Magnetic Resonance Imaging in the Evaluation of the Pancreatic Neoplasms |
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Department of Radiology University of North Carolina Hospitals Chapel Hill | ||||||||||||||
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Abstract The
magnetic resonance imaging (MRI) is a valuable screening tool in the
evaluation of various pancreatic diseases, including pancreatic
neoplasms. A standard MR protocol including non-contrast T1-weighted
fat-suppressed and dynamic gadolinium-enhanced gradient-echo imaging is
sensitive for the assessment of the pancreatic tumors. The usefulness of
MRI in the investigation of pancreatic tumors could be summarized as
follows: (1) detection and characterization of pancreatic tumors,
especially small tumors, (2) evaluation of local extension and vascular
encasement, and (3) determination of the presence of lymph node,
peritoneal, and liver metastases.
Introduction
The pancreatic adenocarcinoma accounts for
95% of all the malignant tumors which occurs in the pancreas. Pancreatic
adenocarcinoma appears as a low signal intensity on T1-weighted fat-suppressed
spin echo (SE) images and has diminished enhancement on dynamic
contrast-enhanced images. Islet-cell tumors arise from the endocrine portion
of the pancreas. They range from benign to malignant. The islet cell tumors
are sub-classified into functioning and nonfunctioning tumors. These tumors
are moderately low in signal intensity on T1- weighted fat-suppressed images,
and demonstrate homogeneous ring or diffuse heterogeneous enhancement on
immediate post-gadolinium gradient-echo image. Pancreatic cystic lesions
appear as well-defined lesions. On MR
images, they do not demonstrate invasion of peripancreatic fat or adjacent
organs. The
objective of this manuscript is to demonstrate MR imaging features of various
pancreatic neoplasms, which are sufficient to detect and characterize
pancreatic tumors. MRI
Technique Our
MRI protocol for the evaluation
of the pancreatic tumors includes transverse and coronal T2-weighted
single-shot echo-train spin-echo (SS-ETSE), transverse T2-weighted fat
suppressed SS-ETSE, transverse T1-weighted spoiled gradient echo (SGE)
in-phase and out-of phase , and transverse T1-weighted fat-suppressed
3-dimentional gradient-echo(3D-GE) images acquired before contrast
administration and during the hepatic arterial-dominant (immediate) phase
(15-20 seconds), the early hepatic venous phase (45 seconds), and the hepatic
venous (interstitial) phase (120 seconds) after contrast administration. MR
cholangiopancreatography (MRCP) images acquired in a coronal oblique
projection to delineate the pancreatic and bile duct is a useful addition.
MRCP permits good demonstration of the biliary and pancreatic ducts to assess
ductal obstruction, dilatation, and abnormal duct pathways. Breath-hold
T1-weighted gradient-echo sequences obtained either as 2D or 3D gradient-echo,
fat-suppression techniques, and dynamic administration of gadolinium chelate
have resulted in image quality of the pancreas sufficient to detect and
characterize focal pancreatic mass lesions. The use of high spatial resolution
MR imaging at 3.0 T improves the detection of small focal lesions,
particularly. MR Imaging
Finding of Normal Pancreas The
normal pancreas is high in signal intensity on T1-weighted fat-suppressed
images because of the presence of aqueous protein in the acini of the pancreas
(1). Normal pancreas is well shown with this technique (Fig. 1A). In elderly
patients, the signal intensity of the pancreas may diminish and be lower than
that of liver. This may reflect changes of fibrosis secondary to the aging
process. The pancreas demonstrates a uniform capillary blush on immediate
postcontrast images (2), which renders it markedly higher in signal intensity
than liver, neighboring bowel, and adjacent fat (Fig. 1B).
Pancreatic
Neoplasms Pancreatic
mass lesions can be detected and successfully characterized with a pattern
recognition approach using T1, T2, and immediate and late post-gadolinium
images. 1.
Adenocarcinoma Adenocarcinoma
of the pancreas refers to carcinoma arising in the exocrine portion of the
gland. Pancreatic ductal adenocarcinoma accounts for 95% of malignant tumors
of the pancreas (3). The lesion is more common in males and blacks. The age
range for tumor occurrence is the fourth through the eighth decade (4, 5),
with incidence peaking in the eighth decade. The tumor has a poor prognosis,
with a 5-year survival of 5% (4). Approximately 60–70% of pancreatic
adenocarcinomas occur in the head (Fig. 2A), 15% in the body, 5% in the tail,
and 10–20% with diffuse involvement (6). Pancreatic adenocarcinoma arising
in the head of the pancreas may cause obstruction of the CBD and pancreatic
duct. This
appearance on MRCP studies results in the “double duct sign,” (Fig. 2B),
which was originally described on ERCP (7). A characteristic imaging
appearance of pancreatic carcinoma consists of enlargement of the head of the
pancreas with dilatation of the pancreatic and common bile duct and atrophy of
the body and tail of the pancreas. Because liver metastases are not common at
initial presentation, the most useful imaging feature for the diagnosis of
pancreatic cancer is the demonstration of a focal hypovascular mass within
pancreatic parenchyma. Immediate post-gadolinium gradient echo image was found
to be the most sensitive approach to detect pancreatic adenocarcinoma,
particularly in the head of the pancreas. Both immediate post-gadolinium
gradient-echo and non-contrast T1-weighted fat-suppressed imaging can be
performed at excluding adenocarcinoma, and both were significantly superior to
spiral CT imaging (8). Pancreatic adenocarcinoma appears as a low signal
intensity mass on non-contrast T1-weighted fat suppressed images (1, 8, 9) and
enhances to a lesser extent than the surrounding normal pancreatic tissue on
immediate post-contrast images. These MRI features are related to their
abundant fibrous stroma and relatively spare tumor vascularity. The appearance
of adenocarcinomas on interstitial phase images is variable and reflects the
volume of extracellular space and venous drainage of cancers compared with the
pancreatic tissue. Surgery remains the main therapeutic treatment of patients
with pancreatic adenocarcinoma (4, 10). Therefore, earlier detection of
potentially curable disease may result in improved patient survival. 2.
Islet Cell Tumors
Islet cell tumors are a subgroup of
gastrointestinal neuroendocrine tumors (11). These tumors are rare and
uncommon. Tumors may be nonfunctioning, or, more commonly, they may present
with an endocrine abnormality resulting from the secretion of hormones (12).
For the functioning tumors, tumor itself is named after the hormone it
secretes (e.g., an insulin- secreting tumor is termed an insulinoma). The most
common pancreatic islet cell tumors are insulinomas and gastrinomas, followed
in frequency by nonfunctional or untyped tumors. Nonfunctional tumors account
for at least 15–20% of islet cell tumors and tend to present with symptoms
due to large tumor mass or metastatic disease (13). Malignancy cannot be
diagnosed on the basis of the histologic appearance of islet cell tumors.
Instead, malignancy is determined by the presence of metastases or local
invasion beyond the substance of the pancreas. Insulinomas are most commonly
benign tumors, gastrinomas are malignant in approximately 60% of cases, and
almost all other types, including nonfunctioning tumors, are malignant in the
great majority of cases. The liver is the most common organ for metastatic
spread. There is also a modest propensity for splenic metastases. In
the MRI investigation for islet cell tumors, pre-contrast T1-weighted
fat-suppressed images, immediate post-gadolinium gradient-echo images, and
T2-weighted fat-suppressed images or breath-hold T2-weighted images are
useful. Tumors are low in signal intensity on T1-weighted fat-suppressed
images, demonstrate homogeneous, ring, or diffuse heterogeneous enhancement on
immediate post-gadolinium gradient echo (Fig. 3), and are high in signal
intensity on T2-weighted fat-suppressed images (14). In rare instances, islet
cell tumors may be very desmoplastic, appear low in signal intensity on
T2-weighted images, and demonstrate negligible contrast enhancement. In these
cases, the tumors may mimic the appearance of pancreatic ductal adenocarcinoma.
Gastrinomas
(G Cell Tumors) Gastrinomas
occur most frequently in the region of the head of the pancreas including
pancreatic head, duodenum, stomach, and lymph nodes in a territory termed the
gastrinoma triangle (15). The anatomic boundaries of the triangle are the
porta hepatis as the superior point of the triangle and the second and third
parts of the duodenum forming the base. Although gastrinomas are usually
solitary, multiple gastrinomas may occur, especially in the setting of
multiple endocrine neoplasia syndrome, type 1 (16, 17). In this setting,
patients have multiple pancreatic and duodenal islet cell tumors. Gastrinomas
are not as frequently hypervascular as insulinomas. Gastrinomas
are low in signal intensity on T1-weighted fat-suppressed images and high in
signal intensity on T2-weighted fat-suppressed images, demonstrating
peripheral ring-like enhancement on immediate post-gadolinium gradient-echo
images (18). Central low signal intensity on post-gadolinium images reflects
central hypovascularity. Occasionally, lesions will be cystic. The enhancing
rim of the primary tumor varies substantially in thickness, with the thickness
of the rim reflecting the degree of hypervascularity of the tumor.
Gastrointestinal imaging findings that may be observed in gastrinomas include
enlargement of the rugal folds of gastric mucosa (hypertrophic gastropathy)
and intense mucosal enhancement on early post-gadolinium gradient-echo images,
increased esophageal enhancement, and abnormal enhancement and/or thickness of
proximal small bowel. These features are reflective of the inflammatory
changes of peptic ulcer disease and gastric hyperplasia due to the effects of
gastrin. Gastrinoma metastases to the liver frequently are relatively uniform
in size and shape (19) and generally hypervascular and possess uniform intense
rim enhancement on immediate post-gadolinium gradient-echo images. Insulinomas
Insulinomas
are one of the most common islet cell tumors and are frequently functionally
active. Patients present with signs and symptoms of hypoglycemia. Insulinomas
are low in signal intensity on T1-weighted images and high in signal intensity
on T2-weighted images. They are well shown on T1-weighted fat-suppressed
images (18). Small insulinomas typically enhance homogeneously on immediate
post-gadolinium gradient-echo images. Larger tumors, measuring more than 2cm
in diameter, often show ring enhancement. Liver metastases from insulinomas
typically have peripheral ring-like enhancement, although small metastases
tend to enhance homogeneously. Enhancement of small metastases frequently
occurs transiently in the capillary phase of enhancement and fades on images
acquired at 1 min after injection. Glucagonoma,
Somatostatinoma, VIPoma, and ACTHoma These
islet cell tumors are considerably rarer than insulinomas or gastrinomas. They
are usually malignant, with liver metastases present at the time of diagnosis
(20-22). The primary pancreatic tumors of glucagonoma and somatostatinoma are
large and heterogeneous on MR images. They are usually moderately low in
signal intensity on T1-weighted fat-suppressed images and moderately high in
signal intensity on T2-weighted fat-suppressed images, enhancing
heterogeneously on immediate post-gadolinium images (23). Liver metastases are
generally heterogeneous in size and shape, unlike gastrinoma metastases, which
are typically uniform (19). Metastases possess irregular peripheral rims of
intense enhancement on immediate post-gadolinium gradient-echo images.
Peripheral spoke-wheel enhancement may be observed in liver metastases on
immediate post-gadolinium images. Hypervascular liver metastases are best
shown on immediate post-gadolinium gradient-echo images, which are superior to
spiral CT images for this determination. Splenic metastases are not uncommon 3.
Carcinoid Tumors Carcinoid
tumors are generally large at presentation, with coexistent liver metastases.
Focal and diffuse involvements of the pancreas have been observed. Tumors are
generally mildly hypointense on T1 and moderately hyperintense on T2 and show
diffuse heterogeneous enhancement on immediate post-gadolinium images (14).
Enhancement of the primary tumor may be mild, despite extensive enhancement of
liver metastases. Liver metastases are variable in size and often exhibit
intense enhancement, similar to islet cell tumor liver metastases. 4.
Cystic Neoplasms In
general, this group of pancreatic tumors arises from the exocrine component of
the gland and is much less common than solid exocrine carcinomas. Serous
Cystadenoma Serous
cystadenomas are usually microcystic and multilocular, and consist of multiple
small cysts less than 1cm in diameter. Uncommonly, serous cystadenomas may be
macrocystic (cysts measuring from 1 to 8cm) including multilocular,
oligolocular or unilocular subtypes. This tumor frequently occurs in older
patients and has an increased association with von Hippel–Lindau disease
(24). Calcifications may occasionally be present. On MR images, the tumors are
well defined and do not demonstrate invasion of fat or adjacent organs (25).
On T2-weighted images, the small cysts and intervening septations may be well
shown as a cluster of small grapelike high-signal-intensity cysts. Relatively
thin uniform septations and absence of infiltration of adjacent organs and
structures are features that distinguish serous cystadenoma from serous
cystadenocarcinoma. Tumor septations usually enhance minimally with gadolinium
on early and late post-contrast images, although moderate enhancement on early
post-contrast images may occur. Delayed enhancement of the central scar may
occasionally be observed (26) and is more typical of large tumors. The central
scar may represent compressed contiguous cyst walls of centrally located
cysts.
Cystic pancreatic masses that contain cysts measuring less than 1cm in
diameter may represent microcystic cystadenoma or side branch type intraductal
papillary mucinous tumor (IPMT), which can be difficult to distinguish. The
presence of a central scar is a feature distinguishing serous cystadenoma from
side branch IPMT, which does not exhibit this finding. Definition of
communication with the pancreatic duct on MRCP images establishes the
diagnosis of side branch IPMT. Serous
Cystadenocarcinoma This
malignant pancreatic tumor is extremely rare. Distinction from benign serous
cystadenoma is difficult on histologic background alone and may only be
established by the presence of metastatic disease or local invasion. The
presence of thick septations and solid components are suggestive signs for
serous cystadenocarcinoma (24). Mucinous
Cystadenoma / Cystadenocarcinoma
These tumors are divided
into benign (mucinous cystadenoma), borderline, and malignant (mucinous
cystadenocarcinoma). However, at many institutions, all cases of mucinous
cystic neoplasms are interpreted as mucinous cystadenocarcinomas of low-grade
malignant potential to reinforce the need for complete surgical resection and
close clinical follow up (24, 25, 27, 28). Mucinous cystic neoplasms occur
more frequently in females (6 to 1), and approximately 50% occur in patients
between the ages of 40 and 60
years.
These
tumors usually are located in the body and tail of the pancreas. They may be
large (mean diameter of 10cm), often multiloculated, and encapsulated. Of
these tumors, 10% may have scattered calcifications. There is a great
propensity for invasion of local organs and tissues. On
gadolinium-enhanced T1-weighted fat-suppressed images, large, irregular cystic
spaces separated by septa are demonstrated (26). Cyst walls and septations are
often thicker in mucinous cystadenocarcinomas than those of mucinous
cystadenomas. Mucinous cystadenomas are well circumscribed, and they show no
evidence of metastases or invasion of adjacent tissues. Mucinous
cystadenocarcinoma may be very locally aggressive malignancies with extensive
invasion of adjacent tissues and organs. Absence of demonstration of tumor
invasion into surrounding tissue does not, however, exclude malignancy. The
presence of solid component is also suggestive of malignancy. Mucin produced
by these tumors may result in high signal intensity on T1- and T2-weighted
images of the primary tumor and liver metastases. Liver metastases are
generally hypervascular and have intense ring enhancement on immediate
post-gadolinium images. Metastases are commonly cystic and may contain mucin,
which results in mixed low and high signal intensity on T1- and T2-weighted
images. Intraductal
Papillary Mucinous Neoplasms (Duct-Ectatic Mucin-Producing Tumor) Intraductal
papillary mucinous neoplasms (IPMN) arise in the pancreatic duct epithelium. IPMN—Main
Duct Type
This tumor can be classified as diffuse or
segmental. Whereas diffuse tumors involve the entire main duct. Segmental
tumors involve one or more segments of the main duct. On MR images, a greatly
expanded main pancreatic duct is demonstrated on T2-weighted images or MRCP
images. Irregular-enhancing tissue along the ductal epithelium is appreciated
on post-gadolinium images, confirming that underlying tumor is the cause of
the ductal dilatation. Total resection is the treatment for this kind of tumor
involving the whole main duct. Local resection may be sufficient for the
treatment of tumors involving a segment of the main duct. IPMN—Side
Branch Type Septations
are generally present, creating a cluster of grapes appearance. Side branch
type IPMN is usually a benign process that appears as a localized cystic
parenchymal lesion (Fig. 4). The majority of side branch IPMNs is located in
the head of the pancreas. MRCP images are able to show communication of the
cystic tumor with the main pancreatic duct in the majority of cases. Another
feature distinguishing from microcystic cystadenoma is that central compacted
septations are not present in IPMNs. Side-branch IPMNs which are less than
2.5cm in size are usually benign and grow very slowly. Conclusion
MR imaging is sensitive for the evaluation
of pancreatic neoplasms especially in the following settings: (1) T1-weighted
fat-suppressed and dynamic gadolinium-enhanced SGE imaging for the detection
of ductal adenocarcinoma and islet cell tumor, (2) T2-weighted fat-suppressed
imaging for the detection of islet-cell tumors. With
MR imaging, you can assess and characterize small pancreatic mass lesions.
MRCP images allow further evaluation of the pancreatic and bile duct.
References 1. Semelka RC,
Ascher SM. MR imaging of the pancreas-state of the art. Radiology
1993;188:593-602. 2. Semelka RC, Kroeker MA, Shoenut JP,
et al. Pancreatic disease: prospective comparison of CT, ERCP, and 1.5-T MR
imaging with dynamic gadolinium enhancement and fat suppression. Radiology
1991;181:785-791. 3. Jemal A, Siegel R, Ward E,
et al. Cancer
statistics, 2008. CA Cancer J
Clin 2008;58:71-96. 4. Warshaw AL, Fernandez-del Castillo C. Pancreatic
carcinoma. N
Engl J Med 1992;326:455-465. 5. Moossa AR. Pancreatic cancer:
approach to diagnosis, selection for surgery and choice of operation. Cancer
1982;50:2689-2698. 6. Clark LR, Jaffe MH, Choyke
PL, et al. Pancreatic
imaging. Radiol Clin North Am 1985;23:489-501. 7. Fayad LM,
Kowalski T, Mitchell DG. MR cholangiopancreatography: evaluation of common
pancreatic diseases. Radiol Clin North Am 2003;41:97-114. 8. Gabata T,
Matsui O, Kadoya M, et al. Small pancreatic adenocarcinomas: efficacy of MR
imaging with fat suppression and gadolinium enhancement. Radiology
1994;193:683-688. 9. Semelka RC,
Kelekis NL, Molina PL, et al. Pancreatic masses with inconclusive findings on
spiral CT: is there a role for MRI? J Magn Reson Imaging 1996;6:585-588. 10. Benassai G, Mastrorilli M, Quarto G, et al.
Factors
influencing survival after resection for ductal adenocarcinoma of the head of
the pancreas. J Surg Oncol 2000;73:212-218. 11. In: R.C.
Semelka, Editor, Abdominal-Pelvic MRI,
Wiley-Liss Inc, New York (2002). 12. Mozell E,
Stenzel P, Woltering EA, et al. Functional endocrine tumors of the pancreas:
clinical presentation, diagnosis, and treatment. Curr Probl Surg
1990;27:301-386. 13. Thompson NW, Eckhauser FE, Vinik
AI, et al. Cystic neuroendocrine neoplasms of the pancreas and liver. Ann
Surg 1984;199:158-164. 14. Semelka RC, Custodio CM, Cem Balci N, et al.
Neuroendocrine
tumors of the pancreas: spectrum of appearances on MRI.
J Magn Reson Imaging 2000;11:141-148. 15. Wittenberg J,
Simeone JF, Ferrucci JT Jr, et al. Non-focal enlargement in pancreatic
carcinoma. Radiology 1982;144:131-135. 16. Mitchell DG,
Cruvella M, Eschelman DJ, et al. MRI of pancreatic gastrinomas. J Comput
Assist Tomogr 1992;16:583-585. 17. Pipeleers-Marichal M,
Donow C, Heitz PU, et al. Pathologic aspects of gastrinomas in patients with
Zollinger-Ellison syndrome with and without multiple endocrine neoplasia type
I. World J Surg 1993;17:481-488. 18. Kraus BB, Ros PR.
Insulinoma:
diagnosis with fat-suppressed MRimaging. AJR Am J
Roentgenol 1994;162:69-70. 19. Semelka RC,
Cumming MJ, Shoenut JP, et al. Islet cell tumors: comparison of dynamic
contrast-enhanced CT and MR imaging with dynamic gadolinium enhancement and
fat suppression. Radiology 1993;186:799-802. 20. Buetow PC, Parrino TV, Buck JL, et
al. Islet cell tumors of the pancreas: pathologic-imaging correlation among
size, necrosis and cysts, calcification, malignant behavior, and functional
status. AJR Am J Roentgenol 1995;165:1175-1179. 21. Kelekis NL, Semelka RC.
Carcinoma
of the pancreatic head area. diagnostic imaging: Magnetic resonance imaging.
Rays 1995;20:289-303. 22. Tjon A Tham
RT, Jansen JB, Falke TH, et al. Imaging features of somatostatinoma: MR, CT,
US, and angiography. J Comput Assist Tomogr 1994;18:427-431. 23. Kelekis NL, Semelka RC.
MRI
of pancreatic tumors. Eur Radiol 1997;7:875-886. 24. Ros PR, Hamrick-Turner JE,
Chiechi MV, et al. Cystic
masses of the pancreas. Radiographics 1992;12:673-686. 25. Lewandrowski
K, Warshaw A, Compton C. Macrocystic serous cystadenoma of the pancreas: a
morphologic variant differing from microcystic adenoma. Hum Pathol.
1992;23:871-875. 26. Semelka RC, Ascher SM. MR imaging
of the pancreas. Radiology 1993;188:593-602. 27. Khurana B, Mortele KJ, Glickman J, et al.
Macrocystic
serous adenoma of the pancreas: radiologic-pathologic correlation. AJR Am J Roentgenol 2003;181:119-123.
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S.I.A.E.C.M.
- Dipartimento di Radiologia Società Scientifica Registrata Ministero della Salute, del Lavoro e delle Politiche Sociali ECM n. 5607 © S.I.A.E.C.M. & UNC All rights reserved |
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