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ISSN: 2165-3259

JAOCR

Official Journal of the American Osteopathic College of Radiology

BODY IMAGING

Guest Editor: Rocky C. Saenz, D.O.

Editor-in Chief: William T. O’Brien, Sr., D.O.

October 2012, Vol. 1, Issue 4

JAOCR About the Journal

Aims and Scope The Journal of the American Osteopathic College of Radiology (JAOCR) is designed to provide praccal up‐to‐ date reviews of crical topics in radiology for praccing radiologists and radiology trainees. Each quarterly issue covers a parcular radiology subspecialty and is composed of high quality review arcles and case reports that highlight differenal diagnoses and important teaching points.

Access to Articles All articles published in the JAOCR are open access online. Subscriptions to the journal are not required to view or download articles. Reprints are not available.

Copyrights Materials published in the JAOCR are protected by copyright. No part of this publication may be reproduced without written permission from the AOCR.

Guide for Authors Submissions for the JAOCR are by invitation only. If you were invited to submit an article and have questions regarding the content or format, please contact the appropriate Guest Editor for that particular issue. Although contributions are invited, they are subject to peer review and inal acceptance.

Editor‐in‐Chief William T. O’Brien, Sr., D.O. San Antonio, TX

Design Editor Jessica Roberts Communications Director, AOCR

Managing Editor Tammam Beydoun, D.O. Farmington Hills, MI

Editorial Board Susann Schetter, D.O. Daniel J. Abbis, D.O. Les R. Folio, D.O. Michael W. Keleher, D.O. Rocky Saenz, D.O. Kipp A. Van Camp, D.O. John Wherthey, D.O.

J Am Osteopath Coll Radiol 2012; Vol. 1, Issue 4 Page i

Table of Contents

Body Imaging

Editor: Rocky C. Saenz, D.O.

Title/Author(s) Page No.

From the Guest Editor 1

Review Arcles MRI of Benign Lesions and Metastac Disease Characterizaon with Gadoxetate Disodium 2 Rocky C. Saenz, D.O.

Pancreac 10 Ruedi Theoni, M.D.

Gallbladder Masses: Mulmodality Approach to Differenal Diagnosis 22 Timothy McKnight, D.O., and Ankit Patel, D.O.

Case Reports Cysc Right Lower Quadrant Mass 32 Tammam Beydoun, D.O., and Sharon Kreuer, D.O.

Non‐Adnexal Cysc Pelvic Mass 35 Reehan M. Ali, D.O.

Pancreac Mass 38 Rocky C. Saenz, D.O.

JAOCR At the Viewbox Acute Necrozing Pancreas 41 Sharon Kreuer, D.O.

Pneumatosis Intesnalis With Evidence of Portal Venous Gas 42 Mahew R. Tommack, D.O.

Portal Vein Thrombosis 43 Reehan M. Ali, D.O., and Daniel J. Cranford, D.O.

Page ii J Am Osteopath Coll Radiol 2012; Vol. 1, Issue 4

From the Guest Editor

In This Issue

Rocky C. Saenz, D.O.

Radiology Residency Program Director, Botsford Hospital, Farmington Hills, MI

As simple as it sounds, this phrase is The “Case Reports” and “Viewbox” especially true in the field of medicine arcles are also stellar. All were wrien and radiology. Lifelong learning is what by the Botsford Hospital Radiology all physicians are commied to. In Residents with the excepon of one. I order to achieve this, one must be authored a case report on granulocyte proacve which takes me and effort. sarcoma of the , which was a This includes reviewing the current case I saw in my recent pracce which literature and praccing cung edge turns out to be very unique case; radiology. With these wise words and Reehan Ali, D.O., authored a case thoughts in mind, I present to you this report on enteric duplicaon ; and wonderful, informave issue. Sharon Kreuer, D.O., and Tammam I feel honored to have been selected Beydoun, D.O., co‐authored a case by the JAOCR to be the Guest Editor of report on Mucocele of the . its inaugural Body Imaging issue. To be The “Viewbox” arcles cover key entrusted with this important academic radiographic findings that are “can’t endeavor is a great honor. With such an miss” cases. These “Viewbox” arcles immense task, I have put together what include cases of pneumointesnalis by I believe is a great first Body Imaging Ma Tommack, D.O., portal vein issue. The review arcles include MRI of thrombosis by Reehan Ali, D.O., and the liver – with the ulizaon of necrozing pancreas by Sharon gadoxec disodium (Eovist) in parcular Kreuer, D.O. – reviewing benign lesions versus I would like to thank William O'Brien, metastac disease, which I authored. D.O., and the AOCR for giving me this The next review arcle covers opportunity. I would also like to thank pancreac lesions and is a very Dr. Paul LaCasse, D.O., Stephan Morse, comprehensive review wrien by Ruedi D.O., and Botsford Hospital’s F. Thoeni, M.D., my prior mentor and Department of Radiology (Including trainer from University of California, Radiology Technicians, Residents, and San Francisco. The final review arcle Aendings). Next, I give special thanks was wrien by Ankit Patel, D.O., and to all of the authors of this issue for Timothy McKnight, D.O., and covers agreeing to share their knowledge and pathology. This arcle was hard work with us, and also for making wrien when Dr. Patel and Dr. all of the deadlines and pung‐up with McKnight were fellows at University of my endless trail of emails. Last and California, Irvine and Dartmouth, most importantly, I would like to thank respecvely. I believe these three my wife Blanca and sons Rocky, Russell, arcles will provide the reader with a Ronin, and Rex. Without my strong great foundaon and understanding of family support, I would not be able to pancreac pathology, gallbladder complete this academic project or any pathology, and the use of gadoxec of my other creave works. disodium in discriminang benign from malignant liver lesions.

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MRI Liver, Saenz MRI of Benign Liver Lesions and Metastac Disease Characterizaon with Gadoxetate Disodium

Rocky C. Saenz, D.O.

Department of Diagnosc Radiology, Botsford Hospital, Farmington Hills, MI

Introducon limitaons. The same restricons and precauons remain with gadoxetate disodium for nephrogenic Imaging characterizaon of liver lesions is of systemic fibrosis as with standard extracellular diagnosc importance with regard to its implicaons gadolinium products.2 on paent treatment. Ulizaon of dynamic MRI has Gadoxetate disodium is best ulized with dynamic, become a common pracce as an adjunct to dynamic gradient echo (GRE) T1 fat saturaon imaging. CT scanning. With the recent FDA approval of Opmally, arterial phase imaging, portal venous gadoxec disodium, this provides another avenue for imaging, and delayed imaging at 20 minutes should be evaluaon and characterizaon of indeterminate liver performed. Typically, liver lesions without lesions. Gadoxec acid was approved for use in the will not accumulate gadoxetate disodium on delayed United States by the FDA in 2008 for detecon and imaging. Therefore, they are hypointense relave to characterizaon of liver lesions in adults with known 1 the nave liver parenchyma on the phase. or suspected focal The purpose of this Since nearly all lack funconing arcle is to review the imaging findings ulizing hepatocytes, they will typically be hypointense on the gadoxec disodium with respect to benign liver lesions hepatocyte phase. The one excepon to this rule is and metastac disease. well‐differenated hepatocellular , which demonstrates enhancement on the hepatocyte phase Gadoxetate Disodium secondary to residual funconing hepatocytes.4‐5 Pre‐ contrast imaging with T1‐weighted, T2‐weighted, and The advantage of ulizing gadoxetate disodium in‐phase and out‐of‐phase imaging are also beneficial comes from its added hepatocyte phase intracellular in characterizing liver lesions. imaging. The prior standard gadolinium agents only provide extracellular informaon with regards to indeterminate liver lesions. Gadoxec disodium with Hepac Cyst its addional hepatocyte phase has the ability to Hepac are seen rounely on diagnosc provide more specific informaon of the hepatocyte imaging studies and usually do not pose a diagnosc funcon/content of an indeterminate liver lesion. dilemma. Histologically, hepac cysts are derived from Gadoxec disodium has two routes of eliminaon: biliary endothelium and contain serous fluid lined by a 2 renal and hepatobiliary. The eliminaon pathways single layer of .6 These benign lesions are 2 are equally distributed. Given its increased T1 more commonly seen in women and may be mulple shortening compared to tradional extracellular in number. Enes such as autosomal dominant gadolinium products, a lower dose of contrast is polycysc kidney disease or tuberous sclerosis have 2 required (0.1 mL per kilogram of body weight). The been known to present with innumerable hepac gadoxetate disodium is transported from the cysts. extracellular space to the intracellular space by ATP‐ CT and MRI imaging of hepac cysts are dependent organic anion transporng polypepde 1 3 complementary in that both modalies show similar (OATP1) and then excreted into the . The findings. Cysts on CT and MRI do not demonstrate intracellular imaging (hepatocyte phase) is obtained 20 contrast enhancement. In addion, T1 and T2‐ minutes aer intravenous injecon. This hepatocyte 2 weighted MR images show the cysts to follow fluid phase lasts up to 120 minutes, which allows for signal. Hepatocyte phase imaging is usually not repeat acquisions on delayed phase imaging to needed in order to characterize these lesions; these correct for paent moon or other potenal technical

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MRI Liver, Saenz

Figure 1. Hepac Cyst. Mulple axial images demonstrate a Figure 2. Hemangioma. Mulple axial images demonstrate a small lesion in segment VII of the right lobe of the liver. The moderately‐sized lesion in segment IVa of the liver. The T1 T1 (A) and T2 fat saturaon (B) images show the lesion to be (A) and T2 fat saturaon (B) images show the lesion to be well circumscribed and of homogeneous low and high signal, well circumscribed and of homogeneous low and high signal, respecvely. The pre‐contrast, fat saturaon GRE (C) shows respecvely. Noce that the T2 signal is “light bulb” bright. the lesion to follow fluid signal. The dynamic poron of the The pre‐contrast, fat saturaon GRE (C) shows the lesion to study shows no enhancement on the arterial phase (D), be of low signal. The dynamic poron of the study shows portal venous phase (E), or hepatocyte phase (F). Noce the peripheral enhancement of the lesion on the arterial phase signal of the lesion follows the signal of cerebrospinal fluid (D) with near total enhancement on the portal venous phase on all sequences. (E). Noce the lesion is slightly hyperintense to the liver on the portal venous phase (E). The hepatocyte phase (F) lesions are hypointense to the surrounding liver demonstrates a hypointense lesion. parenchyma on hepatocyte phase (Fig. 1). In the seng of atypical imaging features, such as mural Hemangioma nodules, debris, or thickened septa, then alternave diagnoses must be considered, including cysc Hemangiomas are the most common benign tumors metastasis.6 of the liver. They are also commonly seen in daily radiology pracce and are more common in females than males. The incidence of these lesions is approximately 5 to 20% of the populaon.6 Histologically, hemangiomas are endothelial lined vascular channels separated by fibrous septa, which

J Am Osteopath Coll Radiol 2012; Vol. 1, Issue 4 Page 3

MRI Liver, Saenz accounts for their dynamic enhancement paern.6 Unlike hepac , it is accepted that these lesions are not associated with oral contracepve use.3,6,7 Hemangiomas are rarely associated with complicaons, such as spontaneous rupture/ hemorrhage;6 therefore, they are usually asymptomac. Symptomac lesions are usually very large (>10cm usually termed giant hemangiomas) and rarely may be associated with platelet sequestraon, resulng in thrombocytopenia, known as Kasabach‐ Merri syndrome.8‐9 Large hemangiomas may also have a central scar, which represents fibrosis secondary to an area of central necrosis produced when the tumor outgrows its blood supply. Since hemangiomas are commonly encountered, radiologists must recognize their imaging features in order to preclude unnecessary workup or invasive procedures. Many lesions are diagnosed via dynamic liver CT based upon their enhancement paerns. Three dominant enhancement paerns have been described in the literature. The most common paern is centripetal, peripheral, nodular enhancement of the lesion on early phases (arterial and portal venous phases).3 The enhancement progressively fills the lesion, resulng in iso‐ to slightly hyperaenuang compared to liver parenchyma on delayed imaging. This enhancement paern typically occurs in hemangiomas 2‐5 cm in size. Once lesions become Figure 3. Hepatocellular . Mulple axial images and a single coronal image demonstrate a lesion in segment I of larger, a similar enhancement paern is seen; the liver. The T1 (A) and T2 (B) images show the lesion to be however, centripetal, peripheral, nodular well circumscribed and hyperintense and intermediate in enhancement of the lesion remains disconnuous signal intensity, respecvely. Noce the lesion has bright T1 centrally. This may occur secondary to the large size of signal secondary to its fat content, which corresponds with the lesion or be related to central scar formaon. its loss of signal on the pre‐contrast, fat saturaon GRE Therefore, the lesion centrally remains image (C). The dynamic poron of the study shows minimal hypoaenuated compared to surrounding liver peripheral enhancement of the lesion on the arterial phase parenchyma on delayed imaging. The final (D) and the portal venous phase (E). The lesion overall enhancement paern usually occurs in small lesions remains hypointense to the liver on the portal venous phase (<2 cm in size). This enhancement paern has been (E). The hepatocyte phase (F) also demonstrates a termed "flash‐filling".3 These lesions typically enhance hypointense lesion. Case courtesy of Ankit B. Patel, D.O. homogeneously between the arterial and early portal venous phases, resulng in increased aenuaon T1 and hyperintense on T2 compared to liver compared to the surrounding liver parenchyma. These parenchyma. Classically, the lesions are hyperintense, smaller hemangiomas also characteriscally become almost “light bulb” bright on T2‐weighted imaging. iso‐aenuated to liver on delayed imaging. This feature helps disnguish them from malignant The MRI characteriscs of hemangiomas are well lesions, which are typically of intermediate signal on documented. The lesions typically are hypointense on

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MRI Liver, Saenz

T2 imaging. The dynamic enhancement paern on MRI with gadolinium agents is similar to the CT paern just described. By ulizing gadoxetate acid, hemangiomas are hypointense on the hepatocyte phase, since they do not contain hepatocytes (Fig 2).

Adenoma

Hepatocellular adenoma is an uncommon benign liver lesion which occurs predominantly in women of reproducve age.6 A direct associaon has been made with the use of oral contracepves and steroids.3,6,7,10 Histologically, adenomas are made up of benign hepatocytes arranged in cords separated by dilated sinusoids.7 They lack bile ducts, which histologically disnguishes them from focal nodular (FNH).6,7 These histologic qualies are responsible for the dynamic enhancement paern seen on imaging. Hepatocellular adenomas also lack portal tracks and hepac veins, which predisposes them to development of necrosis and rupture with spontaneous hemorrhage.6 There is also the potenal for malignant degeneraon with approximately 5% of adenomas differenang into .3 Since the severity of potenal complicaons exists, adenomas are managed differently from other benign liver masses with the majority surgically removed. Therefore, it is important Figure 4. Focal Nodular Hyperplasia. Mulple axial images for radiologists to understand and recognize their demonstrate a moderately sized lesion in segment II of the imaging appearance. liver. On the T1 (A) and T2 fat saturaon (B) images the le‐ The MRI characteriscs of hepatocellular adenomas sion is very subtle and hypointense and slightly hyperintense in signal intensity, respecvely. Noce the lesion has inter‐ may be variable. Typically, these lesions are mediate T2 signal when compared to the hepac cyst and hypointense to liver parenchyma on T1 and hemangioma from Figures 1 and 2. The pre‐contrast fat intermediate to hyperintense compared to liver saturaon GRE (C) shows the lesion to be iso to hypointense parenchyma on T2 weighted images. On occasion, signal. The dynamic poron of the study demonstrates brisk macroscopic fat may be present, which results in areas enhancement of the lesion in the arterial phase (D) and of high T1 signal intensity (Fig. 3). The dynamic MRI slightly hyperintense signal on the portal venous phase (E). The hepatocyte phase (F) shows an iso‐intense lesion. Table 1. DDx Hypervascular Liver Lesions enhancement paern is variable as well; typically, Benign these lesions demonstrate homogeneous, Hepatocellular Adenoma hyperintense enhancement on arterial phase imaging, 10 Focal Nodular Hyperplasia similar to other hepac lesions (Table 1). Hemangioma (Flash‐fill) Hepatocellular adenomas demonstrate this enhancement paern secondary to their vascular Malignant . They typically remain hyperintense to iso‐ Hepatocellular Carcinoma intense to liver parenchyma on portal venous imaging. Metastac Disease The hepatocyte phase characteriscs are a helpful

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MRI Liver, Saenz

Focal Nodular Hyperplasia

Focal nodular hyperplasia (FNH) is the second most common of the liver, and is also more common in females. The incidence is approximately 5% of the general populaon.3 The majority of these lesions are solitary and contain a central scar.3,6 It is controversial in the literature regarding the lesion’s associaon with oral contracepve use, but most studies agree that no direct relaonship exists.3,4 FNH is composed of hyperplasc liver parenchyma superimposed upon a pre‐exisng arterial spiderlike vascular malformaon.7 Histologically, these lesions contain Kupffer cells, hepatocytes, and small bile ductules with surrounding radiang fibrous septa.7 On MRI, FNH is typically of low signal on T1‐ weighted imaging and intermediate signal on T2‐ weighted imaging. Greater than 50% of these lesions demonstrate a central scar, which classically is of high T2 signal. Morphologically, FNH can be differenated from hepatocellular adenoma based upon the tumor margins. Hepatocellular adenoma is typically well circumscribed, whereas FNH has lobulated margins. Arterial phase imaging characteriscally demonstrates marked uptake of gadolinium, making the lesion hyperintense to the surrounding liver parenchyma. On the portal venous phase, the lesion is typically hyperintense or iso‐intense compared to liver Figure 5. Focal Nodular Hyperplasia. Mulple axial images parenchyma. The hepatocyte phase of the dynamic demonstrate a large lesion in the right lobe of the liver. On MR enhancement paern is the most specific the T1 (A) and T2 fat saturaon (B) images the lesion is very radiographic finding in diagnosing FNH.5 On delayed subtle and is hypointense and slightly hyperintense in signal 20 minute imaging, the hepatocyte phase usually intensity, respecvely. Noce the lesion has a central scar demonstrates the lesion to be hyperintense to iso‐ which is of high T2 signal. The pre‐contrast, fat saturaon intense to the remaining liver parenchyma (Fig 4). The GRE image (C) shows the lesion to be hypointense. The dy‐ increased signal during the hepatocyte phase is due to namic poron of the study demonstrates enhancement of the presence of hyperplasc hepatocytes and small the lesion, resulng in a slightly hyperintense appearance on 7 the arterial phase (D) and the portal venous phase (E). The bile ductules. hepatocyte phase (F) shows the lesion to be iso‐intense to Mulple liver lesions including focal nodular the remaining liver. hyperplasia may have a central scar (Table 2). The discriminator with regard to diagnosis of these lesions, as adenomas are usually hypointense compared to Table 2. DDx Liver Lesions with Central Scar liver parenchyma (Fig. 3). The gadoxetate acid hepatocyte phase is instrumental in differenang Giant Hemangioma these lesions from focal nodular hyperplasia, which is Hepatocellular Adenoma typically hyperintense to iso‐intense to liver Focal Nodular Hyperplasia parenchyma.10 Lastly, an addional potenal Hepatocellular Carcinoma (Fibrolamellar) discriminang characterisc of adenomas is peripheral rim enhancement of the pseudocapsule.

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MRI Liver, Saenz

Table 3. Summary MRI Characteriscs Table 4. DDx Hypervascular Liver Metastasis T1 T2 ART PV HC SPEC “MR. CT Craves Peanut Buer” Peripheral Melanoma Hemangioma D B V B/I D nodular CE Renal Cell Fat content, Choriocarcinoma Adenoma V I V V D pseudocapsule Thyroid Central scar T2 FNH D I B B/I B bright Pancreas Breast Heterogeneous Metastac V V B D D signal, errac CE

Abbreviaons: ART‐Arterial Phase, PV‐Portal venous Phase, HC‐ Hepatocyte Phase, SPEC‐Special Characteriscs, B‐Bright, D‐Dark, I‐Intermediate, V‐Variable, CE‐Contrast Enhancement central scar in FNH is unlike the other lesions with benign liver lesions such as hemangiomas, the T2 respect to its bright T2 signal (Fig. 5). Delayed imaging signal intensity of metastac lesions is typically less on CT and MRI with extracelluar, standard gadolinium intense. While hemangiomas have a very similar bright agents usually demonstrates enhancement of the T2 signal compared to hepac cysts, metastac lesions fibrous scar. Hepatocyte imaging with gadoxetate are slightly hyperintense compared to background disodium typically shows non‐enhancement of the liver parenchyma on T2 sequences (Table 3). Rarely, central scar.5 metastac lesions may be bright on T1‐weighted In comparing FNH with hepatocellular adenoma, a imaging, as is seen with hepac metastases from a recent study by Grazioli et al, demonstrated that pancreac ; the increased T1 signal is thought to be related to the effects of insulin hepatocellular adenomas and FNH have different 11 imaging characteriscs on hepatocyte phase imaging promong hepatocyte triglyceride accumulaon. greater than 90% of the me. 10 This study also The majority of metastases have their vascular highlighted the fact that a combinaon of marked supply from the hepac arteries secondary to neo‐ enhancement on arterial phase imaging with angiogenesis; therefore, they demonstrate early corresponding hyperintense to iso‐intense appearance enhancement on arterial phase imaging. This early on hepatocyte phase imaging differenates FNH from enhancement, however, is nonspecific. The differenal the moderate arterial phase enhancement and diagnoses of hypervascular metastac lesions are hypointensity on hepatocyte imaging seen with listed in Table 4. Unlike some of the benign enes hepatocellular adenoma.10 previously discussed, metastases typically do not demonstrate homogeneous enhancement. Lesions from breast carcinoma and gastrointesnal Metastac Disease may have a “target” enhancement Metastac disease represents the most common paern on arterial and early portal venous imaging malignant tumor of the liver. The most common (Fig. 6). Most metastac lesions show “washout” on portal venous imaging (hypointense to liver primary tumors include lung, breast, colon, pancreas, 11 and melanoma.6 The majority are mulple and vary in parenchyma). Hepatocyte phase imaging size as well as appearance.11 Classically, metastac demonstrates low signal intensity compared to lesions are poorly circumscribed with errac behavior surrounding liver parenchyma. Metastac lesions on dynamic CT and MR liver studies. demonstrate no enhancement on the intracellular 20 minute delayed phase, since they do not contain The majority of metastases are heterogeneous but funconing hepatocytes (Fig. 7). low in T1 signal intensity with corresponding intermediate to high T2 signal intensity. Compared to

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MRI Liver, Saenz

Figure 6. Metastac Breast Adenocarcinoma. Mulple axial Figure 7. Metastac . Mulple axial images demonstrate an irregular lesion in segment VIII of images demonstrate an irregular, poorly circumscribed the liver. On the T1 (A) and T2 fat saturaon (B) images the lesion spanning segments V and VI of the liver. On the T1 lesion is heterogeneous but predominantly hypointense and (A) and T2 fat saturaon (B) images the lesion is slightly hyperintense in signal intensity, respecvely. Noce heterogeneous with mixed signal intensity. The pre‐ the lesion has intermediate T2 signal with central high signal contrast, fat saturaon GRE image (C) also shows (B). The pre‐contrast, fat saturaon GRE (C) shows the heterogeneous signal. The dynamic poron of the study lesion to be hypointense. The dynamic poron of the study demonstrates irregular enhancement on the arterial phase demonstrates peripheral rim enhancement with an inner (D) and portal venous phase (E). The hepatocyte phase (F) ring of enhancement resulng in a “target” appearance on shows a predominantly hypointense lesion. the arterial phase (D) and demonstrates central enhancement remaining slightly hyperintense on the portal venous phase (E). The hepatocyte phase (F) shows a hypointense lesion. imaging can provide important informaon in the Summary characterizaon of indeterminate liver lesions. This addional informaon not only assists in making the It is imperave for the radiologist to be familiar with correct diagnosis, but also helps guide management, the different dynamic enhancement paerns of benign to include avoiding unnecessary follow‐up or invasive and malignant liver lesions. With the advent of procedures in some cases. gadoxetate disodium, hepatocyte phase specific

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MRI Liver, Saenz

References 6. Kamel IR and Bluemke DA. MR imaging of liver tumors. Radiol Clin N Am 2003; 41:51–65. 1. Bayer HealthCare Pharmaceuclas website. hp:// 7. Faisal Khosa F, Khan AN, and Eisenberg RL. Hypervascular bayerimaging.com/products/eovist/index.php. Accessed Liver Lesions on MRI. AJR 2011; 197:W204–W220 March 6, 2012. 8. Yuji Kumashiro Y, Kasahara M, Nomoto K, et al. Living Donor 2. Eovist Product Monograph. Bayer Inc, Wayne, NJ. hp:// Liver Transplantaon for Giant Hepac Hemangioma with berlex.bayerhealthcare.com/html/products/pi/Eovist_PI.pdf. Kasabach‐Merrit syndrome With a Posterior Segment Gra. Revised Novemeber, 2011. Accessed March 6, 2012. Liver Transplnt 2002;8:721 ‐724. 3. Ringe KI, Husarik DB, Sirlin CB, et al. Gadoxetate Disodium 9. Brizel HE and raccuglia G. Giant Hemangioma with Enhanced MRI of the Liver: Part 1, Protocol Opmizaon and Thrombocytopenia Radioisotopic Demonstraon of Platelet Lesion Appearance in the Noncirrhoc Liver. AJR 2010; Sequestraon. Blood 1965; 26: 751‐756. 195:13–28. 10. Grazioli L, Bondioni MP, Haradome H , et al. Hepatocellular 4. Jin‐Young Choi JY, Kim MJ, Young NP, et al. Gadoxetate Adenoma and Focal Nodular Hyperplasia: Value of Gadoxec Disodium–Enhanced Hepatobiliary Phase MRI of Acid–enhanced MR Imaging in Differenal Diagnosis. Hepatocellular Carcinoma: Correlaon With Histological Radiology 2012; 262: 520‐529. Characteriscs. AJR 2011; 197:399–405. 11. Alvin C. Silva AC, Evans JM, McCullough AE, et al. MR Imaging 5. Andrei S. Purysko AS, Remer EM, Coppa CP, et al. of Hypervascular Liver Masses: A Review of Current Characteriscs and Disnguishing Features of Hepatocellular Techniques. RadioGraphics 2009; 29:385–402. Adenoma and Focal Nodular Hyperplasia on Gadoxetate Disodium–Enhanced MRI. AJR 2012; 198:115–123.

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Pancrea c Masses, Theoni Pancreac Neoplasms

Ruedi Theoni, M.D.

Department of Radiology and Biomedical Imaging, University of California, San Francisco, CA

Introducon rate of surgical intervenon and overall poor outcome. The tumor serum marker CA 19‐9 is sensive for the This discussion focuses on diagnosing and staging diagnosis of adenocarcinoma of the pancreas, the various pancreac neoplasms with computed although it is not specific. The approach to treatment tomography (CT) and magnec resonance imaging is based upon whether or not the tumor can be (MRI) and addresses endosonography (EUS), positron resected at presentaon. Imaging can stage pancreac emission tomography combined with CT (PET/CT), and adenocarcinoma and plays a crucial role in the somatostan receptor scingraphy (SRS or management of this . Octreoscan) where appropriate. To assess paents If the paent presents with jaundice and the tumor with suspected pancreac disease, ultrasound (US), 1 is located in the head, the inial diagnosis of CT, and MRI have been used. With the introducon of pancreac tumor may be made by US. mul‐detector row CT (MDCT), imaging of the Ultrasonographic signs of pancreac carcinoma pancreas has been further improved and even small include a focal or diffuse pancreac mass, which is lesions now can be diagnosed with a high degree of 2 hypoechoic relave to normal parenchyma, and accuracy. While MRI also has benefied from dilaon of the pancreac duct without or with biliary technological advances and magnec resonance duct distenon (double duct sign). The accuracy of US cholangiopancreatography (MRCP) has helped for detecng the level of obstrucon varies improve assessment of the pancreac and biliary greatly, and US staging of pancreac carcinoma is ducts, MDCT remains the primary tool in evaluang inferior to CT. US oen fails to provide an adequate paents with suspected pancreac disease. EUS and examinaon of the enre gland, resulng in an overall MRI are used as problem‐solving modalies to confirm decrease in its sensivity. Some of these limitaons suspected lesions not idenfied with CT, to find can be overcome by EUS, but tumors in the tail of the addional lesions, and to obtain a definive ssue 3‐8 pancreas are also difficult to visualize by EUS. Contrast diagnosis with EUS‐guided ssue sampling. PET/CT in ‐enhanced transabdominal US shows promise, but the recent year has been increasingly employed for contrast agent is not widely available in the USA.23 assessing paents with suspected pancreac tumors, but its ulmate role awaits further definion.9‐16 Also, MDCT is the modality of choice for opmal SRS has gained popularity in recent years for evaluaon of pancreac neoplasms. A triple‐phase neuroendocrine tumors.17‐20 protocol is recommended that includes thin secons (0.625 or 1.25 mm) through the abdomen, inially

without intravenous contrast followed by a rapidly Ductal Adenocarcinoma delivered bolus of contrast material (at UCSF we use bolus tracking and 150 ml at 5 ml/sec chased by 30 mL Pancreac adenocarcinoma is the fourth leading of saline). It is best to administer a neutral oral cause of death in the United States.21 For 2012, contrast agent (water or VoLumen® [Bracco it is esmated that 43,920 men and women will be Diagnoscs, Inc.]). This approach allows opmal diagnosed with and 37,390 will die from cancer of the determinaon of tumor extension to the stomach and/ pancreas.21 About 90% of all neoplasms of the or and does not interfere with evaluaon pancreas are ductal . The overall of vascular invasion. We use a scan delay of 40‐45 sec relave 5‐year survival rate of only 4.8% is dismal, with (10 sec delay from peak aorc enhancement) for the the median survival me ranging from 6 to 12 late arterial or pancreac phase and a scan delay of 80 months.22 Late clinical presentaon with advanced sec for the hepac or portal‐venous phase. Rarely, an disease and aggressiveness of the tumor leads to a low arterial phase at 20‐25 sec is performed if requested

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Pancreac Masses, Theoni by or for hypervascular pancreac to a small impercepble tumor mass (Fig. 2). Ancillary neoplasms.24,25 In general, arterial involvement and findings are local tumor extension, including direct tumor mass are best detected in the pancreac phase, invasion of neighboring organs such as the liver and whereas the hepac phase serves for opmally stomach, arteries (loss of fat planes surrounding celiac visualizing the liver, veins, and the enre abdomen in axis, superior mesenteric artery [SMA], etc., so‐called the search for liver metastases and peritoneal seeding. vascular “cuffing”), and veins (tear drop sign, One paper demonstrated that a single‐phase thin‐slice flaening, irregularity of margins, etc. of the portal MDCT technique could be sufficient for accurately vein, superior mesenteric vein [SMV] and its assessing resectability of pancreac branches), and metastac disease to local lymph adenocarcinoma.26 nodes, liver, (oen associated with ascites), and more distant sites (Fig. 3). The so‐called “double‐duct sign” (dilataon of the biliary and pancreac ducts) occurs in less than 5% of paents with pancreac carcinoma. Biductal obstrucon is a nonspecific sign and may also be seen in bile duct or ampullary carcinoma, metastases, chronic pancreas, and ampullary stenosis.28 For MRI, dynamic T1‐weighted fat‐suppressed sequences with gadolinium (spoiled gradient recalled [SPGR] pulse sequences) appear to be superior to T2‐ weighted sequences.29 This is related to the fact that most pancreac have a significant desmoplasc reacon that renders the tumor less conspicuous on T2‐weighted images. A gadolinium‐ Figure 1. Pancreac carcinoma in a 65‐year‐old man. The enhanced 3D vascular me of flight SPGR sequence mass is well outlined in the head of the pancreas as an area using an early (arterial) phase provides the best of lower aenuaon (arrows) and was diagnosed as delineaon of the tumor, parcularly if it is a small resectable, which was confirmed at surgery. The duct proximal to the mass is dilated (arrow head). mass which does not change the contour of the pancreas. Diffusion‐weighted MRI appears promising, On MDCT, pancreac adenocarcinoma appears as a especially for metastases to the liver. Oen MRCP low‐density mass oen associated with poorly defined sequences consisng of thin and thick axial and margins (Fig. 1). The pancreac duct proximal to it usually is dilated because the neoplasm originates from the pancreac duct (Fig. 1). The bile duct also may be dilated when the pancreac adenocarcinoma encases it. The low‐density central zone represents hypovascular, scirrhous tumor surrounded by normal parenchyma or inflammatory ssue caused by obstrucve pancreas. Cysc degeneraon rarely appears within the tumor.27 Atrophy of the pancreac parenchyma proximal to the neoplasm frequently is associated with dilaon of the pancreac duct. Tumor obstrucon of the main pancreac duct can lead to rupture of side branches, resulng in formaon of cysts. Occasionally, a low‐density mass cannot be idenfied because the tumor is isodense to the Figure 2. Pancreac carcinoma in a 55‐year‐old man. The surrounding normal parenchyma. In these cases, oen pancreac mass is only faintly seen (arrow head) but the a dilated duct with abrupt cut off can be seen proximal abruptly terminang pancreac duct (arrows) clearly points to the locaon of the tumor distal to the cut off.

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thought to be advantageous for detecng small tumors that do not alter the contour of the gland and for hepac metastases.29 At present, MRI appears to be a problem solving modality. MRI should be considered in paents with suspected pancreac neoplasms in the presence of (1) an allergy to iodine contrast or other contraindicaons for iodine contrast administraon; (2) a MDCT scan with focal enlargement of the pancreas but no definable mass; (3) a clinical history suggesng and MDCT images that are equivocal or difficult to interpret; and (4) a need to disnguish between chronic pancreas with focal enlargement and pancreac cancer. Also, diffusion‐weighted MRI holds great promise for Figure 3. Inoperable pancreas carcinoma in a 74‐year‐old differenang healthy pancreac ssue from 31 man. The low density pancreac mass (short white arrows) pancreac carcinoma. When choosing an imaging with encasement of the superior mesenteric artery and right modality, one must consider that MDCT of the renal artery (black arrows) is clearly seen. Extension into the pancreas takes a small fracon of the me needed for retroperitoneum (long white arrows) with lymphadenopathy is also noted. a complete MRI of the pancreas. Because false posive MDCT diagnoses of coronal sequences with heavy T2‐weighng and pancreac cancer can occur, percutaneous aspiraon breath holding are added to beer assess the are needed if non‐operave treatment is pancreac and biliary ducts. planned, especially in paents with chronic pancreas. Fine‐needle aspiraon (FNA) of Imaging Results for Pancreac Adenocarcinoma pancreac cancer using CT‐guidance frequently is performed; this procedure causes severe pancreas CT imaging results for pancreac carcinoma vary in < 3%.32 The sensivity of percutaneous CT biopsies widely, but a sensivity of >90% for detecng reaches 79% with a posive predicve value of 100%, pancreac carcinoma can be achieved with current a negave predicve value of 47% and an overall generaon scanners and state‐of‐the‐art scanning accuracy of 81%.32,33 Because of possible tumor techniques.1,26 Nevertheless, even with advanced seeding in the needle tract, paents with potenally technology, small metastac implants on the liver and resectable tumors (only 10% of all cases) who are peritoneum can be missed by MDCT. MDCT with a acceptable candidates for surgery should undergo pancreac protocol generally provides accurate exploratory surgery rather than FNA.33 informaon on vascular involvement and sensivies EUS excels in detecng even small pancreac 30 of >80% have been obtained for resectability. The adenocarcinomas, reaching sensivies as high as posive predicve values for unresectability are much 97%. However, it demonstrates poor sensivity and beer than those for resectability. Presently, most specificity for diagnosing vascular involvement by studies show a slight advantage of MDCT over MRI for tumor due to its limited depth penetraon.34,35 Today, detecng and staging pancreac adenocarcinoma. A endoscopic ultrasound‐guided biopsies oen replace meta‐analysis that compared CT, MRI, and US for percutaneous CT biopsies of the pancreas. They have a detecon of pancreac cancer demonstrated sensivity of 95% and a specificity of 98% with a sensivity and specificity of 91% and 85% for helical CT posive predicve value of 99% and a negave and sensivity and specificity of 84% and 82%, for MRI, predicve value of 91%.36 They are parcularly respecvely; but the results of CT and MRI for indicated when CT is equivocal or negave with a 1 resectability were similar. For US, the sensivity for strong clinical suspicion for tumor and when the lesion diagnosing pancreas carcinoma and the specificity for is <3cm in size.33 determining resectability were much lower. MRI is PET/CT has emerged as an important modality for

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A B Figure 4. Insulinoma in a 43‐year‐old women with Whipple triad (hypoglycemia, low blood glucose level [40 to 50 mg/dL], and relief of symptoms aer intravenous administraon of glucose). (A) On this axial scan, a very small (1 cm) hypervascular lesion (arrows) is seen near the neck of the pancreas, which was confirmed at surgery. (B) Same paent as Figure 4A. The hypervascular lesion (arrows) is noted to lightly project off the surface of the pancreas. effecvely managing paents with suspected hyperfunconing pancreac adenomas, cross‐seconal pancreac cancer.37 Nevertheless, more studies are imaging is used only for localizing the pancreac needed to demonstrate its true value and cost‐ neoplasm, since the clinical diagnosis is based on effecveness, since some studies found no benefit clinical data and laboratory tests that usually permit an over CT alone.9 In one study, the diagnosc accuracy accurate diagnosis.39 of 18F‐fluorodeoxyglucose (FDG) PET/CT for pancreac and especially extrapancreac NENs malignancy was 89%, compared to 76% for MDCT and that are small and located in the duodenal or gastric 38 79% for MRI. In 17 paents with advanced pancreac wall (Fig. 4A and B) may be difficult to detect adenocarcinoma analyzed in the same study, FDG‐ preoperavely by any of the radiographic techniques; PET/CT had a sensivity of 30% for N‐ and 88% for M‐ even intraoperave ultrasonography fails to detect staging, whereas both MDCT and MRI had sensivies some of these lesions. Nevertheless, MDCT with 0.625 of 30% for N‐ and 38% for M‐staging. The clinical mm secons has improved these results. These ectopic management was altered in 26% (10 paents) aer lesions are more likely to occur in paents with 38 FDG‐PET/CT. In another PET/CT study, management mulple endocrine adenomatosis (MEA) or mulple was changed in 16% of paents with pancreac cancer endocrine neoplasia (MEN). A combinaon of 10 that inially had been staged as being resectable. In intraoperave palpaon and intraoperave suspected tumor recurrence, PET/CT reliably detected ultrasonography was found to achieve the best results local recurrence and was advantageous in diagnosing for complete resecon. Intraoperave ultrasound is 11 distant disease. parcularly important in paents with mulple lesions and MEN. Neuroendocrine Neoplasms of the Pancreas On MDCT and MRI, funconing NENs generally show intense enhancement in the arterial phase with rapid Hyperfunconing Neuroendocrine Neoplasms. washout in the portal venous phase. The most The term “funconing islet cell tumor of the common NEN, the insulinoma, usually is small (< 2 cm pancreas” has been replaced by “hyperfunconing or in diameter). Metastases occur in only 5‐10% of syndromic neuroendocrine neoplasm” (NEN). Among insulinomas. All other NENs tend to be large and have these NENs, insulinoma is the most common tumor, metastases in 60‐65% of cases. The appearance of liver followed by , , VIPoma, and metastases in paents with funconing NENs is similar other rarely encountered secretory neoplasms. In to that of the primary tumor (intense arterial

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A B Figure 5. Ectopic gastrinoma in a 36‐year‐old woman with Zollinger‐Ellison syndrome (elevated gastrin levels, intractable pepc ulceraons with gastric hypersecreon and hyperacidity). (A) A hypervascular mass (arrows) is idenfied between the pancreas and the caudate lobe which represents the gastrinoma. (B) The SRS (octreode study) of the same paent as Fig. 5A in supine and prone posion confirmed the presence of the hyperfunconing neuroendocrine neoplasm (arrows). enhancement with rapid washout). greater than 85%. Therefore, MRI with state‐of‐the‐art The reported sensivity of convenonal CT for equipment and opmal MRI techniques appears to be detecng insulinomas is low and only slightly higher a useful technique for diagnosing small pancreac for ‐ primarily due to their larger size (Fig. NENs; however, contrast‐enhanced MDCT surpasses 5A). EUS usually allows detecon of even small NENs MRI in diagnosing these small neoplasms with its and their precise locaon. The dual‐phase MDCT superior spaal resoluon and very thin secons. protocol with thin secons improved the detecon SRS ‐ based on various derivaves of long‐acng rate to 94% and reached 100% when combined with somatostan analogues ‐ can be employed for EUS.40 While EUS provides excellent results in the head paents with MEN, small gastrinomas, of the pancreas, detecon rates for lesions in the tail somatostanoma, glucagonoma, carcinoid, and of the pancreas are much lower because of the VIPoma; however, insulinomas may be missed due to distance of the EUS probe from the stomach. Ectopic reduced receptor expression.17,43 While EUS is the gastrinomas may be missed by EUS, but combining it most sensive imaging procedure for the detecon of with SRS increases the overall sensivity for small (< or = 10 mm) NENs, SRS is the procedure of gastrinomas to 86% (Fig. 5A and B).41 The sensivity of choice for the idenficaon of metastases (staging), transabdominal ultrasound for detecng insulinomas parcularly in paents with MEN.43 is low (mean of 46%), and therefore should not be used for this purpose. Non‐Hyperfunconing Neuroendocrine Neoplasms. On MRI, funconing NENs of the pancreas are of Non‐hyperfunconing or nonsyndromic NENs are low signal intensity on T1‐weighted images and high less frequently encountered than insulinomas or signal intensity on T2‐weighted images.4 Occasionally, gastrinomas and represent 15‐25% of all NENs.39 They an insulinoma can be of dark signal intensity on T2‐ arise from alpha or beta cells. These neoplasms are weighted sequences due to a fibrous stroma. In our hormonally quiescent (probably very minimal study, we reached an MRI sensivity of 85% for secreon) and oen present as masses with or detecng funconing NENs of 2 cm or less in diameter, without jaundice or gastric outlet obstrucon. The which is similar to the sensivity achieved by invasive tumors are mostly located in the head of the pancreas procedures.4 For gastrinomas, an MRI sensivity of up and may reach up to 20 cm in diameter (Fig. 6). They to 62% has been reported.42 With present techniques, may consist of solid and necroc components, and MRI should detect lesions >2 cm with a sensivity

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coarse calcificaons are present in up to 25% of cases. Cysc Neoplasms of the Pancreas The masses are hypervascular with a late capillary stain. The tumors do not encase vessels, but in 80‐ Serous and Mucinous Cysc Neoplasms. 100% of cases, they show malignant transformaon Cysc neoplasms of the pancreas account for less with liver metastases and lymphadenopathy. The than 5% of pancreac neoplasms. Pancreac cysc esmated cumulave 5‐year survival with malignant neoplasms are classified into two categories: serous tumors is 52 +/‐ 10%.44,45 The key features of non‐ cysc (usually microcysc, occasionally macrocysc: funconing NENs are large size, hypervascularity, and unilocular [Fig. 7] or oligocysc [Fig. 8]) neoplasms that absence of vascular encasement. Results with CT and usually are benign, and mucinous cysc (macrocysc) MRI are similar. neoplasms that are potenally malignant or already malignant at the me of diagnosis. A rare macrocysc variant is benign but exhibits radiological features similar to those of mucinous . Serous and mucinous cysc neoplasms do not communicate with the pancreac duct, whereas intraductal papillary mucinous neoplasms (IPMN) (discussion to follow) demonstrate communicaon with the pancreac duct. Serous cysc neoplasms of the pancreas are observed in middle‐aged and elderly women. This type of tumor may not require surgical treatment, whereas mucinous cysc tumors should be resected because of their malignant potenal. Nevertheless, some surgeons prefer to resect the serous type as well. In general, the paent’s age, symptoms, overall condion, locaon of the lesion, and growth over me Figure 6. Large non‐hyperfunconing are factors that help in deciding if surgery is in a56‐year‐old man with jaundice. The axial MDCT needed.46,47 Oen, paents with a cyst that increases demonstrates a very large mass in the head and neck of the pancreas (long white arrows) with mulple parally significantly in size over me, is symptomac, or hypervascular metastases in the liver (black arrows) that occurs in older fit paents are selected for surgery. CT produce intrahepac biliary ductal dilaon (short white can accomplish preoperave differenaon of the two arrows). types in many cases.27 Tradionally, the diagnosis of

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Figure 7. Unilocular serous cysc neoplasm in a 61‐year‐old Figure 8. Oligocysc serous cysc neoplasm in a 68‐year‐old woman. One simple appearing cyst (arrows) is present in woman. Three cysc structures (arrows) form one mass in the tail of the pancreas. The wall of the cyst is thin and no the body of the pancreas. septaons are present, as confirmed by ultrasound. serous cysc tumor is made if the number of cysts Mucinous cysc neoplasms of the pancreas (also within the tumor is more than six and the diameters of called “” and “” the cysts are less than 2 cm. A newer nomenclature according to the old nomenclature) have six or fewer prefers to call cysts < 1 cm definitely serous, >1‐ 2 cm cysts; the diameters of the cysts measure more than 2 equivocal and > 2 cm definitely mucinous. Grossly, cm; a central enhancing scar is rarely seen; and these serous tumors appear either as solid tumors calcificaons are peripheral (Table 1).27 The margins with innumerable ny cysts or as honeycombed cysc usually are smooth, and metastac disease may be tumors, depending on the amount of connecve ssue present at the me of diagnosis (Fig. 10). (Table 1). At mes, it is difficult to visualize the cysc Based upon the above‐menoned criteria, a correct areas. The lesions have lobulated margins (Fig. 9). diagnosis of a serous cysc pancreac tumor can be Calcificaons in serous tumors are central in locaon. made in 62% of cases by CT, 74% by US, and 84% using A central enhancing scar may be present and is 48 27 both modalies. In general, results for mucinous characterisc of a serous tumor. cysc tumors are inferior. Pancreac walled‐off necroses and cysc forms of islet cell tumors, ductal carcinomas, solid and papillary tumors, and lymphangioma of the pancreas can be indisnguishable from cysc neoplasms on CT. Thus, EUS needle biopsies of the lesions oen are necessary.49 MRI oen provides beer definion of the internal architecture of cysc neoplasms (Fig. 11) than CT and demonstrates the presence of mucin based on increased signal intensity within the cysts on T1‐ weighted sequences. Also, diffusion‐weighted MRI may become part of the array of tools to differenate mucinous from nonmucinous lesions and may help in the management of pancreac cysc lesions. Septa Figure 9. Serous cysc neoplasm in a 72‐year‐old woman and wall thickness of the lesions are well (microcysc). The lobulated mass (arrows) consists of demonstrated by MRI, but calcificaons are not always mulple ny cysts with septaons barely noceable.

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Intraductal Papillary Mucinous Neoplasms. IPMN (formerly also called “ductectac cystadenoma” or “ductectac ”) is a rare tumor that is considered a subtype of the mucinous cysc neoplasms of the pancreas. IPMNs can be classified as branch duct (side‐branch), main duct, or mixed type depending on the site and extent of involvement.27,50 The cysc changes always demonstrate a connecon to the pancreac duct (Fig. 12), which is a diagnosc feature that can be seen on MDCT and even beer on MRCP (Fig. 13). The branch duct type consists of cysc dilaon of the side branches of the pancreac duct, usually in the Figure 10. Mucinous cysc neoplasm in a 45‐year‐old woman. The mass consists of large cysts (white arrows) with uncinate process. These ducts are lined with atypical, peripheral calcificaons (arrow heads) and thick septaons. hyperplasc, or clearly malignant epithelium. In the The mass is not lobulated. late stages, the tumor nodules of the ducts produce copious mucinous secreons that fill the enre duct. The overall prognosis is good in branch duct type seen. MRI helps disnguish cysc neoplasms from IPMN, because extension into the parenchyma and walled‐off necroses of the pancreas, parcularly if they beyond occurs relavely late in this type of tumor; are mulple. Both MRCP and MDCT with curved planar overall malignant degeneraon is rare. In contrast, reconstrucon can demonstrate the absence of a malignancy is present in 25‐44% of resected connecon to the main pancreac duct. specimens of the other two types, and resecon is the treatment of choice in these paents. CT shows markedly dilated ducts and cysc‐ appearing structures filled with mucinous material that has slightly higher aenuaon than that of water. Based on MDCT scans, a main pancreac duct diameter of 6 mm or larger, a mural nodule of 3 mm or larger, and an abnormal aenuang area are independently predicve of malignancy.50 A mural nodule of 6.3 mm or larger in the main pancreac duct and an abnormal aenuang area are independently predicve of parenchymal invasion. According to these criteria, the sensivity, specificity, and accuracy for idenfying malignancy in paents with IPMN were 83%, 81%, and 82% and for idenfying parenchymal invasion were 90%, 88%, and 89%, respecvely.50 MRI appears to have a slight advantage over CT. MRI can visualize mucin within the cysts and the internal architecture of the lesion, including a solid mass and mural nodules, slightly beer than CT. EUS also is well suited to detecng mural nodules. Figure 11. Mucinous cysc neoplasm in a 47‐year‐old woman. Large cysts (arrows) form a mass in the tail of the pancreas with thick septaons. The main pancreac duct Solid Pseudopapillary Epithelial Neoplasm. (arrow heads) is normal, because there is no communicaon Solid pseudopapillary epithelial neoplasms (SPEN), between the neoplasm and the pancreac duct. previously called “solid and cysc tumors of the

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A B

Figure 12. Mixed‐type IPMN in a 74‐year‐old man. (A) On this axial image, the cysc mass (arrows) clearly communicates with the main pancreac duct (arrow heads). (B) Same paents as 12A. On this coronal image, the dilated main duct and the dilated side branches (arrows) are clearly evident. (C) The ERCP in the same paent as (A) demonstrates a massively dilated main pancreac duct containing large filling defects that represent mucus C (arrows). pancreas”, are rare tumors seen almost exclusively in hemorrhage and cysc spaces filled with necroc young women and are located mostly in the tail of the debris; these characteriscs can be visualized by CT pancreas (Fig. 14). SPEN is a mixed cysc and solid and MRI. On imaging, SPEN appears as sharply mass characterized by a solid peripheral area of tumor defined, heterogeneous, large cysc pancreac masses and a central zone of degeneraon, consisng of with solid components and may have increased vascularity. This type of cysc tumor usually is benign, but it may be malignant in older women.51 Calcificaons are rare and, if present, are located in the capsule or in the inner poron of the mass. EUS also may be helpful in visualizing the nodules and internal architecture of these masses.

Follow‐up Imaging for Cysc Neoplasms of the Pancreas. Small cysc lesions (< 3 cm) that are asymptomac, show no sign of malignancy, and have a negave FNA can be followed every 6 months for one year and then 27 Figure 13. Side‐branch type IPMN. The MRCP demonstrates annually for a total of 4 years. The lesions should be several cysc structures (arrows) arising from side branches surgically removed if they become symptomac; of the main pancreac duct. increase in size during observaon; show malignant

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Pancreac Masses, Theoni features, including a thick wall, mulple irregular septaons, and mural nodules; and/or have increased CEA or CA 19.9, posive cytology or mucin in the aspirate.27,50 Oen, pancreac cysts detected in elderly and fit paents are removed regardless of the features, because of the increased incidence of malignancy in these lesions. For detailed flow chart for cysc lesions, see Table 2.

Figure 14. Solid pseudopapillary epithelial neoplasm in the tail of the pancreas of a 17‐year‐old woman. The solid peripheral area of tumor (long white arrows) and more central zone of degeneraon (short white arrow), consisng of hemorrhage and cysc spaces filled with necroc debris is well visualized by MDCT. Arrow head indicates the normal head of the pancreas.

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Ardengh JC, de Paulo GA, Ferrari AP. EUS‐guided FNA in the 20. Usmani S, Khan HA, Abdulla M, et al. Incremental diagnosc diagnosis of pancreac neuroendocrine tumors before value and impact on paent management of somatostan surgery. Gastrointest Endosc 2004; 60: 378‐384. receptor scingraphy with indium‐111‐pentetreode in gastroenteropancreac neuroendocrine tumors. Med Princ 7. Manfredi R, Graziani R, Moon M, et al. Main pancreac duct Pract 2011; 20: 356‐361. intraductal papillary mucinous neoplasms: accuracy of MR imaging in differenaon between benign and malignant 21. Siegel R, Naishadham D, Jemal A. Cancer stascs, 2012. CA tumors compared with histopathologic analysis. Radiology Cancer J Clin 2012; 62: 10‐29. 2009; 253: 106‐115. 22. Horner MJ, Ries LAG, Krapcho M, et al. (eds) updated on the 8. Ku YM, Shin SS, Lee CH, et al. Magnec resonance imaging of SEER web site November 10, 2011. SEER Cancer Stascs cysc and endocrine pancreac neoplasms. 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Farma JM, Sanllan AA, Melis M, et al. PET/CT fusion scan 28. Ahualli J. The double duct sign. Radiology 2007; 24: 314‐315. enhances CT staging in paents with pancreac neoplasms. 29. Vachiranubhap B, Kim YH, Balci NC, et al. Magnec resonance Ann Surg Oncol 2008; 15: 2465‐247. imaging of adenocarcinoma of the pancreas. Top Magn Reson Imaging 2009; 20: 3‐9.

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30. Klauss M, Mohr A, von Tengg‐Kobligk H, et al. A new invasion 41. Zimmer T, Stolzel U, Bader M, et al. Endoscopic score for determining the resectability of pancreac ultrasonography and somatostan receptor scingraphy in carcinomas with contrast‐enhanced muldetector computed the preoperave localisaon of insulinomas and gastrinomas. tomography. Pancreatology 2008; 8: 204‐210. Gut 1996; 39: 562‐568. 31. Lemke A, Laun FB, Klauss M, et al. Differenaon of pancreas 42. Pisegna JR, Doppman JL, Norton JA, et al. Prospecve carcinoma from healthy pancreac ssue using mulple b‐ comparave study of the ability of MR imaging and other values: comparison of apparent diffusion coefficient and imaging modalies to localize tumors in paents with intravoxel incoherent moon derived parameters. Invest Zollinger‐Ellison syndrome. Dig Dis Sci 1993; 38: 1318‐1320. Radiol 2009; 44: 769‐775. 43. Langer P, Kann PH, Fendrich V, et al. Prospecve evaluaon of 32. Zech CJ, Helmberger T, Wichmann MW, et al. Large core imaging procedures for the detecon of pancreacoduodenal biopsy of the pancreas under CT fluoroscopy control: results endocrine tumors in paents with mulple endocrine and complicaons. J Comput Assist Tomogr 2002; 26: 743‐ neoplasia type 1. World J Surg 2004; 28: 1317‐1322. 749. 44. Schindl M, Kaczirek K, Kaserer K, et al. Is the new classificaon 33. Volmar KE, Vollmer RT, Jowell PS, et al. Pancreac FNA in of neuroendocrine pancreac tumors of clinical help? World J 1000 cases: a comparison of imaging modalies. Gastrointest Surg 2000; 24: 1312‐138. Endosc 2005; 61: 854‐861. 45. Liang H, Wang P,. Wang XN, et al. Management of 34. Maguchi H. The roles of endoscopic ultrasonography in the nonfunconing islet cell tumors. World J Gastroenterol 2004; diagnosis of pancreac tumors. J Hepatobiliary Pancreat Surg 10: 1806‐1809. 2004; 11: 1‐3. 46. Spinelli KS, Fromwiller TE, Daniel RA, et al. Cysc Pancreac 35. Morris‐Sff G, Webster P, Frost B, et al. Endoscopic neoplasms: Observe or operate. Annals of Surgery 2004; 239: ultrasound reliably idenfies chronic pancreas when other 651‐659. imaging modalies have been non‐diagnosc. JOP 2009; 10: 47. Malleo G, Bassi C, Rossini R, et al. Growth paern of serous 280‐283. cysc neoplasms of the pancreas: observaonal study with 36. Uehara H, Ikezawa K, Kawada N, et al. Diagnosc accuracy of long‐term magnec resonance surveillance and endoscopic ultrasound‐guided fine needle aspiraon for recommendaons for treatment. Gut. 2011 Sep 22. [Epub suspected pancreac malignancy in relaon to the size of ahead of print]. lesions. J Gastroenterol Hepatol 2011; 26: 1256‐1261. 48. Procacci C, Graziani R, Bicego E, et al. Serous cystadenoma of 37. Okamoto K, Koyama I, Miyazawa M, et al. Preoperave 18[F]‐ the pancreas: report of 30 cases with emphasis on the fluorodeoxyglucose positron emission tomography/computed imaging findings. Journal of Computer Assisted Tomography tomography predicts early recurrence aer pancreac cancer 1997; 21: 373‐382. resecon. Int J Clin Oncol 2011; 16: 39‐44. 49. Belsley NA, Pitman MB, Lauwers GY, et al. Serous 38. Kauhanen SP, Komar G, Seppänen MP, et al. A prospecve cystadenoma of the pancreas: limitaons and pialls of diagnosc accuracy study of 18F‐fluorodeoxyglucose positron endoscopic ultrasound‐guided fine‐needle aspiraon biopsy. emission tomography/computed tomography, muldetector Cancer 2008; 114: 102‐110. row computed tomography, and magnec resonance imaging 50. Ogawa H, Itoh S, Ikeda M, et al. Intraductal papillary mucinous in primary diagnosis and staging of pancreac cancer. Ann neoplasm of the pancreas: assessment of the likelihood of Surg 2009; 250: 957‐963. invasiveness with mulsecon CT. Radiology 2008; 248: 876‐ 39. Thoeni RF. Imaging of Endocrine Tumors. IN: Pancreac 886. Cancer edited by Heiken J.P. IN: Contemporary Issues in 51. Lee JH, Yu JS, Kim H, et al. Solid pseudopapillary carcinoma of Cancer Imaging Series, Editors. Reznek R.H. & Husband J.E. the pancreas: differenaon from benign solid Cambridge University Press, 2009, pp 104‐129. pseudopapillary tumour using CT and MRI. Clin Radiol 2008; 40. Gouya H, Vignaux O, Augui J, et al. CT, EUS combined protocol 63: 1006‐1014. for preoperave evaluaon of pancreac insulinoma. AJR 2003; 181: 987‐992.

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Gallbladder Masses, McKnight et al. Gallbladder Masses: Mulmodality Approach to Differenal Diagnosis

Timothy McKnight, D.O.,1 and Ankit Patel, D.O.2

1Dartmouth Hitchcock Medical Center, Department of Radiology, Lebanon, NH 2University of California Irvine Medical Center, Department of Radiology, Irvine, CA

Introducon

Gallbladder masses are commonly encountered on diagnosc imaging examinaons. Disnguishing between benign and malignant condions is crical, in terms of clinical significance, management, and follow‐ up. It is important to be familiar with the differenal diagnoses of gallbladder masses, recognize imaging features that are diagnosc for each condion, and understand the ulity and limitaons of each of the cross‐seconal imaging modalies currently available. Gallbladder pathology is a frequent source of paent complaint, to include acute or chronic right upper quadrant pain, jaundice, or dyspepsia. As such, the gallbladder is a rounely imaged structure either directly to exclude or characterize gallbladder pathology or in general abdominal imaging for nonspecific complaints or imaging related to adjacent structures. Gallbladder masses as part of the spectrum of gallbladder pathology are commonly encountered at imaging. It is important for the diagnosc imager to be familiar with the broad differenal of gallbladder masses. While most gallbladder masses are benign and do not present a diagnosc dilemma, they may present with unusual or nonspecific imaging appearances, or on a modality that is not typically over 25 million individuals or about 10% of the U.S. used to characterize gallbladder pathology. adult populaon, affecng women more than men by a rao of 2:1; the risk increases with age.1 The purpose of this arcle is to review the spectrum Consequently, they typically are not a diagnosc of gallbladder masses (Table 1) and mass‐like lesions challenge but remain important to recognize on all on US, CT, and MR, providing the reader with the modalies, so as not to be confused with more ability to recognize benign disease, idenfy worrisome ominous lesions. Common associaons include imaging features, and review the diagnosc diabetes, oral contracepves, estrogen replacement, informaon each cross‐seconal modality may obesity, ileal disease, total parenteral nutrion, provide. , and certain medicaons.2 are present in up to 95% of cases of acute cholecyss, Benign Masses 65% of adenomas, 95% of porcelain , and 90% of gallbladder adenocarcinomas. 3, 4, 5 Eighty Cholelithiasis. percent of stones are cholesterol stones (contain Cholelithiasis, or gallstones, represents the most greater than 50% cholesterol; 10% being pure commonly encountered gallbladder mass. They affect cholesterol), and the remaining 15‐20% are pigmented

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Figure 1. WES sign –Cholelithiasis. Sagial (A) and transverse (B and C) ultrasound images of the gallbladder demonstrate the wall‐echo‐ shadow complex (C) comprised of an outer echogenic line represenng the gallbladder wall (thin white arrow), an outer hypoechoic line represenng the gallbladder lumen (thick open arrow), an inner echogenic line (thin black arrow) represenng the margin of the , and then hypoechoic posterior acousc shadowing. stones (contain <25% cholesterol), which are primarily accuracy of CT characterizaon is significantly composed of calcium bilirubinate and glycoproteins. diminished due to aenuaon overlap between the Ultrasound is the most common modality employed two types of stones, which is aributed to varying for inial evaluaon of the gallbladder. Sonography is calcium content. Another consideraon is that highly sensive and specific for cholelithiasis, decreased tube voltage also decreases CT detecon of detecng >95% for stones over 2mm. Gallstones are choleliths, regardless of stone size. Opmal voltage classically mobile and strongly echogenic with marked for detecng stones has been reported at 140kVp with 6 sensivies of 73‐86%; the sensivity declines to 40‐ posterior acousc shadowing. Demonstrang the 9 posterior acousc shadowing is variable and 68% at 80kVp. This is important to remember when dependent upon technique when imaging the paent. employing low‐dose CT protocols. Some calcified Occasionally numerous or very large stones can fill the stones may contain a triradiate or triangular area of gallbladder, resulng in a wall‐echo‐shadow complex (WES). The anterior wall of the gallbladder is echogenic, followed by a thin hypoechoic line of intraluminal bile, then an echogenic line represenng the superficial margin of the stone. Posterior shadowing obscures the deeper stones (Fig. 1).4,7 The WES complex is specific to gallstones and is important in diagnosing benign stone disease versus a so ssue mass filling the gallbladder lumen. CT sensivity for detecon of gallstones is much less than sonography, typically about 75%‐80% for stones ≥5mm (Fig. 2).8 Calcium containing stones are well seen, even as small as 2mm; however, pure cholesterol stones may be iso‐ or even hypoaenuang to bile, decreasing detecon rates. Considering this finding, aempts have been made to Figure 2. Cholelithiasis. Various CT and MR appearances of characterize stones based on density. Overall, cholelithiasis (A thru E). CT with IV contrast – A and B; Axial pigmented stones tended to have higher Hounsfield LAVA T1 GRE with fat suppression (C); Coronal T2 SSFSE (D); Axial T2 FRFSE‐XL with fat suppression (E). units (HU) than cholesterol stones. However, the

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Gallbladder Masses, McKnight et al. central low or even air density represenng contained nitrogen gas. This has been described as the “Mercedes‐Benz” sign and was originally described as a radiographic finding.10 This may be the only visible feature to suggest the presence of isodense stones.11 MR detecon of gallstones is best appreciated on T2 ‐ weighted images, especially magnec resonance cholangiopancreatography (MRCP) sequences. Overall MR sensivity is approximately 90‐95%. Gallstones are typically hypointense on T1 and T2 weighted images. Less common appearances include a T1 or T2 hyperintense central focus surrounding by low signal or a predominantly T1 hyperintense appearance. The imaging appearance has been aributed to the relave amount of protein or pigment; pure cholesterol stones are typically uniformly low in T2 and T1 signal, and highly pigmented stones are predominantly Figure 3. Gallbladder Polyps. Gray scale US images in two hyperintense in T1 signal.5 This can be an important different paents (A and C) demonstrate focal echogenic, non‐shadowing polyps projecng into the gallbladder lumen: feature for deciding management of impacted stones, one in the fundus (A) and one near the neck (C). Vascular as the pigment stones are soer and may be easier to flow is demonstrated within each on Power (B) and treat endoscopically; pure cholesterol stones are more color (D) Doppler, disnguishing these from avascular solid, making endoscopic treatment more difficult. choleliths.

that adenocarcinomas may arise from benign Gallbladder Polyps. adenomas in an adenoma‐carcinoma sequence similar 12 Another commonly encountered mass is the to that of colonic polyps. This would suggest that gallbladder polyp. Incidence of gallbladder polypoid accurately diagnosing small adenomas (<10mm) may lesions has been reported in 3 ‐ 5% of the adult help in idenfying at risk individuals who require close populaon.12 Gallbladder polyps represent a spectrum follow up or early surgical intervenon. This has been of processes presenng with similar morphology and challenged, however, in several recent studies, which appearance at imaging. Most of these are benign, report that gallbladder are genecally including cholesterol polyps and benign adenomas dissimilar from adenomas and lack residual 17,18 which are discussed here; malignant lesions are adenomatous ssue at pathologic evaluaon. discussed separately. Both cholesterol and adenomatous polyps appear Cholesterol polyps comprise about 50% of sonographically as non‐mobile, echogenic, non‐ gallbladder polyps, are typically less than 10mm in size, shadowing masses. They may be sessile or and are completely benign with no malignant pedunculated, have a stalk which may or may not be potenal. They represent lipid‐laden macrophages visible, and may show internal vascularity (Fig. 3). covered by normal gallbladder epithelium and project Adenomas and cholesterol polyps are usually smooth into the lumen 3, 13. but may also be lobular or cauliflower‐like. One important feature is that the gallbladder wall adjacent Adenomatous polyps of the gallbladder represent to a benign polyp should be normal; any irregularity or true neoplasms and are rather uncommon, focal thickening >3mm should raise the suspicion for represenng about 5% of polyps.14 They have an malignancy. increased incidence in polyposis syndromes, such as Peutz‐Jeghers and familial adenomatous polyposis.15, 16 On unenhanced CT, adenomatous polyps are Subtypes of adenomas include tubular, papillary, and typically iso‐ or hypodense to liver parenchyma and 19 tubulopapillary. Most lesions measure less than 20mm are more easily seen than cholesterol polyps. in size and 10% are mulple.3 It has been theorized Cholesterol polyps are difficult to detect with

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Gallbladder Masses, McKnight et al. unenhanced CT, as their aenuaon characteriscs are similar to bile. Polyps enhance, making them more easily detectable on enhanced CT. However, the stalk may be undetectable, resulng in an appearance idencal to a small stone or tumefacve sludge.20 The MR appearance of polyps is nonspecific with polyps having intermediate signal intensity on T1 and T2 weighted images. The appearance overlaps with gallbladder carcinoma. Irie et al. reported that malignant polypoid lesions more oen have increased signal on diffusion images with lower ADC values than benign polyps at high b‐values.21 Also, it has been described on both MR and CT that while both benign and malignant polypoid lesions enhance in the arterial phase, benign lesions washout while malignant lesions tend to persistently enhance.5,22 Despite the available number of imaging modalies, there remains significant overlap between the Figure 4. Focal Adenomyomatosis. Color Doppler US image appearance of benign polyps and malignant lesions. (A) demonstrates focal gallbladder wall thickening with a polypoid appearance and vascular flow. Contrast‐enhanced There has been considerable controversy over the CT (B) and T2 weighted coronal MR sequences without and years as to the proper follow‐up and management of with fat saturaon (C and D) demonstrate the focal incidentally discovered polyps. Despite lack of gallbladder wall thickening with a characterisc cysc consensus, the most consistently reported appearance (white arrows), favoring adenomyomatosis independent risk factor prompng intervenon is which was confirmed following . 23 size. Many have advocated a strategy of cholesterol deposion that becomes trapped within cholecystectomy for polyps equal to or greater than dilated Rokitansky‐Aschoff sinuses, along with bile 10mm and sonographic imaging follow‐up for those salts, sludge, and calculi. There is associated wall less than 10mm. This results in many unnecessary thickening from hyperplasia of both the mucosa and follow ups and many unnecessary . However, muscularis propria.25 Cholecystosis is the second Corwin et al. recently reported a series of 346 paents benign hyperplasc cholecystosis process, and with gallbladder polyps followed for more than 5 years represents cholesterol and triglyceride deposion in with no progression to carcinoma. The authors the lamina propria. This results in the classically suggested that no addional follow up may be described “strawberry gallbladder” appearance. required for incidental polyps less than 6mm in size.24 Another risk factor that should prompt earlier Adenomyomatosis is commonly encountered on intervenon is polyp morphology. Sessile polyps are ultrasound. The most common findings are nonspecific significantly more likely to represent malignancy than wall thickening (either focal fundal, segmental or diffuse), oen associated with sludge, or calculi; focal pedunculated polyps and should prompt either 3 cholecystectomy or close follow‐up.12,19 fundal mass‐like thickening is most common (Fig. 4). Segmental adenomyomatosis may result in focal luminal narrowing of the gallbladder body. Echogenic Adenomyomatosis. intramural foci with associated V‐shaped comet tail Adenomyomatosis, also known as adenomyomatous reverberaon arfacts are characterisc and represent hyperplasia or divercular disease of the gallbladder, cholesterol crystals within Rokitansky‐Aschoff sinuses. represents one of two acquired benign hyperplasc This is highly specific for adenomyomatosis and should cholecystoses. It is found in approximately 1‐8% of not be confused with the “dirty shadowing” of cholecystectomy specimens.25,26 The pathologic intramural air seen in emphysematous cholecyss, 3 hallmark of adenomyomatosis is intraluminal which is more irregular and linear in configuraon.

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Contrast‐enhanced MDCT is limited in the this finding was rare in a few cases of carcinoma. evaluaon of adenomyomatosis. One retrospecve Diffuse adenomyomatosis showed similarly early review by Ching et al. of 36 cases of either mucosal enhancement with delayed serosal adenomyomatosis or gallbladder carcinoma enhancement, as well as a T2 hyperintense serosal demonstrated a sensivity of only 36% for the twenty‐ layer. These individual findings were demonstrated in two pathologically proven cases of adenomyomatosis 38‐50% of the primary carcinomas; however, these with a negave predicve value of only 44‐48%.26 combined findings were seen in only 13% of However, if wall thickening (focal or diffuse) had a carcinomas.29 In a similar study, Haradome et al., clearly cysc appearance (represenng the Rokitansky reported that contrast enhanced MR demonstrated ‐Aschoff sinuses), the specificity was 79‐93%. It is that enhancement paerns were indisnguishable important to note that there are case reports of between adenomyomatosis and carcinomas in 70% of adenomyomatosis coexisng with gallbladder their paents.28 carcinoma. If suspicious features, such as local organ invasion, adenopathy, or biliary obstrucon are present, carcinoma should remain the primary Tumefacve Sludge. diagnosis.26 So while CT cannot be used to effecvely Biliary sludge represents highly viscous bile with exclude adenomyomatosis, if well‐defined cysc high bilirubin content. It is usually the result of biliary gallbladder wall thickening is encountered in the stasis from prolonged fasng or hyperalimentaon. absence of other suspicious findings, it is reasonable Tumefacve sludge is typically associated with to conclude the diagnosis of adenomyomatosis.26,27 cholelithiasis, and evoluon of tumefacve sludge to 30 The most commonly described feature of calcium bilirubinate stones has been described. adenomyomatosis on MR imaging is the “pearl Tumefacve sludge is most commonly encountered as necklace” sign, which results from the dilated an incidental finding on ultrasound evaluaon for right Rokitansky‐Aschoff sinuses.25,28 A previous study upper quadrant pain. evaluang 66 paents with gallbladder lesions While most biliary sludge presents as a layering demonstrated this finding best on T2 weighted slowly mobile dependent fluid‐fluid level, tumefacve images, ideally using single shot fast spin echo sludge presents as an intraluminal polypoid, techniques or fast spin echo breath hold T2 echogenic, non‐shadowing mass, which may mimic a 31 techniques. The finding could also be seen T1 tumor. The key features separang the two are weighted dynamic contrast enhanced sequences but demonstraon of tumefacve sludge as a mobile mass 3,31 with significantly less sensivity.29 A later study with no internal vascularity. Unfortunately, this is compared 47 paents with either adenomyomatosis not always possible, as sludge can be adherent to the or primary gallbladder carcinoma using single shot fast wall or move very slowly; the lack of vascularity alone spin echo T2‐weighted magnec resonance is not sufficient to effecvely exclude tumor, especially cholangiopancreatography sequences. It was with small masses. It has been suggested that in cases demonstrated that the “pearl necklace” sign could be where tumefacve sludge is suspected on the inial used to diagnose adenomyomatosis and exclude exam but not conclusive, reimaging aer a fay meal carcinoma with a mean sensivity, specificity, and and/or performing a short interval follow‐up accuracy of 62 %, 92%, and 74%, respecvely.28 ultrasound in several weeks may show resoluon or decreased size of the mass, which would exclude a The value of contrast‐enhanced MR to discern 31,32 between adenomyomatosis and carcinoma is highly neoplasm. quesonable. Yoshimitsu et al. described that both Biliary sludge on CT can appear as layering increased adenomyomatosis and primary carcinoma enhance density in the gallbladder or as a tumefacve so from the arterial phase through the delayed phase, ssue aenuaon mass (>25HU). It should not but there were differences in their enhancement enhance; however, vicarious excreon of iodinated 33 distribuon.29 Focal adenomyomatosis showed early, contrast may confound evaluaon for enhancement. smooth, homogeneous mucosal enhancement that CT is limited as a primary evaluaon tool for sludge 33 was connuous around the gallbladder epithelium; with a sensivity between 44‐64%. Tumefacve

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Rare Benign Enes. Addional rare enes that the radiologist should have a passing familiarity with are listed in (Table 1). A detailed discussion of most of these enes is beyond the scope of this arcle and is well described in a review by Levy et al.3 Of these enes, xanthogranulomatous cholecyss (XGC) may be the most important to know. This represents a hisocyte‐ predominant inflammatory process from bile extravasaon into the gallbladder wall through ulcerated Rokitansky‐Aschoff sinuses.3,5 It most oen presents with clinical symptoms idencal to typical cholecyss. Its imaging appearance mimics that of aggressive invasive carcinoma, as the infecon may spread into local adjacent organs. It has also been described as an associated risk factor of primary gallbladder carcinoma3 Wall thickening is the most common finding but is nonspecific. The typical sonographic appearance has been described as wall thickening with mulple hypoechoic bands or nodules. CT findings suggesve of XGC include a low aenuaon nodule involving more than 60% of the thickened gallbladder wall area and a connuous line of mucosal enhancement.3 These same findings are seen on T2 and post‐contrast T1 MRI sequences. Figure 5. Primary Gallbladder Adenocarcinoma. Longitudinal (A) and transverse (B) gallbladder ultrasound images Intramural T2 hyperintense foci correspond to the low demonstrate irregular gallbladder wall thickening. Axial CT density nodules on CT and represent abscesses and images without (C) and with (D) contrast reveal an foci of xanthogranulomatous inflammaon. enhancing eccentric gallbladder wall mass, as well as layering non‐enhancing intraluminal sludge and stones. Mulple rim enhancing hepac lesions are consistent with Malignant Masses hepac metastases (D). F18 FDG‐PET in axial (E) and coronal (F) planes show hypermetabolic acvity associated with the Primary Gallbladder Carcinoma. primary gallbladder carcinoma and mulple hepac metastases. Primary gallbladder carcinoma is uncommon with approximately 7,000 cases reported annually.35 sludge on MR is not separately well described in the Reported risk factors include female gender, advanced literature to our knowledge; however, biliary sludge in age, cigaree smoking, ethnicity (specifically Hispanic, general has been described as iso‐ to mildly Northern Japan, Nave American, and Israeli), and hyperintense on T2 weighted images and hyperintense occupaonal exposure to chemicals from rubber, on T1 weighted images. The T1 hyperintensity results automobile, wood finishing, and metal fabricaon 36,37 from water resorpon and concentraon of industries. Mean age of presentaon is 72 years. cholesterol and bile salts during fasng.5 Similar to CT, More than 90% are adenocarcinomas, and there are any enhancement demonstrated within the mass several histological subtypes, including papillary, clear excludes sludge and is suspicious for neoplasm. The cell, signet cell, and mucinous. Adenosquamous, recent ability to perform subtracon images for post‐ squamous, small cell, and undifferenated types are contrast sequences greatly increases the ability to quite rare. Many gallbladder carcinomas contain a 36,38 idenfy or exclude true enhancement and leads to a mixture of different subtypes. The overall five‐year more confident diagnosis.34 survival rate of gallbladder carcinoma is dismal (less than 5%) with a median survival of 6 months. Papillary

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Gallbladder Masses, McKnight et al. carcinomas have a slightly beer prognosis (median survival 20 months), as they tend to fill the gallbladder before becoming invasive.36 The cross‐seconal appearance of gallbladder carcinoma for US, CT, and MR is that of a mass replacing the gallbladder (40‐65%), focal or diffuse wall thickening (20‐30%), or an intraluminal polypoid mass (15‐25%) (Figures 5‐7).39 Most gallbladder carcinomas present at an advanced stage and are not diagnoscally challenging. There is typically local invasion of liver or adjacent organs, which significantly limits therapeuc opons. It is important to be aware of the ulity of cross seconal imaging in staging and prognosis of gallbladder carcinoma. Sonography is not useful in staging of gallbladder carcinoma; Bach et al. reported that only 37% of paents with advanced disease could be idenfied on US.40 In another study, Tsuchiya described that 30% of early carcinomas may be missed by ultrasound.41 Endoscopic ultrasound improves success in both characterizing local disease and idenfying regional nodal spread versus convenonal ultrasound. CT and MR are more useful in staging, as they more accurately define local extent of disease, regional adenopathy, and distant metastases. CT sensivity for Figure 6. Primary Gallbladder Small Cell Carcinoma. RUQ hepac invasion is 65% if <2cm and 100% if >2cm. transverse ultrasound image with color Doppler (A) Sensivity for nodal spread has been reported as 36% demonstrates an intraluminal echogenic mass with increased color flow and irregular gallbladder wall for N1 and 47% for N2 disease; there is 99% specificity thickening. Unenhanced (B), arterial phase (C and D), and 5 42 for nodes >10mm. CT has a reported an overall T minute delayed (E and F) CT images through the gallbladder stage accuracy of 84% and an accuracy of 85% in show the irregular gallbladder mass directly invading the determining resectability. MR has a variable reported liver parenchyma. Central low density of the mass on all phases likely represents necrosis. Primary small cell sensivity between 67‐100% for hepac invasion, carcinoma was confirmed at biopsy. The prominent although the depth of invasion is underesmated in enhancement on arterial phase with progressive washout approximately 10% of cases. MR sensivity for through the delayed phase is typical of neuroendocrine lymphadenopathy has been reported between 56‐ tumors. 5,39 92%. MR and CT are also useful in detecng Sonographic imaging of gallbladder carcinoma vascular invasion by tumor. typically demonstrates heterogeneous echotexture Diagnosis of early stage gallbladder carcinoma is a within the mass, which reflects varying degrees of disnct challenge. The imaging features of early necrosis, or irregular wall thickening. Echogenic foci gallbladder carcinoma have significant overlap with typically represent gallstones versus the much less 43 those of benign gallbladder diseases previously common (Fig. 8). Both described. There are several features, however, that gallstones and porcelain gallbladder are well described may be useful in characterizing a mass as suspicious risk factors, although the associaon between for malignancy. Malignant polypoid lesions are gallbladder carcinoma and porcelain gallbladder may typically greater than 1cm. Also, any focal or diffuse not be as evident as previously thought. This risk/ wall thickening >1cm or asymmetric thickening are associaon is primarily based on reports from the th suggesve of carcinoma.39 early to mid‐20 century, which found gallbladder carcinoma in 20% of cases of porcelain gallbladder. A

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A B A B

C D C D Figure 7. Primary Gallbladder Adenocarcinoma. Sagial Figure 8. Porcelain Gallbladder. Abdominal AP radiograph grayscale ultrasound image of the RUQ (A) demonstrates (A), transverse RUQ gray scale ultrasound (B), and axial (C) irregular polypoid gallbladder wall thickening. Axial (B and and coronal (D) contrast‐enhanced CT images of the upper C) and coronal (D) contrast‐enhanced CT images of the abdomen each demonstrate thin intramural calcificaon of gallbladder show markedly irregular gallbladder wall the gallbladder wall, diagnosc of porcelain gallbladder. thickening with heterogeneous enhancement and loss of Marked posterior acousc shadowing is seen on US (B). disncon between the gallbladder wall and surrounding liver margin, consistent with direct invasion. Extensive metastac adenopathy is present in the peripancreac and periaorc regions (B and C). recent retrospecve review by Kahn et al. of seven to early washout which is more characterisc of published series encompassing over 60,000 benign polyps.5,22,39 found gallbladder carcinoma in 15% F18‐FDG PET‐CT is a relavely recent addion to the of porcelain gallbladders; gallbladder carcinoma in work‐up of gallbladder malignancies. Several studies itself had an overall incidence of 0.2%. They also have reported a sensivity of 75‐80 % and specificity retrospecvely reviewed an addional 1,200 of 82‐87% for gallbladder malignancy with a high consecuve cholecystectomies with 1.1% having negave predicve value of 90%.45,46 Reported false porcelain gallbladders, as well as an addional series posives include adenomyomatosis, of 35 gallbladder carcinomas; none of the paents in xanthogranulomatous cholecyss, and tuberculoid these two series had both gallbladder carcinoma and granulomatosis.47 False negaves include mucinous porcelain gallbladder. Their conclusion was that carcinoma, which is a well described limitaon of PET. porcelain gallbladder and gallbladder carcinoma are 44 Focal intense increased FDG acvity is the most only weakly associated. commonly described appearance for gallbladder On unenhanced CT, gallbladder carcinoma is malignancy, although rim‐like intense acvity (which is typically hypodense; 40% demonstrate hypervascular more typical of acute cholecyss or chronic foci equal to or greater than liver parenchyma with IV ) has also been described.47 contrast. On MR, gallbladder carcinoma has nonspecific intermediate T1 and moderately hyperintense T2 signal intensity. On both CT and MR, Metastases and Other Rare Malignancies. intense irregular enhancement may occur at the Approximately 98% of gallbladder malignancies 42 periphery of the lesion on arterial phase imaging with represent primary carcinoma. The next most persistent portal venous and delayed enhancement common malignancy is metastases. Malignant from fibrous stromal elements. The persistent delayed melanoma is the most common primary tumor to enhancement is suggesve of malignancy, as opposed metastasize to the gallbladder, represenng just over

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50% of reported cases.48 The sonographic appearance References of melanoma metastases is one or more hyperechoic mural masses >1cm in diameter. Unfortunately, a 1. Zeman RK. Cholelithiasis and cholecyss. In: Gore RM, Levine MS, Laufer I, eds. Textbook of gastrointesnal radiology. study of 464 paents with malignant melanoma by Philadelphia, Pa: Saunders, 1994; 1636–1674. Holloway et al. demonstrated that while 15‐20% of 2. Strom BL, West SL. The epidemiology of gallstone disease. In: paents had gallbladder involvement at autopsy, only Cohen S, Soloway RD. Gallstones. New York, NY: Churchill 4.1% had detectable disease on ultrasound.49 The CT Livingstone, 1985; 1–26. 3. Levy AD, Murakata LA, Abbo RM et al. Benign Tumors and appearance is that of a polypoid enhancing mass or Tumorlike Lesions of the Gallbladder and Extrahepac Bile irregular wall thickening. Most of the lesions are Ducts: Radiologic‐Pathologic Correlaon. Radiographics 2002; serosal, but they may also be intraluminal. The typical 22:387‐413 MR appearance is that of a T1 and T2 hyperintense 4. Bortoff GA, Chen MYM, et al. Gallbladder Stones: Imaging and mass. The T1 hyperintensity has been aributed to Intervenon. Radiographics 2000; 20:751‐766 5. Catalano OA, Sahani DV, et al. MR Imaging of the Gallbladder both the melanin content, which can be variable, as A Pictorial Essay. Radiographics 2008; 28:135‐155. well as hemorrhage or necrosis. Because of the pre‐ 6. McIntosh DM, Penney HF. Gray‐scale ultrasonography as a contrast T1 hyperintensity, post‐contrast imaging may screening procedure in the detecon of . not be helpful. The enhancing gallbladder wall may Radiology 1980; 136 7. MacDonald FR, Cooperberg PL. The WES triad‐ A specific become isointense with the lesions, decreasing sonographic sign of gallstones in the contracted gallbladder. 50 detecon. Other reported metastases to the Gastrointesnal Radiology 1981; 6:39‐41 gallbladder include renal cell carcinoma and 8. Grand D, Horton KM, Fishman, EK. CT of the Gallbladder: hepatocellular carcinoma. Spectrum of Disease. AJR 2004; 183:163‐170. 9. Chan WC, Joe BN, et al. Gallstone Detecon at CT in Vitro: Other rare malignancies reported to occur in the Effect of Peak Voltage Seng. Radiology 2006, 241: 546‐553. gallbladder include primary non‐Hodgkin 10. Meyers MA, O’Donohue N. The Mercedes‐Benz Sign: Insight (approximately 13‐20 cases reported), which typically into the Dynamic of Formaon and Disappearance of Gallstones AJR 1973; 119:63‐70 presents with a nonspecific appearance on US, CT, and 11. Delabrousse E, Bartholomot B et al. Gas‐containing gallstones: MR that mimics gallbladder carcinoma; typical imaging value of the “Merced‐Benz”sign at CT examinaon. J Radiol findings include an intraluminal mass or a mass 2000; 81: 1639‐1641 replacing the gallbladder, along with cholelithiasis, 12. Ishikawa O, Ohhigashi H, Imaoka S, et al. The difference in biliary sludge, porta hepac adenopathy, liver malignancy between pedunculated and sessile polypoid lesions of the gallbladder. Am J Gastroenterol 1989; 84:1386‐ invasion, or biliary obstrucon. MR reveals a T1 1390. hypointense and T2 hyperintense mass relave to liver 13. Albores‐Saavedra J, Vardaman CJ, Vuitch F. Nonneoplasc parenchyma.5,48 There are also case reports of primary polypoid lesions and adenomas of the gallbladder. Pathol gallbladder sarcomas, including Kaposi sarcoma, Annu 1993; 28(pt 1):145–177. 14. Misra S, Chaturvedi A, Misra NC, Sharma ID. Carcinoma of the malignant fibrous hisocytoma, angiosarcoma, 48 gallbladder. Lancet Oncol. 2003; 4:167‐176. , and rhabdomyosarcoma. 15. Wada K, Tanaka M, Yamaguchi K. Carcinoma and polyps of the Summary gallbladder associated with Peutz‐Jeghers syndrome. Dig Dis Sci 1987; 32: 943–946. There are numerous causes of gallbladder masses, 16. Walsh N, Qizilbash A, Banerjee R, Waugh GA. Biliary neoplasia in Gardner’s syndrome. Arch Pathol Lab Med 1987; 111:76– benign much more common than malignant, which are 77. frequently found on imaging. Familiarity with the 17. Wistuba II, Miquel JF , Gazdar AF , Albores‐ Saavedra J . diverse eologies of these masses and their Gallbladder adenomas have molecular abnormalies different presentaons on various cross‐seconal imaging from those present in gallbladder carcinomas. Hum Pathol 1999; 30 (1): 21 – 25. modalies is crical. This knowledge provides the 18. Roa I , de Aretxabala X , Araya JC , Villaseca M , Roa J , radiologist with the ability to make earlier and more Guzmán P . Incipient gallbladder carcinoma: clinical and confident diagnoses and assist referring clinicians in pathological study and prognosis in 196 cases. Rev Med Chil facilitang appropriate management. At mes, costly 2001; 129 (10): 1113 – 1120. diagnosc workups and intervenons may be avoided. 19. Hiroyoshi F, Tomoo K. Small Polypoid Lesions of the Gallbladder: Differenal Diagnosis and Surgical Indicaons by Helical Computed Tomography. Arch Surg. 1998; 133:735‐739.

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20. Yoshimitsu K, Honda H, Dynamic MRI of the gallbladder 36. Henson DE, Albores‐Saavedra J, Corle D. Carcinoma of the lesions: differenaon of benign from malignant. J Magn gallbladder: histologic types, stage of disease, grade, and Reson Imaging. 1997 Jul‐Aug;7(4):696‐701. survival rates. Cancer 1992; 70:1493–1497. 21. Irie H, Kamochi N. High b‐value diffusion‐weighted MRI in 37. Strom BL, Soloway MD, Rios‐Dalenz JL, et al. Risk factors for differenaon between benign and malignant polypoid : an internaonal collaborave case‐control gallbladder lesions. Acta Radiol. 2011 Apr 1; 52(3):236‐40. study. Cancer 1995; 76:1747–1756. Epub 2011 Mar 3. 38. Albores‐Saavedra J, Henson DE, Sobin LH. WHO histological 22. Tseng JH, Wan YL, Hung CF, et al. Diagnosis and staging of typing of tumors of the gallbladder and extrahepac bile gallbladder carcinoma: evaluaon with dynamic MR imaging. ducts. Berlin, Germany: Springer‐Verlag, 1991. Clin Imaging 2002; 26: 177–182. 39. Furlan A, Ferris JV, Gallbladder Carcinoma Update: 23. Park JK, Yoon YB Management Strategies for Gallbladder Mulmodality Imaging Evaluaon, Staging and Treatment Polyps: Is It Possible to Predict Malignant Gallbladder Polyps? Opons. Radiographics 2008; 191:1440‐1447. Gut Liver. 2008 September; 2(2): 88–94. 40. Bach AM, Loring LA, Hann LE, Illescas FF, Fong Y, Blumgart LH. 24. Corwin MT, Siewert B, et al. Incidentally Detected Gallbladder Gallbladder cancer: can ultrasonography evaluate extent of Polyps: Is Follow‐up Necessary? ‐ Long‐term Clinical and US disease? J Ultrasound Med 1998; 17:303–309. Analysis of 346 Paents. Radiology 2011; 258: 277‐282. 41. Tsuchiya Y. Early carcinoma of the gallbladder: macroscopic 25. Boscak AR, Al‐Hawary M, et al. Best Cases of AFIP: features and US findings. Radiology 1991; 179:171–175 Adenomyomatosis of the Gallbladder. Radiographics 2006; 42. Levy AD, Murakata LA, et al. Gallbladder Carcinoma: 26: 941‐946. Radiologic‐Pathologic Correlaon. Radiographics 2001; 21:295 26. Ching BH, Yeh BM, et al. CT Differenaon of ‐314. Adenomyomatosis and Gallbladder Cancer. AJR 2007; 189:62 43. Weiner SN, Koenigsberg M, et al. Sonography and computed ‐66. tomography in the diagnosis of carcinoma of the gallbladder. 27. Yamamoto A, Ozeki Y, et al. Successful Diagnosis of AJR 1984; 142:735–739. Gallbladder Carcinoma Coexisng with Adenomyomatosis by 44. Kahn ZS, Livingstone EH, et al. Reassessing the Need for (18)F‐FDG‐PET‐ Report of a Case. J Gastrointest Cancer. 2011 Prophylacc Surgery in Paents with Porcelain Gallbladder. Dec; 42(2): 252‐6. Arch Surg. 2011; 146(10):1143‐1147. 28. Haradome H, Ichikawa T, et al. The Pearl Necklace Sign: An 45. Rodriguez‐Fernandez A, Gomez‐Rio M. Positron‐emission Imaging Sign of Adenomyomatosis of the Gallbladder at MR tomography with fluorine‐18‐fluoro‐2‐deoxy‐D‐glucose for Cholangiopancreatography. Radiology 2003; 227:80‐88. gallbladder cancer diagnosis. Am J Surg. 2004 Aug; 188(2):171 29. Yoshimitsu K, Honda H, et al. MR Diagnosis of ‐5. Adenomyomatosis of the Gallbladder and Differenaon from 46. Koh T, Tanigichi H, Yamaguchi A, Kunishima S. Differenal Gallbladder Carcinoma. Importance of Showing Rokitansky‐ diagnosis of gallbladder cancer using positron emission Aschoff Sinuses. AJR 1999; 172: 1535‐1540. tomography with fluorine‐18‐labeled fluoro‐deoxyglucose 30. Rosenthal SJ, Cox GG, et al. Pialls and Differenal Diagnosis (FDG PET). J Surg Oncol 2003; 84:74 ‐81 in Biliary Sonography. Radiographics 1990; 10:285‐311. 47. Maldjian PD, Ghesani N, Ahmed S, Liu Y. Adenomyomatosis of 31. Fakhry J. Sonography of Tumefacve Biliary Sludge. AJR 1982; the Gallbladder: Another Cause of a “Hot” Gallbladder. AJR 139:717‐719. 2007; 189: W36‐W38. 32. Hanbidge AE, Buckler PM, et al. From the RSNA Refresher 48. Kim MJ, Kim KW, Kim HC, et al. Unusual Malignant Tumors of Courses: Imaging Evaluaon for Acute Pain in the Right Upper the Gallbladder. AJR 2006; 187:473‐480 Quadrant. Radiographics 2004; 24: 1117‐1135. 49. Holloway BJ, King DM. Ultrasound diagnosis of Metastac 33. Rebner M, Ruggieri PM, et al. CT Evaluaon of Melanoma of the Gallbladder. BJR 1997; 70: 1122‐1125. Intracholecysc Bile. AJR 1985; 145(2): 237‐240. 50. Martel JP, McLean CA, Rankin RN. Best Cases of AFIP: 34. Newaa A, Khatri G, et al. Subtracon Imaging: Applicaons Melanoma of the Gallbladder. Radiographics 2009; 29‐291‐ for Nonvascular Abdominal MRI. AJR 2007; 188(4):1018‐1025. 296. 35. Greenlee RT, Murray T, Bolden S, Wingo PA. Cancer stascs 2000. CA Cancer J Clin 2000; 50:7–33.

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Case Report, Beydoun et al. Cysc Right Lower Quadrant Mass

Tammam Beydoun, D.O., and Sharon Kreuer, D.O.

Department of Diagnosc Radiology, Botsford Hospital, Farmington Hills, MI

Case Presentaon

A 48‐year‐old paent presents for a lumbar spine MRI for low back and hip pain. A 6cm mass was incidentally seen within the right lower quadrant at the level of the cecum (Fig. A‐C). On review of systems, the paent reported intermient right lower quadrant pain over the course of several years. Past medical history was notable for diverculosis with an episode of diverculis in the recent past. Physical examinaon was noncontributory. Further evaluaon with CT including IV and oral contrast was performed. (Fig. D)

A B

C D

Figure. Axial T2 (A), axial T1 (B), and post contrast fat saturated axial T1 (C) images through the level of the cecum demonstrate a fluid signal lesion within the right lower quadrant with thin wall enhancement. Axial post contrast CT image at the same level (D) reveals similar findings, as well as a lack of conspicuous mural calcificaons or surrounding inflammatory changes.

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Key imaging finding depending upon extent of mucin content. Malignant mucinous cystadenocarcinoma contains solid and fluid Cysc right lower quadrant lesion. components and demonstrates irregular, thick, nodu‐ lar walls. Rupture and extravasaon of mucinous con‐ tent may lead to peritoneal seeding and pseudomyxo‐ Differenal diagnoses ma peritonei. Preoperave diagnosis is crucial, as a Mucocele right hemicolectomy is the preferred approach to a or cystadenocarcinoma to Acute appendicis with abscess avoid seeding of the peritoneum. Cysc adnexal tumor Acute appendicis. Discussion Appendicis is a common cause of right lower quad‐ rant pathology and occurs secondary to luminal ob‐ Cysc right lower quadrant lesions encompass a strucon and bacterial overgrowth. Paent presenta‐ large differenal diagnosis and mulple organ systems, on may vary but characteriscally includes general‐ including the genitourinary system in the female pa‐ ized abdominal pain which becomes localized to the ent. Clinical and laboratory findings may narrow the periumbilical region or McBurney point within the list of differenals; however, CT, MR, and US imaging right lower quadrant, as well as voming, anorexia, assist in determining the composion, anatomic origin, and fever. Laboratory values, such as an elevated and aggressiveness of a lesion. A concise and accurate white blood cell count and C‐reacve protein, may be differenal diagnosis is of the utmost importance, helpful along with imaging in guiding the diagnosis.2 guiding the decision for and the extent of surgical in‐ tervenon. In the case of potenal neoplasm, urgency On CT, appendicis classically presents as an en‐ is necessary, as rupture of a malignant lesion involves larged appendix (greater than 6 millimeters) with significant complicaons with the potenal for perito‐ thickened enhancing walls, and surrounding mesenter‐ 3 neal seeding. ic inflammaon. Associated findings include appendi‐ colith, phlegmon, or frank abscess formaon.3 Imaging evaluaon may also be performed using ultrasound, Mucocele. especially in pediatric or pregnant paents. So‐ Mucocele of the appendix is a rare enty demon‐ nographically, the appendix will be dilated and non‐ strated in 0.3% of appendectomy specimens.1 On aver‐ compressible with appendicis. Surrounding fay in‐ age, the diagnosis is made in the sixth decade of life flammaon or fluid collecons are helpful secondary and presents either as an incidentally found right low‐ signs. er quadrant mass or with pain.1 Complicaons include torsion, rupture, and, rarely, intussuscepon. Cysc adnexal tumor. There are three histologic subtypes of mucoceles, There are many types of adnexal masses, which ranging from benign to neoplasc, including simple from benign to malignant, with benign tumors being mucocele, mucinous cystadenoma, and mucinous more common.4 Simple cysc masses of the adnexa cystadenocarcinoma. The most common subtype is are unlikely to be malignant and may be paratubal, benign mucinous cystadenoma, which is indisnguish‐ paraovarian, or ovarian in origin.5 Many women are able from a simple mucocele. Differenaon of these asymptomac, and the adnexal cysts are discovered two enes is based histologically on mucosal hyper‐ incidentally on imaging for other purposes. Cyst rup‐ plasia. Mucoceles are mucin‐containing cysc lesions ture or ovarian torsion may result when adnexal mass‐ with well demarcated thin walls, oen demonstrang es become large; symptoms include pelvic pain, nau‐ mural calcificaons. sea, and voming. Imaging findings are consistent with fluid signal The primary imaging modality when screening for characteriscs on MRI with some variaon on T1WI, adnexal masses is US. The US appearance of cysc ad‐

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Case Report, Beydoun et al. nexal masses varies based upon the eology. Echo‐ References genicity, size, vascular flow, nodularity, and septaons should all be assessed and commented on when evalu‐ 1. Madwed D, Mindelzun R, Jeffery RB. Mucocele of the appendix: imaging findings. Am J Roentgenol 1992 159:69‐71. ang adnexal lesions. Simple cysts are generally ane‐ 2. Curn KR, Fitzgerald SW, Nemcek AA, et al. CT diagnosis of choic, have a thin or impercepble wall, and no inter‐ 5 acute appendicis: Imaging findings. Am J Roentgenol 1995; nal septaons or vascularity. The CT and MR appear‐ 164: 905‐909. ance of simple cysc adnexal lesions is that of fluid 3. Grönroos JM, Paula Grönroos P. Diagnosis of acute aenuaon or signal and a thin wall that enhances appendicis. Radiology 2001; 219: 297. with IV contrast. Complex internal characteriscs, solid 4. Levine D., Brown DL, Andreo RF, et al. Management of components, nodularity, and vascularity are suggesve asymptomac ovarian and other adnexal cysts imaged at US: of malignancy. Society of radiologists in ultrasound consensus conference statement. Radiology 2010; 256: 943‐954. 5. Jeong YY, Outwater EK, Kang HK. From the RSNA refresher Diagnosis courses imaging evaluaon of ovarian masses. RadioGraphics 2000; 20: 1445–1470. Simple mucocele

Summary

US and CT are tradionally the chief imaging modali‐ es used in the work‐up and management of paents with appendiceal pathology. In addion, adjunct imag‐ ing with MR may be ulized to assist with diagnosc decision making in complicated cases. Generally, imag‐ ing is principally used to exclude possible differenal diagnoses, as well as to evaluate for malignant charac‐ teriscs and complicaons prior to resecon. Oen‐ mes, imaging findings are representave of a specific pathology; awareness of these findings is valuable for making an accurate diagnosis.

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Case Report, Ali Non‐Adnexal Cysc Pelvic Mass

Reehan M. Ali, D.O.

Department of Diagnosc Radiology, Botsford Hospital, Farmington Hills, MI

Case Presentaon

A 67‐year‐old woman presented with an incidental pelvic mass that was found during a total abdominal hysterectomy and bilateral salpingo‐oophorectomy (TAH‐BSO). She denied pelvic pain or vaginal discharge. Past medical history and review of systems were non‐contributory. Physical exam was unremarkable. The paent was referred for a CT of the abdomen and pelvis and subsequent pelvic ultrasound for evaluaon of the incidentally found pelvic mass (Fig.).

A B

C

Figure. Coronal (A) and axial (B) CT images through the pelvis demonstrate a well‐circumscribed hypodense cysc lesion in the le pelvis abung a loop of small bowel (arrows). The mass is remote from adnexal structures. Corresponding transabdominal gray‐scale ultrasound image of the pelvis (C) shows a round hypoechoic lesion with a hyperechoic wall.

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Case Report, Ali

Key clinical finding and morphology. In the case of small bowel duplicaon cysts, they will be adjacent to a loop of Incidental pelvic mass on TAH‐BSO. bowel, most oen the . Typically, they will measure simple fluid aenuaon and will have round, 3 Key imaging finding smooth borders and thin, slightly enhancing walls. The characterisc sonographic appearance includes Non‐adnexal cysc pelvic mass abung small a fluid‐filled structure with an inner hyperechoic rim bowel. (mucosa) and outer hypoechoic layer (muscular wall) and posterior acousc enhancement. This “double‐ Differenal diagnoses layered” appearance, however, is not pathognomonic for an enteric duplicaon cyst. Chang, et al., has Enteric duplicaon cyst described an arfact which simulates this “double‐ Peritoneal inclusion cyst layered” appearance in mulple non‐enteric cysts, 4 Cysc lymphac malformaon leading to incorrect diagnoses.

Discussion Peritoneal inclusion cyst: Peritoneal inclusion cysts are seen exclusively in Incidental findings during abdominal and pelvic women and are a fairly common enty. They form surgery are a fairly common occurrence. Surgeons will around an acve ovary in the area of peritoneal subsequently turn to imaging in order to further adhesions. Ovarian fluid resorpon is limited by the characterize the incidental finding. The role of imaging adhesions and an inclusion cyst subsequently forms.5 is to narrow the differenal diagnosis when possible and provide assistance in determining the need for Paents will typically present with pelvic pain or potenal future intervenon. For pelvic masses in pelvic mass. These occur almost exclusively in parcular, CT, MRI, and ultrasound are oen premenopausal women with history of prior 5 complementary modalies. abdominal or pelvic surgery. On ultrasound, this will have an appearance of a complex, mulcysc adnexal mass. They will appear Enteric duplicaon cyst. adherent to the ovarian surface but will not extend to Duplicaon cysts may occur anywhere along the the parenchyma. These can oen mimic other alimentary tract but most commonly occur in the small pathology, including hydro‐ or pyosalpinx. CT findings 1 bowel. A review of 281 cases of GI tract duplicaons include a non‐specific cysc lesion near the adnexae found that 47% occur in the small bowel with the which contains simple or complex fluid.5 majority (33%) in the ileum.2

Duplicaon cysts are hollow, epithelium‐lined, spherical or tubular structures. They share a common Cysc lymphac malformaon. wall and common mesenteric arterial supply with the Pelvic lymphac malformaons are relavely rare adjacent GI tract.1 They do, however, have a separate and are thought to result from abnormal development mucosal lining.3 of venolymphac structures or lymphangioma One‐third of small bowel duplicaons are formaon secondary to injury, inflammaon, or hemorrhage. They are typically congenital and present symptomac in the neonatal period. The majority 6 2 before two years of age with pain. The most common present by two years of age. Complicaons include 6 bowel obstrucon, intussuscepon, abdominal pain, locaon is in the mesentery of the small bowel. and GI bleeding.2 As in our case, they may also be Ultrasound shows a single or mul‐locular lesion silent in presentaon and remain undetected into with a thin wall, which helps to disnguish it from a adulthood. usually thick‐walled duplicaon cyst. The On CT, these cysts are recognized by their locaon malformaon is typically anechoic but may contain some internal echoes.7

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Case Report, Ali

Diagnosis References

Enteric duplicaon cyst 1. Kim SK, Lim HK, Lee SJ, et al. Completely isolated enteric duplicaon cyst: case report. Abdom Imaging 2003; 28: 12‐ 14. Summary 2. Macpherson RI. Gastrointesnal duplicaons: clinical, pathologic, eologic, and radiologic consideraons. Incidental cysc mass lesions found during pelvic Radiographics 1993; 13: 1063‐1080. surgery can present a diagnosc challenge. While 3. Gumus M, Kapan M, Gumus H, et al. Unusual keeping in mind certain pialls, cross‐seconal noncommunicang isolated enteric duplicaon cyst in adults. imaging can help to disnguish between diagnosc Gastr Res and Pract 2011; 2011: 1‐3. consideraons, which include enteric duplicaon cysts, 4. Cheng G, Soboleski D, Daneman A, et al. Sonographic pialls peritoneal inclusion cysts and cysc lymphac in the diagnosis of enteric duplicaon cysts. AJR Am J malformaons. Knowledge of typical imaging paerns Roentgenol 2005; 184: 521‐525. is pivotal for proper interpretaon of these studies. 5. Jain K. Imaging of peritoneal inclusion cysts. AJR Am J Roentgenol 2000; 174(6): 1559‐1563. 6. Losanoff EJ, Richman BW, El‐Sherif A, et al. Mesenteric cysc lymphangioma. J Am Coll Surg 2003; 196: 598‐603. 7. Leven A, Christodoulakis M, Taflampas P, et al. Mesenteric cysc lymphangioma: A case report and literature review. J Surg Radiol 2010; 1: 1.

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Case Report, Saenz Pancreac Mass

Rocky C. Saenz, D.O.

Department of Diagnosc Radiology, Botsford Hospital, Farmington Hills, MI

Case Presentaon

A 48‐year‐old man with a history of recently diagnosed acute myelogenous leukemia (AML) presented to the emergency room with a one‐month history of abdominal pain and bloang. He also reported a twenty‐six pound weight loss. Review of systems was negave for fever, chills, or blood in his stools. Physical exam demonstrated jaundice but was otherwise unremarkable. Laboratory studies revealed elevated conjugated bilirubin, total bilirubin, alkaline phosphatase, gamma‐glutamyl transpepdase (GGT), aspartate aminotransferase (AST), and alanine transaminase (ALT). Amylase, and lipase were normal. The paent then underwent an abdominal ultrasound followed by CT scan (Fig).

A B

C

Figure. Transverse gray scale ultrasound image (A) shows an ill‐defined hypoechoic mass centered in the pancreac head (arrow). Axial CT image with oral and IV contrast at the level of the pancreas (B) demonstrates a large, lobulated, heterogeneous mass centered in the pancreac head (arrow). The mass compresses the adjacent duodenum. Also seen is mesenteric and retroperitoneal adenopathy with a nodal mass in the le para‐aorc space. Axial CT image more cephalad within the upper abdomen (C) reveals splenomegaly with periportal adenopathy.

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Case Report, Saenz

Key imaging finding of 8% in paents with the diagnosis of AML.1 A cytogenec irregularity has been idenfied in some Pancreac mass with adenopathy and splenomegaly leukemic paents with granulocyte sarcoma, and it in a paent with AML. involves the translocaon of chromosomes 8 and 21.5 In this translocaon leukemia, granulocyte sarcoma is 6 Differenal diagnoses seen in 18 to 24% of cases. On CT, granulocyte sarcoma presents as a solid, Granulocyte sarcoma contrast enhancing lesion with associated adenopathy Primary Adenocarcinoma and splenomegaly. These tumors are usually pliable Pancreas and may result in biliary stasis. In a paent with recently diagnosed acute myelogenous leukemia and Metastac disease imaging features discussed above, granulocyte Neuroendocrine neoplasm sarcoma is the leading diagnosis. The paent's described symptoms of abdominal pain and bloang Discussion are likely secondary to duodenal extrinsic compression. Pancreac masses are relavely common in The paent underwent a CT guided biopsy and the abdominal imaging. The most common eologies are ssue samples demonstrated an unusual populaon of pancreac adenocarcinoma and pancreas, which lymphorecular cell elements and patchy atypical may simulate a discrete pancreac mass when focal. lymphoid infiltrates. In order to fully characterize Metastac disease and neuroendocrine tumors are these neoplasc cells, specific immunohistochemical less common. Addional rare masses, such as techniques (such as myeloperoxidase and myeloid granulocyte sarcoma, should be considered in unique associated angens) are required to differenate clinical sengs. Having a basic understanding of the granulocyte sarcoma from malignant lymphoma, imaging manifestaons of these processes will assist in which may otherwise appear similar on pathologic suggesng the correct diagnosis and guiding evaluaon.2,6,7 management and appropriate therapy.

Adenocarcinoma. Granulocyte sarcoma. Adenocarcinoma is the most common primary Granulocyte sarcoma (GS) is also known as myeloid 1 neoplasm of the pancreas and most commonly sarcoma, chloroma, and myeloblastoma. These involves the pancreac head. This enty on CT tumors are composed of extramedullary immature 1 presents as a solid mass. Adenocarcinoma usually myeloid cells. This was inially described by Burns in produces significant mass effect, resulng in dilataon 1811 with King in 1853 using the term chloroma of the and pancreac duct (the (because of the associated gross pathologic green double duct sign). It is not the favored diagnosis in appearance) and Rappaport using the term 1,2 this case given the presence of splenomegaly and granulocyc sarcoma in 1966. Dock made the 2 absence of biliary ductal dilataon. associaon of leukemia with GS. The lesions have been described throughout the body.1‐4 GS is most commonly seen with acute myelogenous Pancreas. leukemia (AML) and less commonly with chronic Pancreas has may occasionally be myelogenous leukemia (CML) or other indisnguishable from a discrete pancreac mass.8‐9 2 myeloproliferave disorders. These lesions typically Focal pancreas involving the head, "groove occur as a manifestaon of leukemia or may occur as a pancreas," may appear mass‐like and is usually sign of AML in a non‐leukemic paent and are interposed between the duodenum and the pancreac associated with a blast crisis or leukemic head.9 Acute inflammaon of the pancreas, diffuse or 3 transformaon. Autopsy series suggest a prevalence focal, classically demonstrates peri‐pancreac fat

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Case Report, Saenz stranding. Paents will also have elevated amylase References and lipase, which were normal in this paent. Chronic pancreas may have normal laboratory values but 1. Servin‐Abad L, Caldera H, Cardenas R, Casillas J. Granulocyc oen demonstrates parenchymal atrophy, sarcoma of the pancreas. A report of one case and review of calcificaons, and ductal enlargement.8 the literature. Acta Haematol 2003;110(4):188‐92. 2. Ravandi‐Kashani F, Estey E, Cortes J, Medeiros LJ, Giles FJ. Granulocyc sarcoma of the pancreas: a report of two cases Metastac disease. and literature review. Clin Lab Haematol 1999 Jun;21(3):219‐ 24. Primary neoplasms prone to pancreac metastases 3. Choi EK, Ha HK, Park SH, et al. Granulocyc Sarcoma of include lung, breast, gastrointesnal tract, renal cell, Bowel: CT Findings. Radiology 2007; 243:752–759. melanoma, lymphoma, and osteosarcoma.9 4. Nishida H, Kinoshita T, Yashiro N, et al. MR findings of Metastac involvement is always a consideraon granulocyc sarcoma of the breasts. BJR 2006;79: e112–15. when a solid lesion is present in a visceral organ. 5. Byrd JC, Edenfield WJ, Shields DS. Extramedullary myeloid cell Typically, metastac disease involves mulple organs tumors in acute nonlymphocyc leukemia: A clinical review. J with a variable appearance. Solitary pancreac Clin Oncol 1995;13:1800–1816. metastac involvement may be seen with metastac 6. Paydas S, Zorludemir S, Ergin M. Granulocyc sarcoma: 32 disease from renal cell, lymphoma, and melanoma.9 cases review of the literature. Leukemia and Lymphoma 2006; 47(12):2527‐41.

7. Chen J, Yanuck RR, Abbondanzo SL, et al. c‐kit (CD 117) Neuroendocrine neoplasms. reacvity in extramedullary myeloid tumor/granulocyc Neuroendocrine neoplasms are pancreac islet cell sarcoma. Arch Pathol Lab Med 2001; 125:1448‐52. tumors (ICT) which produce and secrete hormones.10 8. Kim T, Murakami T, Takamura M, et al. Pancreac Mass Due to Chronic Pancreas: Correlaon of CT and MR Imaging Funconing, syndromic islet cell tumors of the Features with Pathologic Findings. AJR 2001;177: 367–371. pancreas are typically less than three cenmeters in 9. To’o KJ, Raman SS, Yu NC, et al. Pancreac and size, avidly enhance, and have disncve hormonally Peripancreac Diseases Mimicking Primary Pancreac 10 related symptoms. In contrast, the non‐syndromic Neoplasia. RadioGraphics 2005; 25:949–965. ICTs are usually larger than five cenmeters and 10. Horton KM, Hruban RH, Yeo C, et al. Mul–Detector Row CT hypoaenuated in appearance due to their necroc, of Pancreac Islet Cell Tumors. RadioGraphics 2006; 26:453– cysc nature.10 464.

Diagnosis

Granulocyte Sarcoma of the Pancreas

Summary

In conclusion, it is important to consider granulocyte sarcoma when confronted with a pancreac mass with associated abdominal adenopathy and splenomegaly in a paent with a known history of AML, especially in the absence of biliary ductal dilataon. Although rare, recognizing this diagnosis as a disnct possibility may assist the pathologist in making the correct diagnosis on biopsy specimens and facilitate appropriate chemotherapy treatment with improvement or resoluon of tumor burden.

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Sharon Kreuer, D.O.

Department of Diagnosc Radiology, Botsford Hospital, Farmington Hills, MI

Acute Necrozing Pancreas.

This axial CT image with oral and intravenous contrast demonstrates a fluid collecon containing moled air occupying the pancreac body and tail with extensive peripancreac fat stranding. Classically, necrozing pancreas is characterized by a diminished or lack of parenchymal enhancement on IV contrast‐enhanced CT. When evaluang necrozing pancreas, it is important to determine the extent of necrosis and to differenate this enty from a pancreac abscess or infected pseudocyst. The extent of necrosis can be quanfied either by using the percent of gland involvement or the anatomic secons involved. Addionally, the Balthazar computed tomography severity index (CTSI), an imaging prognosc index, can be used to assess morbidity and mortality. Secondary infecon of necroc ssue is a recognized sequela in necrozing pancreas. Differenang sterile necrosis from abscess or infected pseudocyst is difficult, and in some cases impossible. Therefore, CT or US‐guided ssue sampling may be necessary. Secondary infecon in this unfortunate paent with necrozing pancreas and high CTSI was confirmed upon CT‐guided aspiraon.

J Am Osteopath Coll Radiol 2012; Vol. 1, Issue 4 Page 41

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Mahew R. Tommack, D.O.

Department of Diagnosc Radiology, Botsford Hospital, Farmington Hills, MI

Pneumatosis Intesnalis With Evidence of Portal Venous Gas.

This single axial CT image with oral and intravenous contrast demonstrates portal venous gas in the le lobe of the liver, air in the main portal vein, and air in the wall of the splenic flexure. Pneumatosis intesnalis is a “can’t miss” finding in radiology. Although there are benign causes of this enty, it can be associated with life threatening pathology, such as bowel necrosis. Bowel necrosis is caused by bowel ischemia due to an interrupon of the blood supply. Common eologies include emboli, thrombosis, vasoconstricon, stenosis, and closed‐loop obstrucon. This may also be seen in sepsis, typhlis, or in pediatric cases of necrozing enterocolis. Radiographic findings include intramural gas, commonly seen along the non‐dependent poron of bowel. As bowel ischemia ensues, linear streaks of air may be found within the mesenteric veins and eventually in the portal venous system, as in this case. Portal venous gas within the liver may be differenated from pneumobilia by its locaon along the periphery of the liver, as opposed to pneumobilia which is more centrally located. When bowel necrosis is the causave factor of pneumatosis intesnalis, other findings such as bowel wall thickening, inflammatory changes, bowel dilataon, and free fluid may be seen. These paents are generally crically ill with elevated lacc acid levels and a metabolic acidosis. Addional causes of pneumatosis intesnalis include disrupon of the bowel mucosa from a recent procedure, pepc ulcers, or inflammatory bowel disease; increased permeability of bowel mucosa secondary to immunosuppression (e.g. AIDS, chemotherapy, and immunosuppressive therapy); and a variety of pulmonary condions, such as COPD and asthma, which may allow air to dissect through the bronchopulmonary intersum and into the bowel wall.

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Reehan M. Ali, D.O., and Daniel J. Cranford, D.O.

Department of Diagnosc Radiology, Botsford Hospital, Farmington Hills, MI

Portal Vein Thrombosis.

What are the common causes and serious complicaons of this condion? This single coronal reformaed CT image with oral and intravenous contrast demonstrates a filling defect in the main portal vein, consistent with portal venous thrombosis (PVT). Paents with PVT most oen present with nonspecific abdominal pain; fever, , and weight loss are less common clinical presentaons. PVT may also be an incidental finding, especially in cases of chronic thrombosis. Typical causes of PVT include hypercoagulable states, cirrhosis, inflammatory condions such as pancreas, and invasion or compression by tumor. On unenhanced CT, thrombus typically appears hyperdense. On contrast‐enhanced studies, bland thrombus presents as a hypodense filling defect, while tumor thrombus may demonstrate enhancement. Non‐visualizaon of the portal vein is also suggesve of the diagnosis. In chronic cases, collateral veins develop in the porta hepas, which is referred to as cavernous transformaon. On US, PVT has a variable appearance. Color Doppler images are instrumental in confirming suspected thrombus seen on gray scale images by demonstrang absence of flow within the involved segment (some flow may be seen within tumor thrombus). Color Doppler may also demonstrate reversal of flow within the portal vein in the opposite direcon of the hepac artery, termed hepatofugal flow. PVT leads to and associated sequelae, to include varices, splenomegaly, and ascites, which may be difficult to manage. More concerning complicaons include rupture of , hepac infarcon, and in some instances, bowel infarcon from mesenteric thrombosis.

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