Author: Idoia Corcuera
NECT CECT (Arterial & Venous) MRI - T1 MRI - T2 MRCP MRI - Post-contrast T1 (arterial & venous) Diffusion/ADC Radionuclide Gross pathology Histology Additional comments
Adenocarcinoma Isodense mass. Dilated pancreatic duct and obliteration of retropancreatic fat. Cystic or necrotic areas and calcifications may occur when associated with chronic pancreatitis Arterial: Poorly enhancing, heterogeneous mass. Parenchymal atrophy and ductal dilatation. Local invasion into porta hepatis or mass in head may also obstruct CBD producing "double duct sign". Arterial phase important to assess vascular involvement which determine resectability

Venous: Hypodense heterogeneous mass. Vascular invasion: teardrop-shaped SMV
Hypointense Variable signal intensity depending on the degree of desmoplastic reaction, hemorrhage, necrosis, and associated inflammatory change May define level and degree of obstruction. Dilatation of both the pancreatic and bile ducts (the double duct sign) Arterial: Little ringlike enhancement or no enhancement. Hypointense relative to the normal pancreas

Venous: Hypointense. Sometimes exhibit delayed enhancement
Increased signal intensity and relatively low ADC values because of the restricted diffusion associated with fibrosis PET: Moderate to marked increased FDG uptake Small focal mass (average diameter, 2-3 cm), solid without significant necrosis or hemorrhage. Hypovascular. Fibrosis. Cystic areas Most common exocrine pancreas primary malignancy. Scirrhous and hypovascular with an associated marked desmoplastic response, as well as local infiltration. Often produces mucin. Cystic areas.
Islet cell tumors - Functioning islet cell tumor: Small or large in size. Small lesions usually undetectable. Iso, hypodense or mixt; ±Ca. ±Cystic and necrotic areas (usually non-insulin tumors). - Non-functioning islet cell tumor: Usually large and complex. Iso, hypodense o mixt. Calcification, cystic and necrotic areas (large tumors). Arterial: - Functioning islet cell tumor: Most are hyperdense. Enhancing metastases in liver and lymph nodes. - Non-functioning islet cell tumor: Usually hypervascular; nonenhancing cystic or necrotic areas. Calcifications. Enhancing viable tumor and metastases; liver metastases often extensive even in relatively healthy patient

Venous: - Functioning islet cell tumor: hypo, iso or hyperdense. Delayed solid/ring-enhancement (insulinoma). - Non-functioning islet cell tumor: hypo, iso, hyperdense. Nonenhancing areas representing cysts and necrosis.
- Functioning islet cell tumor: hypointense. - Non-functioning islet cell tumor: small tumors isointense; large tumors heterogeneous (cystic and necrotic) - Functioning islet cell tumor: hyperintense. - Non-functioning islet cell tumor: small tumors isointense; large tumors hyperintense (cystic and necrosis) -Functional tumors: small tumors (less than 2cm) homogeneous enhancement, larger lesions tend to show heterogeneous enhancement.-Non functioning tumors: small tumors hyperintense, large tumors nonenhancing cystic+necrotic areas Varying ADC values as a result of variable underlying histopathologic characteristics. May be helpful in distinguishing endocrine carcinomas without hemorrhage or cystic degeneration from benign endocrine neoplasms by ADC values, with low ADC values and high signal intensity on diffusion-weighted images obtained by using high b values in endocrine carcinomas In-111-DTPA-D-Phe octreotide uptake Well demarcated, solid, and firm to rubbery on palpation. Variable color depending on the amount of stroma, the degree of vascutarity, and the presence of hemorrhage or cystic degeneration, and may range from pale yellow to pink or red. Larger islet cell tumors tend to demonstrate cystic changes and necrosis. ±Gritty calcification in the larger tumors. The histologic characteristics of functioning and clinically silent lesions are identical. Three patterns are observed: (1) a solid, diffuse pattern; (2) a ribbonlike, trabecular pattern; and (3) an acinar or ductlike pattern. More than one of these architectural patterns may occur in the same neoplasm. Composed of sheets of small round cells, uniform nuclei/cytoplasm. Mitoses are unusual. The amount of intervening stroma is extremely variable, and the stroma may appear dense and hyalinized. There is a well-organized relationship between the neoplastic cells and the numerous stromat vessels. These vessels are responsibte for the hypervascular nature of the lesions
Lymphoma Arterial: Little enhancement. ± encasement of peripancreatic vessels (Image shows secondary lymphoma of the pancreas in a 54-year-old man with abdominal pain. Coronal oblique postcontrast arterial phase maximum intensity projection image shows local invasion of the pancreatic tail (curved arrow) from lymphomatous infiltration of the spleen (straight arrow) and extensive confluent retroperitoneal lymphadenopathy)

Venous example 1: Diffuse, homogeneous enlargement of the pancreas with little enhancement.± encasement of peripancreatic vessels

Venous example 2: Image shows primary pancreatic lymphoma in a 56-year-old woman with right upper quadrant pain who had undergone renal transplantation 10 years earlier for chronic renal insufficiency (note the atrophic kidneys [*]). US showed a gallstone but failed to adequately depict the pancreas. Endoscopic retrograde cholangiopancreatography showed abrupt narrowing of the CBD, which was treated with placement of a metallic stent. Postcontrast portal phase CT scan shows a focal hypoattenuating tumor (straight arrow) in the pancreatic head, a finding that was confirmed to be lymphoma at biopsy. A gallstone (arrowhead) and the biliary stent (curved arrow) are also noted.

Metastases Venous: Variable: mimics primary tumor. Hypervascular: usually renal cell cancer. Hypovascular: lung, breast, melanoma, colon Venous: Rim of enhancement in larger hypovascular mets. Homogeneous enhancement in renal cell mets.
Mucinous cystic pancreatic tumor Venous: Multilocular cystic lesion: well-defined, round, hypoattenuating mass. Fine internal septa and cyst wall enhancement ± calcification. -Unilocular cystic lesion: enhancement of cyst wall. Variable signal intensity based on cyst content: hypointense if fluid-like material, hyperintense if proteinaceous or hemorrhagic. Focal calcifications: hypointense Cyst: hyperintense. Internal septations and focal calcifications: hypointens Venous: Enhancement of septations and cyst wall bright in diffusion-weighted image and high signal intensity in ADC Large mass encapsulated by thick fibrous capsule (2-12 cm in diameter), smooth and round; lobulated surface may be seen. Multi-/unilocular large cyst; thin septa. Solid papillary projections protrude into interior of tumor sign of cancer Tall, mucin-producing columnar cells. Substended by densely cellular mesenchymal stroma. Characteristic ovarian-type stroma with spindle cells.
Pancreatic serous cystadenoma Microcystic: -Serous microcystic adenomas: Honeycomb or sponge-like mass with enhancement of septa delineating small cyst. Enhancing septa may predominate over cystic spaces, mimicking solid neoplasm. capsular enhancement. Dilatation of pancreatic duct and/or CBD. ± Calcification within central scar or septa.

Macrocystic: Macrocystic ("oligocystic") serous cystadenoma: Thin nonenhancing, imperceptible wall.
Microcystic: Tumor: hypointense. Blood within cysts: varied intensity. Central scar and calcification: hypointense

Macrocystic: Tumor: hypointense. Blood within cysts: varied intensity. Central scar and calcification: hypointense
Microcystic: Tumor hyperintense. Central scar and calcification: hypointense

Macrocystic: Tumor hyperintense. Central scar and calcification: hypointense
Microcystic: Capsular enhancement. Enhancement of septa delineating small cysts. The thin fibrous septa between the small cysts may show delayed enhancement.

Macrocystic: Capsular enhancement. Enhancement of septa delineating small cysts. The thin fibrous septa between the small cysts may show delayed enhancement.
Macrocystic: relatively high signal intensity and an ADC value of 2.52 × 10−3 mm2/sec. Microcystic: Well-circumscribed, round/ovoid, cystic, multilocular. Lobulated edges secondary to bulging cyst. Honeycombed or spongy appearance. Thin fibrous septa radiating from central scar. Distrophic calcification within central scar.

Macrocystic: Well-circumscribed, round/ovoid, cystic, multilocular. Lobulated edges secondary to bulging cyst. Honeycombed or spongy appearance. Thin fibrous septa radiating from central scar. Distrophic calcification within central scar.
Microcystic: Cyst are lined by cuboidal/flat epithelial cells separated by fibrous septa. Cells and fluis are glycogen rich. No cytologic atypia nor mitotic figures. Areas of calcium. Cholesterol clefts. Hemosiderin-laden macrophagues.

Macrocystic: Cyst are lined by cuboidal/flat epithelial cells separated by fibrous septa. Cells and fluis are glycogen rich. No cytologic atypia nor mitotic figures. Areas of calcium. Cholesterol clefts. Hemosiderin-laden macrophagues.
Solid-Pseudopapillary Tumor (formerly SPEN tumor) Venous: Heterogeneous mass hypovascular with no contrast-enhancement. Low density areas of variable size within the lesion; depends on degree of hemorrhage and necrosis. ± Calcification. Thick enhancing "capsule".±vascular invasion . Large well-demarcated mass with central areas of low and high signal intensity. High signal intensity secondary to hemorrhage.Capsule appears as rim of low intensity slightly hyperintense and not clearly cystic. Arterial: Mild heterogeneous arterial enhancement

Venous: Progressive fill-in and enhancement during the delayed phase. Enhancement of the capsule and some of the solid portions of the tumor.
Neoplasm composition—solid debris versus cystic or hemorrhagic fluid—determines the degree of diffusion and the ADC values. The solid component of the neoplasm may account for the relatively low ADC values. Thick, fibrous, hypervascular capsule surrounding a mixture of solid and cystic areas. Well-formed, thick peripheral capsule. Degenerative pseudopapillae and noncohesive tumor cells with round nuclei and eosinophilic cytoplasm. Hemorrhagic degeneration and cystic areas.
Branched IPMT multiple intrapancreatic cystlike lesions with thin, irregular, peripheral ring-enhancing

Thin, irregular, peripheral ring-enhancing "multicystic" lesion. Not spherical cysts, but arcs & tubes. Bulging ampulla at duodenal sweep with thin rim enhancement.
Hypointense branch duct cysts. Hyperintense dilated branch duct cyst, may show papillary excrescence in cystic lesions of pancreatic head Lobulated clustered cysts. Reveals communication between cystic lesions and duct Lobulated clustered cysts. Reveals communication between cystic lesions and duct Cystically dilated branch ducts with rough internal surface. Few to multiple intraductal elevated papillary tumors (adenomas). Communicating channels between cystic spaces Simple hyperplasia, papillary adenomas, dysplasia, in situ carcinoma. Papillary projections covered with columnar epithelial cells. Septa that separate mucin-filled lacuna
Main duct IPMT Polypoid lesions/mural nodule isodense Hypointense tortuous dilated MPD Hyperintense dilated MPD. ± papillary excrescence along MPD Diffuse dilatation of the main pancreatic duct with a tortuous path. Intraductal mucin and papillary tumors: may be detected as nodular filling defects. contrast enhancement of the main pancreatic duct walls. Enhancement of papillary nodules Increased ADC value most likely due to fluid in the duct Dilated main pancreatic duct filled with mucin. Flat elongated tumor (hyperplasia to malignancy) with rough surfaces. classified as adenomas, borderline tumors, or carcinomas depending on the degree of cytoarchitectural atypia
Abscess Heterogeneous hypoattenuating fluid collection confined by enhancing wall or rind of inflammatory tissue. Nonenhancing contents. Purulent exudate. Little to no necrotic tissue. Positive smear/culture for bacteria/fungi. (image shows a surgical specimen shows greenish purulent fluid replacing pancreatic parenchyma)
Pseudocyst Homogeneous, hypodense lesion with near-water density ("mature" pseducyst). -Hemorrhagic, infected pseudocyst: heterogeneous, mixed density contents. ± pancreatic calcification; MPD and CBD dilatation. Low-attenuation fluid collection with a well-defined thin wall. Enhancement of thin fibrous capsule; not of contents. Gas within pseudocyst=superimposed infection or descompression into adjacent duct. Hypointense. Increased T1 signal intensity may be secondary to hemorrhage, protein deposition, or both Hyperintense (fluid), mixed intensity (fluid + debris) Hyperintense encapsulated collections contiguous with dilated pancreatic duct. no internal enhancement Collection of fluid, tissue, debris, pancreatic enzymes, and blood sorrounded by fibrous capsule
True pancreatic cyst No enhancement True epithelial lining
Lipomatous Pseudohypertrophy No enhancement Increased signal intensity, signal loss with fat-suppressed sequences Enlargement of pancreas. Local or diffuse fatty replacement of normal pancreatic tissue Marked atrophy and loss of exocrine glandular elements. Replacement by mature adipose tissue. Preservation of ducts and islets of Langerhans
Chronic pancreatitis Atrophy of body-tail parenchyma. Dilated MPD with ductal calculi. Intra- and peripancreatic pseudocyst. Venous: Mass due to chronic pancreatitis: varied enhancement due to presence or abscence of fibrosis: fibroinflammatory mass (common in pancreatic head), hypoenhanced mass (due to fibrosis), isodense enhancing mass (lack of fibrosis) Dilated MPD..Splenic vein thrombosis. Varices. Hypointense Pseudocyst and necrotic areas hyperintense. Intraductal calculi hypointense or signal void Well-depicted fluid containing structures. Side-branch ectasia and dilated MPD. Multifocal dilatations and strictures; irregular contour; pseudocysts; and filling defects from calculi, mucinous plugs, or debris. Stones as small as 2 mm in diameter can be detected. More gradual enhancement compared to that of the normal pancreas. Heterogeneous enhancement pattern of parenchyma. Nonenhancing decreased signal areas: necrosis, pseudocyst. Well-depicted pancreatic pseudocyst contiguous with dilated MPD. Vascular occlusions sometimes demostrated

More gradual enhancement compared to that of the normal pancreas. Heterogeneous enhancement pattern of parenchyma. Nonenhancing decreased signal areas: necrosis, pseudocyst. Well-depicted pancreatic pseudocyst contiguous with dilated MPD. Vascular occlusions sometimes demostrated
Lower ADC