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(Radiographics. 2002;22:e2.)
© RSNA, 2002

MR Imaging of the Pancreas: A Pictorial Tour1

Celso Matos, MD, Olivier Cappeliez, MD, Catherine Winant, MD, Emmanuel Coppens, MD, Jacques Devière, MD and Thierry Metens, PhD

1 From the Department of Radiology, Hôpital Erasme, Université Libre de Bruxelles, 808 Route de Lennik, B-1070 Brussels, Belgium. Received March 14, 2001; revision requested September 12; revision received and accepted October 22. Address correspondence to C.M. (e-mail: cmatos@ulb.ac.be)



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Figure 1.   For the main pancreatic duct, the resolution of MRCP approaches that of ERCP. This comparative MRCP (A) and ERCP (B) data obtained in an 80-year-old patient with senescent changes of the pancreatic duct clearly illustrates this assertion.

 


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Figure 2.   Normal MRCP performed during secretin stimulation shows a slight and temporary increase in the caliber and signal intensity of the main pancreatic duct in A (arrow) and, concomitantly, progressive and complete duodenal filling (arrowheads in B). Complete filling of the Santorini duct (arrowhead in A) is also seen.

 


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Figure 3.   Patient with acute necrotizing pancreatitis, a peripancreatic exudate, and ascites. Suboptimal visualization of the common bile duct and pancreatic duct (arrows) due to increased signal intensity of the background tissue is observed on this MRCP image. To avoid suboptimal visualization in such conditions, a 2D or 3D multisection acquisition with a targeted MIP can be used.

 


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Figure 4.   MRCP before (A) and after (B) administration of a "negative" oral contrast agent. Better visualization of the pancreatic duct in the tail (arrowhead) and the peripancreatic collection (arrows) is seen after suppression of background fluid in the stomach (*) in B.

 


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Figure 5.   Patient with obstructive chronic calcified pancreatitis. (A) Plain radiograph show a calcified stone (arrowhead) in the pancreatic area. (B) The MRCP shows dilatation of the main pancreatic duct and the side branches (arrowheads) and the level of obstruction. The obstructive intraductal stone may be suggested (arrow), but its visualization is suboptimal because it is only partially surrounded by fluid. (C) The location of the stone in the main pancreatic duct is clearly shown at ERCP (arrow).

 


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Figure 6.   Chronic calcified pancreatitis and pseudocysts demonstrated on MRCP (A), ERCP (B) and axial (C) and coronal (D) thin-section single-shot TSE T2-weighted images. In A, the damaged portion of the pancreatic duct (arrowheads) and the pseudocyst (arrow) are clearly depicted. However, ductal content and pseudocyst septation and content are better depicted in B, C, and D (arrows).

 


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Figure 7.   Chronic calcified pancreatitis and multiple calculi in the main pancreatic duct demonstrated on MRCP (A) and coronal multisection thin-slab TSE T2-weighted images obtained with a shorter echo time (80 msec) (B, C, D). Filling defects corresponding to calculi in the pancreatic duct are better visualized in B, C, and D (arrowheads); however, the whole pancreatic duct anatomy is better displayed in A. The "filling defect" at the hilum of the liver (arrow) corresponds to a vascular impression.

 


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Figure 8.   Acute necrotizing pancreatitis demonstrated on MRCP (A) and coronal thin-section single-shot TSE T2-weighted (B) images. In A, a distal common bile duct stricture (arrow), abnormal pancreatic duct side branches (solid arrowheads) and indirect signs of duodenal wall thickening (open arrowheads) are visualized. The peripancreatic fluid collections detected in B (arrows) are not detected in A, because of the shorter T2 relaxation time of the fluid in the peripancreatic collections. However, because of intrinsic limitations in signal-to-noise ratio and spatial resolution, this sequence is not useful for detection of solid lesions within the pancreas or the liver (Fig 9)

 


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Figure 9.   Coronal thin-section single-shot TSE T2-weighted image obtained in a patient with a pancreatic tumor (*) and liver metatstases (arrows). Contrast between lesions and normal adjacent liver is suboptimal.

 


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Figure 10.   (A, B) MRCP images obtained before (A) and after (B) secretin administration, (C) axial thin-section single-shot TSE T2-weighted image, and (D) axial TSE T1-weighted image obtained with a fat suppression spectral prepulse. Patient presented with a hemorrhagic pseudocyst (arrowheads) and suspicion of pancreatic duct rupture (arrow in A). In B, the full length of the pancreatic duct is delineated and a main duct rupture can be ruled out.

 


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Figure 11.   Dynamic MRCP during secretin stimulation in a patient presenting with a pancreas divisum configuration. Fast repetition of data acquisition allows clear visualization of the intramural portion of the common bile duct and the pancreatic duct (arrowheads in B).

 


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Figure 12.   MRCP images obtained before (A) and 10 minutes after (B) secretin administration in a patient with recurrent episodes of pancreatitis and pancreas divisum. In A, the ventral duct is not visible, while in B it is clearly delineated (arrowhead). The dorsal duct (arrows) shows a prolonged increase in caliber related to outflow impairment of pancreatic fluid.

 


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Figure 13.   Dynamic MRCP images (A obtained before secretin administration, B and C obtained 2 and 5 minutes, respectively, after secretin administration) in a patient with an ampullary tumor shows an increase in the caliber of the pancreatic duct (arrow) and an incomplete recovery of the baseline value 10 minutes (D) after the administration of secretin. Associated biliary tract dilatation is seen (arrowheads).

 


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Figure 14.   Dynamic MRCP images obtained in a patient with mild changes of chronic pancreatitis before (A) and after (B) secretin administration. Improved visualization of side branches (arrowheads) is seen in B.

 


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Figure 15.   (AD) Dynamic MRCP images obtained in a patient with progressive enhancement of the pancreatic parenchyma (arrowheads) after secretin administration. A was acquired before the administration of secretin, and B was acquired 2 minutes after. (13) Corresponding ERCP images show a progressive increase in pancreatic duct caliber during retrograde injection of contrast material, which might be related to pancreatic tissue hypertension. Side-branch morphology (arrows) is compatible with early changes due to chronic pancreatitis.

 


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Figure 16.   (A) MRCP image obtained in a patient with enhancement of pancreatic parenchyma (arrowheads) after secretin stimulation. B After endoscopic pancreatic sphincterotomy, parenchymal enhancement is no longer detected.

 


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Figure 17.   (A) MRCP image obtained 10 minutes after secretin administration in a patient with normal duodenal filling. (B) MRCP image in another patient with chronic pancreatitis shows reduced duodenal filling (arrows).

 


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Figure 18.   Patient with acute pancreatitis and peripancreatic exudate. Non-fat-suppressed (A, C) and fat-suppressed (B, D) axial and coronal HASTE T2-weighted images. Increased signal intensity of peripancreatic fat tissues (arrows) is better demonstrated in B and D.

 


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Figure 19.   Normal pancreas demonstrated on four contiguous sections obtained with a TSE T1-weighted sequence with a fat-suppression spectral prepulse. The pancreatic parenchyma has homogeneously high intensity, and delineation of pancreatic contours (arrowheads) is improved.

 


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Figure 20.   Neuroendocrine tumor involving the tail of the pancreas shown on (A) MRCP, (B) axial respiratory-triggered TSE T2-weighted, and (C) fat-suppressed TSE T1-weighted images obtained at the level of the tumor. In A, a stricture with upstream dilatation of the pancreatic duct is displayed (arrow). In B, no difference in signal intensity is detected between the tumor (arrow) and the adjacent pancreas. In C, the tumor is clearly delineated (arrowhead).

 


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Figure 21.   Normal pancreas (A, B) and chronic pancreatitis (C, D) demonstrated with an axial GRE T1-weighted sequence with a water-stimulation prepulse. As with fat-suppression sequences, spectral water stimulation suppresses the fat signal and normal pancreas has high intensity. In chronic pancreatitis, the signal is dramatically reduced (*) because of the diffuse fibrosis in the gland.

 


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Figure 22.   Normal pancreas demonstrated on coronal 3D GRE T1-weighted images obtained after an IV bolus injection of a gadolinium chelate in the (A) arterial, (B) early portal venous, and (C) delayed phases. Progressive and homogeneous pancreatic enhancement is seen (arrows). MIP images (D, E) calculated from data obtained in A and B, respectively, nicely demonstrate the arterial and venous networks.

 


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Figure 23.   Adenocarcinoma of the head of the pancreas demonstrated on a coronal 3D GRE T1-weighted image obtained after an IV bolus of a gadolinium chelate in the portal venous phase (A) and the correponding MIP (B). The small tumor (arrow) is displayed in A, and no venous invasion is detected.

 


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Figure 24.   Positioning (A, B) and resultant axial (C) and coronal (D) single-shot MRCP projections obtained according to the anatomic angulation of the pancreas.

 


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Figure 25.   Acute necrotizing pancreatitis is demonstrated with MRCP before (A) and after (B) secretin administration. In B, the "ductal defect" visualized in A is completely filled (arrows), allowing main pancreatic duct disruption to be ruled out. Fat-suppressed TSE T1-weighted images before (C) and after administration of IV gadolinium chelate (D) clearly demonstrate the extent of glandular damage (arrowheads). The extent of necrosis is better evaluated in D.

 


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Figure 26.   Pancreatic duct disruption and pseudocyst complicating acute pancreatitis demonstrated with MRCP before (A) and after (B, C) secretin administration and a coronal HASTE T2-weighted sequence (D). In C, a more targeted projection clearly demonstrates the communication (arrow) of the pseudocyst with a pancreatic fistula originating in the tail (arrowhead). Note that the pancreatic duct appears normal (arrow in B) downstream to the rupture. In B, the pseudocyst (*) increased in volume compared to that seen in A, suggesting a communication with the pancreatic duct. In D, the topography of the fistula (arrow) is better demonstrated.

 


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Figure 27.   Acute pancreatitis and pancreatic duct disruption with peripancreatic fluid collection. (A) Axial HASTE T2-weighted image demonstrates the anteriorly located fluid collection (*). (B) MRCP after secretin administration depicts a bright spot (arrow) in the pancreatic duct overlapping the fluid collection (*) and corresponding to the site of disruption (Movie 2). Morphologic changes involving the side branches in the tail are also depicted (arrowhead).

 


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Figure 28.   Acute pancreatitis, pancreatic duct disruption, and pseudocyst demonstrated with MRCP after administration of secretin (A) and with coronal (B) and axial (C, D) HASTE T2-weighted sequences with fat suppression. In A, a pancreatic duct defect (arrow) not filled by secretin is seen in conjunction with a heterogeneous pseudocyst (*) and an upstream dilatation of the pancreatic duct (arrowhead). The pseudocyst wall, internal septation (arrowhead in D), and topography are better depicted in BD.

 


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Figure 29.   Chronic pancreatitis with a pancreatic duct rupture and a pseudocyst with necrotic debris in the tail of the pancreas demonstrated with MRCP (A) and corresponding axial (B) and coronal (C, D) HASTE T2-weighted sequences. The pseudocyst "wall", the necrotic debris, and the relationship with the wall of the stomach (*) are better visualized in B, C, and D (black arrows). The morphologic changes in the pancreatic duct (arrowheads) and a small fistula tract (white arrow) are better depicted in A.

 


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Figure 30.   Acute pancreatitis with local hemorrhage around the head of the pancreas. (A) MRCP shows a normal pancreatic duct and a cystic lesion (arrow) in the tail. (B) Axial HASTE T2-weighted image also shows the cystic lesion (arrow). (C) On an axial HASTE T2-weighted image, the head of the pancreas (*) seems enlarged. (D) Fat-suppressed TSE T1-weighted image shows a focal area of hyperintensity (arrow) corresponding to hemorrhage.

 


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Figure 31.   Pancreas divisum and acute pancreatitis. (A, B) Unenhanced CT scans obtained at the level of the body (A) and head (B) of the pancreas clearly demonstrate glandular enlargement (*) with diffuse hypoattenuating areas related to inflammatory changes. (C, D) Corresponding MRCP images obtained before (C) and after (D) secretin administration. Improved delineation of the pancreatic duct and minor ampulla dilatation (arrow) are seen in D.

 


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Figure 32.   Pancreas divisum and pancreatitis. (A) Contrast-enhanced helical CT shows an enlarged dorsal duct (arrowhead) anterior to the common bile duct (arrow). (B, C) Corresponding unenhanced (B) and secretin-enhanced (C) MRCP images demonstrate dorsal duct enlargement (arrow), abnormal side branches (arrowheads), and reduced duodenal filling.

 


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Figure 33.   Intraductal papillary mucinous tumor in patient presenting with recurrent pancreatitis. (A) Unenhanced CT at the level of the head of the pancreas shows a well-delineated hypoattenuating lesion (arrow) not extending to the peripancreatic fat. (B) Corresponding MRCP image shows a pancreas divisum with a minute communication (arrow) in conjunction with a homogeneous, hyperintense lobulated lesion (*) in the ventral pancreas. (C) Coronal fat-suppressed HASTE T2-weighted image more clearly demonstrates communication of the lesion with the duct (arrow).

 


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Figure 34.   Intraductal papillary mucinous tumor in patient presenting with recurrent pancreatitis. (A) MRCP after secretin administration demonstrates a pancreas divisum with minute communication and an irregular fluid-filled lesion (arrow) communicating with the ventral portion of the duct. (B, C) Corresponding ERCP images obtained after selective retrograde iodine contrast material injection fails to demonstrate the cystic tumor. In C, selective catheterization of the ventral portion of the pancreatic duct is shown.

 


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Figure 35.   Intraductal papillary mucinous tumor in patient presenting with recurrent pancreatitis. (A, B) Contrast-enhanced CT scan (A) and corresponding axial HASTE T2-weighted iamge (B) clearly demonstrate a ventral pancreatic duct enlargement (arrows) and no tumor. (C, D) MRCP (C) and corresponding ERCP (D) better demonstrate the extent of the intraductal lesion, its irregular margins, and filling defects (arrows), corresponding to mucus production and papillary hyperplasia.

 


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Figure 36.   Chronic calcified pancreatitis. (A) Plain radiograph of the pancreatic area shows multiple calcified stones. (B) ERCP with the catheter placed in the ventral pancreatic duct shows that stones are partially broken (arrowhead) after extracorporeal shockwave lithotripsy. Stones are located in the Santorini duct. (C, D) MRCP in the axial (C) and coronal (D) planes clearly demonstrates the exact location of the filling defects (arrows) in the Santorini duct and the marked ductal alterations of chronic pancreatitis (enlargement of the main duct, irregularities, and side branch dilatation). This case illustrates the potential of MRCP as a guide for endoscopic therapy and for follow-up studies.

 


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Figure 37.   Obstructive chronic calcified pancreatitis. (A) MRCP shows characteristic alterations with marked ductal dilatation, filling defects, and a smooth common bile duct stricture (arrowhead). (B, C) Corresponding cross-sectional MR images demonstrate glandular enlargement and decreased signal intensity on the water-stimulated GRE T1-weighted image (arrowheads in C). Extrinsic gastric wall compression (arrows) due to glandular enhancement is also displayed on both MRCP (A) and coronal HASTE T2-weighted (B) images.

 


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Figure 38.   Chronic calcified pancreatitis. (A) Unenhanced CT scan shows the calcified stones (arrow) in the head of the pancreas. (B) Axial HASTE T2-weighted image does not show the stones. (C) MRCP shows the extent of ductal damage and side-branch involvement (arrowheads) but does not clearly demonstrate the stones and their distribution, nor the exact morphology of the ducts in the head of the pancreas.

 


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Figure 39.   Intraductal mucus-producing lesions mimicking chronic pancreatitis. (A) MRCP shows a mild dilatation of the pancreatic duct and side branches (arrowheads) and no filling defects. (B) Fat-suppressed TSE T1-weighted image through the pancreas shows a subtle decrease in signal intensity in the tail (arrow). (C, D) ERCP at the level of the head and body (C) and tail (D) of the pancreas shows that the duct was partially filled with mucus (arrows).

 


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Figure 40.   Chronic pancreatitis with obstructive stones. (A) Contrast-enhanced CT section at the level of the head of the pancreas shows the stones and pancreatic duct dilatation (arrowheads). (B) MRCP performed before endoscopic stone extraction reveals the filling defect (arrow) and the marked pancreatic duct dilatation; no anatomic variant is seen, and the common bile duct is slightly enlarged. (C) After stone removal, MRCP shows a substantial decrease in pancreatic duct and common bile duct caliber.

 


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Figure 41.   Chronic pancreatitis with pseudocyst in the head of the pancreas. (A, B) Coronal (A) and axial (B) HASTE T2-weighted images show the pseudocyst in the head of the pancreas and its relationship with the ventral pancreatic duct (arrow). (C, D) MRCP images obtained before (C) and after (D) endoscopic stent insertion clearly demonstrate the distention of the pancreatic duct and side branches (arrowheads in C), as well as the pseudocyst (arrow in C) and the dramatic reduction in the caliber of the pancreatic duct and disappearance of the pseudocyst after stent insertion (arrow in D).

 


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Figure 42.   Mild chronic pancreatitis. Comparative study with unenhanced CT, MR imaging, and secretin-enhanced MRCP. At unenhanced CT (A), no calcifications, pancreatic duct enlargement, or glandular atrophy are depicted. Cross-sectional T2-weighted image (B) and MRCP (C) demonstrate main pancreatic duct and side-branch enlargement (arrowheads) compatible with mild chronic pancreatitis changes.

 


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Figure 43.   Chronic pancreatitis with an increase in pancreatic lipase and amylase in a symptom-free patient. (A, B) Contrast-enhanced CT scans in the delayed phase shows a homogeneous pancreas without calcifications and a subtle enlargement of the pancreatic duct in the head (arrow). (C, D) Secretin-enhanced MRCP images obtained 2 (C) and 8 (D) minutes after secretin administration show pancreatic duct dilatation, irregularities of the borders, and side-branch dilatation (arrowheads) compatible with chronic pancreatitis changes.

 


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Figure 44.   Chronic pancreatitis. Unenhanced (A) and secretin-enhanced (B) MRCP, ERCP (C), and axial HASTE T2-weighted image (D). Ductal changes are clearly depicted in AC (arrowheads), while they are less conspicuous on the cross-sectional MR study (D). This case illustrates the need for MRCP studies even in the absence of ductal dilatation at cross-sectional MR imaging.

 


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Figure 45.   Chronic pancreatitis and main pancreatic duct stricture in the body of the pancreas. (A, B) Secretin-enhanced MRCP demonstrates that at the level of the stricture, side branches are located close to the stricture (arrowhead). Duodenal filling is normal. (C, D) Axial HASTE T2-weighted (C) and axial fat suppressed TSE T1-weighted (D) images confirm the absence of a space-occupying lesion (arrows). Moreover, in D, the hyperintense normal pancreas is clearly differentiated from the hypointense fibrotic parenchyma (arrowheads).

 


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Figure 46.   Complication of acute pancreatitis. Unenhanced (A) and secretin-enhanced (B) MRCP images. In A, a single distal pancreatic duct stricture and proximal dilatation are visualized (arrowheads). In B, complete filling of the stricture (arrowheads) was obtained after IV secretin administration.

 


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Figure 47.   Groove pancreatitis. (A) MRCP demonstrates a "double duct" stricture with proximal dilatation of the common bile duct and pancreatic duct (arrow). A cystic lesion (arrrowhead) is seen between the common bile duct and the duodenal wall. (B) Axial fat-suppressed TSE T1-weighted image at the level of the head of the pancreas shows the normal hyperintense pancreas (arrow) and no tumor. However, the pancreas is medially shifted because of the presence of a hypointense lesion (*) located between the head of the pancreas and the gallbladder. (C, D) Axial unenhanced (C) and delayed gadolinium-enhanced (D) GRE T1-weighted images, demonstrate diffuse enhancement (arrow) of the sheetlike mass, which corresponded to fibrotic tissue (40).

 


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Figure 48.   Pancreatic cancer. (A) Unenhanced (left) and secretin-enhanced (right) MRCP images show a focal defect (arrowhead) of the pancreatic duct not filled after secretin administration, with proximal dilatation and chronic pancreatitis-related changes. (BD) Axial HASTE T2-weighted (B) and unenhanced (C) and gadolinium-enhanced (D) fat-suppressed TSE T1-weighted contiguous images do not demonstrate the tumor.

 


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Figure 49.   Pancreatic cancer with venous invasion. Staging with "all-in-one" MR imaging. (A) MRCP shows a double-duct stricture in the head of the pancreas (arrows). (B) Unenhanced axial fat-suppressed TSE T1-weighted image demonstrates the hypointense pancreatic tumor (arrow). (C, D) Coronal gadolinium-enhanced dynamic 3D GRE T1-weighted image (C) and corresponding MIP (D) nicely demonstrate superior mesenteric vein invasion (arrows).

 


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Figure 50.   Coronal 3D GRE T1-weighted images obtained after an IV bolus of a gadolinium chelate in the arterial (A) and portal venous (B) phases in a patient with pancreatic cancer (arrows in A), hepatic metastases (arrowheads in A), and splenic vein invasion (arrow in B).

 


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Figure 51.   Incidental diagnosis of serous cystadenoma in a patient with gallstones and chronic pancreatitis. MRCP (A) and axial (B) and coronal (C, D) HASTE T2-weighted images show a lobulated "microcystic" mass in the head of the pancreas (arrows). No definite communication with the pancreatic duct is demonstrated. Mild chronic pancreatitis changes (arrowheads) are also seen in A.

 


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Figure 52.   Intraductal mucin-producing tumor (side-branch duct type). Secretin-enhanced MRCP studies (A, C) and comparative ERCP (B). Both examinations demonstrate multiple irregular cystic lesions (arrowheads) in the head of the pancreas, communicating with a normal pancreatic duct (arrows). The more distal cystic lesion (*) seen at MRCP is not completelly filled at ERCP.

 


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Figure 53.   Intraductal mucin-producing tumor with malignant transformation. (A) MRCP shows main pancreatic duct dilatation (branch duct type) (arrowheads). (B) Axial HASTE T2-weighted image at the level of the head of the pancreas shows the continuity of the ventral duct with the cystic dilatation (arrow).

 


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Figure 54.   Carcinoid tumor of the uncinate process. Contrast-enhanced CT (A), coronal fat-suppressed HASTE T2-weighted image (B), and MRCP after secretin administration (C) before and (D) after duodenopancreatectomy. In A, a hypoattenuating lesion (arrow) with peripheral enhancement is seen. B and C show the cystic nature of the lesion and its irregular margins (arrows). No definite communication with the pancreatic duct is demonstrated. The caliber of the pancreatic duct and duodenal filling are normal. The suggested diagnosis before surgery was a cystadenoma or an intraductal papillary mucinous tumor invoving a side branch. In D, we see an enlargement of the main pancreatic duct (arrowheads) with marked changes of chronic pancreatitis. In this clinical setting and in accordance with previous studies (50), we use cystic fluid aspiration with cytologic evaluation, measurement of viscosity, and analysis for tumor markers and enzymes as an ancillary diagnostic tool.

 





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