd Berg
Dept Radiology
Kimberley hospital
13/4/2012
Pancreas:
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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-cells
Islets clustered together crossed by network of capillaries
Exocrine part:
Acinar cells producing & secreting digestive enzymes
Alkaline juice secreted by ductal cells
Secreted into duodenum for digestion with bile
Imaging classification:
Solid lesions
Malignant
Benign
 Cystic lesions
Unilocular simple
Small cystic
Septated
 Solid with cystic components
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Solid Pancreas lesions:
Malignant:
1.AdenoCA*
2.Neuroendocrine*
3.Solid Pseudopapillary*
4.Panceaticoblastoma
5.Lymphoma
6.Mets to Pancreas*
7.Very rare:
Epthelial: Acinar cell, Giant cell & Colloid
CA
Mesenchymal: Granular cell CA,
Fibrous histiocytoma, Juvenile
hemangioendothelioma,
Fibroma, Inflam Myoblastic tumor
& Sarcoma*
Mixed: Squamous cell & Mixed endoexocrine tumors
*May have cystic degeneration
Benign:
1.Focal Pancreatitis
2.Fatty infiltration/replacement
3.Intrapancreatic accessory spleen
4.Pancreas lobulation/Cong anomalies
5.Miscellaneous:
Pancreatic Sarcoidosis
Castleman’s Disease
Malignant & Potentially Malignant
Solid Pancreas tumours
Pancreatic Adenocarcinoma
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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 phase
Porto-venous phase to detect mets & evaluate surrounding veins
10% 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 & T2
Often thin peritumour ring of increased enhancement
Superior to CT for detecting small tumours & Mets
Accuracy for detecting & staging of AdenoCA 90-100%
Endoscopic US:
Role in detecting small tumours (2-3mm) and help clarify equivocal CT & MR
findings
Ill-defined, heterogenous hypoechoic mass
98% sensitivity in detecting adenoCA
However operator dependent & narrow field of view for assessing local
invasion
PET:
Increased uptake & retention of FDG
Sensitivity 85-100%, Specificity 84-93%
Biggest impact ability to detect small metastases
False negatives: Mucinous tumours, Necrotic tumours, Peritoneal mets < 1cm
& hyperglyceamia
False positives: Inflammatory tissue
Criteria for defining the respectability of Pancreatic
AdenoCA
Resectible:
1. No mets
2. No abutment, distortion, tumour
thrombus or encasement of SMV/PV
3. 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. Mets
2. Lymphnode mets beyond the field of
resection
3. >180° Encasement of SMA
4. Unreconstructable occlusion of SMV/PV
5. Aortic invasion/ encasement
National Comprehensive Cancer Network- Radiographics, July 2011
Pancreatic Neuroendocrine tumours
Previously Islet cell tumours
1-5% of all Pancreas tumours, Age 51-57y, Equal both genders
Mostly sporadic, but may be associated with MEN type 1, Von Hippel-Lindau,
Neurofibromatosis type 1 & Tuberous Sclerosis
Classified into Functioning & Non-functioning
Further 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 NET
CT:
Most distinctive feature: rich blood supply – enhancing more rapid + intense than
surrounding tissue in arterial phase
Homogenous enhancement of tumours < 2cm & more heterogenous for larger tumours
which can be ring-like
Porto-venous phase show no typical pattern
Metastases often follow same enhancement pattern as primary
Sensitivity 94%
MR:
Generally have longer T1&T2 relaxation than other tumours and normal pancreas
Low on T1 and intermediate to high on T2
Sensitivity 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 insulinomas
Sensitivity 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 tumour
Solid cystic papillary epithelial-, Papillary cystic-, Solid and cystic-/ Franz tumour
1-2% of Pancreas tumours
Age range 10-74y (mostly young adults), female predominance (9:1), African & Asian
Low malignant potential with excellent prognosis post resection
Mets uncommon (7-9%): Liver, omentum, peritoneum
Typically large (mean 9cm), slow-growing, well encapsulated mass
Common 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 level
30% Peripheral calcifications
MR:
Capsule low T1&T2
Internal 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
Pancreatoblastoma
0.2% 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 diagnose
Rarely cause bile/ duodenal obstruction due to soft gelatinous consistency
Metastases: Liver, lymphnodes, lung, bone, mediastinum, peritoneum & omentum
US:
Heterogeneous mass with hypoechoic cystic spaces (necrosis) and hyperechoic internal
septae
Occasionally only hypoechoic solid mass
CT:
Generally multiloculated heterogeneous mass with enhancing septae
Calcifications if present rimlike or clustered
Mild contrast enhancement
MR:
Low-interm T1 & High T2
Pancreatoblastoma in 5y old:
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
Pancreatic Lymphoma
Most commonly B-cell type of Non-Hodgkin lymphoma
Primary: <2% of Extranodal lymphomas & 0.5% of Pancreatic tumours
Secondary: In 30% of widespread NH Lymphomas
Age 35-75y, Immunocompramised
Two morphological patterns:
1.Focal well circimscribed: 80% in head
Mean size 8cm
CT: Uniform hypodense
MR: Low T1, Interm T2
Faint contrast enhancement
2.Diffuse form:
CT: Infiltrative with enlargement & poorly defined of pancreas
MR: Low T1 + T2
Homogeneous 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 transplant
Focal hypodense tumour in head
Secondary Pancreas Lymphoma:
Local invasion of pancreas tail from
lymphomatous infiltration of the spleen
Also extensive retroperitoneal
lymphadenopathy
Metastases to the Pancreas
2-5% of Pancreatic neoplasms
Mostly from: Renal cell CA, Lung CA, Breast CA, Colorectal CA & Melanoma
US:
Hyper- / hypoechoic
CT:
Hypo-/Isodense
MR:
Low T1 & high on T2
Follow enhancement pattern of primary
>1.5cm mostly peripheral enhancement with central necrotic area & smaller lesions mostly
homogeneous enhancement
Renal cell CA hypervascular, need to differentiate from NET
Rest mostly hypovascular, need to diff from AdenCA
Past medical history very important
Mets from Renal cell CA
Asymptomatic pt had nephrectomy 20y ago
Hypervascular tumour with cystic-necrotic degeneration &
intratumour vessels
Benign solid Pancreatic masses
Focal Pancreatitis
Chronic pancreatitis:
Focal inflammatory mass, often in head
Account for 5-10% of pancreatectomies for presumed malignancy
Difficault to distinguish from AdenoCA, even histologically
Shared features
Favour focal
Pancreatitis
US: Hypoechoic
Duct penetrating sign: Non
Abrupt interruption of dilated
dilated/ smooth tapering duct pancreas duct
through mass
CT: Hypodense
Non-abrupt gradual
narrowing of ducts
Calcifications
MR: Low T1&T2
Double duct sign
Ductal strictures
Infiltration of adjacent fat
Arterial encasement
Peripancreatic venous
obstruction
Modest atrophy
Favour AdenoCA
Upstream pancreas atrophy
High ratio of duct diameter to
gland diameter
Focal chronic pancreatitis
Focally enlarged head with irregular contour & internal
calcifications
Remained stable over 3y after follow up imaging
Autoimmune Pancreatitis: (AIP)
25% of focal pancreatits
May occur alone or with other autoimmune disorders; most patients have increased IgG
and antinuclear antibody levels
US: focal hypoechoic, diffuse enlargement (“sausage”)/ normal
CT: 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 groove
Two 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 T2
Associated with smooth stricture of
pancreatic part of CBD & Wall
thickening + cystic dysplasia of
duodenum
Fatty infiltration-replacement
Common finding in elderly & obese, but usually diffuse
Also associated with chronic pancreatitis & Cystic fibrosis
Has predilection for anterior part of head, sparing posterior part & uncinate process
US:
Fat – Hyperechoic & spared areas hypoechoic
CT:
If macroscopic will show negative HU on uncontrasted scan (contrast spread between fat increasing
attenuation)
Absence of mass effect
MR:
Modality of choice
Macroscopic fat easily detected on fat-sat sequences
Microscopic fat detected with chemical shift imaging
Dual phase T1 weighted GRE series: Areas show high on the in-phase & signal loss on opposedphase sequence
Hypoechoic area of
fatty sparing in
hyperechoic fatty
pancreas
Intrapancreatic accesory spleen
Failed fusion of splenic anlage in dorsal mesogastrium
Typically 1-3cm, well-defined ovoid mass in tail
US:
Homogeneous, mildly echogenic.
May show posterior acoustic enhancement
Vascular hilum sometimes seen with doppler
CT:
Greater enhancement similar to spleen with same tigroid pattern
MR:
Lower on T1, Higher on T2
Need 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 anomalies
Pancreatic lobulation:
Bifid pancreas tail:
Tuber omentale:
Focal prominence of anterior pancreatic
surface left of sup mesenteric vessels
Very rare solid masses
Sarcoidosis:
Idiopathic systemic granulomatous disorder
Pancreatic involvement very rare, only 19 biopsy-proven cases in literature
Solitary/ multiple masses, may reach 6-7cm
Peripancreatic lymphnode enlargent
US: Hypoechoic
CT: Hypodense & non-enhancing
MR: Low T1, High T2 & Hypoenhancing
History & other findings
Castleman Disease:
Rare angiofollicular lymphnode hyperplasia
Only 10 cases of pancreatic involvement documented
CT: Solid, well-encapsulated mass with strong enhancement (may be ringlike)
May have calcifications & cystic changes
Cystic pancreatic lesions
Benign:
Serous cystadenoma
Cystic teratoma
Inflammatory:
Pseudocyst, Abscess,
Echinococcus
True epithelial cysts:
Von Hippel-Lindau
Adult PCKD
Cystic fibrosis
Rare:
Lymphangioma
Hemangioma
Paraganglioma
Malignant/ Potentially malignant:
Mucinous cystic neoplasm
Intraductal papillary mucinous
neoplasm (IPMN)
Solid with cystic degeneration:
AdenoCa
Solid pseudopapillary tumour
Neuroendocrine tumours
Mets
Sarcoma
Cystic teratoma
Morphological classification
Pseudocyst,
IPMN,
Serous cystadenoma,
Epithelial cysts
Mucinous cyst adenoma,
IPMN
Serous Cystadenoma
Mucinous cystic neoplasm
IPMN
AdenoCa
Solid pseudopapillary tumour
Neuroendocrine tumours
Mets
Sarcoma
Cystic teratoma
Inflammatory cysts
Pseudocyst:
No epithelial lining, but fibrous wall surrounding pancreatic fluid, cellular debris & blood
Most common cystic mass
Complication of acute or chronic pancreatitis or pancreatic trauma
US:
Usually well defined, smooth-walled anechoic cyst
May be multilocular with internal septations with internal echoes or fluid-fluid levels if
heamorrhage or infected
CT:
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 common
Uni-/multilocular
Peripheral enhancement
Peripheral calcifications my be present
True epithelial cysts
Ussually multiple small simple cysts
PCKD with cyst in pancreas
Von Hippel-Lindau disease
Benign cystic lesions
Serous cystadenoma (Microcystic adenoma)
Glycogen containing hypervascular tumour
Female predominance (4.5:1), Mean age 60y
Usually micro-/polycystic pattern (from 2mm up to 2cm)
May appear solid (due to vascularity & honeycomb appearance) with multiple
surrounding cysts
Enhancing septa & cyst wall
30% 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:
Rare
Difficult to distinguish from Mucinous cystic neoplasm
Usually more lobular outline & less peripheral enhancement
Cystic teratoma:
Very rare
Well defined mostly cystic & solid components
Well defined cystic mass with thick walls &
septations. Areas of fat
Malignant & Potentially malignant
Mucinous cystic neoplasms:
Includes Mucinous cystadenoma & Cystadenocarcinoma
Female predominence, Average age 60y
70-90% occur in body & tail
Usually hypovascular thick-walled multilocular (occasionally unilocular) with a few
compartments (>2cm)
Septations usually very thin walled
Occasionally peripheral calcifications (↑ chance of malignancy)
Contain mucin, sometimes debris/ haemorrhage
CT show enhancement of wall & septations
MR show the content with variable signal intensity probably due to proteinaceous fluid/
blood
VS
Multilocular
serous
cystadenoma
Peripheral calcifications
Endoscopic US: Septated cyst
Intraductal papillary mucinous neoplasms (IPMN):
Potentially malignant
Characterized by papillary proliferation of pancreatic ductal epithelium & production of
mucin
3 Types:
Main duct (70% chance of malignancy)
Branch duct (20% chance of malignancy)
Mixed
More common in older men
CT:
Cystic dilatation of a main or a side branch duct that contains thick mucoid secretions
Mural 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
drainage
Pancreatoscopy also possible
MRCP:
Less invasive
More sensitive than ERCP for differentiating mural nodules from mucin (mucin has
same signal intensity as pancreatic fluid)
Cysts with solid components
AdenoCa
Solid pseudopapillary tumour
Neuroendocrine tumours
Mets
Sarcoma
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-yearold girl who presented with mid epigastric
pain.
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:
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
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References:
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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 Nonpseudocyst, 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