Computed TomographyAngiography of the

Hepatic, Pancreatic, andSplenic Circulation Melissa Price, MDa, Manuel Patino, MDa,Dushyant Sahani, MDb,*

KEYWORDS

� Liver � Pancreas � Spleen � CT angiography � Dual-energy CT

KEY POINTS

� MDCTA allows acquisition of data with enhanced spatial and temporal resolution that can be recon-structed for robust preoperative road mapping.

� MDCTA can detect normal and variant vascular anatomy as well as allow accurate lesion charac-terization within the liver and pancreas.

� Using dual-energy CT, virtual unenhanced images can be generated, thereby reducing overall ra-diation dose. In addition, material composition allows for robust delineation of enhancement.

MULTIDETECTOR COMPUTED TOMOGRAPHYANGIOGRAPHY TECHNIQUES

Multidetector computed tomography angiography(MDCTA) of the hepatic, pancreatic, and spleniccirculations delineates both vascular anatomyand parenchymal pathology. This has importantimplications for preoperative planning and tumorstaging. With the advent of modern multidetectorCT scanners, it is now possible to temporally ac-quire fast multiphasic acquisitions of abdominalorgans in the optimal phase of enhancement withenhanced 2-dimensional (2D) and 3D imagedisplay. In general, rapid acquisition with thin sli-ces and scanning delays are critical componentsof an optimal MDCTA protocol.1

Technical Factors

Adequate distention of the stomach and duo-denum is obtained by having patients drink 500

a Division of Abdominal Imaging, Massachusetts Gener02114, USA; b Division of Abdominal Imaging, MassachFruit Street, White 270, Boston, MA 02114, USA* Corresponding author.E-mail address: dsahani@mgh.harvard.edu

Radiol Clin N Am 54 (2016) 55–70http://dx.doi.org/10.1016/j.rcl.2015.08.0090033-8389/16/$ – see front matter � 2016 Elsevier Inc. All

to 1000 mL of water 20 to 30 minutes before thescan and an additional 300 to 500 mL immediatelybefore the scan. Water is preferred to radio-opaque contrast, as the latter may make identifi-cation of high-attenuation structures, such ashyperenhancing tumors and vessels in the vicinityof stomach and duodenum, on the 2D and 3D im-age display difficult. Moreover, the natural densityof water on CT also clearly delineates the periam-pullary anatomy and adjacent lesions.1

Hepatic Phases

The liver has a dual blood supply from the hepaticartery and portal vein, with the portal vein supply-ing most blood to the liver (75%–80%). Biphasichepatic CT protocols include an arterial phase aswell as a portal venous phase to detect tumorsthat have arterial neovascularization and relativelydiminished portal supply, such as hepatocellular

al Hospital, 55 Fruit Street, White 270, Boston, MAusetts General Hospital, Harvard Medical School, 55

rights reserved. radiologic.th

eclinics.com

Price et al56

carcinoma (HCC).2 Biphasic hepatic CT improvessensitivity in detecting hypervascular primary andmetastatic hepatic tumors compared with a singleportal venous phase, although the greatest tumor-to-liver contrast typically occurs in the portalvenous phase, in both patients with and withoutcirrhosis.3

At our institution, the timing of the arterial phasein MDCTA of the liver is determined with automaticbolus tracking: contrast is injected and 15 secondsafter the attenuation of the abdominal aorta rea-ches 150 Hounsfield units (HU), image acquisitionstarts. The portal venous phase images are ac-quired 55 to 70 seconds after the contrast material(CM) injection. A delayed phase also can be addedfor a triple-phase hepatic CT, which has beenshown to have improved sensitivity for detectionof HCC over biphasic CT. When automated bolustracking is used, scanning for the delayed phaseoccurs 180 seconds after injection of the CM2

(Table 1).

Pancreatic Protocol

For accurate detection and staging of pancreaticadenocarcinoma, it is important to perform abiphasic pancreatic protocol CTA that includes apancreatic parenchymal phase at 40 to 50 seconds(if using a fixed delay) and a portal venous phase.The pancreatic parenchymal phase allows foroptimal pancreatic parenchymal enhancementand provides maximal contrast difference

Table 1Sample liver computed tomography angiography

Noncontrast (Only 4 SlicesThrough Mid Liver) Art

Scan delay — Bol

Ref kV 120 120

Quality ref mAs 180 220

Slice thickness 5 mm 1 m

Slice increment 5 mm 0.6

Pitch 0.95 0.9

Rotation time 0.5 0.5

ACQ 128 � 0.6 128

Kernel I30F medium smooth I30

Liver multidetector computed tomography angiography: Siemlutions, Malvern, PA, USA).

Intravenous (IV) contrast: 370 mg/mL.Weight-based dose: <135 lb: 80 mL, 135–200 lb: 90 mL, >200IV gauge: 18 gauge.IV contrast rate: 4 mL/s.Oral contrast: water.Bolus tracking: 150 HU of abdominal aorta measured at the

scan delay of 15 seconds for arterial phase.

between normal pancreatic parenchyma and tu-mor; for pancreatic ductal adenocarcinoma, thetumor is hypoattenuating versus background pa-renchyma. The pancreatic phase also allowsdepiction of the arterial anatomy. The portalvenous phase delineates the portal and mesen-teric venous anatomy and hepatic parenchymalpathology4 (Tables 2 and 3).Recently, utilization of split-bolus injection in

conjunction with spectral CT has been shown toimprove pancreatic tumor conspicuity and reduceradiation dose by combing the pancreatic and por-tal venous phases into one scan. This is done byinitially administering 100 mL iodinated intrave-nous contrast before the CT for the portal venousphase and then injecting an additional 40 mL ofcontrast 35 seconds later to enhance the pancre-atic phase. Bolus tracking initiates scanning15 seconds after the abdominal aorta reaches anattenuation of 280 HU. Images are then recon-structed at 60 and 77 keV. This scanning protocoloffers marked reduction in radiation dose andhigher tumor conspicuity with the 60 keVcompared with a standard pancreatic protocolCT.5

Dual-Energy Computed Tomography and LowPeak Kilovoltage Imaging

Dual-energy CT (DECT) can now be used inconjunction with MDCTA to provide additional in-formation about tissue composition and enhance

erial Phase Portal Venous

us tracking 70 s after contrast injection

120

200

m 5 mm

mm 5 mm

5 0.95

0.5

� 0.6 128 � 0.6

F medium smooth I30F medium smooth

ens Definition Edge 128 CT scanner (Siemens Medical So-

lb: 120 mL.

level of the mid liver, monitored delay of 10 seconds and

Table 2Sample pancreatic computed tomographyangiography (CTA) protocol

Pancreatic CTAPortal VenousPhase

Delay (fixed) 50 s 70 s

Care kV Ref 120 Ref 120

Quality ref mAs 220 200

Slice thickness 2 mm 5 mm

Slice increment 2 mm 5 mm

Pitch 0.95 0.95

Rotation time 0.5 0.5

Collimation 128 � 0.6 mm 128 � 0.6 mm

Kernel I30F mediumsmooth

I30F mediumsmooth

Pancreatic multidetector computed tomography angiog-raphy: Siemens Definition Edge 128 CT scanner.

Intravenous (IV) contrast: 370 mg/mL.Weight-based dose: <135 lb: 80 mL, 135–200 lb:

90 mL, >200 lb: 120 mL.IV gauge: 18–20 gauge.IV contrast rate: 4 mL/s.Oral contrast: water.

Hepatic, Pancreatic, and Splenic Circulation 57

contrast resolution by imaging at 2 different en-ergies: 80 and 140 kVp. Iodinated contrast demon-strates increased attenuation at lower energylevels because the K-edge of iodine (33.2 KeV) iscloser to the lower energy of 80 kVp than thehigher energy level. Imaging at a lower energy of80 kVp can improve hypervascular lesion conspi-cuity as well as reduce the effective radiationdose, and the amount of iodinated contrastrequired for an examination. The disadvantage ofusing a lower kVp is that image noise increases

Table 3Protocol for pancreatic CTA reconstruction andreformatted images

CTA ThinReconstructions

3D MPR: CTASagittal andCoronalReformats

Kernel I31F S3 I31F S3

Thickness 1 mm 3 mm

Interval 0.6 mm 3 mm

Pancreatic multidetector computed tomography angiog-raphy: Reconstruction and Reformats.

Siemens Definition Edge 128 CT scanner.Abbreviations: 3D, three dimensional; CTA, computed to-

mography angiography; MPR, multiplanar reconstruction.

due to attenuation of the x-ray beam by the pa-tient, which is exacerbated in larger patients.Certain structures, such as gallstones and urinarystones, also demonstrate greater conspicuitywhen imaged at a higher kVp. By imaging at the2 energy levels, the benefits of both low and higherenergy levels can be achieved in a singleexamination.6,7

With DECT, 80 kVp and 140 kVp datasets areacquired with a single acquisition, and virtual un-enhanced and weighted average images (WAIs)are then created from these raw datasets. WAIscombine the HU data acquired by the 80 kVpand 140 kVp datasets to simulate a 120 kVp acqui-sition. This results in optimal lesion conspicuity,high contrast, low noise, and artifact reduction.The quality of vascular imaging can be improvedwith the lower kVp dataset.8,9

Dual-Energy Computed Tomography ImageReconstruction and PostprocessingTechniques

Material-specific applications in DECT allow forthe generation of images based on differences inattenuation and changes in attenuation at differentenergy levels, which help to differentiate thecomposition of materials. With dual-source dual-energy CT, a 3-material decomposition algorithmof iodine, soft tissue, and fat is used, and separatematerial-specific images can be generated basedon them. Single-source dual-energy CT uses a2-material decomposition algorithm composed ofiodine and water.10

Dual-energy techniques can reduce effective ra-diation dose by reconstructing virtual unenhancedimages, which obviate the need for an unen-hanced scan in multiphase MDCTA. The virtual un-enhanced images are obtained by digitallysubtracting iodine from the data set of contrast-enhanced images.6 The iodine-specific images indual-energy CT are derived from material decom-position and demonstrate true iodine content oftissues. These images are not dependent oninherent tissue attenuation and therefore canmore reliably demonstrate true tissue enhance-ment. The iodine content of each voxel isquantified in iodine-specific maps, allowing fordetection of very small amounts ofenhancement.10

Virtual monochromatic (VMC) images arecreated from material-specific algorithms andpostprocessed from the dual-energy data set.The selected VMC energy level depicts structuresas though they were acquired from a monochro-matic beam. Low-energy VMC images showgreater attenuation of iodine leading to better

Price et al58

contrast between structures, although at theexpense of higher noise.10

Volumetric material-specific datasets acquiredwith DECT can be reconstructed as axial imagesor even processed by conventional 3D applica-tions like maximum intensity projection (MIP),multiplanar reconstruction (MPR), and volume-rendered reformation. MPR, MIP, and volume-rendered reconstructions of the iodine-specificmaps make virtual bone subtraction possible,which in turn helps visualization of the vesselswith removal of bones and calcified plaques. Vir-tual nonenhanced images aid in the detection ofvascular calcification by removing contrast fromimages, although they contain higher noise andlower resolution.9

ARTERIAL ANATOMY

The vascular anatomy of the liver and pancreas in-fluences surgical decisions for tumor resection soas to minimize surgical morbidity. Moreover,because primary and metastatic hepatic malig-nancies are increasingly being treated with mini-mally invasive interventional and surgicaltechniques, MDCTA has become an essential mo-dality to accurately define hepatic arterial anat-omy. It is crucial for interventional radiologistsand surgeons to be familiar with variant arterialanatomy to avoid procedural and surgicalcomplications.11

CELIAC AXIS

The celiac artery is the first major anterior infra-diaphragmatic branch of the abdominal aorta, fol-lowed by the superior mesenteric artery (SMA) andinferior mesenteric artery. With the most commonbranching pattern of the celiac axis, the left gastricartery branches first and the celiac trunk then di-vides into the common hepatic and splenic ar-teries. This pattern is seen in approximately 70%of individuals. Several other variants have beendescribed, such as a true trifurcation of all 3 ves-sels from the terminal portion of the celiac axis,and combined trunks when one vessel is replacedfrom a different arterial bed.12

HEPATIC ARTERY

The common hepatic artery (CHA) originates fromthe celiac trunk, giving off the gastroduodenal ar-tery as the first branch, and continues to the portahepatis as the proper hepatic artery. The rightgastric artery originates from the proper hepaticartery at the portal hilum. The proper hepatic arterythen finally divides into its 3 terminal branches: theright, middle, and left hepatic arteries.12

The proper hepatic artery is located anterior tothe portal vein within the porta hepatis and to theleft of the common bile duct. Following its take-off from the proper hepatic artery, the right hepaticartery courses between the common bile duct andthe portal vein.13

Classic branching of the hepatic artery isobserved in approximately 60% of people.12

Variant origins of the CHA are rare and seen inonly approximately 4% of individuals. In peoplewith a replaced CHA, 50% have an origin fromthe SMA and the remainder are usually replacedto the abdominal aorta.11 In patients who have aCHA that arises from the SMA, the artery typicallymaintains a suprapancreatic position but coursesposterior to the main portal vein and superiormesenteric vein (SMV), unlike in the normal CHAanatomy. The CHA maintains a suprapancreatic,preportal pathway when it arises from the abdom-inal aorta14 (Fig. 1).The most frequent anatomic variation of the he-

patic arterial system is a replaced right hepatic ar-tery arising from the SMA, present in up to 18% ofpatients (Fig. 2). The next most common variationis a replaced left hepatic artery arising from the leftgastric artery.14

Pancreatic Arterial Anatomy

The pancreatic blood supply is derived frombranches of the celiac trunk and the SMA. The dor-sal pancreatic artery and pancreatica magna ar-tery arise from the splenic artery, which alsogives off distal arterial branches to supply thepancreatic tail. The SMA branches off the abdom-inal aorta just inferior to the celiac trunk and poste-rior to the neck of the pancreas. The SMA coursesanterior to the pancreatic uncinate and to the leftof the SMV.1,15

The gastroduodenal artery originates from theCHA and gives off the anterior and superior pan-creatoduodenal arteries, which form an anasto-mosis with the inferior pancreaticoduodenalartery. This anastomosis creates an arterial arcadethat surrounds the head and uncinate process ofthe pancreas. The transverse pancreatic arteryforms a connection between pancreaticoduodenalarcade and the dorsal pancreatic and pancreaticamagna arteries.1

Splenic Artery

The splenic artery has the most torturous course ofall the branches of the celiac axis and is usually thelargest branch, with a diameter of approximately 6to 10 mm and an average length of 13 cm. Aber-rant origins of the splenic artery are uncommonand seen in fewer than 1% of individuals. When

Fig. 1. A 62-year-old man with a replaced CHA arising from the SMA. (A, B) Three-dimensional volume-renderedimages. (C, D) Axial contrast-enhanced CTA images. (E, F) Sagittal and coronal reformatted images. A bilobedaneurysm (arrows) with calcification and mural thrombus (arrowhead) arises from the CHA. (G, H) CTA imagesfollowing coil embolization of the aneurysm.

Hepatic, Pancreatic, and Splenic Circulation 59

present, the most common variant origins of thesplenic artery are the abdominal aorta, SMA, andright hepatic artery.12

The splenic artery courses along the superiormargin of the pancreas, anterior and superior tothe splenic vein. At the hilum, the splenic artery di-vides into superior and inferior terminal branches,which then subsequently divide into segmental in-trasplenic branches. The superior terminalbranches are the dominant arterial supply to thespleen and tend to be longer than the inferior ter-minal branches. As previously mentioned, thesplenic artery supplies multiple arterial branchesto the pancreas. The dorsal pancreatic artery isthe first branch and is followed by the pancreaticamagna, which typically arises from the middleportion of the splenic artery.16

VENOUS ANATOMYPortal Venous Anatomy

The portal vein forms posterior to the pancreaticneck when the superior mesenteric and splenicveins converge. Within the porta hepatis, the portalvein is located posterior to the proper hepatic ar-tery and common bile duct and normally has adiameter of 11 to 13 mm.13

Conventional Anatomy

� Main portal vein branches into the right andleft portal veins

� Right portal vein divides into the anterior andposterior branches

� Right anterior branch supplies hepatic seg-ments V and VIII

Fig. 2. A 35-year-old woman beforeliver donor evaluation. MultiplanarMIP images. (A) Celiac artery (CA),CHA, and left hepatic artery (LHA).(B) Replaced right hepatic artery(RHA) arising from the SMA.

Price et al60

� Right posterior branch supplies segments VIand VII

Variant Anatomy

� “Z type” variant: right posterior portal vein isthe first branch to arise from the main portalvein and is subsequently followed by the rightanterior and finally the left portal veins

� Trifurcation: right anterior, right posterior, andleft portal veins share a common origin fromthe main portal vein17

Hepatic Venous Anatomy

� The liver is conventionally drained via 3 hepat-ic veins that converge into the inferior venacava

� Right hepatic vein drains segments V to VIII� Middle hepatic vein drains segments IV, V,and VIII

� Left hepatic vein drains segments II and III18

LIVER MULTIDETECTOR COMPUTEDTOMOGRAPHY ANGIOGRAPHYPreoperative Assessment for HepaticTransplantation

MDCTA is an excellent modality for demonstratinga patient’s hepatic vascular anatomy before livertransplantation and has become the first-line im-aging modality for surgical planning of living donorliver transplantation.Hepatic vascular variants are important to iden-

tify with preoperative imaging, as they can dramat-ically impact surgical technique and rarely result indonor exclusion. In adult-to-adult living donor pre-operative imaging, it is essential to identify thelocation of and course of the middle hepatic veinbecause the hepatectomy plane is typically alongthe gallbladder fossa, approximately 1 cm to theright of the middle hepatic vein.19

The middle hepatic artery, supplying segmentIV, is also included in the hepatectomy plane of

Fig. 3. A 64-year-old man 10 days status post orthotopic livarterial-phase CTA image and (B) coronal arterial-phase im(white arrows). (C) Angiographic image after surgical throhepatic artery (black arrows).

adult-to-adult live donor liver transplantation, andits origin and course are important to delineativepreoperatively. One variant that has important sur-gical implications is a middle hepatic artery arisingfrom the right hepatic artery, as this crosses theplanned hepatectomy line.18

Postoperative Evaluation for LiverTransplantation

MDCTA has a critical role in detecting arterial com-plications after liver transplantation, and iscommonly used as the next imaging modalitywhen abnormalities are detected on liver Dopplerultrasound. Hepatic arterial complicationsfollowing transplantation that can be diagnosedwith MDCTA include the following:

� Thrombosis� Dissection� Stenosis� Pseudoaneurysm formation

Hepatic Artery Thrombosis

Hepatic arterial thrombosis (HAT) is a potentiallydevastating arterial complication following trans-plantation and also the most common vascularcomplication. Undetected HAT can result in biliaryischemia, necrosis, bilomas, sepsis, fulminant he-patic necrosis, and graft failure. Although earlydiagnosis of HAT may enhance the success of at-tempts at revascularization with surgical throm-bectomy or thrombolysis, most patients withHAT will require retransplantation.20 Absence ofhepatic arterial flow on Doppler ultrasonographyshould raise concern for hepatic arterial throm-bosis and prompt further evaluation with CTA,magnetic resonance angiography, or catheterangiography (Fig. 3).

� “Early” HAT is defined as occurring within thefirst month following transplantation

er transplant with hepatic artery thrombosis. (A) Axialage demonstrating abrupt cutoff of the hepatic arterymbectomy showing multifocal stenosis of the proper

Hepatic, Pancreatic, and Splenic Circulation 61

� “Late” HAT occurs 1 month or more aftertransplantation

� HAT is more common in the early posttrans-plant period and may present with fulminanthepatic failure21

Hepatic Artery Stenosis

The incidence of hepatic artery stenosis in livertransplant recipients is 5% to 11%.20,22,23 Hepaticartery stenosis most commonly occurs at the siteof anastomosis within the first 3 months aftertransplantation. It is critical to detect hepatic arte-rial stenosis, as it can lead to graft dysfunction, he-patic artery thrombosis, and biliary structuring ifuntreated. When detected early with imaging mo-dalities such as MDCTA, there is a greater likeli-hood that hepatic artery stenosis can besuccessfully treated with catheter angioplasty orsurgical reconstruction so that retransplantationis not required.22,23

Hepatic Artery Aneurysms

MDCT serves as an excellent noninvasive imagingmodality for diagnosis and surveillance of hepaticartery aneurysms (HAAs). HAAs are the secondmost common type of visceral artery aneurysm,after splenic artery aneurysms.24 Most HAAs areincidentally detected with cross-sectional imagingand patients will be asymptomatic unless theaneurysm ruptures. Unlike splenic artery aneu-rysms, HAAs most frequently occur in men.25

When imaging HAAs, it is critical to assess forthe presence of any anatomic vascular variants,particularly in the presence of planned endovascu-lar or surgical intervention (see Fig. 1).

Hepatocellular Carcinoma

HCC most frequently occurs in individuals withhepatitis or cirrhosis. HCC classically demon-strates arterial enhancement with washout on theportal venous phase and may show delayedcapsule appearance. Although HCC can presentas a well-defined lesion at imaging, it can alsodiffusely infiltrate the liver and invade hepatic and

Fig. 4. An 80-year-old man with HCC. (A, B) Arterial-phasean arterially enhancing tumor infiltrating most of the righthe right portal vein (arrowhead).

portal veins. The sensitivity of MDCT for detectionof HCC varies by tumor size. In larger lesions, itcan exceed 70%; however, when tumors aresmaller than 20 mm, the sensitivity of MDCT de-creases to approximately 50% in patients withcirrhosis undergoing multiphase CT examinationswith unenhanced, arterial, and portal venousphases.26 (Fig. 4)

Although HCC most frequently develops in thesetting of cirrhosis, in the United States approxi-mately 22% of HCC will occur in noncirrhoticlivers. Individuals who develop HCC withoutcirrhosis are more likely to present with a symp-tomatic solitary or dominant hepatic mass, andthe tumor is typically moderately or well differenti-ated at pathology. Most of these lesions in patientswithout cirrhosis show necrosis, and approxi-mately one-quarter will have hemorrhagiccomponents.27

The United Network for Organ Sharing (UNOS),which administers the Organ Procurement andTransplant Network (OPTN), gives increased prior-ity on the transplant waitlist to individuals whohave HCC and remain within the Milan Criteria;namely, 1 HCC that is 5 cm or smaller, or asmany as 3 HCCs that are all 3 cm or smaller.UNOS allows for the diagnosis of HCC to bemade with imaging alone, either with dynamiccontrast-enhanced MDCT or MR. In 2011, theUNOS/OPTN board of directors issued anamended policy delineating the technical parame-ters that should be followed for dynamic liver pro-tocols and the criteria required to diagnose HCCwith imaging, with an emphasis on specificityover sensitivity. OPTN Class 5 lesions in cirrhoticlivers meet radiologic criteria for HCC, which areoutlined in Table 4.28

There are several advantages of using dual-energy CT in conjunction with MDCTA for imagingevaluation of HCC. Hypervascular hepatic tumorssuch as HCC have enhanced conspicuity whenimaged at 80 kVp rather than 140 kVp, and theeffective radiation dose is also lower at 80 kVp.6

The low-energy VMC images, which are availablewith both single-source and dual-source DECT,

axial images. (C) Coronal arterial-phase image. There ist hepatic lobe (arrows). Tumor thrombus extends into

Table 4OPTN imaging guidelines for class 5 nodules in cirrhotic livers

OPTN class 5A � Nodule <2 cm and �1 cm in size� Late arterial hyperenhancement relative to hepatic parenchyma� Washout on the later contrast phases and pseudocapsule formation (peripheralrim enhancement)

OPTN class 5A-g(growth)

� Nodule <2 cm and �1 cm in size� Late arterial hyperenhancement relative to hepatic parenchyma� Lesion growth by 50% or greater on serial CT or MRI examinationsperformed �6 mo apart (not applicable to ablated lesions)

OPTN class 5B � Nodule �2 cm and �5 cm in size� Late arterial hyperenhancement relative to hepatic parenchyma� One of the following criteria:

� Portal venous or delayed phase washout� Late capsule or pseudocapsule formation� Lesion growth by 50% or greater on serial CT or MRI examinationsperformed �6 mo apart

� Biopsy proven

OPTN 5T (treated) � OPTN class 5 lesion or biopsy-proven HCC that has been treated withlocoregional therapy

� Findings suggestive of residual or recurrent tumor, such as nodular enhancementalong the ablation zone can be present

Abbreviations: CT, computed tomography; HCC, hepatocellular carcinoma; OPTN, Organ Procurement and TransplantNetwork.

From HRSA/OPTN. OPTN policy 9: allocation of livers and liver-intestines. 2015. Available at: http://optn.transplant.hrsa.gov/resources/by-organ/liver-intestine. Accessed June 27, 2015.

Price et al62

increase the contrast-to-noise ratio (CNR) be-tween hypervascular hepatic tumors and the adja-cent liver.10 Iodine-specific image maps increasethe conspicuity of the ablation zone margincompared with the blended VMC images in pa-tients who have undergone radiofrequency abla-tion and can be particularly useful whenassessing for local tumor recurrence29,30 (Fig. 5).

SPLENIC MULTIDETECTOR COMPUTEDTOMOGRAPHY ANGIOGRAPHYSplenic Artery Aneurysms

Splenic artery aneurysms (SAAs) are the mostcommon type of visceral artery aneurysm, makingup 60% of cases, and have a prevalence of 0.04%

Fig. 5. Contrast-enhanced dual-energy CT images of a 62-ySingle-energy CT image 140 kVp. (B) Virtual monochromNote the increase in iodine attenuation and high imagecompared with the conventional single-energy image.

to 0.10% at autopsy.16,25,31 They are typicallyasymptomatic and incidentally diagnosed at imag-ing. By definition, SAAs occur when the artery sizeexceeds 1 cm and involves dilatation of all layersof the artery wall. Women are more commonlyaffected than men. When SAAs exceed 2 cm insize, intervention is usually favored, either with en-dovascular or open surgical repair due to the riskof rupture; however, there are no definitive man-agement guidelines.32 In addition, enlargement ofthe aneurysm, pregnancy or planned pregnancy,or the presence of symptoms also may promptintervention.25

SAAs are usually saccular and tend to occureither at the distal aspect of the artery or at a bifur-cation in the middle or distal segment of the

ear-old showing HCC in hepatic segment II (arrow). (A)atic image 50 keV. (C) Material-density iodine image.contrast observed on the low-keV and iodine images,

Hepatic, Pancreatic, and Splenic Circulation 63

artery.16,33 Multiparous women and individualswith portal hypertension have the most frequentincidence of SAAs. The association with multipar-ity has been postulated to be due to hormonal al-terations that result in intimal hyperplasia andsubsequent aneurysm formation.16,34 (Fig. 6)

PANCREATIC MULTIDETECTOR COMPUTEDTOMOGRAPHY ANGIOGRAPHYPancreatic Cancer

Pancreatic ductal adenocarcinoma (PDA) is anaggressive cancer with high mortality. Accuratestaging of PDA at the time of diagnosis is impor-tant to triage patients to surgical resection orchemotherapy, as well as help determine overallprognosis. Evaluation with imaging plays a primaryrole in the initial decision-making process of pa-tients with PDA by providing staging information.4

MDCTA has been shown to have positive predic-tive value of 89% for preoperative prediction ofresectability of PDA across multiple generationsof CT scanners.35

Achieving high CNR and lesion conspicuity areparticularly critical in pancreatic imaging, asPDAs can appear relatively inconspicuous and insome cases isoattenuating to pancreatic paren-chyma on CT.6 It has been shown that imagingwith a lower voltage (80 kVp) and higher tube cur-rent results in greater pancreas-to-tumor CNR.36

The iodine-specific maps in dual-energy CT canimprove conspicuity of hypoattenuating PDAsand the low-voltage dataset can better delineate

tumor margins due to the increased tumor-to-pancreas CNR.37 (Fig. 7)

Based on imaging features of PDA demon-strated at MDCTA, these tumors are classified asresectable, borderline resectable, or unresectable.The National Comprehensive Cancer Networkcriteria for placing patients in 1 of these 3 cate-gories is outlined in Table 5. The pertinent findingsrecommended in the Consensus Statement of theSociety of Abdominal Radiology and AmericanPancreatic Association on the pancreatic radi-ology reporting template should be included inthe imaging report for patients with known or sus-pected PDA, as summarized in Table 64 (Figs. 8and 9).

Hypervascular Pancreatic Tumors

The differential diagnosis of focal hypervascularpancreatic lesions includes primary neuroendo-crine tumors, metastases, intrapancreatic acces-sory spleen, and vascular lesions, such asarteriovenous fistulas or aneurysms of the splenicartery.

Although pancreatic neuroendocrine tumorscomprise fewer than 5% of all primary pancreaticmalignancies,38 they are the most common hyper-vascular tumors of the pancreas. These lesions areusually well demarcated and usually show avidenhancement on the early arterial-phase images,owing to the rich capillary network present withinthe lesions (Fig. 10).39 Smaller functioning tumorsshow homogeneous enhancement, whereas

Fig. 6. A 54-year-old woman withan SAA. (A–C). Multiplanar MIPimages show the aneurysm at thesplenic hilum with mural thrombusand peripheral rim calcification.(D) Three-dimensional volume-rendered image.

Fig. 7. A 79-year-old man with PDA involving the head and invading the duodenum. Dual-energy axial CTA im-ages show a hypoattenuating tumor within the pancreatic head (arrows) that appears more conspicuous on themonochromatic 50-keV and iodine-specific images. (A) Single-energy CT (SECT) 140 kVp arterial-phase image. (B)Monochromatic 50 keV image. (C) Material-density iodine image.

Price et al64

larger nonfunctioning lesions may show heteroge-neity and necrosis. It is crucial to perform pancre-atic protocol MDCTA in patients with a knownneuroendocrine lesion so as to assess the primarylesion within the pancreas as well as evaluate theliver for hypervascular metastases (Fig. 11).

Pancreatic Metastases

Metastatic lesions to the pancreas are uncommonand account for fewer than 5% of all pancreaticmalignancies.40 Primary tumors of the kidney, thy-roid, lung, and breast, as well as melanoma havebeen reported to metastasize to the pancreatic pa-renchyma. It is important to note that becausethese metastatic lesions can invade the ductal

Table 5National Comprehensive Cancer Network Guidelines

Stage Arterial Findings Venou

Resectable Preserved fat planes aroundceliac axis, SMA, and hepaticartery

No SMinvo

Borderlineresectable

� Gastroduodenal arteryencasement up to the hepaticartery or direct abutment ofhepatic artery

� Tumor abutment of SMAshould be <180�

SMV indistosuffproxrese

Unresectable � Aortic invasion orencasement

� Pancreatic head tumors: SMAencasement of more than180�, celiac axis abutment, orinferior vena cava invasion

� Pancreatic body/tail tumors:SMA or celiac axis encasementof more than 180�

SMV aunsu

Abbreviations: PDA, pancreatic ductal adenocarcinoma; SMA,From Al-Hawary MM, Francis IR, Chari ST, et al. Pancreat

consensus statement of the Society of Abdominal Radiolog2014;270(1):248–60.

epithelium, they may produce ductal dilatationand mimic pancreatic adenocarcinoma.41 Metas-tases from renal cell carcinoma (RCC) may befound at the time of primary tumor diagnosis or,more frequently, during follow-up after surgery,42

and though these lesions can be solitary, theyhave been reported to be multiple in 20% to 45% of patients.43 RCC is the most common primarytumor leading to solitary pancreatic metastases.44

These lesions are usually round or ovoid masses,well-delineated, and show brisk enhancement inthe pancreatic late arterial phase and washout ondelayed phase images.45 Based on enhancementalone, it can be difficult to differentiate these met-astatic lesions from hypervascular neuroendocrinetumors of the pancreas (Fig. 12).

for PDA Staging

s FindingsNodal and DistantMetastases

V or portal veinlvement

—

volvement or portal veinrtion or narrowing with

icient vessel lengthimal and distal for safection and reconstruction

nd portal vein occlusionitable for reconstruction

Distant metastases;metastases to lymphnodes beyond fieldof resection

superior mesenteric artery; SMV, superior mesenteric vein.ic ductal adenocarcinoma radiology reporting template:y and the American Pancreatic Association. Radiology

Table 6Pancreatic ductal adenocarcinoma reporting template: Society of Abdominal Radiology and AmericanPancreatic Association

Tumor location � Right of superior mesenteric vein (SMV): pancreatic head or uncinateprocess

� Left of SMV: pancreatic body or tail

Tumor size —

Presence and extent ofvascular involvement:arterial

Celiac axis, superior mesenteric artery and common hepatic artery:� �180� vessel contact� >180� vessel contact

Presence and extent ofvascular involvement:venous

Portal vein and SMV:� Circumferential degree of tumor vessel contact� Focal caliber narrowing� Contour abnormality� Presence of bland thrombus

Presence of arterial anatomicvariants

—

Extrapancreatic tumorextension

� Local (to adjacent organs): stomach, small bowel, spleen, colon/mesocolon

� Distant: liver, peritoneum, abnormal-appearing lymph nodesoutside local drainage pathway

Data from Al-Hawary MM, Francis IR, Chari ST, et al. Pancreatic ductal adenocarcinoma radiology reporting template:consensus statement of the Society of Abdominal Radiology and the American Pancreatic Association. Radiology2014;270(1):248–60.

Hepatic, Pancreatic, and Splenic Circulation 65

Vascular Complications of Pancreatitis

Acute pancreatitis is associated with trypsin acti-vation within pancreatic acinar cells with resultingautodigestion of the pancreas. When severe, theenzymatic autodigestion can extend beyond thepancreatic parenchyma and result in vascularand hemorrhagic complications. Reports in the

Fig. 8. CTA images for staging of a 65-year-old man with loand uncinate process of the pancreas. (A–C) Arterial and pencasement of celiac artery and common hepatic artery byphase axial and coronal images showing encasement of(black arrows).

literature state that major vascular complicationsfollowing pancreatitis occur with a greater inci-dence in individuals with chronic pancreatitiscompared with acute pancreatitis.46

As the pancreas is anatomically associated withthe splenic, superior mesenteric, and portal veins,these can be involved in pancreatitis. Thrombosis

cally advanced adenocarcinoma arising from the headortal venous phase axial and coronal images showingtumor (white arrows). (D–F) Arterial and portal venousthe superior mesenteric and common hepatic arteries

Fig. 9. A 68-year-old man with adenocarcinoma of the pancreatic tail. (A) Hypodense lesion in the body of thepancreas (arrow) without associated pancreatic duct dilatation or enhancing mural nodules, consistent with anintraductal papillary mucinous neoplasm (IPMN). (B, C) Ill-defined soft tissue mass in the tail of the pancreas(arrowhead), invading the splenic hilum and left anterior pararenal space (white arrows). The patient underwentdistal pancreatectomy and splenectomy; pathology confirmed pancreatic ductal adenocarcinoma with splenicinvolvement.

Fig. 10. Dual-energy CTA images from a 68-year-old man with an 8-mm enhancing lesion in the pancreatic tail.(A) A 140-kVp image. (B) Virtual monochromatic 65-keV image. (C) Material-density iodine image. The pancreatictail lesion (arrow) is most conspicuous on the low-keV and iodine-specific images. The patient underwent endo-scopic ultrasound and transgastric biopsy. Histopathology confirmed a well-differentiated endocrine neoplasm,strongly positive for chromogranin and synaptophysin.

Fig. 11. Dual-energy CTA images ofa 64-year-old woman with a hypo-attenuating pancreatic head mass(arrows). (A) Axial, SECT 140-kVpimage. (B) Axial, monochromatic65-keV image. (C) Material-densityiodine image. (D) Coronal arterial-phase image. The lesion bordersare delineated best on the iodine-specific images. The patient under-went a Whipple resection andpathology confirmed a well-differentiated neuroendocrine tu-mor, World Health OrganizationGrade 2 of 3.

Price et al66

Fig. 12. A 74-year-old woman with history of RCC. (A–C) Axial arterial-phase images. (D–F) Coronal arterial-phaseimages. The images show arterially enhancing metastases involving the greater curvature of the stomach, left ad-renal gland, and pancreas (arrows).

Fig. 13. A 61-year-old man with ahistory of pancreatitis. There is ahematoma involving the pancre-atic head (white arrows) with agastroduodenal artery pseudoa-neurysm (black arrows). (A) Axialarterial-phase image. (B) Axialdelayed-phase image. (C) Coronalarterial-phase image. (D) Angio-graphic image.

Fig. 14. A 55-year-old man with history of chronic pancreatitis. (A) Coronal portal venous phase image. (B) Axialportal venous phase image. Note the presence of punctate calcifications in the pancreas (arrowheads). There is ahematoma involving the head and uncinate process of the pancreas (black arrow), and a pseudoaneurysm (whitearrows) arising from the middle colic artery. (C) Angiographic image.

Hepatic, Pancreatic, and Splenic Circulation 67

Fig. 15. A 54-year-old man with hemorrhagic, necrotizing pancreatitis. (A) Axial arterial-phase CTA image. (B)Coronal arterial-phase CTA image. (C) Angiographic image. The CTA images show extensive pancreatic necrosisand a heterogeneous collection (white arrows). There is a complex arteriovenous fistula (arrowhead) in theneck of the pancreas with branches from the celiac artery, left gastric artery, and SMV. Angiographic image (C)shows the arteriovenous fistula (black arrow) draining into the splenoportal junction (black arrowhead).

Price et al68

of the splanchnic veins, defined as the portal,splenic, or SMVs, either in combination or isola-tion, occurs in approximately 1.8% of individualswith acute pancreatitis. Isolated splenic veinthrombosis (SPV) is the most common form ofsplanchnic vein thrombosis.47 SPV is more likelyto occur in the presence of pancreatic fluid collec-tions with severe necrotizing pancreatitis and canbe caused by inflammation or compression froman adjacent fluid-collection.48 When present,these complications are important to accuratelydiagnosis, because in some cases untreatedsplenic vein thrombosis can result in gastric vari-ces, and SMV occlusion may lead to small bowelischemia.47

Direct vascular injuries, although rare, can lead topseudoaneurysm formation and, rarely, arterialrupture into the gastrointestinal tract.49 Pseudoa-neurysm formation is a severe complication ofpancreatitis and can be identified at MDCTA as afocal outpouching arising from the involved artery,typically in a region of pancreatic necrosis.50 Themost common sites of pseudoaneurysm formationsecondary topancreatitis inorderof decreasing fre-quency are the splenic, gastroduodenal, pancreati-coduodenal, hepatic, and left gastric arteries50,51

(Fig. 13). Rarely, superior mesenteric, jejunal, orcolic arterial branches are affected52 (Fig. 14).In rare cases of severe hemorrhagic pancrea-

titis, more complex vascular injuries may occur(Fig. 15).CTA allows accurate diagnosis of arterial injures

and can demonstrate the extent of a pseudoa-neurysm along with the degree of thrombosiswithin the pseudoaneurysm. The 3D postprocess-ing of images, with MIPs and volume rendering,assist with surgical planning and interventionalprocedures.

SUMMARY

MDCTA of the hepatic, pancreatic, and splenic cir-culations is a highly effective noninvasive imaging

modality that delineates complex vascular anat-omy and anatomic variants as well as paren-chymal organ pathology with high spatialresolution. Newer imaging techniques, such asDECT, can increase contrast resolution andenhance diagnostic capabilities while limiting radi-ation dose.

REFERENCES

1. Perez-Johnston R, Lenhart DK, Sahani DV. CT angi-

ography of the hepatic and pancreatic circulation.

Radiol Clin North Am 2010;48(2):311–30, viii.

2. Iannaccone R, Laghi A, Catalano C, et al. Hepato-

cellular carcinoma: role of unenhanced and delayed

phase multi-detector row helical CT in patients with

cirrhosis. Radiology 2005;234(2):460–7.

3. Foley WD, Mallisee TA, Hohenwalter MD, et al. Multi-

phase hepatic CT with a multirow detector CT scan-

ner. AJR Am J Roentgenol 2000;175(3):679–85.

4. Al-Hawary MM, Francis IR, Chari ST, et al. Pancre-

atic ductal adenocarcinoma radiology reporting

template: consensus statement of the Society of

Abdominal Radiology and the American Pancreatic

Association. Radiology 2014;270(1):248–60.

5. Brook OR, Gourtsoyianni S, Brook A, et al. Split-

bolus spectral multidetector CT of the pancreas:

assessment of radiation dose and tumor conspi-

cuity. Radiology 2013;269(1):139–48.

6. Heye T, Nelson RC, Ho LM, et al. Dual-energy CTap-

plications in the abdomen. AJR Am J Roentgenol

2012;199(5 Suppl):S64–70.

7. Yeh BM, Shepherd JA, Wang ZJ, et al. Dual-energy

and low-kVp CT in the abdomen. AJR Am J Roent-

genol 2009;193(1):47–54.

8. Macari M, Spieler B, Kim D, et al. Dual-source dual-

energy MDCT of pancreatic adenocarcinoma: initial

observations with data generated at 80 kVp and at

simulated weighted-average 120 kVp. AJR Am J

Roentgenol 2010;194(1):W27–32.

9. Vlahos I, Chung R, Nair A, et al. Dual-energy CT:

vascular applications. AJR Am J Roentgenol 2012;

199(5 Suppl):S87–97.

Hepatic, Pancreatic, and Splenic Circulation 69

10. Agrawal MD, Pinho DF, Kulkarni NM, et al. Onco-

logic applications of dual-energy CT in the

abdomen. Radiographics 2014;34(3):589–612.

11. Covey AM, Brody LA, Maluccio MA, et al. Variant he-

patic arterial anatomy revisited: digital subtraction

angiography performed in 600 patients. Radiology

2002;224(2):542–7.

12. Hazirolan T, Metin Y, Karaosmanoglu AD, et al.

Mesenteric arterial variations detected at MDCT

angiography of abdominal aorta. AJR Am J Roent-

genol 2009;192(4):1097–102.

13. Tirumani SH, Shanbhogue AK, Vikram R, et al. Imag-

ing of the porta hepatis: spectrum of disease. Radio-

graphics 2014;34(1):73–92.

14. Song SY, Chung JW, Yin YH, et al. Celiac axis and

common hepatic artery variations in 5002 patients:

systematic analysis with spiral CT and DSA. Radi-

ology 2010;255(1):278–88.

15. Johnson PT, Heath DG, Kuszyk BS, et al. CTangiog-

raphy with volume rendering: advantages and appli-

cations in splanchnic vascular imaging. Radiology

1996;200(2):564–8.

16. Madoff DC, Denys A, Wallace MJ, et al. Splenic arte-

rial interventions: anatomy, indications, technical

considerations, and potential complications. Radio-

graphics 2005;25(Suppl 1):S191–211.

17. Covey AM, Brody LA, Getrajdman GI, et al. Inci-

dence, patterns, and clinical relevance of variant

portal vein anatomy. AJR Am J Roentgenol 2004;

183(4):1055–64.

18. Sahani D, Mehta A, Blake M, et al. Preoperative he-

patic vascular evaluation with CT and MR angiog-

raphy: implications for surgery. Radiographics

2004;24(5):1367–80.

19. Singh AK, Cronin CG, Verma HA, et al. Imaging of

preoperative liver transplantation in adults: what ra-

diologists should know. Radiographics 2011;31(4):

1017–30.

20. Itri JN, Heller MT, Tublin ME. Hepatic transplantation:

postoperative complications. Abdom Imaging 2013;

38(6):1300–33.

21. ParejaE,CortesM,NavarroR, et al.Vascularcomplica-

tions after orthotopic liver transplantation: hepatic ar-

tery thrombosis. Transplant Proc 2010;42(8):2970–2.

22. Caiado AH, Blasbalg R, Marcelino AS, et al. Compli-

cations of liver transplantation: multimodality imag-

ing approach. Radiographics 2007;27(5):1401–17.

23. Quiroga S, Sebastia MC, Margarit C, et al. Compli-

cations of orthotopic liver transplantation: spectrum

of findings with helical CT. Radiographics 2001;

21(5):1085–102.

24. Horton KM, Fishman EK. CT angiography of the

mesenteric circulation. Radiol Clin North Am 2010;

48(2):331–45, viii.

25. Horton KM, Smith C, Fishman EK. MDCT and 3D CT

angiography of splanchnic artery aneurysms. AJR

Am J Roentgenol 2007;189(3):641–7.

26. Addley HC, Griffin N, Shaw AS, et al. Accuracy of

hepatocellular carcinoma detection on multidetector

CT in a transplant liver population with explant liver

correlation. Clin Radiol 2011;66(4):349–56.

27. Brancatelli G, Federle MP, Grazioli L, et al. Hepato-

cellular carcinoma in noncirrhotic liver: CT, clinical,

and pathologic findings in 39 U.S. residents. Radi-

ology 2002;222(1):89–94.

28. Wald C, Russo MW, Heimbach JK, et al. New OPTN/

UNOS policy for liver transplant allocation: standard-

ization of liver imaging, diagnosis, classification, and

reporting of hepatocellular carcinoma. Radiology

2013;266(2):376–82.

29. Lee SH, Lee JM, Kim KW, et al. Dual-energy

computed tomography to assess tumor response

to hepatic radiofrequency ablation: potential diag-

nostic value of virtual noncontrast images and iodine

maps. Invest Radiol 2011;46(2):77–84.

30. Morgan DE. Dual-energy CT of the abdomen. Ab-

dom Imaging 2014;39(1):108–34.

31. Abbas MA, Stone WM, Fowl RJ, et al. Splenic artery

aneurysms: two decades experience at Mayo clinic.

Ann Vasc Surg 2002;16(4):442–9.

32. Hogendoorn W, Lavida A, Hunink MG, et al. Open

repair, endovascular repair, and conservative man-

agement of true splenic artery aneurysms. J Vasc

Surg 2014;60(6):1667–76.e1.

33. Liu Q, Lu JP, Wang F, et al. Visceral artery aneu-

rysms: evaluation using 3D contrast-enhanced MR

angiography. AJR Am J Roentgenol 2008;191(3):

826–33.

34. Mattar SG, Lumsden AB. The management of

splenic artery aneurysms: experience with 23 cases.

Am J Surg 1995;169(6):580–4.

35. Zamboni GA, Kruskal JB, Vollmer CM, et al. Pancre-

atic adenocarcinoma: value of multidetector CT

angiography in preoperative evaluation. Radiology

2007;245(3):770–8.

36. Marin D, Nelson RC, Barnhart H, et al. Detection of

pancreatic tumors, image quality, and radiation

dose during the pancreatic parenchymal phase: ef-

fect of a low-tube-voltage, high-tube-current CT

technique–preliminary results. Radiology 2010;

256(2):450–9.

37. De Cecco CN, Darnell A, Rengo M, et al. Dual-en-

ergy CT: oncologic applications. AJR Am J Roent-

genol 2012;199(5 Suppl):S98–105.

38. Bhosale PR, Menias CO, Balachandran A, et al.

Vascular pancreatic lesions: spectrum of imaging

findings of malignant masses and mimics with

pathologic correlation. Abdom Imaging 2013;

38(4):802–17.

39. Lewis RB, Lattin GE Jr, Paal E. Pancreatic endocrine

tumors: radiologic-clinicopathologic correlation. Ra-

diographics 2010;30(6):1445–64.

40. Crippa S, Angelini C, Mussi C, et al. Surgical treat-

ment of metastatic tumors to the pancreas: a single

Price et al70

center experience and review of the literature. World

J Surg 2006;30(8):1536–42.

41. Scatarige JC, Horton KM, Sheth S, et al. Pancreatic

parenchymal metastases: observations on helical

CT. AJR Am J Roentgenol 2001;176(3):695–9.

42. Koide N, Yokoyama Y, Oda K, et al. Pancreatic

metastasis from renal cell carcinoma: results of the

surgical management and pathologic findings.

Pancreas 2008;37(1):104–7.

43. Law CH, Wei AC, Hanna SS, et al. Pancreatic resec-

tion for metastatic renal cell carcinoma: presenta-

tion, treatment, and outcome. Ann Surg Oncol

2003;10(8):922–6.

44. Tsitouridis I, Diamantopoulou A, Michaelides M,

et al. Pancreatic metastases: CT and MRI findings.

Diagn Interv Radiol 2010;16(1):45–51.

45. Vincenzi M, Pasquotti G, Polverosi R, et al. Imaging

of pancreatic metastases from renal cell carcinoma.

Cancer Imaging 2014;14:5.

46. Sharma PK, Madan K, Garg PK. Hemorrhage in

acute pancreatitis: should gastrointestinal bleeding

be considered an organ failure? Pancreas 2008;

36(2):141–5.

47. Harris S, Nadkarni NA, Naina HV, et al. Splanchnic

vein thrombosis in acute pancreatitis: a single-

center experience. Pancreas 2013;42(8):1251–4.

48. Flati G, Andren-Sandberg A, La Pinta M, et al.

Potentially fatal bleeding in acute pancreatitis: path-

ophysiology, prevention, and treatment. Pancreas

2003;26(1):8–14.

49. Barge JU, Lopera JE. Vascular complications of

pancreatitis: role of interventional therapy. Korean J

Radiol 2012;13(Suppl 1):S45–55.

50. Shyu JY, Sainani NI, Sahni VA, et al. Necrotizing

pancreatitis: diagnosis, imaging, and intervention.

Radiographics 2014;34(5):1218–39.

51. Kirby JM, Vora P, Midia M, et al. Vascular complica-

tions of pancreatitis: imaging and intervention. Car-

diovasc Intervent Radiol 2008;31(5):957–70.

52. Verde F, Fishman EK, Johnson PT. Arterial pseudoa-

neurysms complicating pancreatitis: literature re-

view. J Comput Assist Tomogr 2015;39(1):7–12.