Magnetic Resonance Imaging
in the Evaluation of the Pancreatic Neoplasms 
Wassim Asfari, M.D. Sang Soo Shin, M.D. Richard C. Semelka MD
Department of Radiology University of North Carolina Hospitals Chapel Hill

   

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.

28. Friedman AC, Lichtenstein JE, Dachman AH. Cystic neoplasms of the pancreas. Radiological-pathological correlation. Radiology 1983; 149:45-50.

 


Corresponding author :
Richard C. Semelka, M.D.
Department of Radiology  UNC  Chapel Hill CB 7510 – 2001 Old Clinic Bldg Chapel Hill, NC 27599-7510 Phone: (919) 966-9676
Fax: (919) 843-7147
E-mail: richsem@med.unc.edu

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



Bookmark Edited & Powered by A1 ITT Digital Strategisit