Magnetic Resonance Cholangiopancreatography: Pearls, Pitfalls, and Pathology

Nyree Grifn, MD, FRCR,* Dominic Yu, BA, FRCR, and Lee Alexander Grant, FRCR
Magnetic resonance cholangiopancreatography is a method of evaluating the pancreaticobiliary tree through the use of heavily T2-weighted magnetic resonance images. Despite being introduced approximately 2 decades ago, it remains the best noninvasive diagnostic tool for this purpose, facilitated by advances in imaging acquisition and technique. The purpose of this review is to describe the protocol at our institution, highlight the pitfalls the reader needs to be aware of when interpreting magnetic resonance cholangiopancreatography images, and demonstrate the different pathologies that it can be used to investigate. Semin Ultrasound CT MRI 34:32-43 C 2013 Elsevier Inc. All rights reserved.

agnetic resonance cholangiopancreatography (MRCP) was introduced approximately 2 decades ago. It highlights uid-lled biliary structures through the use of heavily T2-weighted sequences and has an essential role in the noninvasive evaluation of pancreaticobiliary pathology. The technique has evolved with time, with improvements in the speed of acquisition and spatial resolution. T2-weighted images of the biliary tree were traditionally obtained through the use of balanced gradient-echo steady state free precession sequences.1,2 Nowadays, fast spin-echo (FSE) pulse sequences with long echo times are used, which have higher signal to noise and contrast to noise ratio and lower sensitivity to motion and susceptibility artifacts. Modied sequences have been developed, such as the rapid acquisition with rapid enhancement, fast-recovery FSE, and the half-Fourier acquisition single-shot turbo spin-echo (HASTE) sequences.3-5 The purpose of this pictorial review is rst to describe how MRCP is performed at our institution, second to discuss potential pitfalls the reader needs to be aware of, and third to discuss the myriad indications for this technique. The normal biliary anatomy and variants will not be discussed, as these have been comprehensively described in the rst review paper in this Seminars issue.

MRCP Protocol
The patient is usually fasted 4-6 hours prior to the procedure to reduce uid secretions within the stomach and duodenum, reduce peristalsis, and promote gallbladder lling. Initial axial T2-HASTE breath hold sequences are performed through the upper abdomen, imaging from the diaphragm down to the duodenal ampulla. This allows initial evaluation of the biliary tree and also of the solid organs in the upper abdomen. Two 3-dimensional respiratory-triggered heavily T2-weighted FSE sequences are then obtained in the coronal oblique plane, with 1 acquisition aligned to the common bile duct (CBD) in the head of the pancreas, and 1 aligned to the main pancreatic duct at approximately 901 to the rst imaging plane. Respiratory triggering is achieved using a navigator sequence where the navigator is placed over the edge of the diaphragm on the coronal and sagittal localizers. Diaphragmatic motion can then be tracked as the patient is asked to breathe regularly, allowing the acquisition to be triggered when the position of the diaphragm interface with the lung falls within a prespecied acceptance window. In this way, artifact from respiratory motion can be minimized. Each 3-dimensional navigator sequence takes between 3-7 minutes to acquire and results in a stack of 40 contiguous coronal oblique slices, each of 1.5 mm in thickness. The data are then postprocessed to generate a maximum intensity projection (MIP) reformat (Fig. 1), where only the pixel with the highest signal intensity along a ray perpendicular to the plane of projection is displayed. Hence, an image of the pancreaticobiliary tree is reconstructed with suppression of the background tissue. Multiplanar reformats are also then created with 18 MIP reformats displayed at 101 intervals to

*Department of Radiology, Guys and St Thomas NHS Foundation Trust, London, UK. Department of Radiology, Royal Free Hospital, Hampstead, London, UK. Address reprint requests to Nyree Grifn, Department of Radiology, Guys and St Thomas NHS Foundation Trust, Westminster Bridge Road, London SE1 7EH, UK. E-mail: nyree.grifn@gstt.nhs.uk

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0887-2171/$-see front matter & 2013 Elsevier Inc. All rights reserved. doi:http://dx.doi.org/10.1053/j.sult.2012.11.003

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Figure 3 Aerobilia within the common bile duct. The signal void within the common bile duct has a nondependent position (arrow), conrming the presence of aerobilia.

Figure 1 MRCP MIP reformat demonstrating the normal biliary anatomy. The left hepatic ducts (LHD) and right hepatic ducts (RHD) join to form the common hepatic duct (CHD). The cystic duct (CD) drains the gallbladder (GB). The common bile duct (CBD) is formed after the insertion of the cystic duct with the common hepatic duct. The pancreatic duct (PD) shares a common drainage with the CBD into the major duodenal papilla.

If the patient is unable to breathe regularly, an alternative to the respiratory-triggered thin collimation slices is to obtain a single breath-hold thick-collimation slab. This is achieved using a fat-saturated HASTE sequence where a single slab of

each other, over a 1801 radial array. In this way, the biliary tree can be rotated off adjacent uid-lled structures, which may otherwise obscure parts of it.

Figure 2 Distended intrahepatic bile ducts (arrow). Apparent lling defects (n) are caused by inspissated mucin within the dilated ducts.

Figure 4 Pulsation artifact from the right hepatic artery. (A) MRCP MIP image demonstrating an apparent signal void at the midpoint of the common hepatic duct (arrow). (B) Coronal T2 image conrms this is in fact a result of the right hepatic artery crossing the midcommon hepatic duct (arrow).

34 data between 4-8 cm in thickness is acquired in the coronal oblique plane in a 1- to 2-second breath hold. The sequence has a very long echo time, making it heavily T2-weighted. In this way, the entire pancreatico-biliary tree is displayed with no postprocessing required. In recent years,secretin-stimulated MRCP has been introduced6 to investigate pancreatic exocrine function. Other indications include assessing for sphincter of Oddi dysfunction, the detection and characterization of pancreatic ductal anomalies and strictures, detection of early chronic pancreatitis, and evaluating the integrity of the pancreatic duct. Secretin is an endogenous hormone usually produced by the duodenum. When given as an intravenous injection, it promotes pancreatic exocrine secretion, resulting in increased secretions within the duodenum and increased dilatation of the main pancreatic duct over a period of 10 minutes, with peak effect between 2-5 minutes.

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The technique of functional cholangiography using hepatobiliary-specic contrast agents has also been developed,7 where intravenous contrast is taken up by the hepatocytes and subsequently excreted in the biliary tree, allowing demonstration of the bile ducts on T1 fat-saturated sequences. This technique is further described in a separate review on hepatocyte-specic contrast agents included in this Seminars issue.

Pearls and Pitfalls

When reporting MRCP images, the reader needs to be aware of a number of artifacts that can affect interpretation. Partial voluming artifacts may arise with the use of MIP reformats and with thick slab acquisitions, meaning that small intraductal lling defects or strictures may be overlooked. Breathing artifact can also result in a bizarre

Figure 5 Von Meyerburg complexes. (A) MRCP MIP and (B) axial T2 images conrming the presence of multiple tiny (o1.5 cm) cystic lesions that do not appear to communicate with the biliary tree.

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Table 1 Todani Classication of Choledochal Cysts Type Type I (80%-90%) Type IA Type IB Type IC Type II (2%) Type III (1.5%-5%) Type IV (10%) Type IVA Type IVB Type V Description

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Cystic dilatation of the common bile duct Focal segmental CBD dilatation Fusiform CBD dilatation True choledochal diverticulum Choledochocele Multiple intrahepatic and extrahepatic duct cysts Multiple extrahepatic duct cysts Saccular or fusiform dilatation of the intrahepatic bile ducts

Figure 6 Caroli disease. (A) MRCP MIP and (B) axial T2 images demonstrating the presence of multiple fusiform or saccular areas of intrahepatic biliary dilatation (arrows). Calculi are often seen within the areas of dilatation (arrowhead).

appearance of the MIP reformats, with ducts appearing disconnected, stenotic, or duplicated. Reference to the thin collimation slices and axial images is always strongly recommended to avoid these pitfalls. In addition, a number of pathologies can mimic choledocholithiasis. For example, lling defects in the biliary tree can

also be produced by normal ow voids, aerobilia, and the presence of debris, mucin (Fig. 2), hemorrhage, or tumor within the biliary tree. Normal ow voids may occur where the cystic duct inserts into the common hepatic duct, resulting in a central lling defect on axial images at this site. Aerobilia can easily be distinguished from CBD stones, as signal voids are seen in a nondependent (rather than dependent) position within the bile ducts on axial images (Fig. 3). If T2-weighted MRCP is performed after administration of a hepatocytespecic contrast agent, the contrast will shorten T2 relaxation times and thus reduce the signal intensity of bile, resulting in spurious intraductal lling defects. A common pitfall is the misdiagnosis of common hepatic duct strictures on the MIP reformats. This is often due to pulsation artifact from the right hepatic artery as it crosses the posterior aspect of the common hepatic duct (Fig. 4A and B). The absence of proximal biliary dilatation and careful examination of the source images will allow correct interpretation. Susceptibility artifact from metallic clips and bowel gas may also limit interpretation of MRCP images, as well as uid from structures overlying the biliary tree (eg, duodenum). The latter can be overcome by review of the multiplanar reformats where any overlying structures can be projected off the biliary tree.

Figure 7 Todani classication of choledochal cysts. (A) Type Ifusiform dilatation of the CBD, (B) Type IIa true choledochal diverticulum (arrow), (C) Type IIIa choledochocele (arrow), and (D) Type IVamultiple intrahepatic and extraheptic cysts. LHD, left hepatic duct.

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the angle of ductal union. Complications arising from both choledochal cysts and Caroli disease include choledocholithiasis, pancreatitis, intrahepatic abscesses, biliary cirrhosis, portal hypertension, and cholangiocarcinoma.

Indications for MRCP

Congenital Biliary Pathologies
MRCP has a high sensitivity in demonstrating congenital anomalies related to the biliary tree and pancreatic duct. Congenital malformation of the ductal plate8 arises when there is arrest of or a derangement in the normal embryologic remodeling of bile ducts. It results in a variable amount of destructive inammation and segmental biliary dilatation. When there is failure of involution of the small interlobular bile ducts within the liver, Von Meyerburg complexes (biliary hamatomas) may arise. On MRCP , these lesions appear as multiple tiny (o1.5 cm) cystic lesions that do not appear to communicate with the biliary tree (Fig. 5A and B). If contrast is given, variable enhancement can be seen within these lesions, from rim enhancement through to homogenous enhancement. When there is malformation of the larger intrahepatic bile ducts, this results in Caroli disease. This is a rare autosomal recessive condition, which is characterized by fusiform or saccular dilatation of the intrahepatic biliary tree (Fig. 6A and B). It can be associated with congenital hepatic brosis, autosomal polycystic kidney disease, medullary sponge kidney, medullary cystic disease, and choledochal cysts. Choledochal cysts arise when there is malformation of the large (predominantly) extrahepatic bile ducts. Todani et al.9 classied choledochal cysts into 5 types (Fig. 7A-D) as dened in Table 1. They can be associated with an anomalous union of the pancreaticobile duct in 10%-58% of cases. Usually the CBD and the main pancreatic duct unite (at an acute angle) within the sphincter of Oddi to form a common channel between 0.2-1 cm in length. When these 2 ducts unite outside the duodenal wall and proximal to the sphincter of Oddi, it is postulated that reux of pancreatic uid into the CBD leads to inammation and eventual dilatation of the bile ducts. Komi et al.10 classied anomalous union of the pancreaticobile duct into 3 types depending on

Congenital Pancreatic Duct Anomalies

One of the commonest pancreatic duct variants is pancreas divisum, which is a recognized cause of recurrent pancreatitis. Usually the dorsal pancreatic duct fuses with the ventral pancreatic duct in the head of the pancreas, to drain into the major duodenal papilla along with the CBD. The remnant of

Figure 8 Pancreas divisum. The main pancreatic duct (MPD) drains into the minor duodenal papilla (MP), while the accessory pancreatic duct (APD) drains into the major duodenal papilla (MDP) along with the CBD.

Figure 9 Annular pancreas. (A) MRCP MIP image demonstrating the annular biliary drainage tract (arrow) encircling the second part of the duodenum (n), which is constricted as it passes though the annular component. Incidentally, the main pancreatic duct (PD) is prominent with a number of dilated side branches, but in addition an intraductal papillary mucinous neoplasm (IPMN) is also seen arising from the main pancreatic duct (arrowhead). (B) Axial CT. The second part of the duodenum (n) can be seen passing medial to the annular component of the pancreas (arrows) surrounding its lateral aspect.

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Figure 10 MIP MRCP image. Multiple gallstones (arrow) are seen as lling defects within the common bile duct.

the dorsal pancreatic duct in the head of the pancreas may remain patent and drain into the minor duodenal papilla in 40% of cases. In pancreas divisum (Fig. 8), there is failure of fusion of these ventral and dorsal pancreatic ducts. The main pancreatic duct thus drains the tail, body, and superior head of the pancreas into the minor duodenal papilla, while the accessory pancreatic duct drains the uncinate process and inferior head of the pancreas into the major duodenal papilla along with the CBD. This variant is easily detected on MRCP . Another variant of pancreatic ductal anatomy is the ansa pancreatica. This is when the accessory duct remains patent but enters the minor duodenal papilla by forming an arch like a reverse S character. Again, this is a recognized cause of recurrent pancreatitis. Annular pancreas is a rare congenital anomaly when there is failure of the ventral pancreatic bud to rotate with the duodenum, resulting in either partial or complete encasement of the duodenum by the ventral bud. It can also be associated with pancreas divisum. It may present in the neonate with duodenal obstruction, sometimes in conjunction with other congenital anomalies, for example, Down syndrome. If unrecognized in children, up to 50% may present in the third to sixth decade of life, with abdominal pain, postprandial satiety, vomiting, peptic ulcers, recurrent pancreatitis, and rarely biliary obstruction. In a review of 24 cases of annular pancreas,11 the presence of pancreatic tissue posterolateral to the second part of the duodenum had a high sensitivity and specicity for the presence of annular pancreas. In this study,11 the annular duct joined the main pancreatic duct in the majority of cases, with the remainder draining into the

Figure 11 Calculi within a cystic duct remnant. (A) MIP MRCP image demonstrating the calculi as multiple lling defects (arrows) within a dilated cystic duct. (B) Axial T2 MR image demonstrating these calculi as dependent signal voids (arrow) within the cystic duct.

accessory duct. MRCP is the best noninvasive way of demonstrating the ductal conguration (Fig. 9A and B).

Acquired Pathologies
Choledocholithiasis is one of the commonest indications for MRCP . It is either performed in a patient (often with known gallstones) presenting with acute obstructive jaundice or in a patient following cholecystectomy who presents with recurrent biliary symptoms. CBD stones appear as dependent intraductal lling defects causing proximal CBD obstruction (Figs. 10 and 11). Stones as small as 2 mm may be detected, although MIP reformats may obscure smaller stones due to partial voluming effects as described earlier. Mirizzi syndrome12 is a rare complication of gallstone disease, arising when an impacted gallstone within the neck of the gallbladder or cystic duct causes extrinsic compression to the common hepatic duct (Fig. 12). When the obstruction is simple, it is classied as type 1. Type 2 is when there is erosion of the wall

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of high-signal structures, called the pearl necklace sign. On ultrasound (Fig. 13D), a comet-tail artifact is seen due to acoustic shadowing from the echogenic cholesterol crystals within the Rokitansky-Aschoff sinuses. This is highly specic for adenomyomatosis. Chronic pancreatitis (Fig. 14A and B) can lead to a pancreatic duct dilatation or strictures on MRCP , with the presence of pancreatic intraductal stones and pseudocysts. A chain of lakes appearance may be seen with alternating stenosis and dilatation of the main pancreatic duct. Early ductal changes can be exaggerated with the use of secretin, which stimulates pancreatic duct dilatation as described previously. Pseudocysts are encapsulated uid collections, which develop in the setting of both acute and chronic pancreatitis and are often seen within the lesser sac. They usually appear as unilocular cysts on MRCP . A communication with the pancreatic duct may be demonstrated. Benign biliary strictures may be due to a number of causes, with the commonest being postsurgical (eg, following laparoscopic cholecystectomy, liver transplantation [Fig. 15], hepatic resection, and biliary enteric anastomoses [Fig. 16]). For example, if aberrant insertion of the right posterior duct into the common hepatic duct is not recognized at the time of cholecystectomy, there may be accidental transection of this duct instead of the cystic duct. This may lead to a biliary leak in the acute setting with the subsequent development of a biliary stricture. Other causes for benign strictures include both primary and secondary sclerosing cholangitis. Primary sclerosing cholangitis (PSC) is an autoimmune brosing inammatory process of the bile ducts, typically presenting in the fourth and fth decades and with a male predominance. It is associated with inammatory bowel disease (especially ulcerative colitis) in 60%-80% of patients. Intrahepatic and extrahepatic bile duct strictures develop over time (usually at the bifurcation of ducts), with up to 10% of patients eventually developing cholangiocarcinoma. The classical imaging appearances of PSC on MRCP are irregular beading of the intrahepatic and extrahepatic bile ducts (Fig. 17) with multifocal strictures, ductal wall thickening, and segmental ectasia.13,14 MRCP is useful in demonstrating established PSC, although early changes are better appreciated by endoscopic retrograde cholangiopancreatography (ERCP). Usually peripheral bile ducts should extend

Figure 12 Mirizzi syndrome due to an impacted gallstone within the cystic duct (arrow) causing extrinsic compression to the common hepatic duct (n).

of the common hepatic duct resulting in a cholecystocholedochal stula. Adenomyomatosis12 of the gallbladder is seen in up to 9% of cholecystectomy specimens and is often an incidental nding with no intrinsic malignant potential. It is more common in women, usually presenting in the fth decade of life. It is associated with gallstones in between 25%-75% of cases, cholesterolosis (33%), and pancreatitis. It is characterized by hyperplasia of the gallbladder wall with the development of intramural mucosal diverticula (Rokitansky-Aschoff sinuses). Three morphological types are recognized: generalized (diffuse), segmental (annular), and fundal (localized). On MRCP (Fig. 13A-C), these types give rise to diffuse mural thickening, hour-glass conguration, or a focal sessile mass of the gallbladder correspondingly. The latter may be difcult to differentiate from gallbladder carcinoma. The uid-lled intramural diverticula will appear as a curvilinear arrangement

Figure 13 Adenomyomatosis. (A) MIP MRCP image demonstrating segmental adenomyomatosis (arrow). (B) Corresponding axial T2 image demonstrating segmental annular adenomyomatosis with an hour-glass conguration (arrows). (C) Corresponding coronal T2 image demonstrating the pearl necklace sign due to the curvilinear arrangement of the uidlled intramural diverticula (arrow). (D) Ultrasound demonstrating the comet tail artifact (arrows) from cholesterol crystals.

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Figure 14 Chronic pancreatitis. (A) MIP MRCP image demonstrating a distended pancreatic duct (PD) with dilated pancreatic side branches (arrow). (B) In a different patient, a lling defect is seen within the proximal pancreatic duct (arrow) in keeping with a small calculus.

to the periphery of the liver and form acute angles with the central ducts on ERCP . As PSC progresses, the ducts become obliterated so that the peripheral ducts are no longer visualized, leading to a pruned tree appearance; the acute angles formed with the central ducts also become more obtuse. Secondary sclerosing cholangitis13,14 includes a spectrum of diseases such as recurrent pyogenic cholangitis, autoimmune pancreatitis, ischemic cholangiopathy, eosinophilic cholangiopathy, and acquired immunodeciency syndrome cholangiopathy. Pyogenic cholangitis (also known as oriental cholangiohepatitis) is a chronic parasitic infection of the bile ducts, endemic in South East Asia. The initiating pathogen may include Ascaris lumbricoides, Fasciola hepatica, and Clonorchis sinensis. Recurrent infections may result in the development of pigmented calculi, biliary abscesses, ductal wall thickening, and inammatory strictures, with a predilection for the lateral segment of the left lobe, posterior segment of the right lobe, and extrahepatic duct (Fig. 18).

Cholangiocarcinoma may develop in up to 5% of patients. Autoimmune pancreatitis is a rare cause of chronic pancreatitis, which can be associated with systemic lymphadenopathy and other autoimmune conditions such as retroperitoneal brosis, chronic thyroiditis, sialadenitis, and interstitial nephritis. It is associated with focal or diffuse enlargement of the pancreas and with focal or diffuse strictures of the pancreatic duct and bile ducts. Ischemic cholangiopathy (Fig. 19) may arise following liver transplantation. Strictures may occur at the site of anastomosis due to iatrogenic trauma with resultant ischemia and stricture formation. Thrombosis of the hepatic artery occurs in 4%-8% of liver transplants and is the cause of up to 50% of nonanastomotic strictures. Eosinophilic cholangiopathy (Fig. 20) is a very rare disorder of the biliary tract where there is dense transmural eosinophilic inltration of the bile ducts resulting in intrahepatic and extrahepatic biliary strictures. Multi-organ involvement is seen in the majority of patients. Acquired immunodeciency syndrome

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Figure 15 MIP MRCP image demonstrating a tight stricture (arrow) at the anastomosis between the donor and recipient biliary trees following liver transplantation. The remnant cystic duct is also present (n).

Figure 17 Primary sclerosing cholangitis (PSC). MIP MRCP image demonstrating the typical irregular beading involving the intrahepatic ducts (arrowheads).

cholangiopathy is associated with an opportunistic organism, for example, Cryptosporidium or Cytomegalovirus, in 50% of patients. It may result in papillitis, acalculous cholecystitis, and cholangitis, with strictures of the distal CBD or of the intrahepatic bile ducts simulating PSC. Cholangiocarcinoma14 is a cause for malignant biliary strictures, accounting for 30% of hepatic primary malignancies. Up to 70% are Klatskin tumors, which are located at the porta hepatis (Fig. 21A and B). Risk factors include liver uke infestation, congenital anomalies of the pancreatico biliary tree, cirrhosis, PSC, and hepatitis B or C virus infection. MRCP features suggestive of malignancy include the rapid progression of strictures, high-grade biliary stenoses with shouldered margins, marked proximal bile duct dilatation, and intraductal polypoid lesions. Periportal changes of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images may be seen. If contrast is

Figure 16 MIP MRCP image demonstrating a stricture at the hepaticojejunostomy anastomosis. The intrahepatic biliary tree (arrowheads) is distended due to a stricture at the anastomosis between the biliary tree and bowel (arrow). The small bowel leading up to the anastomosis can easily be seen (n).

Figure 18 Pyogenic cholangitis (oriental cholangiohepatitis). Axial T2 MR image demonstrating the dilated (arrow) and strictured ducts, together with large intraductal calculi (arrowheads).

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Figure 19 Ischemic cholangiopathy. MIP MRCP in a patient following liver transplantation. The intrahepatic bile ducts are irregular, demonstrating multiple strictures (arrowheads) as a result of ischemic damage to the intrahepatic biliary tree. A caliber change (arrow) can also be seen at the anastomotic junction between the donor common hepatic duct and recipient common bile duct.

given, delayed enhancement may be demonstrated within the tumor due to the large brous component. Pancreatic adenocarcinoma arises in the head of the pancreas in 70% of cases. It classically gives rise to the double-duct sign where there is dilatation of both the CBD and main pancreatic duct. MRCP is not routinely used for identifying or staging pancreatic cancers, but can be a useful noninvasive

Figure 21 Hilar cholangiocarcinoma. (A) MIP MRCP image demonstrating disassociation and dilatation of the left and right hepatic ducts due to a stricture at the liver hilum (n). PD, pancreatic duct; LHD, left intrahepatic duct; RHD, right intrahepatic duct. (B) Axial T2 image demonstrating the large intermediate signal intensity hilar cholangiocarcinoma (arrows) causing disassociation of the left and right intrahepatic ducts and obstruction (arrowhead). There is associated liver decompensation as evidenced by the ascites (n).

Figure 20 Eosinophilic cholangiopathy. MIP MRCP image demonstrating severe irregularity of the intrahepatic biliary ducts with multiple strictures present (arrows). There is also irregularity of the extrahepatic biliary tree that is less evident on this image. GB, gallbladder; PD, pancreatic duct.

investigation in demonstrating the level of obstruction in patients presenting with painless obstructive jaundice. Cystic pancreatic neoplasms include both microcystic and macrocystic lesions.15 Microcystic lesions are usually benign serous cystadenomas, characterized by a collection of cysts (usually 46), measuring up to 2 cm in size and separated by thin septations. They usually occur in older women (460 years) with a predilection for the head of the pancreas. A brous central scar with or without calcication (better appreciated on computed tomography (CT)) is seen in 30% of cases. Macrocystic lesions include mucinous cystic neoplasms and intraductal papillary mucinous neoplasms (IPMNs). These lesions have less numerous and larger (42 cm) cysts compared with serous cystadenomas. The mucin results in high signal on T1-weighted images, and intermediate signal on T2-weighted images. Mucinous cystadenomas usually involve the body and tail of the pancreas and occur in a younger age group (between 30-50 years) than serous tumors, and again are more common in females. There is no communication with the main pancreatic duct, but the lesion may cause partial pancreatic duct obstruction. Cysts

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often resected, although the risk is low in cysts o3 cm in size. Other features of malignancy include the presence of solid nodules, thick enhancing walls or septae or both, and a wide (41 cm) connection between the side branch lesion and the main pancreatic duct. The main branch variant (Fig. 23) is characterized by either segmental or diffuse involvement of the main pancreatic duct, with the segmental form mimicking the appearances of a mucinous neoplasm (cystadenoma or cystadenocarcinoma). However, differentiation can be made, as the former is often associated with dilatation of the rest of the main pancreatic duct due to the secretion of mucin. When the whole of the main pancreatic duct is dilated, atrophy of the pancreas is seen, making it difcult to distinguish from chronic pancreatitis. In advanced (malignant) main duct IPMN, diffuse wall thickening and enhancement of the main pancreatic duct are seen with enhancing mural nodules.

Conclusion
Figure 22 Side branch IPMN. MIP MRCP demonstrating a septated cystic lesion within the uncinate process (arrows) with a clear communication with the main pancreatic duct (arrowhead). PD, pancreatic duct.

may contain debris or hemorrhage. If egg-shell calcication is seen on CT, this nding is highly predictive of malignancy. IPMNs16 can be classied as main duct, side branch, or mixed. A side branch IPMN or mixed tumor (where there is a side branch tumor that extends to the main pancreatic duct) will appear as a septated cyst that communicates with the main pancreatic duct (Fig. 22). Side branch tumors are often seen in the uncinate process, although they can occur elsewhere in the pancreas. These lesions have malignant potential and thus are

MRCP remains a very useful tool in the noninvasive investigation of pathologies related to the biliary tree and pancreas. The sequences rely on heavily T2-weighted images to demonstrate these uid-lled structures. This review has highlighted the pitfalls the reader needs to be aware of when interpreting MRCP images, and the numerous benign and malignant indications for which this technique continues to be employed.

References
1. Wallner BK, Schumacher KA, Weidenmaier W , et al: Dilated biliary tract: Evaluation with MR cholangiography with a T2-weighted contrastenhanced fast sequence. Radiology 181:805-808, 1991 2. Morimoto K, Shimoi M, Shirakawa T, et al: Biliary obstruction: Evaluation with three-dimensional MR cholangiography. Radiology 183:578-580, 1992 3. Laubenberger J, Buchert M, Schneider B, et al: Breath-hold projection magnetic resonance cholangiopancreaticography (MRCP): A new method for the examination of the bile and pancreatic ducts. Magn Reson Med 33:18-23, 1995 4. Miyazaki T, Yamashita Y, Tsuchigame T, et al: MR cholangiopancreatography using HASTE (half-Fourier acquisition single-shot turbo spinecho) sequences. Am J Roentgenol 166:1297-1303, 1996 5. Sodickson A, Mortele KJ, Barish MA, et al: Three-dimensional fastrecovery fast spin-echo MRCP: Comparison with two-dimensional single shot fast spin echo techniques. Radiology 238:549-559, 2006 6. Lee NJ, Kim KW , Kim TK, et al: Secretin-stimulated MRCP . Abdom Imaging 31:575-581, 2006 7. Seale MK, Catalano OA, Saini S, et al: Hepatobiliary-specic MR contrast agents: Role in imaging the liver and biliary tree. Radiographics 29:1725-1748, 2009 8. Brancatelli G, Federle MP , Vilgrain V , et al: Fibropolycystic liver disease: CT and MR imaging ndings. Radiographics 25:659-670, 2005 9. Todani T, Watanabe Y, Narusue M, et al: Congenital bile duct cysts: Classication, operative procedures, and review of thirty-seven cases including cancer arising from choledochal cyst. Am J Surg 134 (2):263-269, 1977; [PubMed PMID: 889044] 10. Komi N, Takehara H, Kunitomo K, et al: Does the type of anomalous arrangement of pancreaticobiliary ducts inuence the surgery and prognosis of choledochal cyst? J Pediatr Surg 27:728-731, 1992 11. Sandrasegaran K, Patel A, Fogel EL, et al: Annular pancreas in adults. Am J Roentgenol 193:455-460, 2009

Figure 23 Main branch IPMN. MIP MRCP demonstrating dilatation of the entire main pancreatic duct (arrows). There is also minimal side branch dilatation (arrowhead). Unlike a proximal obstruction, with a tendency to progressive dilatation toward the pancreatic tail, a main branch IPMN tends to cause obstruction that is more prominent proximally, as can be seen here.

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12. Catalano OA, Sahani DV , Kalva SP , et al: MR imaging of the gallbladder: A pictorial essay. Radiographics 28:135-155, 2008 13. Vitellas KM, Keogan MT, Freed KS, et al: Radiologic manifestations of sclerosing cholangitis with emphasis on MR cholangiopancreatography. Radiographics 20:959-975, 2000 14. Menias CO, Surabhi VR, Prasad SR, et al: Mimics of cholangiocarcinoma: Spectrum of disease. Radiographics 28:1115-1129, 2008

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15. Sahani DV , Kadavigere R, Saokar A, et al: Cystic pancreatic lesions: A simple imaging-based classication system for guiding management. Radiographics 25:1471-1484, 2005 16. Pedrosa I, Boparai D: Imaging considerations in intraductal papillary mucinous neoplasms of the pancreas. World J Gastrointest Surg 2 (10):324-330, 2010