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Magnetic Resonance Cholangiopancreatography:

Pearls, Pitfalls, and PathologyNyree Griffin, MD, FRCR,* Dominic Yu, BA, FRCR, and Lee Alexander Grant, FRCR

Magnetic resonance cholangiopancreatography is a method of evaluating the pancreatico-

biliary 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.

Magnetic resonance cholangiopancreatography (MRCP)was introduced approximately 2 decades ago. It high-lights fluid-filled biliary structures through the use of heavilyT2-weighted sequences and has an essential role in thenoninvasive evaluation of pancreaticobiliary pathology. Thetechnique has evolved with time, with improvements in thespeed of acquisition and spatial resolution. T2-weightedimages of the biliary tree were traditionally obtained throughthe use ofbalanced gradient-echo steady state free precession

sequences.1,2 Nowadays, fast spin-echo (FSE) pulsesequences with long echo times are used, which have highersignal to noise and contrast to noise ratio and lower sensitivityto motion and susceptibility artifacts. Modified sequenceshave been developed, such as the rapid acquisition with rapidenhancement, fast-recovery FSE, and the half-Fourier acqui-sition single-shot turbo spin-echo (HASTE) sequences.3-5

The purpose of this pictorial review is first to describe howMRCP is performed at our institution, second to discusspotential pitfalls the reader needs to be aware of, and third todiscuss the myriad indications for this technique. The normalbiliary anatomy and variants will not be discussed, as these

have been comprehensively described in the first reviewpaper in this Seminars issue.

MRCP Protocol

The patient is usually fasted 4-6 hours prior to the procedureto reduce fluid secretions within the stomach and duode-num, reduce peristalsis, and promote gallbladder filling.Initial axial T2-HASTE breath hold sequences are performedthrough the upper abdomen, imaging from the diaphragmdown to the duodenal ampulla. This allows initial evaluationof the biliary tree and also of the solid organs in the upper

abdomen. Two 3-dimensional respiratory-triggered heavilyT2-weighted FSE sequences are then obtained in the coronaloblique plane,with 1 acquisition aligned to the commonbileduct (CBD) in the head of the pancreas, and 1 aligned to themain pancreatic duct at approximately 901 to the firstimaging plane. Respiratory triggering is achieved using anavigator sequence where the navigator is placed over theedge of the diaphragm on the coronal and sagittal localizers.Diaphragmatic motion can then be tracked as the patient isasked to breathe regularly, allowing the acquisition to betriggered when the position of the diaphragm interface withthe lung falls within a prespecified acceptance window. In

this way, artifact from respiratory motion can be minimized.Each 3-dimensional navigator sequence takes between 3-7minutes to acquire and results in a stack of 40 contiguouscoronal oblique slices, each of 1.5 mm in thickness. The dataare then postprocessed to generate a maximum intensityprojection (MIP) reformat (Fig. 1), where only the pixel withthe highest signal intensity along a ray perpendicular to theplane of projection is displayed. Hence, an image of thepancreaticobiliary tree is reconstructed with suppression ofthe background tissue. Multiplanar reformats are also thencreated with 18 MIP reformats displayed at 101 intervals to

32 0887-2171/$-see front matter& 2013 Elsevier Inc. All rights reserved.doi:http://dx.doi.org/10.1053/j.sult.2012.11.003

*Department of Radiology, Guys and St Thomas NHS Foundation Trust,

London, UK.

Department of Radiology, Royal Free Hospital, Hampstead, London, UK.

Address reprint requeststo Nyree Griffin, Department of Radiology, Guys and

St Thomas NHS Foundation Trust, Westminster Bridge Road, London

SE1 7EH, UK. E-mail: [email protected]
http://localhost/var/www/apps/conversion/tmp/scratch_9/dx.doi.org/10.1053/j.sult.2012.11.003mailto:[email protected]:[email protected]://localhost/var/www/apps/conversion/tmp/scratch_9/dx.doi.org/10.1053/j.sult.2012.11.003http://localhost/var/www/apps/conversion/tmp/scratch_9/dx.doi.org/10.1053/j.sult.2012.11.003http://localhost/var/www/apps/conversion/tmp/scratch_9/dx.doi.org/10.1053/j.sult.2012.11.003


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each other, over a 1801 radial array. In this way, the biliarytree can be rotated off adjacent fluid-filled structures, which

may otherwise obscure parts of it.

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

Figure 1 MRCP MIP reformat demonstrating the normal biliaryanatomy. The left hepatic ducts (LHD) and right hepatic ducts

(RHD) join to form thecommonhepatic duct (CHD). Thecystic duct(CD) drains the gallbladder (GB). The common bile duct (CBD) is

formed after the insertionof thecysticduct with thecommonhepaticduct. The pancreatic duct (PD) shares a common drainage with the

CBD into the major duodenal papilla.

Figure 2 Distended intrahepatic bile ducts (arrow). Apparent

filling defects (n

) are caused by inspissated mucin within the dilatedducts.

Figure 3 Aerobilia within the common bile duct. The signal void

within the common bile duct has a nondependent position (arrow),confirming the presence of aerobilia.

Figure 4 Pulsation artifact from the right hepatic artery. (A) MRCPMIP image demonstrating an apparent signal void at the midpoint of

the common hepatic duct (arrow). (B) Coronal T2 image confirms

this is in fact a result of the right hepatic artery crossing the mid-common hepatic duct (arrow).

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data between 4-8 cm in thickness is acquired in the coronaloblique plane in a 1- to 2-second breath hold. The sequencehas a very long echo time, making it heavily T2-weighted. Inthis way, the entire pancreatico-biliary tree is displayed withno postprocessing required.

In recent years,secretin-stimulated MRCP has beenintroduced6 to investigate pancreatic exocrine function.

Other indications include assessing for sphincter of Oddidysfunction, the detection and characterization of pan-creatic ductal anomalies and strictures, detection of earlychronic pancreatitis, and evaluating the integrity of thepancreatic duct. Secretin is an endogenous hormoneusually produced by the duodenum. When given as anintravenous injection, it promotes pancreatic exocrinesecretion, resulting in increased secretions within theduodenum and increased dilatation of the main pancrea-tic duct over a period of 10 minutes, with peak effectbetween 2-5 minutes.

The technique of functional cholangiography usinghepatobiliary-specific contrast agents has also been devel-oped,7 where intravenous contrast is taken up by thehepatocytes and subsequently excreted in the biliary tree,allowing demonstration of the bile ducts on T1 fat-saturatedsequences. This technique is further described in a separatereview on hepatocyte-specific contrast agents included in this

Seminars issue.

Pearls and Pitfalls

When reporting MRCP images, the reader needs to beaware of a number of artifacts that can affect interpretation.Partial voluming artifacts may arise with the use of MIPreformats and with thick slab acquisitions, meaning thatsmall intraductal filling defects or strictures may be over-looked. Breathing artifact can also result in a bizarre

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

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appearance of the MIP reformats, with ducts appearingdisconnected, stenotic, or duplicated. Reference to the thincollimation slices and axial images is always stronglyrecommended to avoid these pitfalls.

In addition, a number of pathologies can mimic choledo-cholithiasis. For example, filling defects in the biliary tree can

also be produced by normal flow voids, aerobilia, and thepresence of debris, mucin (Fig. 2), hemorrhage, or tumor

within thebiliary tree. Normal flow voids mayoccur where thecysticduct inserts into thecommon hepatic duct, resulting in acentral filling defect on axial images at this site. Aerobilia caneasily be distinguished from CBD stones, as signal voids areseen in a nondependent (rather than dependent) positionwithin the bile ducts on axial images (Fig. 3). If T2-weightedMRCP is performed after administration of a hepatocyte-specific contrast agent, the contrast will shorten T2 relaxationtimes and thus reduce the signal intensity of bile, resulting inspurious intraductal filling defects.

A common pitfall is the misdiagnosis of common hepaticduct strictures on the MIP reformats. This is often due to

pulsation artifact from the right hepatic artery as it crosses theposterior aspect of the common hepatic duct (Fig. 4A and B).The absence of proximal biliary dilatation and carefulexamination of the source images will allow correct inter-pretation. Susceptibility artifact from metallic clips and bowelgas may also limit interpretation of MRCP images, as well asfluid from structures overlying the biliary tree (eg, duode-num). The latter can be overcome by review of the multi-planar reformats where any overlying structures can beprojected off the biliary tree.

Figure 6 Caroli disease. (A) MRCP MIP and (B) axial T2 imagesdemonstrating the presence of multiple fusiform or saccular areas of

intrahepatic biliary dilatation (arrows). Calculi are often seen withinthe areas of dilatation (arrowhead).

Figure 7 Todani classification of choledochal cysts. (A) Type Ifusiform dilatation of the CBD, (B) Type IIa true

choledochal diverticulum (arrow), (C) Type III

a choledochocele (arrow), and (D) Type IVa

multiple intrahepatic andextraheptic cysts. LHD, left hepatic duct.

Table 1 Todani Classification of Choledochal Cysts

Type Description

Type I (80%-90%)

Type IA Cystic dilatation of the common bile

duct

Type IB Focal segmental CBD dilatation

Type IC Fusiform CBD dilatation

Type II (2%) True choledochal diverticulumType III (1.5%-5%) Choledochocele

Type IV (10%)

Type IVA Multiple intrahepatic and extrahepatic

duct cysts

Type IVB Multiple extrahepatic duct cysts

Type V Saccular or fusiform dilatation of the

intrahepatic bile ducts



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Indications for MRCP

Congenital Biliary PathologiesMRCP has a high sensitivity in demonstrating congenitalanomalies related to the biliary tree and pancreatic duct.

Congenital malformation of the ductal plate8 arises whenthere is arrest of or a derangement in the normal embry-ologic remodeling of bile ducts. It results in a variableamount of destructive inflammation and segmental biliarydilatation. When there is failure of involution of the smallinterlobular bile ducts within the liver, Von Meyerburgcomplexes (biliary hamatomas) may arise. On MRCP, theselesions appear as multiple tiny (o1.5 cm) cystic lesionsthat do not appear to communicate with the biliary tree(Fig. 5A and B). If contrast is given, variable enhancementcan be seen within these lesions, from rim enhancementthrough to homogenous enhancement.

When there is malformation of the larger intrahepatic bileducts, this results in Caroli disease. This is a rare autosomal

recessive condition, which is characterized by fusiform orsaccular dilatation of the intrahepatic biliary tree (Fig. 6A andB). It can be associated with congenital hepatic fibrosis,autosomal polycystic kidney disease, medullary spongekidney, medullary cystic disease, and choledochal cysts.

Choledochal cysts arise when there is malformation of thelarge (predominantly) extrahepatic bile ducts. Todani et al.9

classified choledochal cysts into 5 types (Fig. 7A-D) asdefined in Table1. They can be associated with an anomalousunion of the pancreaticobile duct in 10%-58% of cases.Usually the CBD and the main pancreatic duct unite (at anacute angle) within the sphincter of Oddi to form a common

channel between 0.2-1 cm in length. When these 2 ductsunite outside the duodenal wall and proximal to thesphincter of Oddi, it is postulated that reflux of pancreaticfluid into the CBD leads to inflammation and eventualdilatation of the bile ducts. Komi et al.10 classified anomalousunion of the pancreaticobile duct into 3 types depending on

the angle of ductal union. Complications arising from bothcholedochal cysts and Caroli disease include choledocho-lithiasis, pancreatitis, intrahepatic abscesses, biliary cirrhosis,portal hypertension, and cholangiocarcinoma.

Congenital Pancreatic Duct Anomalies

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

Figure 8 Pancreas divisum. The main pancreatic duct (MPD) drains

into theminor duodenal papilla (MP), while the accessory pancreatic

duct (APD) drainsinto themajor duodenal papilla (MDP) along withthe CBD.

Figure 9 Annular pancreas. (A) MRCP MIP image demonstratingthe annular biliary drainage tract (arrow) encircling the second

part of the duodenum (n), which is constricted as it passesthough the annular component. Incidentally, the main pan-

creatic duct (PD) is prominent with a number of dilated sidebranches, but in addition an intraductal papillary mucinous

neoplasm (IPMN) is also seen arising from the main pancreaticduct (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 lateralaspect.

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the dorsal pancreatic duct in the head of the pancreas mayremain patent and drain into the minor duodenal papilla in40% of cases. In pancreas divisum (Fig. 8), there is failureof fusion of these ventral and dorsal pancreatic ducts. The

main pancreatic duct thus drains the tail, body, and superiorhead of the pancreas into the minor duodenal papilla,while the accessory pancreatic duct drains the uncinateprocess and inferior head of the pancreas into the majorduodenal papilla along with the CBD. This variant is easilydetected on MRCP.

Another variant of pancreatic ductal anatomy is the ansapancreatica. This is when the accessory duct remains patentbut enters the minor duodenal papilla by forming an arch likea reverse S character. Again, this is a recognized cause ofrecurrent pancreatitis.

Annular pancreas is a rare congenital anomaly when there isfailure of the ventral pancreatic bud to rotate with the

duodenum, resulting in either partial or complete encasementof the duodenum by the ventral bud. It can also be associatedwith pancreas divisum. It may present in the neonate withduodenal obstruction, sometimes in conjunction with othercongenital anomalies, for example, Down syndrome. Ifunrecognized in children, up to 50% may present in the thirdto sixth decade of life, with abdominal pain, postprandialsatiety, vomiting, peptic ulcers, recurrent pancreatitis, andrarely biliary obstruction. In a review of 24 cases of annularpancreas,11 the presence of pancreatic tissue posterolateral tothe second part of the duodenum had a high sensitivity andspecificity for the presence of annular pancreas. In this

study,11

the annular duct joined the main pancreatic duct inthe majority of cases, with the remainder draining into the

accessory duct. MRCP is the best noninvasive way ofdemonstrating the ductal configuration (Fig. 9A and B).

Acquired Pathologies

Choledocholithiasis is one of the commonest indications forMRCP. It is either performed in a patient (often with knowngallstones) presenting with acute obstructive jaundice or in apatient following cholecystectomy who presents with recur-rent biliary symptoms. CBD stones appear as dependentintraductal filling 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 topartial voluming effects as described earlier. Mirizzi syn-drome12 is a rare complication of gallstone disease, arisingwhen an impacted gallstonewithintheneck of the gallbladderor cystic duct causes extrinsic compression to the common

hepatic duct (Fig. 12). When the obstruction is simple, it isclassified as type 1. Type 2 is when there is erosion of the wall

Figure 10 MIP MRCP image. Multiple gallstones (arrow) are seen as

filling defects within the common bile duct.

Figure 11 Calculi within a cystic duct remnant. (A) MIP MRCP image

demonstrating the calculi as multiple filling defects (arrows) within adilated cystic duct. (B) Axial T2 MR image demonstrating these

calculi as dependent signal voids (arrow) within the cystic duct.



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of the common hepatic duct resulting in a cholecystochole-dochal fistula.

Adenomyomatosis12 of the gallbladder is seen in up to 9% ofcholecystectomy specimens and is often an incidental findingwith no intrinsic malignant potential. It is more common in

women, usually presenting in the fifth decade of life. It isassociated with gallstones in between 25%-75% of cases,cholesterolosis (33%), and pancreatitis. It is characterized byhyperplasia of the gallbladder wall with the development ofintramural mucosal diverticula (Rokitansky-Aschoff sinuses).Three morphological types are recognized: generalized (dif-fuse), segmental (annular), and fundal (localized). On MRCP(Fig. 13A-C), these types give rise to diffuse mural thickening,hour-glass configuration, or a focal sessile mass of thegallbladder correspondingly. The latter may be difficult todifferentiate from gallbladder carcinoma. The fluid-filledintramural diverticula will appear as a curvilinear arrangement

of high-signal structures, called the pearl necklace sign. Onultrasound (Fig. 13D), a comet-tail artifact is seen due toacoustic shadowing from the echogenic cholesterol crystalswithin the Rokitansky-Aschoff sinuses. This is highly specificfor adenomyomatosis.

Chronic pancreatitis(Fig. 14A and B) canlead to a pancreaticduct dilatation or strictures on MRCP, with the presence of

pancreatic intraductal stones and pseudocysts. A chain of lakesappearance may be seen with alternating stenosis anddilatation of the main pancreatic duct. Early ductal changescan be exaggerated with the use of secretin, which stimulatespancreatic duct dilatation as described previously. Pseudo-cysts are encapsulated fluid collections, which develop in thesetting of both acute and chronic pancreatitis and are oftenseen within the lesser sac. They usually appear as unilocularcysts on MRCP. A communication with the pancreatic ductmay be demonstrated.

Benign biliary strictures may be due to a number of causes,with the commonest being postsurgical (eg, following laparo-

scopic cholecystectomy, liver transplantation [Fig. 15], hepa-tic resection, and biliary enteric anastomoses [Fig. 16]). Forexample, if aberrant insertion of the right posterior duct intothe common hepatic duct is not recognized at the time ofcholecystectomy, there may be accidental transection of thisduct instead of the cystic duct. This may lead to a biliary leakin the acute setting with the subsequent development of abiliary stricture. Other causes for benign strictures includeboth primary and secondary sclerosing cholangitis.

Primary sclerosing cholangitis (PSC) is an autoimmunefibrosing inflammatory process of the bile ducts, typicallypresenting in the fourth and fifth decades and with a male

predominance. It is associated with inflammatory boweldisease (especially ulcerative colitis) in 60%-80% of patients.Intrahepatic andextrahepatic bile duct strictures develop overtime (usually at the bifurcation of ducts), with up to 10% ofpatients eventually developing cholangiocarcinoma. Theclassical imaging appearances of PSC on MRCP are irregularbeading of the intrahepatic and extrahepatic bile ducts(Fig. 17) with multifocal strictures, ductal wall thickening,and segmental ectasia.13,14 MRCP is useful in demonstratingestablished PSC, although early changes are better appre-ciated 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 commonhepatic duct (n).

Figure 13 Adenomyomatosis. (A) MIP MRCP image demonstrating segmental adenomyomatosis (arrow). (B) Correspond-

ing axial T2 image demonstrating segmental annular adenomyomatosis with an hour-glass configuration (arrows). (C)

Corresponding coronal T2 image demonstrating the pearl necklacesign due to the curvilinear arrangement of the fluid-filled intramural diverticula (arrow). (D) Ultrasound demonstrating thecomet tailartifact(arrows) from cholesterol crystals.

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to the periphery of the liver and form acute angles with thecentral ducts on ERCP. As PSC progresses, the ductsbecome obliterated so that the peripheral ducts are no longervisualized, leading to a pruned tree appearance; the acuteangles formed with the central ducts also become more

obtuse.Secondary sclerosing cholangitis13,14 includes a spectrum of

diseases such as recurrent pyogenic cholangitis, autoim-mune pancreatitis, ischemic cholangiopathy, eosinophiliccholangiopathy, and acquired immunodeficiency syndromecholangiopathy. Pyogenic cholangitis (also known as orientalcholangiohepatitis) is a chronic parasitic infection of the bileducts, endemic in South East Asia. The initiating pathogenmay include Ascaris lumbricoides, Fasciola hepatica, andClonorchis sinensis. Recurrent infections may result in thedevelopment of pigmented calculi, biliary abscesses, ductalwall thickening, and inflammatory strictures, with a pre-

dilection for the lateral segment of the left lobe, posteriorsegment 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 pancrea-titis, which can be associated with systemic lymphadeno-pathy and other autoimmune conditions such asretroperitoneal fibrosis, chronic thyroiditis, sialadenitis,

and interstitial nephritis. It is associated with focal or diffuseenlargement of the pancreas and with focal or diffusestrictures of the pancreatic duct and bile ducts. Ischemiccholangiopathy (Fig. 19) may arise following liver transplan-tation. Strictures may occur at the site of anastomosis due toiatrogenic trauma with resultant ischemia and strictureformation. Thrombosis of the hepatic artery occurs in4%-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 tractwhere there is dense transmural eosinophilic infiltration ofthe bile ducts resulting in intrahepatic and extrahepatic

biliary strictures. Multi-organ involvement is seen in themajority of patients. Acquired immunodeficiency syndrome

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 filling defect is seen within the proximal pancreatic duct(arrow) in keeping with a small calculus.



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cholangiopathy is associated with an opportunistic organism,for example, Cryptosporidium or Cytomegalovirus, in 50%of patients. It may result in papillitis, acalculous cholecys-titis, and cholangitis, with strictures of the distal CBD or ofthe intrahepatic bile ducts simulating PSC.

Cholangiocarcinoma14 is a cause for malignant biliarystrictures, accounting for 30% of hepatic primary malignan-cies. Up to 70% are Klatskin tumors, which are located at the

porta hepatis (Fig. 21A and B). Risk factors include liver flukeinfestation, congenital anomalies of the pancreatico biliarytree, cirrhosis, PSC, and hepatitis B or C virus infection.MRCP features suggestive of malignancy include the rapidprogression of strictures, high-grade biliary stenoses withshouldered margins, marked proximal bile duct dilatation,and intraductal polypoid lesions. Periportal changes of lowsignal intensity on T1-weighted images and high signalintensity on T2-weighted images may be seen. If contrast is

Figure 15 MIP MRCP image demonstrating a tight stricture (arrow) at

the anastomosis between the donor and recipient biliary treesfollowing liver transplantation. The remnant cystic duct is also

present (n).

Figure 16 MIP MRCP image demonstrating a stricture at the hepati-cojejunostomy anastomosis. The intrahepatic biliary tree (arrow-

heads) is distended due to a stricture at the anastomosis between the

biliary tree and bowel (arrow). The small bowel leading up to theanastomosis can easily be seen (n).

Figure 17 Primary sclerosing cholangitis (PSC). MIP MRCP imagedemonstrating the typical irregular beading involving the intrahepa-

tic ducts (arrowheads).

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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given, delayed enhancement may be demonstrated within thetumor due to the large fibrous component.

Pancreatic adenocarcinoma arises in the head of the pancreasin 70% of cases. It classically gives rise to the double-duct signwhere there is dilatation of both the CBD and main pancreatic

duct. MRCP is not routinely used for identifying or stagingpancreatic cancers, but can be a useful noninvasive

investigation in demonstrating the level of obstruction inpatients presenting with painless obstructive jaundice.

Cystic pancreatic neoplasms include both microcystic andmacrocystic lesions.15 Microcystic lesions are usually benignserous cystadenomas, characterized by a collection of cysts(usually46), measuring up to 2 cm in size and separated bythin septations. They usually occur in older women (460

years) with a predilection for the head of the pancreas. Afibrous central scar with or without calcification (betterappreciated on computed tomography (CT)) is seen in 30%of cases. Macrocystic lesions include mucinous cystic neo-plasms and intraductal papillary mucinous neoplasms(IPMNs). These lesions have less numerous and larger(42 cm) cysts compared with serous cystadenomas. Themucin results in high signal on T1-weighted images, andintermediate signal on T2-weighted images. Mucinous cystade-nomas usually involve the body and tail of the pancreas andoccur in a younger age group (between 30-50 years) thanserous tumors, and again are more common in females. There

is no communication with the main pancreatic duct, but thelesion may cause partial pancreatic duct obstruction. Cysts

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.

Figure 20 Eosinophilic cholangiopathy. MIP MRCP image demon-strating 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.

Figure 21 Hilar cholangiocarcinoma. (A) MIP MRCP image demon-strating 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) AxialT2 image demonstrating the large intermediate signal intensity hilarcholangiocarcinoma (arrows) causing disassociation of the left and

right intrahepatic ducts and obstruction (arrowhead). There isassociated liver decompensation as evidenced by the ascites (n).



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may contain debris or hemorrhage. If egg-shell calcification isseen on CT, this finding is highly predictive of malignancy.IPMNs16can be classified as main duct, side branch, or mixed.

A side branch IPMN or mixed tumor (where there is a sidebranch tumor that extends to the main pancreatic duct) will

appear as a septated cyst that communicates with the mainpancreatic duct (Fig. 22). Side branch tumors are often seen intheuncinateprocess, although they can occur elsewhere in thepancreas. These lesions have malignant potential and thus are

often resected, although the risk is low in cystso3 cm in size.Other features of malignancy include the presence of solidnodules, thick enhancing walls or septae or both, and a wide(41 cm) connection between the side branch lesion and themain pancreatic duct. The main branch variant (Fig. 23) ischaracterized by eithersegmental or diffuse involvementof themain pancreatic duct, with the segmental form mimicking the

appearances of a mucinous neoplasm (cystadenoma orcystadenocarcinoma). However, differentiation can be made,as the former is often associated with dilatation of the rest ofthe main pancreatic duct due to the secretion of mucin. Whenthe whole of the main pancreatic duct is dilated, atrophy of thepancreasis seen, making it difficultto distinguish from chronicpancreatitis. In advanced (malignant) mainduct IPMN, diffusewall thickening and enhancement of the main pancreatic ductare seen with enhancing mural nodules.

ConclusionMRCP remains a very useful tool in the noninvasive investiga-tion of pathologies related to the biliary tree and pancreas. Thesequences rely on heavily T2-weighted images to demonstratethese fluid-filled structures. This review has highlighted thepitfalls the reader needs to be aware of when interpretingMRCP images, and the numerous benign and malignantindications for which this technique continues to beemployed.

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Figure 22 Side branch IPMN. MIP MRCP demonstrating a septatedcystic lesion within the uncinate process (arrows) with a clear

communication with the main pancreatic duct (arrowhead). PD,pancreatic duct.

Figure 23 Main branch IPMN. MIP MRCP demonstrating dilatation of

the entire main pancreatic duct (arrows). There is also minimal sidebranch dilatation (arrowhead). Unlikea proximal obstruction, with a

tendency to progressive dilatation toward the pancreatic tail, a main

branch IPMN tends to cause obstruction that is more prominentproximally, as can be seen here.

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