JBR 2012-4 by office

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WETTEREN 1

P 702083

Volume 95 Page 191-278 July-August

Bimonthly

–

2012

DIAGNOSTIC AND INTERVENTIONAL IMAGING, RELATED IMAGING SCIENCES, AND CONTINUING EDUCATION

ORGANE DE LA SOCIETE ROYALE BELGE DE RADIOLOGIE (SRBR) ORGAAN VAN DE KONINKLIJKE BELGISCHE VERENIGING VOOR RADIOLOGIE (KBVR)

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Subscribers’ information The JBR-BTR is published 6 times a year. Subscription of members of the Belgian Society of Radiology are included in membership dues and are handled by the Society. Non-members’ subscriptions are available from the ARSMB-KVBMG. The rate is valid to date and can be amended without notice according to fluctuation of printing and material costs. Annual subscriptions or single issue orders should be made promptly. The publishers cannot guarantee supply of back issues. Change of address must be notified 60 days in advance. RATES: Annual Belgium 150 € Other Countries 175 € All amounts are net and include postal and handling charges.

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You are kindly invited to address all your correspondence to Mrs A. Hirsch and execute all payments to ARSMBKVBMG (see below).

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JBR-BTR ♦ 95/4 ♦ 2012 Journal Belge de ♦ Belgisch Tijdschrift voor ♦ RADIOLOGIE

Founded in 1907 A bimonthly journal devoted to diagnostic and interventional imaging, related imaging sciences, and continuing education Contents

Hernias of the greater omentum through the antero-superior abdominal wall: an extensive pictorial MDCT review with emphasis on typical anatomic landmarks. A pictorial essay B. Coulier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191 The relation between pelvic varicose veins and lower extremity venous insufficiency in women with chronic pelvic pain A. Bora, S. Avcu, H. Arslan, E. Adali, M.D. Bulut . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215 Intramyocardial paravalvular abscess after aortic valve replacement B. Lutin, Y. Van Belleghem, D. Devos . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 222 Left vein of Labbé thrombosis associated with ipsilateral dural sinus thrombosis: non-enhanced CT and contrast-enhanced CT (CTV) findings D.I. Styblo-Sramek, G. De Temmerman, B.M. Verbist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226 The association of intramammarian arterial calcifications detected on mammography with coronary artery disease and its risk factors B. Hekimoglu, B. Demirler Simsir, E. Ozturk, C. Yucesoy, R. Akdemir . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229 A rare tumor mimicking breast carcinoma A.S. Celebi, G. Toksoy, A. Ozel, K.C. Caliskan, F. Kabukcuoglu . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235 GI tract wall visualization and distension during abdominal and pelvic multidetector CT with a neutral barium sulphate suspension: comparison with positive barium sulphate suspension and with water M.R. Oliva, S.M. Erturk, T. Ichikawa, T. Rocha, P.R. Ros, S.G. Silverman, K.J. Mortele . . . . . . . . . . . . . . . . . . . . . 237 Milwaukee shoulder syndrome. L. Dewachter, P. Aerts, I. Crevits, R. De Man . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 243 Erdheim-Chester disease detected with 99MTC MDP bone SPECT/CT G. Ceulemans, M. Keyaerts, L. Verbruggen, A. Hoorens, C. Boulet, D. Verdries, M. De Maeseneer, B. Ilsen, H. Everaert . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245 Single left coronary artery with the right coronary artery arising from the mid-portion of the left anterior descending artery. Diagnosis with MDCT. P. Mailleux, Th. Muller . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 249 Double contrast percutaneous transhepatic cholangiographic CT in patients with obstructive jaundice: an initial experience of 7 cases. C.L. Wang, Q. Shi, X.J. Xiang, Z.Z. Chen, Z.D. Yuan, Q.H. Deng, H.Y. Zhou, X.X. Ren, L. Cheng, Y.X.J. Wang . 251 Combination of partial situs inversus, polysplenia and annular pancreas with duodenal obstruction and intestinal malrotation Y. Ben Ahmed, S. Ghorbel, T. Chouikh, F. Nouira, H. Louati, A. Charieg, B. Chaouachi . . . . . . . . . . . . . . . . . . . . 257 Managing coronary artery vein bypass graft stump pseudoaneurysm: a novel approach V. Rachapalli, R. Evans, D. Roberts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261 Chronic recurrent multifocal osteomyelitis mimicking osteoid osteoma Z. Jibri, M. Sah, R. Mansour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263 Inflammatory myofibroblastic tumor of the pancreatic head L. Lacoste, Ch. Galant, J.F. Gigot, B. Lacoste, L. Annet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267 CONTINUING EDUCATION MRI of myelitis J. Hodel, O. Outteryck, P. Jissendi, M. Zins, X. Leclerc, J.P. Pruvo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 270

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In Memoriam: Prof. emeritus P. Bodart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277 Forthcoming Courses and Meetings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Instructions to Authors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Subscribers information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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Advertising index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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The terms used for indexation of subjects were developed by the Radiological Society of North America (RSNA) over a period of years. Their use here is by permission of the RSNA. The terms may not be used in any other index, print or electronic, except by specific permission of RSNA. ◆◆ Indexed in Index Medicus and in Zentralblatt Radiologie. Evaluated for Medline User, EMBASE and CANCERNET. Abstracted in Excerpta Medica Journals. ◆

MR Angiography with MultiHance ® :

detection of significant steno-occlusive disease of the abdominal or peripheral arteries • MultiHance® is now also indicated for Contrast-enhanced MR-angiography where it improves the diagnostic accuracy for detecting clinically significant steno-occlusive vascular disease in patients with suspected or known vascular disease of the abdominal or peripheral arteries.(1)

MH_MRA_3-03-08ADV

• The recommended dose of MultiHance® injection in adult patients is 0.1 mmol/kg body weight. This corresponds to 0.2 mL/kg of the 0.5 M solution.(1)

Reference: 1. Multihance Spc Please consult locally approved information.

1. NAAM VAN HET GENEESMIDDEL: MultiHance, 0.5 M oplossing voor injectie. 2. KWALITATIEVE EN KWANTITATIEVE SAMENSTELLING: 1 ml oplossing voor injectie bevat: 334 mg gadobeenzuur (0,5 M) als het dimeglumine-zout [gadobeendimeglumine 529 mg = gadobeenzuur 334 mg + meglumine 195 mg]. Voor hulpstoffen, zie 6.1. 3. FARMACEUTISCHE VORM: Oplossing voor injectie. Heldere waterige oplossing, afgevuld in kleurloze glazen flacons. Osmolaliteit bij 37 ºC: 1,97 osmol/kg. Viscositeit bij 37 ºC: 5,3 mPa.s. 4. KLINISCHE GEGEVENS: Therapeutische indicaties: Dit geneesmiddel is uitsluitend bestemd voor diagnostisch gebruik. MultiHance is een paramagnetische contrastvloeistof die wordt gebruikt voor de magnetische resonantie tomografie (MRI) geïndiceerd voor: MRI van de lever voor de detectie van focale leverlaesies bij patiënten met bekende of verdachte primaire leverkanker (b.v. hepatocellulair carcinoom) of metastasen. MRI van de hersenen en het ruggenmerg, waar het de detectie van laesies verbetert en aanvullende diagnostische informatie kan geven op de informatie uit de niet contrast-versterkte MRI. Contrastversterkte MR-angiografie (MRA) bij patiënten met verdachte of bekende vasculaire ziekten van de abdominale of perifere arteriën. Dosering en wijze van toediening: MRI van de lever: de aanbevolen dosis MultiHance bij volwassenen bedraagt 0,05 mmol/kg lichaamsgewicht, hetgeen overeenkomt met 0,1 ml/kg van de 0,5 M oplossing. MRI van de hersenen en het ruggenmerg: de aanbevolen dosis MultiHance bij volwassenen is 0,1 mmol/kg lichaamsgewicht hetgeen overeenkomt met 0,2 ml/kg van de 0,5 M oplossing. MRA: de aanbevolen dosis MultiHance bij volwassenen is 0,1 mmol/kg lichaamsgewicht hetgeen overeenkomt met 0,2 ml/kg van de 0,5 M oplossing. MultiHance moet onmiddellijk voor het gebruik in de injectiespuit worden opgezogen en mag niet worden verdund. Eventuele ongebruikte restanten contrastvloeistof moeten worden vernietigd, en mogen niet worden gebruikt voor ander MRI onderzoek. Om de mogelijke risico’s van extravasatie van MultiHance in het spierweefsel te voorkomen dient men erop toe te zien dat de i.v. naald of canule zorgvuldig in de vena wordt aangebracht. Lever en hersenen en ruggenmerg: de oplossing dient intraveneus te worden toegediend als bolus of als langzame injectie (10 ml/min.). MRA: de oplossing dient intraveneus als een bolus injectie te worden toegediend, handmatig of gebruikmakend van een automatisch injecteersysteem. Na de injectie dient een spoeling met fysiologische zoutoplossing plaats te vinden. Post-contrast tomogrammen acquisitie: Lever

Dynamische tomografie:

Onmiddellijk na een bolus injectie.

Vertraagde tomografie:

Tussen de 40 en 120 minuten na de injectie, afhankelijk van de individuele tomografische behoefte.

1. DENOMINATION: MultiHance 0,5 mmol/ml solution injectable. 2. COMPOSITION QUALITATIVE ET QUANTITATIVE: MultiHance 0,5 mmol/ml solution injectable. COMPOSITION QUALITATIVE ET QUANTITATIVE : 1 mL de solution contient : acide gadobénique 334 mg (0,5 M) sous forme de sel de diméglumine. [529 mg de gadobénate de diméglumine = 334 mg d’acide gadobénique + 195 mg de dimglumine]. Pour les excipients, cf. 6.1. 3. FORME PHARMACEUTIQUE: Solution injectable. Solution aqueuse limpide, incolore, remplie dans des flacons de verre incolore. Osmolalité à 37°C : 1,970 Osmol/kg. Viscosité à 37°C : 5,3 mPa.s. 4. DONNEES CLINIQUES: Indications thérapeutiques: Ce médicament est à usage diagnostique uniquement. Produit de contraste paramagnétique utilisé dans l’imagerie par résonance magnétique (IRM) et indiqué dans : IRM du foie pour la détection des lésions hépatiques lorsqu’un cancer hépatique secondaire ou primitif (carcinome hépatocellulaire) est suspecté ou connu. IRM du cerveau et de la moelle épinière où il améliore la détection des lésions et apporte des informations diagnostiques supplémentaires comparativement à une IRM sans produit de contraste. Angiographie par résonance magnétique (ARM) où il améliore l’exactitude diagnostique pour la détection de la maladie vasculaire sténo-occlusive cliniquement significative lorsqu’une pathologie vasculaire des artères abdominales ou périphériques est suspectée ou connue. Posologie et mode d’administration: IRM du foie: La dose recommandée chez l’adulte est de 0,05 mmol/kg de poids corporel, soit 0,1 ml/kg de la solution 0,5 M. IRM du système nerveux central: La dose recommandée chez l’adulte est de 0,1 mmol/kg de poids corporel, soit 0,2 ml/kg de la solution 0,5 M. ARM: La dose recommandée chez l’adulte est de 0,1 mmol/kg de poids corporel, soit 0,2 ml/kg de la solution 0,5 M. MultiHance doit être introduit dans la seringue immédiatement avant l’injection et ne doit pas être dilué. Tout reliquat éventuel doit être jeté et ne doit pas être utilisé pour d'autres examens IRM. Pour diminuer le risque d’extravasation de MultiHance dans les tissus mous environnants, il est conseillé de s’assurer de la bonne disposition de l’aiguille ou de la canule dans la veine. Foie et système nerveux central : le produit doit être administré par voie intraveineuse soit en bolus soit en injection lente (10 mL/min). ARM: le produit doit être administré par voie intraveineuse en bolus, soit manuellement soit à l’aide d’un injecteur automatique. L’injection doit être suivie d’un bolus de chlorure de sodium à 0,9%. Acquisition des images post-contraste: Foie

Imagerie dynamique

Immédiatement après l’injection en bolus

Imagerie retardée

Entre 40 et 120 minutes après l’injection (IRM retardée), en fonction du type d’imagerie nécessaire

Hersenen en ruggenmerg

Tot 60 minuten na toediening.

Système nerveux central

Jusqu’à 60 minutes après administration

MRA

Onmiddellijk na toediening, met scan vertraging die op basis van de testbolus of automatische bolus detectie techniek wordt berekend.Indien een automatische contrastdetectie puls-sequentie niet wordt gebruikt voor bolus timing, dan dient een test bolus injectie <2 ml van de oplossing gebruikt te worden om de geschikte scan vertraging te berekenen.

ARM

Immédiatement après l’administration, avec un délai d’acquisition calculé sur la base du bolus test ou par la technique de détection automatique du bolus. Si la détection automatique du contraste en séquence pulsée n’est pas utilisée, alors l’injection d’un bolus test de 2 mL de produit au maximum devra être réalisée pour calculer le timing d’acquisition adéquat.

De veiligheid en de werkzaamheid van MultiHance zijn niet vastgesteld bij patiënten beneden 18 jaar. Het gebruik van MultiHance bij deze patiëntengroep wordt derhalve niet aanbevolen. Contra-indicaties: MultiHance dient niet te worden toegepast bij patiënten met een overgevoeligheid voor één van de bestanddelen. MultiHance mag eveneens niet worden toegepast bij patiënten die eerder allergische reacties of andere bijwerkingen ondervonden ten gevolge van andere gadoliniumchelaten. 5. HOUDER VAN DE VERGUNNING VOOR HET IN DE HANDEL BRENGEN: Bracco Imaging Deutschland GmbH, Max-Stromeyer-Straße 116, 78467 Konstanz, Duitsland. 6. NUMMER VAN DE VERGUNNING VOOR HET IN DE HANDEL BRENGEN: MultiHance 5 ml: BE199963, MultiHance 10 ml: BE199972, MultiHance 15 ml: BE19998, MultiHance 20 ml: BE199997. 7. DATUM VAN EERSTE VERLENING VAN DE VERGUNNING/HERNIEUWING VAN DE VERGUNNING: Datum eerste verlening van de vergunning: 22 juli 1997. Datum laatste renewal: 21 juli 2007. 8. DATUM VAN HERZIENING VAN DE TEKST: Augustus 2008. Goedkeuringsdatum: 09/2008. 9. AFLEVERINGSWIJZE: Geneesmiddel op medisch voorschrift.

La sécurité d’emploi et l’efficacité de MultiHance n’ont pas été établies chez les sujets de moins de 18 ans. Par conséquent, l’utilisation de MultiHance dans cette population n’est pas recommandée. Contre-indications: MultiHance est contre-indiqué chez les patients présentant une hypersensibilité à l’un de ses constituants. MultiHance ne doit pas être utilisé chez les patients ayant des antécédents d’allergie ou d’effet indésirable liés à d’autres chélates de gadolinium. 5. TITULAIRE DE L’AUTORISATION DE LA MISE SUR LE MARCHE: Bracco Imaging Deutschland GmbH Max-Stromeyer-Straße 116, 78467 Konstanz Allemagne. 6. NUMERO(S) D’AUTORISATION DE MISE SUR LE MARCHE: MultiHance 5 ml: BE199963, MultiHance 10 ml: BE199972, MultiHance 15 ml: BE199981, MultiHance 20 ml: BE199997. 7. DATE DE PREMIERE AUTORISATION/DE RENOUVELLEMENT DE L’AUTORISATION: Date de première autorisation: 22 juillet 1997. Date de dernier renouvellement: 21 juillet 2007. 8. DATE DE MISE A JOUR DU TEXTE: Août 2008. Date d’approbation: 09/2008. 9. STATUT LEGAL DE DELIVRANCE: Médicament soumis à préscription médicale.

www.bracco.com

02-voorblz-12-6_Opmaak 1 21/08/12 13:06 Pagina 2

Editor: J. Pringot

Royal Belgian Society of Radiology: Http://www.rbrs.org

Managing Editor: P. Seynaeve

President: J.F. De Wispelaere Vice-Presidents: R. Hermans, D. Henroteaux

Editorial Board: B. Appel, F. Avni, P. Beeckman, L. Breysem,N. Buls, P. Clapuyt, B. Coulier, B. Daenen, E. Danse,H. Degryse, P. Demaerel, B. Ghaye, J. Gielen, P. Habibollahi, N. Hottat, M. Laureys, F. Lecouvet, M. Lemmerling, B. Lubicz, J.F. Monville, T. Mulkens, J.F. Nisolle, B. Op de Beeck, R. Oyen, S. Pans, V.P. Parashar (USA), P. Parizel, P. Peene, H. Rigauts, N. Sadeghi, S. Sintzoff Jr, M. Smet, A. Snoeckx, J. Struyven, H. Thierens, P. Van Dyck, F. Vanhoenacker, Ph. Van Hover, J. Verschakelen, K. Verstraete.

Past-President: B. Desprechins General Secretaries: M. Lemort, J. Verschakelen Meeting Secretaries: M. Spinhoven, Y. Lefebvre Treasurers: D. Brisbois, A. Van Steen Coordinators of continuing education: Ph. Clapuyt, G. Villeirs Coordinators of professional defence: C. Delcour, D. Bielen Webmasters: J. de Mey, J. Struyven

Sections of the Royal Belgian Radiological Society (SRBR-KBVR): Abdominal and digestive imaging

B. Op de Beeck, E. Danse

Bone and joints

P. Van Dyck, J.F. Nisolle

Breast imaging

C. Van der Merckt, A. Van Steen

Cardiac imaging

R. Salgado, O. Ghekière

Cardiovascular and interventional radiology

G. Maleux, M. Laureys

Chest radiology

B. Ghaye, W. De Wever

Head and neck radiology

J. Widelec, R. Hermans

Neuroradiology

P. Demaerel, N. Sadeghi

Pediatric radiology

B. Desprechins, L. Rausin

For addresses and particulars, see website at http://www.rbrs.org

Instructions to authors The purpose of The Belgian Journal of Radiology is the publication of articles dealing with diagnostic radiology and related imaging techniques, therapeutic radiology, allied sciences and continuing education. All — new and revised — manuscripts and correspondence should be addressed to JBR-BTR Edito rial Office, Avenue W. Churchill 11/30, B-1180 Bruxelles, tel.: 02-374 25 55, fax: 32-2-374 96 28. Please note that the following instructions are based on the “Uniform Requirements for manuscripts Submitted to Biomedical Journals” adopted by the International Committee of Medical Journal Editors (Radiology, 1980,135: 239-243). It should however be noted that presentation modifications may be introduced by the Editorial Office in order to conform with the JBR-BTR personal style. Authors should specify to which of the following headings their manuscript is intended: Original Article, Review Article, Case Report, Pictorial Essay, Continuing Education, Technical Note, Book Review, Opinion, Letter to the Editor, Comment, Meeting News, in Memoriam, News. Authors should consider the following remarks and submit their manuscripts accordingly. All articles must contain substantive and specific scientific material. – Original articles are articles dealing with one specific area of Radiology or allied science related through the personal experience of the author. – Review articles are special articles reporting the experience of the author considered in

–

the general perspective of the literature over the topic. Case reports are short descriptions of a particular case providing a message directly linked to an individuel patient investigated. No more than one case should be described in detail and clinical description should be kept to a minimum. Case reports should invest the usual headings of articles but should focus on the particular radiologic procedure that contributed to the diagnosis. References should be present, though limited in number. Tables and acknowledgements are usually omitted. Pictorial essays are articles presenting information through illustrations and legends. The presentation remarks stated in the paragraph dealing with case reports apply to pictorial essays. Continuing education articles are designed in accordance with the general guidelines for articles published in the JBR-BTR in particular they are divided into introduction, material and methods, results, discussion, references, and are provided with an abstract. However, papers addressing the continuing education may have only additionnally to their contents an introduction (stating the aim of the article and providing any background information useful to understand why the topic is relevant, and describing the subtopics covered by the study), references, and an abstract. Tables should be limited to a maximum of one table per 6 pages of manuscript. Illustrations should also be limited to a maximum of one illustration (1010 cm)

(possibly made up of different parts) per 3 pages of manuscript. All the material should be made available to the JBR- BTR editorial office (2 copies of the manuscript with 2 sets of illustrations) with the corresponding diskette though there will not be peer review. – Images in Clinical Radiology are short (max. 1 typed page) case reports designed to illustrate with max. 3 figures a specific entity. The report should not include abstract nor discussion but consist of a synthetic description of the clinical and radiological features as well as the final diagnosis and one major reference. Technical notes are short descriptions of a specific technique, procedure or equipment of interest to radiologists. Technical notes may originate from radiologists having experience of the item presented or from commercial firms (these should contact the Editorial Office to obtain specific guidelines for publication). The manuscript length should be inferior to 1 typed page, original language should be English, the manuscript may be accompanied by maximum 1 b/w figure, and include one major reference. – Book reviews should be limited to one typed page, mention full references of the book, including number of pages, of illustrations (when available), and price. The author should specify to whom the book is intended and give a personal appreciation. They will be published with the initial letters of the signature. (continued on JBR-BTR 2012, 95-2: p. VI)

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Gadovist®1.0

Gadobutrol

able l i a v A Now en* r d l i h C for

The Power of Contrast Gadovist 1.0 mmol/ml solution for injection in prefilled syringe/cartridge. QUALITATIVE AND QUANTITATIVE COMPOSITION: 1 ml of solution for injection contains 604.72 mg gadobutrol (equivalent to 1.0 mmol gadobutrol containing 157.25 mg gadolinium). 1 prefilled syringe with 5.0 ml contains 3023.6 mg gadobutrol, 1 prefilled syringe with 7.5 ml contains 4535.4 mg gadobutrol, 1 prefilled syringe with 10 ml contains 6047.2 mg gadobutrol, 1 prefilled syringe with 15 ml contains 9070.8 mg gadobutrol, 1 prefilled syringe with 20 ml contains 12094.4 mg gadobutrol. 1 cartridge with 15 ml contains 9070.8 mg gadobutrol, 1 cartridge with 20 ml contains 12094.4 mg gadobutrol, 1 cartridge with 30 ml contains 18141.6 mg gadobutrol. 1 ml contains 0.00056 mmol (equivalent to 0.013 mg) of sodium. PHARMACEUTICAL FORM: Solution for injection in prefilled syringe/cartridge. Clear, colourless to pale yellow liquid. Physico-chemical properties: Osmolality at 37°C: 1603Osm/kg H2O, Viscosity at 37°C: 4.96 mPa•s. CLINICAL PARTICULARS Therapeutic indications: This medicinal product is for diagnostic use only. Gadovist is indicated in adults, adolescents, and children aged 72 years and older for: Contrast enhancement in cranial and spinal magnetic resonance imaging (MRI). Contrast enhanced MRI of liver or kidneys in patients with high suspicion or evidence of having focal lesions to classify these lesions as benign or malignant. Contrast enhancement in magnetic resonance angiography (CE-MRA). Posology and method of administration: Gadovist should only be administered by healthcare professionals experienced in the field of clinical MRI practice. Method of administration: This medicinal product is for intravenous administration only. The dose required is administered intravenously as a bolus injection. Contrast-enhanced MRI can commence immediately afterwards (shortly after the injection depending on the pulse sequences used and the protocol for the examination). Optimal signal enhancement is observed during arterial first pass for CE-MRA and within a period of about 15 minutes after injection of Gadovist for CNS indications (time depending on type of lesion/tissue). T1 -weighted scanning sequences are particularly suitable for contrastenhanced examinations. Intravascular administration of contrast media should, if possible, be done with the patient lying down. After the administration, the patient should be kept under observation for at least half an hour, since experience shows that the majority of undesirable effects occur within this time. Instructions for use: This product is intended for single use only. This medicinal product should be visually inspected before use. Gadovist should not be used in case of severe discolouration, the occurrence of particulate matter or a defective container. Prefilled syringes: The prefilled syringe must be taken from the pack and prepared for the injection immediately before the administration. The tip cap should be removed from the prefilled syringe immediately before use. Cartridges: Administration of contrast media should be performed by qualified personnel with the appropriate procedures and equipment. Sterile technique must be used in all injections involving contrast media. The contrast medium must be administered by means of a MEDRAD Spectris® type injector. Instructions of the device manufacturer must be followed. Dosage: Adults: CNS indications: The recommended dose for adults is 0.1 mmol per kilogram body weight (mmol/ kg BW). This is equivalent to 0.1 ml/kg BW of the 1.0 M solution. If a strong clinical suspicion of a lesion persists despite an unremarkable MRI or when more accurate information might influence therapy of the patient, a further injection of up to 0.2 ml/ kg BW within 30 minutes of the first injection may be performed. CE-MRI of liver and kidneys: The recommended dose for adults is 0.1 mmol per kilogram body weight (mmol/kg BW). This is equivalent to 0.1 ml/kg BW of the 1.0 M solution. CE-MRA: Imaging of 1 field of view (FOV): 7.5 ml for body weight below 75 kg; 10 ml for body weight of 75 kg and higher (corresponding to 0.1-0.15 mmol/kg BW). Imaging of >1 field of view (FOV): 15 ml for body weight below 75 kg; 20 ml for body weight of 75 kg and higher (corresponding to 0.2-0.3 mmol/kg BW). Special Populations: Impaired renal function: Gadovist should only be used in patients with severe renal impairment (GFR < 30 ml/min/1.73m2) and in patients in the perioperative liver transplantation period after careful risk/benefit assessment and if the diagnostic information is essential and not available with non-contrast enhanced MRI. If it is necessary to use Gadovist, the dose should not exceed 0.1 mmol/kg body weight. More than one dose should not be used during a scan. Because of the lack of information on repeated administration, Gadovist injections should not be repeated unless the interval between injections is at least 7 days. Paediatric population: For children aged 2 years and older and for adolescents the recommended dose is 0.1 mmol Gadovist per kg body weight (equivalent to 0.1 ml Gadovist per kg body weight). Gadovist is not recommended for use in children below age 2 years due to a lack of data on efficacy and safety. Elderly (aged 65 years and above): No dosage adjustment is considered necessary. Caution should be exercised in elderly patients. Contraindications: Hypersensitivity to the active substance or to any of the excipients. Undesirable effects: The overall safety profile of Gadovist is based on data from more than 4,500 patients in clinical trials, and from post-marketing surveillance. The most frequently observed adverse drug reactions ( 0.5 %) in patients receiving Gadovist are headache, nausea, injection site reactions, dysgeusia and feeling hot. The most serious adverse drug reactions in patients receiving Gadovist are cardiac arrest, respiratory arrest and anaphylactoid shock. Delayed anaphylactoid reactions (hours later up to several days) have been rarely observed). Most of the undesirable effects were of mild to moderate intensity. The adverse drug reactions observed with Gadovist are represented in the table below. They are classified according to System Organ Class (MedDRA). The most appropriate MedDRA term is used to describe a certain reaction and its synonyms and related conditions. Adverse drug reactions from clinical trials are classified according to their frequencies. Frequency groupings are defined according to the following convention: common: 1/100 to < 1/10; uncommon: 1/1,000 to < 1/100; rare: 1/10,000 to < 1/1,000. The adverse drug reactions identified only during post-marketing surveillance, and for which a frequency could not be estimated, are listed under ‘not known’. Within each frequency grouping, undesirable effects are presented in order of decreasing seriousness. Table 1: Adverse drug reactions reported in clinical trials or during post-marketing surveillance in patients treated with Gadovist Frequency System Organ Class

Common

Uncommon

Immune system disorders

Nervous system disorders

Headache

Dizziness, Dysgeusia, Paresthesia

Cardiac disorders

Not known

Loss of consciousness, Convulsion, Parosmia Tachycardia, Palpitations

Respiratory, thoracic and mediastinal disorders Gastrointesti-nal disorders

Rare Hypersensitivity /anaphylactoid reaction (e.g. anaphylactoid shock§*, circulatory collapse§*, respiratory arrest§*, bronchospasm§, cyanosis§, oropharyngeal swelling§*, laryngeal oedema§, hypotension*, blood pressure increased§, chest pain§, urticaria, face oedema§, angioedema§, conjunctivitis§, eyelid oedema§, flushing, hyperhidrosis§, cough§, sneezing§, burning sensation§, pallor)

Cardiac arrest*

Dyspnoea* Nausea

Vomiting

Skin and subcutaneous tissue disorders

Erythema, Pruritus (including generalized pruritus), Rash (including generalized, macular, popular, pruritic rash)

General disorders and administration site conditions

Injection site reaction0, Feeling hot

Dry mouth Nephrogenic Systemic Fibrosis (NSF) Malaise, Feeling cold

L.BE.07.2012.0923

§ Hypersensitivity / anaphylactoid reactions identified only during post-marketing surveillance (frequency not known) * life-threatening and/or fatal cases have been reported; 0 Injection site reactions (various kinds) comprise the following terms: Injection site extravasation, injection site burning, injection site coldness, injection site warmth, injection site erythema or rash, injection site pain, injection site hematoma. Patients with an allergic disposition suffer more frequently than others from hypersensitivity reactions. Isolated cases of nephrogenic systemic fibrosis (NSF) have been reported with Gadovist. Available on medical prescription only. MARKETING AUTHORISATION HOLDER Bayer SA-NV , J.E. Mommaertslaan 14 1831 Diegem (Machelen). MARKETING AUTHORISATION NUMBER(S) Gadovist 1,0 mmol/ml, prefilled syringe 7,5 ml: BE266323 Gadovist 1,0 mmol/ml, prefilled syringe 10 ml: BE266332 Gadovist 1,0 mmol/ml, prefilled syringe 15 ml: BE221094 Gadovist 1,0 mmol/ml, prefilled syringe 20 ml: BE266341 Gadovist 1,0 mmol/ml, vial 15 ml: BE320686 Gadovist 1,0 mmol/ml vial 20 ml: BE320695 Gadovist 1,0 mmol/ml vial 30 ml: BE320704 DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION: 12 februari 2001 DATE OF REVISION OF THE TEXT: 01/2012 Date of approval: 05/2012

www.ri.bayer.be

* Gadovist® 1.0 is indicated in adults, adolescents, and children aged 2 years and older for CNS, liver and kidneys and for MR angiography.

GE Healthcare

At GE, we are committed to helping increase access to healthcare while improving its quality and lowering its cost. Just like physicians everywhere. So by investing in new innovations, we are empowering the world’s healthcare professionals to do what they do best: caring for patients around the world. Every day, doctors are bringing better health to more people — and GE Healthcare technologies are behind them.

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e l t a d Up e dica g in mimag in

Update in Abdominal and Urogenital Imaging Congress Centre Oud Sint-Jan Bruges, Belgium 6-8 September 2012

2012 ABDOMINAL & UROGENITAL

Organising Committee Bart Claikens (Ostend, Belgium) President Pablo R Ros (Cleveland, USA) Visiting-President Patrick Van Wettere (Ostend, Belgium) Vice-President

Faculty Members

Pablo R Ros (Cleveland, OH, USA) Carlo Bartolozzi (Pisa, Italy) Julia Fielding (Chapel Hill, NC, USA) Jurgen Fütterer (Nijmegen, the Netherlands) Bernd Hamm (Berlin, Germany) Koen Mortelé (Boston, MA, USA) Julien Puylaert (The Hague, the Netherlands) Richard Semelka (Chapel Hill, NC, USA) Thomas Vogl (Frankfurt, Germany)

Freddy Avni (Brussels, Belgium) Etienne Danse (Louvain-la-Neuve, Belgium) Filip Deckers (Antwerp, Belgium) Philippe Lefere (Roeselare, Belgium) Bart Op de Beeck (Antwerp, Belgium) Lieven Van Hoe (Aalst, Belgium) Dirk Vanbeckevoort(Leuven, Belgium) Filip Vanhoenhacker (Antwerp-Mechelen, Belgium) Geert Villeirs (Ghent, Belgium)

www.update-medical-imaging.be 15:11

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ANNOUNCEMENT and CALL FOR ABSTRACTS

3rd International CAA Conference

CEREBRAL AMYLOID ANGIOPATHY AND RELATED MICROANGIOPATHIES October 24-26, 2012 Leiden University Medical Center, Leiden, The Netherlands The goal of the conference is to bring together leading international experts in Î˛-amyloid metabolism, vascular biology, neuropathology, stroke genetics, brain imaging, and the clinical manifestations of cerebrovascular disease to present and discuss cutting-edge data in this rapidly developing field. A special focus will be moving the field towards clinical trials of candidate diseasemodifying treatments, in particular by establishing consensus on preclinical animal data and human biomarkers for CAA trials. Other topics of discussion will be early detection methods for presymptomatic CAA and the biological and clinical interactions between CAA and Alzheimerâ&#x20AC;&#x2122;s disease. The atmosphere for discussion is anticipated to be informal and lively, with ample opportunities for forming new collaborations and relationships within the growing CAA scientific and clinical communities.

Registration and information: Registration and information: www.boerhaavenascholing.nl www.boerhaavenascholing.nl Details: www.rbrs.org

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JBR–BTR, 2012, 95:

XII.

FORTHCOMING COURSES AND MEETINGS NATIONAL MEETINGS 06-08.09.12 UPDATE IN ABDOMINAL AND UROGENITAL IMAGING Bruges, Congress Centre Oud Sint-Jan Information: www.update-medical-imaging.be 17.09.12 RBRS – Neuroradiology Section Information: nsadeghi@ulb.ac.be 19-22.09.12 22ND ANNUAL MEETING MUSOC – MUSCULOSKELETAL ULTRASOUND SOCIETY Leuven Information: www.musoc.com 22.09.12 ACADEMISCHE ZITTING OVER MRI EN SPECTROSCOPIE VAN DE PROSTAAT Gent, UZ Information: geert.villeirs@Ugent.be

RBRS – Neuroradiology Section 17.09.12, 05.11.12 RBRS – Chest Radiology 20.11.12

11.10.12 PICC-LIJNEN: HOE, WAT, WAAROM? Leuven, Meeting Center 3 hoog Information: linda.meersman@uzleuven.be 11-13.10.12 HRCT TEACHING COURSE Leuven, Groot Begijnhof Information: www.everyoneweb.com/radiology 05.11.12 RBRS – Neuroradiology Section Information: nsadeghi@ulb.ac.be

20.11.12 RBRS - Chest Section Brussels, Cliniques Universitaires St Luc Information: benoit.ghaye@uclouvain.be 10-12.01.13 5TH LEUVEN COURSE ON EAR IMAGING Leuven, Huis van Chièvres Information: Monika.Philips@uzleuven.be 01-23.10.13 HRCT TEACHING COURSE Leuven, Groot Begijnhof Information: www.everyoneweb.com/radiology

10.11.12 LUNG CANCER IMAGING IN 2012: UPDATES AND INNOVATIONS Tervueren, Palais des colonies / Koloniënpaleis Organization: Dr B Ghaye, Pr E Coche Information: martine.vanwambeke@uclouvain.be

Miscellaneous 06-08.09.12, 19-22.09.12, 22.09.12, 11-13.10.12, 11.10.12, 19-20.10.12, 10.11.12, 10-12.01.13, 01-23.12.13

Detailed and real time information is available on RBRS website at www.rbrs.org

INTERNATIONAL MEETINGS DIPLOME INTERUNIVERSITAIRE D’IMAGERIE VASCULAIRE NON INVASIVE Année 2012-2013 Paris, France Info: veronique.rey@bct.aphp.fr

27-30.09.12 5TH IDKD INTENSIVE COURSE IN GREECE Diseases of the Chest and Heart Myconos, Greece Information: www.idkd.org

07.09.12 HEPATOCELLULAR CARCINOMA – DIAGNOSIS AND TREATMENT Amsterdam, The Netherlands Information: www.epgs.nl

19-23.10.12 60ÈMES JOURNEES FRANÇAISES DE RADIOLOGIE Paris, France Information: sfr@sfradiologie.org

12-15.09.12 39TH ANNUAL MEETING AND MUSCULOSKELETAL IMAGING COURSE: BASIC PRINCIPLES TO ADVANCED CONCEPTS Information: www.internationalskeletalsociety.com

24-26.10.12 CEREBRAL AMYLOID ANGIOPATHY AND RELATED MICROANGIOPATHIES Leiden, The Netherlands, Information: www.boerhaavenascholing.nl

15-19.09.12 CIRSE 2012 Lisbon, Portugal Information: www.cirse.org

25-27.10.12 ANNUAL MEETING EUROPEAN SOCIETY OF CARDIAC RADIOLOGY (ESCR) Barcelona, Spain Information: www.escr.org

20-23.09.12 36TH EUROPEAN SOCIETY OF NEURORADIOLOGY ANNUAL MEETING Edinburgh, Scotland Information: esnr2012@in-conference.org.uk

14-16.11.12 34EMES JOURNEES DE LA SOCIETE FRANCAISE DE SENOLOGIE ET DE PATHOLOGIE MAMMAIRE 2012 France, Paris Information: www.senologie.com

25-30.11.12 RSNA 2012 Chicago, USA Information: www.rsna.org 02-06.04.13 45TH IDKD 2013 DAVOS Musculoskeletal Diseases Davos, Switzerland Information: www.idkd.org 09-12.05.13 3RD IDKD INTENSIVE COURSE IN HONG KONG Diseases of the Chest and Heart Hong Kong, China Information: www.idkd.org

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HERNIAS OF THE GREATER OMENTUM THROUGH THE ANTERO-SUPERIOR ABDOMINAL WALL: AN EXTENSIVE PICTORIAL MDCT REVIEW WITH EMPHASIS ON TYPICAL ANATOMIC LANDMARKS. A PICTORIAL ESSAY* B. Coulier1 Thanks to its very high performances in term of spatial resolution, table speed and multiplanar reconstructions (MPR), 64-row MDCT today produces unrivalled high quality images of the entire abdominal wall (AW) during a single short breath hold. It appears thus particularly useful for the evaluation of AW hernias, allowing accurate identification of their contents, differentiation from other abdominal masses, planning of optimal surgical repair and detection of pre- or post-operative complications. The greater omentum (GO) is another structure that can also be clearly identified, localized and characterized with 64-row MDCT. The identification of its numerous vessels, which predominantly have a vertical course, is the essential key for its delineation. AW hernias implicating the GO are therefore exquisite situations that can also be optimally diagnosed by MDCT. The very high contrast provided by the mostly predominant fatty content of the GO offers a unique opportunity to clearly illustrate the classical anatomic landmarks of almost nearly each type of hernia of the antero-superior AW. The cases presented in this extensive pictorial review were collected in our department during a 5-year-period. Key-words: Omentum – Hernia.

Thanks to its very high performances in term of spatial resolution, table speed and multiplanar reconstructions (MPR) 64-row MDCT today produces unrivalled high quality images of the entire abdominal wall (AW) during a single short breath hold (1). 64-row MDCT appears thus particularly useful for the evaluation of AW hernias, allowing accurate identification of their contents, differentiation from other abdominal masses, planning of optimal surgical repair and detection of pre- or postoperative complications. The greater omentum (GO) is another structure that can also be clearly identified, localized and characterized with 64-row MDCT in all patients (2). The identification of its numerous vessels, which predominantly have a vertical course, is the essential key for its delineation. AW hernias implicating the GO are therefore exquisite situations that can be optimally diagnosed by MDCT. The GO is not only perfectly identified but the very high contrast provided by its mostly predominant fat content offers a unique opportunity to clearly identify, illustrate and finally remember the anatomic landmarks of nearly each type of hernia of the anterior and superior AW.

Discussion MDCT anatomy of the GO The GO is a large free-hanging apron arising from the gastric greater curvature (GGC), crossing the transverse colon and descending in front of the hollow viscera (2-3). After a distance that usually ranges from 14 to 36 cm, it turns superiorly on itself to drape over the transverse colon and extend to the retroperitoneal pancreas. These descending and ascending portions usually fuse to form a four layer fatty apron. A persisting space continuous with the lesser sac sometimes separates the two sets of layers. The GO is composed of a trabecular connective tissue framework that carries arteries, veins, lymphatics and fat pads. Its arterial supply is determined by the right and left gastroepiploic arteries receiving their blood supply from the celiac trunk, the left one by the lineal artery and the right, a stronger one, from the gastroduodenal artery. Both arteries pass tortuously along the GGC and decrease in diameter by giving off gastric and epiploic arteries. 5 to 13 epiploic arteries originate from the right gastroepiploic artery and only one main epiploic

From: 1. Department of Diagnostic Radiology, Clinique St Luc, Bouge (Namur) Belgium. Address for correspondence: Dr B. Coulier, M.D., Department of Diagnostic Radiology, Clinique St Luc, Rue St Luc 8, B-5004 Bouge (Namur) Belgium. E-mail: bcoulier@skynet.be * This pictorial review is respectfully and kindly dedicated to the memory of Professor Emeritus Pierre Bodart who was my Master of Radiology from 1983 to 1987 in the Cliniques Universitaires Saint-Luc (UCL), Brussels, Belgium.

artery emerges from the left. These vertical epiploic arteries descend mostly at right angles from the GGC and bifurcate close to the GO margin, where they eventually anastomose. The venous drainage parallels the arteries and empties into the portal system. The identification of this rich vascular network and particularly that of the essentially vertical epiploic vessels – particularly the veins which are generally twice as large as the arteries – constitutes the main landmark for current prompt identification of the GO during abdominal MDCT. These vessels may be clearly identified in 100% of patients (2). Because the GO represents the most superficial fatty intraperitoneal apron, its free edge can be easily identified during scrupulous up and down cine view analysis of the abdomen. It is found just at the level where the fatty omental apron abruptly disappears allowing the intestines to lie directly beneath the AW. The GO has considerable mobility and may move all around the peritoneal cavity. It functions as a visceral fixation and serves to shield an abnormality and limit its spread (3). However, it is also a common location for neoplastic intraperitoneal seeding and infectious processes because it is bathed in the peritoneal fluid (3). The GO has anatomic variations (2). Some of these are related to sex and first concern the length and shape (2). The average length of the GO is very statistically significantly longer in females than in males, particularly his left portion.

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Fig. 1. — Coronal (A, B), axial (C) MPR views and selected volume rendering view (d) of a very large hiatal hernia (HH). A 180° vertical volvulus of the stomach (white star) induces a secondary incarceration of a major portion of the GO. It is situated in front of the inverted antrum (black stars). The main gastroepiploic arcade is projected in the upper pole of the hernia (white arrow) and the right and left main lateral epiploic veins are clearly seen penetrating the neck of the hernia (black arrows).

As a result the GO could be expected being more frequently implicated in hypogastric or inguinal hernias in females. Because of its mobility, length and the fact that it is the most superficial intraperitoneal structure the GO also represents an organ being massively exposed to herniation through the AW. When a hernia pro-

duces, the GO is the statistically most exposed structure to protrude first and for this reason it also plays a fundamental protective role for the gut. Hiatal hernia (HH) The common sliding (type 1) and the less common paraesophageal (types 2, 3 and 4) HHs are caused by

a weakened or torn phrenoesophageal membrane (4). The GO is potentially commonly implicated in the paraesophageal types (particularly in the type 4) in which variable portions of the stomach herniate into the chest (the gastroesophageal junction classically remaining below the diaphragm). This situation predisposes to gastric volvulus or

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Fig. 2. — Chest plain film (A), coronal (B), axial (C, D), sagittal (E) MPR views and selected VR view (F) of a very large omental paraesophageal hiatal hernia (HH). The gastroesophageal junction remains under the diaphragm (black arrow). A large portion of the transverse colon herniates within the posterior mediastinum (white arrow) together with a major portion of the GO (white star). Small black arrows delineate the diaphragmatic ring. Epiploic veins are clearly seen penetrating within the hernia.

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Fig. 3. — Chest plain film (A), posterior coronal (B), axial (C) and anterior coronal (D) MPR views obtained in a 70 year old woman presenting with a major acquired diaphragmatic hernia (DH). The stomach and a great portion of the transverse portion and of the splenic flexure of the colon are herniated within the thorax through a 7 centimeter large diaphragmatic defect — black arrows on C) and dotted white line on D) -. Because anatomically inserted on these organs a major portion of the GO (white star) is concomitantly forced through the hernia constituting a major portion of the volume of the hernia.

torsion (5). Because it is firmly attached along the GGC, the GO is forced to follow the stomach into the thorax when a sufficiently great portion of its GGC migrates in the hernia (Fig. 1). In extensive cases the colon (especially its transverse portion) may secondarily – or primarily – (Fig. 2) accompany (6). Cases of iso-

lated paraesophageal intrathoracic herniations of the GO through the esophageal hiatus have also rarely been described (7-9). In these cases the differential diagnosis is that of mediastinal lipoma or liposarcoma. The identification of the herniating omental vessels represents the key of the diagnosis.

Non-hiatal diaphragmatic hernia (DH) Most DHs have a traumatic origin (10-11). Traumatic diaphragmatic rupture is reportedly seen in 0.8%5.8% of all blunt trauma cases, 2.5%5% of abdominal blunt traumas and 1.5% of thoracic blunt traumas (10).

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Fig. 4. — Axial (A), coronal (B), axial oblique (C), sagittal (F) MPR views and selective VR views (D, E) illustrating a rare case of right Morgagni-Larrey hernia (MH) of the GO (white star). Epiploic veins (white arrow) clearly protrude through a 25 × 33 mm right anterior paramedian diaphragmatic hiatus (C) to expand in the right cardiophrenic space. The ligamentum teres of the falciform ligament (black arrow) is forced through the hernia.

Most ruptures occur in the posterolateral area of the left diaphragm, which is structurally weak. The right diaphragm is congenitally stronger and may also be protected by the liver. A review article found left sided ruptures in 68.8% of patients, compared to right sided ones in only 24.2%, bilateral in 1.5%, pericardial in 0.9%, and unclassified in 4.9% (12). The diaphragm may also be altered by age and/or by previous surgery especially of the left upper quadrant. Although most DHs are diagnosed and successfully repaired at the time of initial injury, the correct diagnosis can often be delayed because blunt traumatic DH is relatively uncommon, and because patients may remain asymptomatic

– sometimes for an extremely long time – or display various nonspecific symptoms. Nevertheless the diaphragm doesn’t heal spontaneously and the diameter of the orifice will progressively increase allowing intrathoracic prolapse of larger amount of abdominal organs (11). Due to its great mobility and large anatomic insertion on the stomach the GO can largely prolapse within the hernia (Fig. 3). Morgagni hernia (MH) The anteromedial subcostosternal diaphragmatic MHs accounts for only 3% of all surgically treated diaphragmatic hernias (13-16). It produces through a defect described

by both Morgagni and Larrey that is a triangular space caused by a failure of fusion between the musculofibrotendinous elements of the diaphragm that originate from the xiphisternum and the costal margin and insert on the central tendon of the diaphragm (14). This potential space is referred to as the foramen of Morgagni or the space of Larrey. The internal mammary artery – with its associated vein and lymphatics – passes through this space, as it becomes the epigastric artery. Congenital MH often is considered as being only a pediatric condition. However there have been many case reports and small series of acquired MH involving adults. Nevertheless MH remains a rare entity among

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Fig. 5. — Volume rendering view (A, B), axial (C), sagittal (D) and coronal (E) MPR views of a very proximal painful incarcerated epigastric hernia EH (white star) situated just below the xyphoid process. A portion of the GO is incarcerated and the result is an upper attraction of the main gastroepiploic vein (white arrow). The herniation produces through a very tiny orifice of about 1 cm in diameter (black arrow) and the protrusion of the GO induces a displacement of the ligamentum teres of the falciform ligament (small black arrows). Within the hernia the peritoneal omental inflammatory fat appears surrounded by another sheet of fat constituted by properitoneal fat (black asterisks).

adults with a prevalence of only 0,17%, a not well established natural history, a clinical presentation which may be confusing and no definitive management strategies. 70% of the patients are women. MH is far most common on the right (90% of cases) despite protection of the liver (13, 16-17). The defect has classically a

greater transverse than anteroposterior diameter (18) (Fig. 4). Almost any peritoneal abdominal organs may be found within a MH (13, 17) but the GO alone (31%) or accompanied by the colon (29%) represents the most common contents. The stomach (15%), small bowel (11%) and liver (4%) may also be found

within the hernia sac (14). Those patients with a herniated stomach are considered potentially having serious symptoms when compared to others. Pregnancy, chronic cough, trauma, obesity, chronic constipation are common predisposing conditions cited in the literature (13, 16). Most MHs are usually asymptomatic

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Fig. 6. â&#x20AC;&#x201D; Sagittal (A) and coronal (B) MPR views and oblique volume rendering view (C) show two small superposed omental epigastric hernias (EH) (white arrows) producing through the linea alba in very obese female. The epiploic vessels are clearly identified.

and symptoms occur mainly in patients who have a hollow viscus included in the herniation (14, 16). In reality most hernias are discovered incidentally (19-21). Traditional teaching states that repair of MH is invariably indicated after diagnosis because the risk of incarceration or strangulation of abdominal organs. Even if the hernia sac appears to only contain the GO, repair is considered clearly indicated (13, 19, 22). Epigastric hernias (EH) EH is caused by a defect in the linea alba between the xiphoid process and the umbilicus (Fig. 5),

and it usually occurs just superior to the umbilicus (23-26). During cadaver studies, the linea alba has been found having a varying make-up: in 30% of cases it is constituted by the confluence of only one anterior and only one posterior rectus sheath layer; in 10% only one anterior and three posterior layers are concerned and finally in 60% of cases there are three anterior and three posterior layers that constitute the linea alba. Moreover the decussation that constitutes the linea alba has a low tensile strength with a low density of collagen fibers. This variability in the already generally weak fascia is undoubtedly one of the factors

determining spontaneous ventral hernias. EH occur in 3 to 5% of the population and are most likely to affect men 20 to 50 years of age. 20 to 30% of patients have multiples defects. Most patients are asymptomatic but the hernia may become incarcerated and painful. Generally, properitoneal fat, blood vessels or the GO (Fig. 6 & 7) protrude through the defect (27). Sometimes hollow viscera may also protrude especially in patients in which the GO has a prehepatic configuration (Fig. 8). Hernia producing in the linea alba below the umbilicus are hypogastric ventral hernias and are much less common (24).

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Fig. 7. — Axial (A) and sagittal (C) volume rendering views and coronal (B) and sagittal (D) MPR views illustrating a series of four superposed omental epigastric hernias producing through centrimetric orifices of the linea alba in a very obese female.

Umbilical hernia (UH) UHs are usually congenital and result from incomplete closure of the AW after ligation of the umbilical cord (15, 27). Closure of the umbili-

cal stump involves circumferential granulation tissue formation which results in fusion of skin, single fascial layer and peritoneum, a process leading to complete closure by 4 years of age in the majority of cases.

UHs that persist are usually small and rarely demonstrate incarceration. Acquired UHs – developing after the normal closure of the umbilical ring – account for 4% of all hernias

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C Fig. 8. — Sagittal (A) and coronal (B) MPR views illustrating another case of multiple epigastric hernias (EHs). In this case the multiple superposed EHs (white star) contain intestinal loops with a permanent risk of incarceration and occlusion. The GO is constitutionally permanently developed in a right supra and pre-hepatic position — a situation found in about 30% of males — and doesn’t play its classical midline protective role. A selected volume rendering view (C) confirms the prehepatic development of the GO (black arrows).

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Fig. 9. — : Sagittal (A) and axial (B) MPR views and volume rendering (C, D) views of an enormous umbilical hernia (UH) exclusively constituted by more than 50% of the GO: the GO is globally concentrated on the midline of the abdomen (white arrows) and massively herniates in the UH (white star).

and are more common in women (24, 27-28). They usually occur secondary to obesity (Fig. 9), multiple pregnancies, intraabdomianal masses, liver failure, and a weak abdominal wall (29). They may become large and strangulation is more common (Fig. 10). Rectus sheath hernia (RSH) Superior to the arcuate line are classically found the strong complete rectus sheaths, which are continuous structures housing the rectus muscle and the epigastric vessels (30). At this level the rectus sheath is classically composed by a central splitting of the aponeurosis of the internal

oblique muscle inclosing the rectus muscle itself (1). This aponeurotic complex is anteriorly covered by the aponeurosis of external oblique muscle and posteriorly by that of transverse abdominis muscle. Thoracic and intercostal perforating vessels can enter the posterior sheath only at the costal margin (25). As a rule spontaneous RSHs producing above the arcuate line appear exceedingly rare (Fig. 11). Only about 8 cases have been reported (30, 31). The pathophysiology of spontaneous RSH is not well understood. A combination of thinner posterior aponeurotic components and defects due to posterior perfo-

rating vessels or nerves (i.e., intercostal nerves and the transition of internal thoracic to superior epigastric arteries) could contribute to these rare interstitial RSH (26, 31). Linea arcuata hernia (LAH) LAH is a rather recently described and peculiar type of interstitial parietal hernia of the AW which consists of a generally asymptomatic ascending protrusion of intraperitoneal structures under the linea arcuata (LA) or arcuate line of Douglas (1, 32). In most cases this type of hernia appears fortuitously demonstrated during abdominal CT obtained for various other pathological conditions

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C Fig. 10. — Axial (A) and sagittal (B) MPR views illustrating a case of inflammatory necrotic umbilical hernia (black star). Volume rendering view (C) of the GO vasculature (black arrows) clearly demonstrates the convergence and incarceration of epiploic vessels (white arrow).

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Fig. 11. — Rectus sheath hernia (RSH): sagittal (A), axial oblique (B) and coronal oblique (D) MPR views of an exceptionally rare right interstitial hernia of the right portion GO (white star) through a defect (black arrow) of the posterior aponeurosis (white arrow) of the rectus muscle (black star) above the level of the arcuate line. The orifice of the hernia is in oval shape. Volume rendering (C) perfectly identify the GO thanks to its typical epiploic vessels (small white stars).

(Fig. 12). Three grades (G1 to G3) of LAH have been described (1, 32): G1 is a single delineation of the LA due to a minimal bulging of intraperitoneal fat (generally the GO), G2 represents a minimal but more substantial real herniation of fat and/or intestinal loops under the LA and G3

represents clearly prominent hernias of abdominal structures (essentially the GO and/or intestinal loops) (Fig. 12). G2 and G3 have an combin ed incidence of only 1,42% and most cases remain asymptomatic (1). There is a major male prevalence (M:F sex ratio 12,5:1) and patients

older than 71 years represent 76% of patients (1). Up to now, only 4 cases of surgically treated LAH have been reported: one was treated with laparoscopic mesh repair, two with open mesch repair and more recently one with laparoscopic without mesh repair (32-34).

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Fig. 12. — 2 cases of linea arcuata hernia (LAH) : coronal (A) and sagittal (B) MPR and axial (C) views of a typical right interstitial hernia of the GO (white star) under the arcuate line of Douglas (black arrow). The omental nature of the herniating process is clearly confirmed by the identification of the protruding epiploic veins. Axial (E), coronal (D) and sagittal (F) MPR views of another typical left case. The semeiology is exactly the same.

Spigelian hernia (SH) SH is considered rather rare affecting less than 1% of the population with hernia defects (35-36). It classically develops under the level of the arcuate line of Douglas or Linea Arcuata (LA). Under this LA, all three aponeurosis of the lateral abdominal muscles do not more equally distribute anteriorly and posteriorely around the rectus muscle to constitute a firm circumferential sheath but abruptly pass exclusively anteriorly to the muscle, thus creating a weakness of the posterior rectus sheath. The LA corresponds to the brutal anatomic concave ending of the transverse abdominis and posterior sheet of internal oblique aponeu-

rosis on the posterior side of the rectus muscle sheath (35). This weakness is amplified by the fact that, at this level, the internal oblique and transverse muscles do not more constitute solid muscular bands but only fascias or thin musculo-aponeurotic bands separated by fascias and running in a parallel instead of perpendicular way. 95% of SH produce through these slitting defects (Fig. 13). Transversally this area of weakness is situated between the rectus muscle and the lateral abdominal muscles on a curvilinear vertical line called the line of Spiegel (35-36). SH mostly affects a population in the fifth and sixth decades of life and usually occurs on abdominal walls that have undergone traumas or pre-

vious surgical operations. It is usually localised on the right side (36). SHs are usually identified once there is pain or obstruction from incarceration (37). Presentation and symptoms are variable and related to the nature of the incarcerating structure. Moreover SH are also clinically difficult to diagnose because a typical mass is not always palpable. Diagnosis is thus notoriously difficult and CT is the imaging modality of choice (27). It is reported that only 50% of all SHs are diagnosed in the preoperative period (37). These difficulties make it all the more important to determine whether repair of incidentally identified SHs is justifiable and under what circumstances one should proceed with repair.

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Fig. 13. — Spigelian interstitial hernia (SH) implicating the right inferior angle of the GO (white star) : axial (A), sagittal oblique (B) and coronal oblique (C) views of the right inferior abdominal wall demonstrate a large orifice producing through the conjoint aponeurosis of the transverse and internal oblique muscles (black arrows). Selective VR views (D, E) of the GO perfectly illustrate long right epiploic veins (white arrows) protruding through the well delineated oval orifice. The herniated process remains recovered by the distended aponeurosis of the great oblique muscle (white arrowhead). Black star = Rectus muscle.

Incarceration and strangulation with occlusive syndrome is reported in as many as 24% of these hernias. This high percentage of complications is essentially due to a generally small size of their orifice (0,5 to 2 cm). SHs always contain a peritoneal sac, rarely

exceed a diameter more than 2 or 3 cm and remain covered by the aponeurosis of the external oblique (Fig. 13). The GO (Fig. 13), small bowel, sigmoid colon or caecum are the most implicated organs but cases implicating a strangulated appendix, the

gallbladder, an ovary or a testis, the round ligament or the fallopian tube, the stomach, the Meckel’s diverticulum, an uterine fibroma or endometric nodules, and epiploic appendage have also rarely been reported (35-36).

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Fig. 14. — Association of indirect inguinal (IIH) and incisional (IH) omental hernias: coronal oblique and sagittal oblique MPR views of the anterolateral abdominal wall of an old man presenting clinically with a parietal mass: an IIH of the GO (black star) coexists with an omental IH of another portion of the GO (white star) and producing through an old Mc Burney scar. The long elongated epiploic veins which are running just under the anterior abdominal wall are clearly protruding through the orifices and unequivocally identify the GO nature of the herniated fat tissue.

Incisional (IH), trocar and drain site hernia (TSH) IHs are iatrogenic and occur in a weak area in the abdominal wall after abdominal surgery (27, 38). Infection of the wound or obesity are major etiologic factors. They may manifest anywhere in the abdominal wall and are more commonly encountered in association with vertical than with transverse incisions. They may also be peristomal. IH commonly manifests in the first year after surgery, although a small percentage may be clinically occult. Their reported prevalence ranges from 0.5% to 13,9% for most abdominal surgeries but may be as high as 41% after aortic surgery. Typically properitoneal fat or the GO protrudes

first through the hernia defect (Fig. 14). If IH is left untreated, bowel loops may be incorporated and become incarcerated or strangulated. Laparoscopic surgery has quickly developed, becoming in some cases the gold standard procedure as the preferred mode of access to the peritoneal cavity (39-40). Despite the minimal invasiveness, some laparoscopic procedures-related complications can be directly attributed to abdominal access with laparoscopic trocars. The postoperative port-site hernia formation, which is defined as the development of a hernia at the canula insertion site, is one of them. TSH is a rare but potentially dangerous complication of laparoscopic surgery ranging from early small omental herniations (Fig. 15) to

delayed hernia formation with or without bowel entrapment. The incidence of TSH has been shown to be 0,65% to 2,8% and an incidence of 1,5 to 1,8% would be reasonably standard (41-42). TSHs are classified into 3 types (27, 40) : the “early onsettype” that occurs immediately after the operation (within two weeks), with a small-bowel obstruction frequently developing, the “late-onset type” that occurs several months after surgery, mostly with local abdominal bulging with no small bowel obstruction and the “special type” indicating dehiscence of the whole abdominal wall with protrusion of the intestine and other tissue (eg, greater omentum). TSHs with facial defects of 10 mm or larger should be closed, including

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Fig. 15. — 2 cases of omental “trocar” hernias (TH): sagittal (A), axial (B) and oblique (C) MPR views in a case of symptomatic painful omental TH (white arrow) through a “trocar site” of the right upper quadrant (recent cholecystectomy). Ultrasound (D), axial (E) and oblique (F) CT views in another case of small omental hernia (black arrow) through a very small “trocar” site of the right upper quadrant (post- cholecystectomy).

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the peritoneum. Opinions vary if a 5-mm trocar site defect should be closed. The main pathogenesis appears not related to host factors but rather to technical factors: eg, a large trocar size and stretching of the port site. Groin hernias Groin hernias may be divided into two main categories: inguinal hernia (IH) and femoral hernia (FH). IHs are the most common and are subdivided into direct (DIH) and indirect (IIH) types. The ring of IH and the ring of FH are located above and below the inguinal ligament, respectively (43).

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★ B Fig. 16. — CT anatomy of the inguinal area: these two coronal MDCT views (A, B) obtained in a 60 year old patient presenting with a left mild indirect inguinal hernia (IIH) illustrate the classical anatomic landmarks of the inguinal area. The femoral area (1) — where a femoral hernia may produce medially to the femoral vessels (white arrowhead) — is separated from the inguinal area by the inguinal ligament (B, open arrow). The epigastric vessels (A, black arrow) — contained in the external umbilical fold separating the medial from the external inguinal fossa — represent the landmarks between the anatomic sites where direct (internal inguinal fossa =2) and indirect (external inguinal fossa = 3) hernias may produce. Rectus muscle = white star. Internal oblique muscle = white arrow.

The inguinal ligament of Poupart, which represents the folded-up lower border of the external oblique muscle, constitutes the floor of the inguinal canal. It joins the anterosuperior iliac spine to the pubic tubercle (44-45). Just lateral to this tubercle a V-shaped gap in the external oblique aponeurosis forms the external inguinal ring. The transverse abdominis and internal oblique muscles joint medially to form the conjoint tendon that has a free edge arching over the spermatic cord and round ligament before attaching to the pectineal line. Thus this tendon conjoint forms the posterior wall and roof of the inguinal canal. The inferior epigastric artery (IEA) lies on the surface of the tendon conjoint immediately medial to the spermatic cord and defines the medial border of the inguinal internal ring. Medially to the IEA is the important triangle of Hesselbach formed by the IEA laterally, the lateral border of the rectus muscle medially and the inguinal ligament inferiorly. MDCT produces images of the inguinal region with detail not available with previous generations of CT (44). When multiplanar reconstructions are performed in the sagittal , coronal and axial plane 100% identification of the key anatomic structures can be achieved (Fig. 16). For the evaluation of groin hernias, physical examination is most important in clinical practice, although it is sometimes difficult to distinguish FHs from IHs. CT has recently been proved being useful to make this differential diagnosis (43, 46). The demonstration of a compression of the femoral vein by the hernia sac is common in FH (46). Additionally the relationship between the hernia sac

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Fig. 17. — Giant indirect inguinal hernia (IIH) : axial (A, B), curvilinear sagittal (C) MPR views and Volume Rendering view (D) of a giant IIH of the GO (white star). The calcified spermatic artery is identified at the internal border of the hernia. Long epiploic veins (black arrows) can be followed from the hernia to the greater curvature of the stomach.

and pubic tubercle on CT images represents another key to the differentiation of FHs from IHs (Fig. 16). If the hernia sac is located lateral and posterior to the horizontal line drawn from the pubic tubercle, the probability of a FH is high (43, 46). If the hernia is anterior to this line it is more likely an IH.

b) Inguinal Hernias (IHs) Among groin hernia, IH is undoubtedly the commonest hernia type and accounts for 75% of abdominal wall hernias with a lifetime risk of 27% in man and 3% in women (24, 47-48). IH is at risk of irreducibility or incarceration, which

may result in strangulation and obstruction (47). However unlike with FH, strangulation is rare with an estimated lifetime risk of strangulation of 0.27% for an 18 year old man and 0.03% for a 72 year old man (49). IHs are classically classified as direct (DIH) or indirect (IIH) depending on whether the hernia sac bulges

➝ Fig. 18. — Another case of incarcerated indirect inguinal hernia (IIH) of the GO: A,B: curvilinear coronal MPR CT views and C,D: selected ultrasound pictures. An elongated inflammatory fatty omental mass passes through the inguinal canal (white arrow). Ascitic fluid is trapped below the hernia (black star) and the long epiploic veins are typically attracted to the inguinal area (black arrow). This attraction induces an unusual angulation of the main gastroepiploic arcade (white star).

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Fig. 19. — Incarcerated indirect inguinal hernia (IIH): Right sagittal inguino-scrotal ultrasound view (A) and corresponding curvilinear sagittal oblique MPR CT view (B) illustrate an inflammatory incarcerated omental IIH (white arrow). The long epiploic veins of the GO are clearly identified and the incarceration induces an attraction of the gastric antrum to the hypogastric area (black star); white star = right testis surrounded by reactive fluid.

directly through the posterior wall of the inguinal canal (DIH) or passes through the internal inguinal ring alongside the spermatic cord, following the coursing of the inguinal canal itself (IIH) (24). Congenital hernias are usually IIHs – protrusion through a patent processus vaginalis – and the hernia

content includes bowel loops, omental fat or peritoneal fluid (24, 38, 45). Fluid may become encysted. They classically produce in the lateral umbilical fold thus laterally to the inferior epigastric vessels. They have a course along the inguinal canal toward the scrotum or labia and run at an angle (Fig. 16-19) to the peri-

toneal fossa rather than extending directly inferiorly like DIHs (38). In addition, the neck of the hernia tends to be narrow as it passes through the internal inguinal ring. DIHs are generally believed to be acquired (38). They are unusual in women. They occur as a generalized bulge through an area of potential

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Fig. 20. — Direct type of inguinal hernia (DIH): axial (A, D, E), coronal (B) and sagittal (C) MPR views illustrate a typical right DIH of the GO (white star). The hernia produces at the level of the medial inguinal fossa through an orifice (black arrow) located medially to the epigastric ascending vessels (white arrow) — contained in the lateral umbilical fold. The protruding epiploic vessels are clearly delineated (grey arrow). The obliterated umbilical artery which is contained in the medial umbilical fold and represents the inner border of the medial inguinal fossa (white arrowheads) is partially forced through the medial margin of the hernia. Within the hernia the peritoneal omental fat appears surrounded by another sheet of fat constituted by properitoneal fat (black asterisk). Black arrowheads represent the spermatic cord. Another DIH is visible on the left and only contains properitoneal fat (black star).

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Fig. 21. â&#x20AC;&#x201D; Another typical direct inguinal hernia (DIH) of the GO illustrated by a series of axial view (A), a coronal MPR view (B) and a selective volume rendering view (C). The vertically descending epiploic veins (black arrows) of the GO typically converge to herniate through the abdominal wall (white arrow) at the level of the medial inguinal fossa. The epigastric vessels classically remain outside the direct hernia (small white arrows).

weakness called the Hesselbach triangle in the posterior wall of the inguinal canal (Fig. 16) (38). The clinical symptoms are undistinguishable from those of IIHs and groin pain is the primary symptom. Unlike IIHs incarceration is uncommon in DIH because they are characterized by a broad neck (38). They occur medial to the lateral umbilical fold. There are two types of DIHs: one extends inferiorly from the medial umbilical fossa (Figs. 20 & 21) and the other extends inferiorly from the supravesical fossa (38). It is not uncommon to find synchronous DIHs and IIHs in a patient, either unilaterally or contralaterally.

c) Femoral hernia (FH) In adult FHs (Fig. 22) are much less common, occur more commonly in females and account for between 5,3 to 8,2% of all groin hernias (38, 44-45, 50). They are relatively rare in children (less than 1% of all pediatric groin hernias) (50). They are thought to be congenital arising from a defect in the attachment of the transverse fascia of the pubis (45). They protrude through the femoral canal medial to the femoral vein in the potential empty space and posterior to the inguinal ligament. Clinically apparent FHs may be reducible, irreducible, incar-

cerated or strangulated (50). The hernia is initially quite small, internal and asymptomatic because it is contained within the femoral canal. However, it can be enlarged by passing through the saphenous opening into the subcutaneous tissue of the thigh. Incarceration or strangulation has been reported to occur in 15-20% of the hernias at this stage. The protruded viscus undergoes strangulation and necrosis more often in FH than in other hernias due to the narrower opening of the former. The majority of incarcerated and all strangulated FHs are considered to be surgical emergencies.

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Fig. 22. — Typical femoral hernia (FH) of a right portion of the GO: axial (A, B), coronal oblique and sagittal oblique (C, D) MPR views illustrate an herniation of a portion of the GO (white star) typically producing under the inguinal arcade (small white arrows) at the level of the internal angle of the scarpa’s triangle (white arrow), just internally to the femoral vessels. On the axial (A) view the hernia typically produces below a horizontal line drawn from the pubic tubercule (black arrowhead). Pectineus muscle (black star). The vertically descending epiploic veins (black arrows) of the GO typically converge to the herniation.

References 1. Coulier B.: Multidetector computed tomography features of linea arcuata (arcuate-line of Douglas) and linea arcuata hernias. Surg Radiol Anat, 2007, 29: 397-403. 2. Coulier B.: 64-row MDCT review of anatomic features and variations of

the normal greater omentum. Surg Radiol Anat, 2009, 31: 489-500. 3. Yoo E., Kim J.H., Kim M.J., et al.: Greater and lesser omenta: normal anatomy and pathologic processes. Radiographics, 2007, 27: 707-720. 4. Lee G.H., Cohen A.J.: CT imaging of abdominal hernias. AJR Am J Roentgenol, 2003, 161: 1209-13.

5. Coulier B., Ramboux A.: Acute obstructive gastric volvulus diagnosed by helical CT. JBR-BTR, 2002, 85: 43. 6. Golash V.: Laparoscopic reduction of acute intrathoracic herniation of colon, omentum and gastric volvulus. J Minim Access Surg, 2006, 2: 7678.

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214 7. Maruyama R., Miyamoto T., Shoji F., et al.: Intrathoracic omental herniation through the esophageal hiatus in a young patient. Jpn J Thorac Cardiovasc Surg, 2005, 53: 452-454. 8. Kubota K., Ohara S., Yoshida S., Nonami Y., Takahashi T.: Intrathoracic omental herniation through the esophageal hiatus: a case report. Radiat Med, 2001, 19: 307-311. 9. Kato N., Iwasaki H., Rino Y., et al.: Intrathoracic omental herniation through the esophageal hiatus: report of a case. Surg Today, 1999, 29: 347350. 10. Kitada M., Ozawa K., Satoh K., Hayashi S., Sasajima T.: Recurrent diaphragmatic hernia 3 years after initial repair for traumatic diaphragmatic rupture: a case report. Ann Thorac Cardiovasc Surg, 2010, 16: 273-275. 11. Coulier B., Ramboux A., Mailleux P., Broze B.: Diagnosis of non-hiatal diaphragmatic hernia using helical computed tomography. JBR-BTR, 1999, 82: 1-5. 12. Shah R., Sabanathan S., Mearns A.J., Choudhury A.K.: Traumatic rupture of diaphragm. Ann Thorac Surg, 1995, 60: 1444-1449. 13. Horton J.D., Hofmann L.J., Hetz S.P.: Presentation and management of Morgagni hernias in adults: a review of 298 cases. Surg Endosc, 2008, 22: 1413-1420. 14. Coulier B., Broze B.: Gastric volvulus through a Morgagni hernia: multi detector computed tomography diagnosis. Emerg Radiol, 2008, 15: 197-201. 15. Gossios K.J., Tatsis C.K., Lykouri A., Constantopoulos S.H. Omental herniation through the foramen of Morgagni. Diagnosis with chest computed tomography. Chest, 1991, 100: 1469-1470. 16. Altinkaya N., Parlakgümü A., Koc Z., Ulusan S.: Morgagni hernia: diagnosis with multidetector computed tomography and treatment. Hernia, 2010, 143: 277-281. 17. Machtelinckx C., De Man R., De Coster M., Ghillebert G., Provoost V.: Acute torsion and necrosis of the greater omentum herniated into a foramen of Morgagni. Abdom Imaging, 2001, 26: 83-85. 18. Ackroyd R., Watson D.I.: Laparoscopic repair of a hernia of Morgagni using a suture technique. J R Coll Surg Edinb, 2000, 45: 400-402. 19. Minneci P.C., Deans K.J., Kim P., Mathisen D.J.: Foramen of Morgagni hernia: changes in diagnosis and treatment. Ann Thorac Surg, 2004, 77: 1956-1659. 20. Kamiya N., Yokoi K., Miyazawa N., et al.: Morgagni hernia diagnosed by MRI. Surg Today, 1996, 26: 446-448.

JBR–BTR, 2012, 95 (4) 21. Lanteri R., Santangelo M., Rapisarda C., Di Cataldo A., Licata A.: Bilateral Morgagni-Larrey hernia: a rare cause of intestinal occlusion. Arch Surg, 2004, 139: 1299-1300. 22. Ipek T., Altinli E., Yuceyar S., et al.: Laparoscopic repair of a MorgagniLarrey hernia: report of three cases. Surg Today, 2002, 32: 902-905. 23. Shastri N., Gilmer L.: Periumbilical swelling in an infant. Epigastric hernia. Am Fam Physician, 2008, 77: 1151-1152. 24. Aguirre D.A., Santosa A.C., Casola G., Sirlin C.B. Abdominal wall hernias: imaging features, complications, and diagnostic pitfalls at multi-detector row CT. Radiographics, 2005, 25: 1501-1520. 25. Askar O.M. A new concept of the aetiology and surgical repair of paraumbilical and epigastric hernias. Ann R Coll Surg Engl, 1978, 60: 4248. 26. Korenkov M., Beckers A., Koebke J., et al.: Biomechanical and morphological types of the linea alba and its possible role in the pathogenesis of midline incisional hernia. Eur J Surg, 2001, 167: 909-914. 27. Miller P.A., Mezwa D.G., Feczko P.J., Jafri Z.H., Madrazo B.L.: Imaging of abdominal hernias. Radiographics, 1995, 15: 333-347. 28. Khati N.J., Enquist E.G., Javitt M.C. : Imaging of the umbilicus and periumbilical region. Radiographics, 1998, 18: 413-431. 29. Zarvan N.P., Lee F.T. Jr., Yandow D.R., Unger J.S.: Abdominal hernias: CT findings. AJR, 1995, 164: 1391-1395. 30. Whitson B.A., Ose K.J.: Spontaneous posterior rectus sheath hernia: a new clinical entity? Hernia, 2007, 11: 445447. 31. Losanoff J.E., Basson M.D., Gruber S.A.: Spontaneous hernia through the posterior rectus abdominis sheath: case report and review of the published literature 1937-2008. Hernia, 2009, 13: 555-558. 32. Abasbassi M., Hendrickx T., Caluwé G., Cheyns P.: Symptomatic linea arcuata hernia. Hernia, 2011, 15: 229-231. 33. Cappeliez O., Duez V., Alle J.L., Leclercq F.: Bilateral arcuate-line hernia. AJR Am J Roentgenol, 2003, 180: 864-865. 34. von Meyenfeldt E.M., van Keulen E.M., Eerenberg J.P., Hendriks E.R.: The linea arcuata hernia: a report of two cases. Hernia, 2010, 14: 207-209. 35. Coulier B., Ramboux A., Mailleux P.: Strangulated intestinal Spigelian hernia. JBR-BTR, 1997, 80: 68-70. 36. Campanelli G., Pettinari D., Nicolosi F.M., Avesani E.C.: Spigelian hernia. Hernia, 2005, 9: 3-5.

37. Nagarsheth K.H., Nickloes T., Mancini G., Solla J.A.: Laparoscopic repair of incidentally found Spigelian hernia. JSLS, 2011, 15: 81-85. 38. Harrison L.A., Keesling C.A., Martin N.L., Lee K.R., Wetzel L.H.: Abdominal wall hernias: review of herniography and correlation with cross-sectional imaging. Radio graphics, 1995, 15: 315-332. 39. Dulskas A., Lunevi ius R., Stanaitis J.: A case report of incisional hernia through a 5 mm lateral port site following laparoscopic cholecystectomy. J Minim Access Surg, 2011, 7: 187-189. 40. Tonouchi H., Ohmori Y., Kobayashi M., Kusunoki M.: Trocar site hernia. Arch Surg, 2004, 139: 1248-1256. 41. Mayol J., Garcia-Aguilar J., OrtizOshiro E., et al.: Risks of the minimal access approach for laparoscopic surgery: multivariate analysis of morbidity related to umbilical trocar insertion. World J Surg, 1997, 21: 529533. 42. Nassar A.H., Ashkar K.A., Rashed A.A., Abdulmoneum M.G.: Laparoscopic cholecystectomy and the umbilicus. Br J Surg, 1997, 84: 630-633. 43. Delabrousse E., Denue P.O., Aubry S., et al.: The pubic tubercle: a CT landmark in groin hernia. Abdom Imaging, 2007, Mar 27. [Epub ahead of print] 44. Cherian P.T., Parnell A.P.: Radiologic anatomy of the inguinofemoral region: insights from MDCT. AJR, 2007, 189: 177-183. 45. Shadbolt C.L., Heinze S.B., Dietrich R.B.: Imaging of groin masses: inguinal anatomy and pathologic conditions revisited. Radiographics, 2001, 21: 261-271. 46. Suzuki S., Furui S., Okinaga K., et al.: Differentiation of femoral versus inguinal hernia: CT findings. AJR, 2007, 189: 78-83. 47. Jenkins J.T., O'Dwyer P.J.: Inguinal hernias. BMJ, 2008, 336: 269-272. 48. Dabbas N., Adams K., Pearson K., Royle G.: Frequency of abdominal wall hernias: is classical teaching out of date? JRSM Short Rep., 2011, 19: 5. 49. Fitzgibbons RJ., Jonasson O., Gibbs J., et al.: The development of a clinical trial to determine if watchful waiting is an acceptable alternative to routine herniorrhaphy for patients with minimal or no hernia symptoms. J Am Coll Surg, 2003, 196: 737742. 50. Natsis K., Totlis T., Papadopoulou A.L., Apostolidis S., Skandalakis P.: Bilateral femoral hernia in a male cadaver with vascular variations: case report and review of the literature. Hernia, 2006, 10: 347-349.

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THE RELATION BETWEEN PELVIC VARICOSE VEINS AND LOWER EXTREMITY VENOUS INSUFFICIENCY IN WOMEN WITH CHRONIC PELVIC PAIN A. Bora1, S. Avcu1, H. Arslan1, E. Adali2, M.D. Bulut1 Purpose: To determine the relation between pelvic varicose veins and lower extremity venous insufficiency in women with chronic pelvic pain. Methods and Materials: This study was done in Yuzuncu Yil University Faculty of Medicine, Department of Radiology, with patients who were referred for abdominal and pelvic imaging between January 2007 and April 2008. A total of 1029 women with pelvic imaging study were included in the study. The presence of venous dilatations (diameter > 5 mm) in parauterine and paraovarian localizations were accepted as pelvic varicose veins. In all patients, endometrial thickness was measured and lower extremity venous system was examined with Doppler ultrasonography to assess possible associated venous insufficiency. All patients were undergone questionnaire for frequency of delivery, age, and chronic pelvic pain. Results: Pelvic varicose veins were discovered with transabdominal ultrasound and computerized tomography in 56 of 1029 patients. Various degrees of associated lower extremity venous insufficiency were also discovered in 44 of 56 patients (78,6%) with pelvic venous dilatation. Of the 44 patients with lower extremity venous insufficiency, 21 were bilateral, 9 were right-sided, and 14 were left-sided. Endometrial thickness was significantly increased in patients with pelvic venous dilatation. Conclusion: The presence of pelvic varicose veins is significantly associated with lower extremity venous insufficiency. Since the diagnosis of lower extremity venous insufficiency plays an important role in deciding the course of treatment, lower extremity Doppler ultrasonography examination would be useful to include in the evaluation of pelvic varicose veins. Key-word: Veins, extremities.

Pelvic congestion syndrome (PCS), is defined as dilatation of veins of the broad ligament and the ovarian plexus. PCS is one of the important causes of chronic pelvic pain affecting women of reproductive age, especially multiparas (1, 2). Pain in PCS is generally defined as tension, fullness and dullness. The duration and severity of the pain which is variable, can radiate to the hip and the thigh. Accompaning symptoms are irritable bladder, dyspareunia, and painful micturation (3). It is diagnosed by eliminating the other pelvic pathologies by several imaging techniques in suspected cases at the clinic, since there are many clinical situations that mimic the symptoms of PCS (4). Disorders to be eliminated in the differential diagnoses include pelvic inflammatory, endometriosis, pelvic tumors, interstitial cystitis and inflammatory bowel syndrome (5). PCS is a clinical syndrome of chronic pelvic pain asscoiated with typical radiological features of insufficient ovarian vein and dilated paraovarian veins. PCS is diagnosed by history, physical examination and

use of imaging techniques. In the imaging techniques, transabdominal and transvaginal ultrasonography (US) are the first prefered procedures because they are easy and non-invasive. Meanwhile, computed tomography (CT), magnetic resonance imaging (MRI) and venography are the other diagnostic tools (6, 7). Normally, the diameter of the parauterine and paraovarian veins which are tubular structures, is smaller than 5 mm. The specific imaging finding of pelvic venous congestion is a dilated and tortuous structure of the ovarian and parauterine veins, the diameters of which are larger than 5 mm (8-10). Pelvic varicose veins generally accompany vulvar, perineal and lower extremity varicose veins (11, 12). There is limited data in the literature regarding the level and the rate at which pelvis varicose veins accompany lower extremity venous insufficiency (11-13). Our aim in this study is to evaluate whether there is a relation between pelvic varicose veins and lower extremity venous insufficiency in patients with chronic pelvic pain.

From: 1. Department of Radiology, 2. Department of Obstetrics and Gynaecology, Yuzuncu Yil University School of Medicine, Van, Turkey. Address for correspondence: Dr S. Avcu, M.D., Yuzuncu Yil University School of Medicine, Department of Radiology, Van, Turkey. E-mail: serhatavcu@hotmail.com

Materials and methods A total of 1029 female patients who had been referred to the Radiology Department of the Yüzüncü Yıl University School of Medicine between January 2007October 2008 from several departments (Gynecology and Obstetrics, General Surgery, Internal Medicine, Urology) for abdomino-pelvic imaging (725 transabdominal US and 402 CT) were included in this prospective study. The study protocol was performed according to the Helsinki Committee requirements and Ethics Committee approval was obtained for the study. Also, informed consent was signed by the patients. The clinical features were questioned and it was evaluated whether or not there was venous insufficiency in the main femoral vein in both lower extremities in patients whose ovarian and parauterine venous structures had been seen to be dilated during pelvic imaging. On transabdominal ultrasonographic evaluation, a PHILIPS HD11 (Bothell, Washington, USA) with 3.5 MHz convex probe was used. The images were obtained in supine and semi-erectile position. Uterine and paraovarian pathologies were noted. In order to find the ovarian veins, the transducer was placed in the transverse plane through the left upper abdomen. The left renal and ovarian veins were viewed in this position.

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Then inferior vena cava was observed by placing the transducer in the middle of the abdomen. The transducer was then slid to tha lateral in order to view the right ovarian vein. The intraluminal diameter of the ovarian veins were measured and recorded. The flow direction of blood in the ovarian veins were interpreted by Coloured Duplex Doppler US. Duplex wave changes were recorded during the valsalva maneuver on the patients. The images of US were analysed by an experienced investigator. The endometrial thickness was also measured. Circular or linear, non-pulsative, anechoic parauterine and paraovarian structures greater than 5 mm were accepted as pelvic varicosis. CT imaging and scaning were performed by 4 channel MDBT scanner (SOMATOM Sensation 4; Siemens, Erlangen, Germany). The portal phase was used for evaluation of venous structures. Portal phase images were recorded 70 sec following the infusion of 100 ml ionic contrast agent at a rate of 2.5 ml/s. The abdomen was scanned from the superior part of the diaphragm to the pelvic floor with the patient holding his/her breath. The scanning paramteres were: collimation: 2.5 mm, pitch value: 1.25, kVp: 120, mA: 100. Data collecting and imaging recordings were performed at a study station where there was suitable software (Leonardo, Siemens Medical Systems). Images of each patient were evaluated by an investigator experienced in abdominal radiology. The diameter of ovarian and parauterine veins were measured in the axial plane. Nutcracker syndrome and the relation between ovarian vein and left renal vein were evaluated by coronal and sagittal mutiplanar reformate images. The widest vein diameter which was greater than 5 mm at any plane was defined as dilated and accepted as pelvic varicosis (Fig. 1).

Fig. 1. â&#x20AC;&#x201D; Abdominal tomography of a 40-year-old female patient who had abdominal pain. A. Dilatation was seen in the left ovarian vein at the point of drainage to the renal vein in the axial images. B. Bilaterally dilated venous structures, the diameters of which were greater than 5 mm in the axial pelvic images and a 4 cm cyst in the right ovary. C. Bilaterally dilated venous structures, the diameters of which were greater than 5 mm in the bilateral Multiplanar Reformat (MPR) coronal images.

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Fig. 2. — It was seen that the main femoral vein flow was not ceased during the valsalva and an opposite flow consistent with reflux was seen in the lower extremity Spectral Doppler evaluation. The actual appearance was in favor of venous insufficiency.

Lower extremity venous system was evaluated by high resolution 7.5 MHz linear probe of Philips HD11 (Bothell, Washigton, USA) in the second step examnation of patients who had dilated ovarian and parauterine veins on the transabdominal US and CT imagings. Vein wall texture, intraluminal echogeneity and compressibility of bilateral main femoral veins were investigated in the supine position. The related venous structures were then evaluated according to their color and spectrum. As the reflux time changes according to the position of the patient, to the diameter of the lumen, and according to the numbers and locations of the valves, a definite limit has not been set for the venous reflux time in the literature, and a reflux time greater than 0.5-1 sec was accepted as pathological (14). We also accepted a reciprocal flow of over 0.7 sec during the valsalva and mechanical com-

B Fig. 3. — In the Doppler US investigation of a 28-year-old female patient with pelvic pain, A: wide venous structures, the diameters of which were greater than 5 mm in pelvic region. B. It was seen that the main femoral vein flow was not ceased during the valsalva and opposite flow consistent with reflux was seen in the Spectral Doppler evaluation. The actual appearance was in favor of venous insufficiency.

pression as pathological in our study (Fig. 2). Statistical analysis All data were analyzed using the Statistical Package for the Social

Sciences for Windows 10.0 software (SPSS, Chicago, IL, USA). Data were presented as mean ± SD or percentage. Comparisons between groups were analyzed by Student’s t-test and chi-square test. Statistical significance was defined as p < 0.05.

Table I. — Distribution of the patients according to the imaging methods. Ultrasonography

Computed Tomography

Total

Dilatation of pelvic veins (+) Dilatation of pelvic veins (-)

21 704

35 367

56 973

Total

725

402

1029

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Table II. — The clinical features of the patients.

Age (year) Chronic pelvic pain, n (%) PCS, n (%) Endometrial thickness (mm) Gravida (n)

Dilatation of pelvic veins (+) (n = 56)

Dilatation of pelvic veins (-) (n = 973)

P value

36.9 ± 7.6 51 (91%) 51 (91%) 9.9 ± 1.8 4.8 ± 2.5

40.4 ± 9.2 78 (8%) 0 (0%) 6.2 ± 2.1 2.1 ± 1.7

0.44 < 0.001 < 0.001 0.048 < 0.001

PCS, pelvic congestion syndrome.

Table III. — Lower extremity venous insufficiency in women with pelvic venous dilatation.

Pelvic venous dilatation, n(%)

Results Lower extremity venous system insufficiency was found in 44 of 56 patients who had pelvic venous dilatation. Lower extremity venous system insufficiency was found in 12 cases even though they had pelvic vein diameter of lower than 5mm. Pelvic veins whose diameters were greater than 5 mm, were seen bilaterally in 21 cases, on the right side in 9 cases, and on the left side in 14 cases (Fig. 3). The mean number of births was 4.8 ± 2.5 (0-10) in the study group which was composed of 4 nulliparous and 52 multiparous cases. In the statistical analysis, there was a positive relationship between the number of births and pelvic venous dilatation (p < 0.001). Furthermore, as the number of births increased, the frequency of low extremity venous insufficiency increased. The number of births of cases which had pelvic venous dilatation and low extremity venous insufficiency were compared with the number of births of cases which had only pelvic venous dilatation. The mean number of births was higher in the lower extremity venous insufficiency group (5,1 ± 2,5 v.s 3,7 ± 2,4, p = 0.084). The distribution of the patients according to the imaging methods has been displayed in Table I. The clinical features of the cases whose pelvic vein diameter was greater than 5 mm has been demonstrated in Table II. Table III reports the lower extremity venous insufficiency in women with pelvic venous dilatation.

lower extremity venous insufficiency (+)

lower extremity venous insufficiency (-)

Total

44 (78.6%)

12 (21.4%)

56 (100%)

Among the 56 patients with pelvic congestion, it was found that 2 had left renal vein progressing between the aorta and the superior mesenteric artery, and 3 were found to have the left renal vein progressing in the retro-aortic area. The frequency of nutcracker syndrome was 0.1% in the study group and 3.6% in patients with PCS. The mean endometrial thickness was measured to be 9.9 ± 1.8 mm in the group in which pelvic dalatation was seen, and was measured as 6.2 ± 2.1 mm in the group in which pelvic varicosis was not found. Endometrial thickness was significatly higher in the patients who had pelvic dilatation in the parauterine and pelvic areas (p = 0.048). Discussion The results of the current study revealed that lower extremity venous insufficiency accompanies pelvic venous dilatation. Since the diagnosis of lower extremity venous insufficiency plays an important part in deciding the course of treatment, lower extremity Doppler US examination should be included in the evaluation of pelvic varicous veins. Widening of the veins of the broad ligament and the ovarian plexus, and the presence of an incompetent ovarian vein are specific findings of PCS (15). It has been shown that PCS is found in 10% of the general population and in half of the women who have chronic pelvic pain (8, 16, 17). A hormonal component is thought to be present in the etiology of the PCS, because the symptoms disappear after menopause. In recent studies,

the relationship between polycystic ovarian syndrome and PCS has been demonstrated (18). Estrogen is a potent vasodilator. The presence of estrogens receptors in human vascular cells is widely known. The vasodilatory effect of estrogen come out through different mechanisms. Excess estrogen leads to relaxation of smooth muscles by stimulation of nitric oxide synthetase and secretion of nitric oxide (19, 20). Nitric oxide not only dilates the uterine vessels, but also blocks the nitric oxide inhibitors and results in venous pain. Although several imaging methods have been used to diagnose pelvic venous dilatation, transabdominal US is frequently used due to its noninvasiveness and easy applicability (5, 10). US can detect other pathologies related with PCS, such as polycystic ovary syndrome. In the light of this information, ultrasonography should be the first imaging technique for the diagnosis of PCS (13). Doppler US is used succesfully in the evaluation of blood flow in venous structures. Retrograde flow in ovarian and parauterine veins suggests PCS in Doppler US (11). Displaying dilated pelvic veins is not sufficient fort he diagnosis of the syndrome, and decreased blood flow in the ovarian vein should also be present in order to make the diagnosis. Pelvic varicosis can be missed when ultrasonographic investigation is performed in the supine position as this position renders easier venous drainage. The sensitivity of US in the supine position is low for pelvic varicosis (20). In order to increase the sensitivity of US for the

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diagnosis of PCS, the procedure should be performed in a semi-erectile position. It is important to view the retrograde flow in the pelvic vein during the valsalva maneuver for the diagnosis (12). Chronic pelvic pain was described in 129 of 1029 women who had undergone abdominal and pelvic evaluation. PCS was found in 52 (39.5%) of the patients who had described chronic pelvic pain. Our results were similar with the findings of Gultasli et al (13). Diseases which may be be reasons for chronic pelvic pain, such as polycystic ovary syndrome, and myoma uteri were found in 72 (7%) of the patients in our study. The diameter of the pelvic veins were found to be greater than 5 mm in 3 of the patients. Pelvic venous dilatation was investigated by US evaluation with the patients in supine position first and then in the semi-erectile position. Retrograde flow was probed in ovarian and parauterine veins during the valsalva maneuver in patients with pelvic venous dilatation. Retrograde flow in the ovarian vein by Doppler US indicates PCS (11). Imaging of the widened pelvic veins is not sufficient for the diagnosis of the syndrome, but retrograde ovarian vein flow during valsalva should also be demonstrated. Dynamic imaging tests are necessary for the correct diagnosis (12). Pelvic venous dilatation and retrograde flow during the Valsalva were detected in 21 of 725 patients who had undergone pelvic US examination. The patients who showed pelvic dilatation by US examination were evaluated by CT. CT is an important imaging tool for the diagnosis of PCS and detecting the pathologies related with PCS. Furthrmore, contrast imaging has an important place in the diagnosis of venous insufficiency when there is venous contrast uptake during the arterial phase (6). The disadvantages of CT are radiation exposure, ineffective determination of venous changes in the supine and stable positions during the evaluation (7). Pelvic venous dilatation was found in 35 of 402 patients who had undergone CT examination in our study. US evaluation was performed in the semi-erectile position in patients in whom pelvic dilatation was found on the CT examination. Retrograde flow was seen in the Doppler US examination of pelvic veins of 30 patients in whom pelvic venous dilatations were found by CT examination. Retrograde flow was

not seen in 5 patients. We thought that pelvic CT which had been performed in patients with chronic pelvic pain for different reasons had an important place in the diagnosis of PCS, contrary to the literature. Although invasive techniques such as vulvar phlebogaphy, transuterine venography, retrograde phlebogaphy, and selective ovarian venography have been used in the past, these techniques are not utilized anymore, with the exception of selective ovarian venography. Selective ovarian venography is the gold standard for the diagnosis of PCS and should only be used for in patients who undergo the endovascular approach (7). Selective ovarian venography can be performed under local anaesthesia. Following exclusion of pregnancy, the femoral vein is catheterized using the Seldinger technique. After selective catheterization of the left ovarian vein draining into the left renal vein under flouroscopy, nonionic contrast agent with low osmalality is injected and radiograms are obtained with the patient in the semi-erectile position (7). The patients who had been found to have pelvic venous dilatation on the imaging techniques which had been requested by several departments, underwent evaluation by US, which would not pose additional risks and which would be non-invasive for pelvic vein examination and detection of insufficient flow in main femoral vein. There were no cases planned for endovascular treatment. Pelvic congestion is generally diagnosed in multiparas. During pregnancy, the ovarian vein widens in order to compensate the increased blood flow, which is 60 times greater than normal. This is thought to be one of the most important reasons for the appearnce of venous insufficiency (9). A significant relationship was found between pelvic venous dilatation and the mean number of births in the statistical evaluation in our study group, in which the mean number of births was 4.8 ± 2.5 (0-10) (p < 0,001). The mean number of births in 56 patients who had pelvic venous dilatation and lower extremity venous insufficiency was 5.1 ± 2.5; but the mean number of births who did not have lower extremity venous insufficiency was 3.7 ± 2.4 (p = 0.084). In the autopsy series, it was found that there were no valves in the superior portion in 6% of the right and 15% of the left ovarian veins. It is

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thought that the absence of valves is congenital, because pelvic varicosis is seen in nulliparous women, too (9). Four of the 56 patients with pelvic venous dilatation in our study were nulliparous. No other reason that could result in pelvic venous congestion was found in these patients. Another cause of PCS is compression of the left renal vein between the superior mesenteric artery and the aorta. As a result of the compression of the left reanl vein, venous hypertension occurs and collaterals are formed around the renal pelvis. This situation is defined as the Nutcracker syndrome. In the early phase, venous hypertension occurs when the left renal vein is compressed between the aorta and the superiror mesenteric artery. Venous collaterals are also formed around the renal capsule. During the venous hypertension period in the Nutcracker syndrome, reflux is not observed, because the valves of the left ovarian vein are sufficient. The increase in the pressure of the left renal vein results in dilatation of the veins neighboring the calyx. Hematuria and flank pain are seen due to the dilated veins around the calyx (21, 22). Nutcracker syndrome is diagnosed by symptoms like pelvic congestion, left flank pain, hematuria and observation of vulvar and pelvic varicosis on the US due to renal vein compression. MRI and CT examinations are also important for the diagnosis (23). Among the 56 patients with pelvic congestion, it was found that 2 had a left renal vein progressing between the aorta and the superior mesenteric artery, and 3 (0.3%) were found to have a left renal vein progressing in the retroaortic area. The frequency of nutcracker syndrome was 0.1% in the study group and 3.6% in patients with PCS. Nutcracker syndrome is stated to be rare in the literature (23). When the effect of estrogen is blocked by drugs like medroxyprogesterone acetate in the treatment of PCS, radiological and clinical improvements are achieved (24). It has been shown that high dose medroxyprogesterone acetate would improve the symptoms in 40% of the patients and decrease the congestion venographically (25). Although this effect would make one consider hormonal factors in the etiology, there has been no proof on the increased blood estrogen levels in women with pelvic congestion; however, there has been an indirect

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effect of estrogen in pelvic organs (13). It has been shown that endometrial thickness and uterine size are increased significantly in pelvic congestion (13). In our study, the mean endometrial thickness was 9.9 ± 1.8 mm in patient who had pelvic varicosis and 6.2 ± 2.1 mm in patients who did not have pelvic varicosis (p = 0.048). This supports the idea that hormonal factors have an effect in pelvic congestion. This supports the findings of Gultasli et al. (13), who had shown that endometrial thickness of 30 patients with pelvic venous dilatation was greater than that of normal people (endometrial thickness was 9.2 mm in the pelvic dilatation group and 6.7 mm in normal people). Pelvic varicosis is generally seen with vulvar, perineal and lower extremity varicosis (9, 10). Valvular insufficiency in other pelvic venous systems like the internal and external iliac veins have an important place in the pathophysiology of pelvic venous congestion (9). Despite the mention of lower extremity varicosis accompanying pelvic varicosis in the literature, there has been a limited number of studies that mention the rate. Gultasli et al. (13) found that 70% of the patients with pelvic venous dilatation had lower extremity insufficiency. Peripheral venous insufficiency was found in 21 (70%) of 30 patients whose pelvic vein diameter was greater than 5 mm. Peripheral venous insufficiency was mostly seen in main femoral vein (52%) and in other lower extremity venous structures at different rates. In our study, in order to evaluate lower extremity venous insufficiency in cases with pelvic vein dilatation, main femoral vein was selected. The reason for this decision was due to the study of Gultasli et al. (13) who had mostly found main femoral vein insufficiency in patients with PCS. In the study group, it was found that main femoral vein insufficiency was seen in 44 of 56 patients whose pelvic vein diameter was greater than 5 mm and the relation between pelvic varicosis and lower extremity venous insufficiency was prominent. This finding is consistent with the results of Gultasli et al. (13). PCS is treated by medical, interventional radiological techniques and surgical procedures. Current randomized controlled studies have given proofs about the supportive effect of medroxyprogesterone acetate or gosereline in the treat-

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ment (26). Medical treatment is noninvasive, and progesterone, gosereline and daflon are useful for symptomatic treatment (24). In cases resistant to medical treatment, interventional radiology seems to be less invasive when compared with surgical treatment (6, 27). The greatest advantage of interventional radiology is the production of obstruction of ovarian veins with different embolizing agents in a single session and avalibility of the diagnostic procedure and treatment in the same sesession. The iliac veins can also be embolized. PCS to left renal vein stenosis or Nutcracker syndrome can be treated by stent installation. The results of endovascular treatment are more favorable than medical treatment and at least as successful as surgery (6, 27). Although complications are rare, metalic coils may extend through the main iliac vein and lead to pelvic pain (28). In the study performed by Kim et al. (29) it was seen that the symptoms of 127 patients in whom bilateral ovarian vein embolization and iliac vein embolization had been assessed with regard to effectiveness, had improved in 83%, not changed in 13%, and worsened in 4% of the cases. These results supported the fact that internal iliac vein embolization would improve the symptoms significantly and the success of embolization would be high. In this study, the right ovarian vein was embolized when there was prominent reflux in the left and the right ovarian vein. Internal iliac vein embolization was performed when the symptoms did not improve 6 weeks after the embolization of the ovarian vein (29). Surgery should be attempted if the interventional radiological techniques have failed. Laparoscopic or open ovarain vein or internal iliac vein ligation are among the surgical alternatives. As a result, PCS has an important place amongst the causes of chronic pelvic pain, which is frequently seen in women. In our study, we found that lower extremity venous insufficiency in great part accompanies pelvic venous dilatation. It would be beneficial to evaluate the lower extremity venous system by Doppler US when pelvic varicosis is detected by different imaging procedures. References 1. Stones R.W.: Pelvic vascular congestion-half a century later. Clin Obstet Gynecol, 2003, 46: 831-836.

2. Coakley F.V., Varghese S.L., Hricak H.: CT and MRI of pelvic varices in women. J Comput Assist Tomogr, 1999, 23: 429-434. 3. Grossman S.A., Sheidler V.R., McGuine D.B., Geer C., Santor D., Piastodisi S.: A comparison of the Hopkins Pain Rating Instrument with standard visual analogue and verbal descriptor scales in patients with cancer pain. J Pain Symptom Manage, 1992, 7: 196-203. 4. Reginal P.W., Adams S., Frankes S., Wadworth J., Beard R.W.: Medroxyprogesterone acetate in the treatment of pelvic pain due to venous congestion. Br J Obstet Gynaecol, 1989, 96: 1148-1152. 5. Stones R.W., Rae T., Rogers V., Fry R., Beard R.W.: Pelvic congestion in women: evaluation with transvaginal ultrasound and observation of venous pharmacology. Br J Radiol, 1990, 63: 710-711. 6. Nicholson T., Basile A.: Pelvic congestion syndrome, who should we treat and how? Tech Vasc Interv Radiol, 2006, 9: 19-23. 7. Beard R.W., Highman J.H., Pearce S., Reginald P.W.: Diagnosis of pelvic varicosities in women with chronic pelvic pain. Lancet, 1984, 2: 946949. 8. Giacchetto C., Cotroneo G.B., Marincolo F.: Ovarian varicocele: ultrasonic and phlebographic evaluation. J Clin Ultrasound, 1990, 18: 551-555. 9. Rozenblit A.M., Ricci Z.J., Tuvia J., Amis E.S. Jr.: Incompetent and dilated ovarian veins: a common CT finding in asymptomatic parous women. AJR, 2001, 176: 119-122. 10. Kennedy A., Hemingway A.: Radiology of ovarian varices. Br J Hosp Med, 1990, 44: 38-43. 11. Hobbs J.T.: The pelvic congestion syndrome. Br J Hosp Med, 1990, 43: 200-206. 12. Desimpelaere J.H., Seynaeve P.C., Hagers Y.M., Appel B.J., Mortelmans L.L.: Pelvic congestion syndrome: demonstration and diagnosis by helical CT. Abdom Imaging, 1999, 24: 100-102. . 13. Gültas¸ lı N.Z., Kurt A., Ipek A., Gümüs¸ M., Yazıcıog˘lu K.R., Dilmen G., et al.: The relation between pelvic varicose veins, chronic pelvic pain and lower extremity venous insufficiency in women. Diagn Interv Radiol, 2006, 12: 34-38. 14. Labropoulos N., Tiongson J., Pryor L., Tassiopoulos A.K., Kang S.S., Ashraf Mansour M., et al.: Definition of venous reflux in lower-extremity veins. J Vasc Surg, 2003, 38: 793798. 15. Hodson T.J., Reed M.W., Peck R.J., Hemingway A.P.: Case report: the ultrasound and Doppler appearances of pelvic varices. Clin Radiol, 1991, 44: 208-209. 16. Park S.J., Lim J.W., Ko Y.T., Lee D.H., Yoon Y., Oh J.H., et al.: Diagnosis of pelvic congestion syndrome using transabdominal and transvaginal sonography. AJR, 2004, 182: 683-688.

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PELVIC VARICOSE VEINS AND LOWER EXTREMITY VENOUS INSUFFICIENCY â&#x20AC;&#x201D; BORA et al 17. Belenky A., Bartal G., Atar E., Cohen M., Bachar G.N.: Ovarian varices in healthy female kidney donors: incidence, morbidity, and clinical outcome. AJR, 2002, 179: 625-627. 18. Anonymous. Pelvic congestion. Lancet, 1994, 337: 398-400. 19. Van Buren G.A., Yang D.S., Clark K.E.: Estrogen-induced uterine vasodilatation is antagonized by L-nitroarginine methyl ester, an inhibitor of nitric oxide synthesis. Am J Obstet Gynecol, 1992, 167: 828-833. 20. Foong L.C., Gamble J., Sutherland I.A., Beard R.W.: Altered peripheral vascular response of women with and without pelvic pain due to congestion. BJOG, 2000, 107: 157-164. 21. MacMahon H.E., Lattoraca R.: Essential renal hematuria. J Urol, 1954, 71: 667-676.

22. Pytel A.: Renal fornical hemorragies: Their pathogenesis and treatment. J Urol, 1960, 83: 783-789. 23. Ahmed K., Sampath R., Khan M.S.: Current trends in the diagnosis and management of renal nutcracker syndrome: a review. Eur J Vasc Endovasc Surg, 2006, 31: 410-416. 24. Soysal M.E., Soysal S., Vicdan K., Ozer S.: A randomized controlled trial of goserelin and medroxyprogesterone acetate in the treatment of pelvic congestion. Hum Reprod, 2001, 16: 931-939. 25. Farquhar C.M., Rogers V., Franks S., Pearce S., Wadsworth J., Beard R.W.: A randomized controlled trial of medroxyprogesterone acetate and psychotherapy for the treatment of pelvic congestion. Br J Obstet Gynaecol, 1989, 96: 1153-1162.

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26. Cheong Y., William Stones R.: Chronic pelvic pain: aetiology and therapy. Best Pract Res Clin Obstet Gynaecol, 2006, 20: 695-711. 27. Sichlau M.J., Yao J.S., Vogelzang R.L.: Transcatheter embolotherapy for the treatment of pelvic congestion syndrome. Obstet Gynecol, 1994, 83: 892896. 28. Park S.J., Lim J.W., Ko Y.T., Lee D.H., Yoon Y., Oh J.H., et al.: Diagnosis of pelvic congestion syndrome using transabdominal and transvaginal sonography. AJR, 2004, 182: 683688. 29. Kim H.S., Malhotra A.D., Rowe P.C., Lee J.M., Venbrux A.C.: Embolotherapy for pelvic congestion syndrome: long-term results. J Vasc Interv Radiol, 2006, 17: 289-297.

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INTRAMYOCARDIAL PARAVALVULAR ABSCESS AFTER AORTIC VALVE REPLACEMENT B. Lutin1, Y. Van Belleghem2, D. Devos1 Myocardial abscess is a rare but life-threatening disease with various clinical presentations. We describe the case of a paravalvular abscess distending intramurally 7 years post surgery for aortic valve replacement. Early detection and urgent surgical intervention is essential for this otherwise fatal disease entity. Key-words: Myocardium Heart, valves.

Case presentation A 59-year-old man was transferred to our radiology department because of general deterioration and a left ventricular ejection fraction of 50%. Besides diabetes mellitus type II, his medical history included a significant aortic valve stenosis and ischemic heart disease for which a combined intervention was performed with prosthetic aortic valve replacement (ON-X-23) and coronary artery bypass grafting 7 years previously. Three weeks earlier he had been admitted at a general hospital for atrial fibrillation with a fast ventricular response. After successful pharmacological reconversion to sinus rhythm he was discharged from hospital within a week. Because of prostatitis he had been taking ciprofloxacin for 7 days, 250 mg twice a day. Eight days later he was admitted again because of poor general condition, confusion and dyspnoea with intermittent fever, up to 38,5°C. Pleural fluid and a consolidation were seen on chest computed tomography. Combined antibiotic therapy was started. Blood cultures and culture of the pleural fluid were negative. Despite this therapy, blood sedimentation and C-reactive protein remained high. No vegetations were seen on transesophageal echocardiography but empirical amikacin was started because of suspected prosthetic valve endocarditis. Left ventricular ejection fraction was 50%. On admission in our university hospital he was alert and oriented, but ill. He had lost 10 kg of weight in the last 2 months. He was apyrexial, had a regular heart rhythm of 90 bpm and a blood pressure of

B Fig. 1. — A. First CT-evaluation in the referring hospital shows pleural fluid left and a hypodense thickening of the left ventricular wall. No pericardial fluid is seen. B. Imaging 2 weeks later shows enlargement and organisation of the lesion in the left ventricular wall: abscess formation. The abscess can be seen to dissect the myocardial wall.

141/90 mmHg. There were some crepitations in the left lung base and

From: Department of 1. Radiology, 2. Cardiac Surgery, Ghent University Hospital, Ghent, Belgium. Address for correspondence: Dr D. Devos, M.D., Department of Radiology, Ghent University Hospital, De Pintelaan 185, B-9000 Ghent, Belgium. E-mail: daniel.devos@uzgent.be

there was limited lower extremity oedema. An electrocardiogram showed a left bundle branch block. A PET-CT was performed for two reasons: to find an infectious origin of the suspected endocarditis and, because of his weight loss, nicotine (36 pack years) and alcohol abuse (56 U/day), to exclude a neoplasm.

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Radiological examination CT findings On CT, a large multiloculated mass was seen, with a hypodense, non-contrast enhancing content. This mass was largely located in the left ventricular wall, reaching from the aortic valve, over the proximal anterior LV wall to the apical lateral wall (Fig. 1B and 2). A small portion of this mass touched the prosthetic aortic valve. Compared with the first CT 2 weeks earlier, the speedy evolution as well as the organisation (central liquefaction) were strongly suggestive for abscess formation (Fig. 1A). The patient was referred for semiurgent surgical intervention. Surgery consisted of a repeat thoracotomy and opening of the pericardium. On the lateral apical wall of the left ventricle, a bulging intramyocardial abscess was found ready to rupture. This abscess was cut open along the entire length up to the level of the pulmonary trunk, thereby transecting an already occluded diagonal coronary branch. The close spatial relationship of the abscess with the prosthetic valve was confirmed. After opening the ascending aorta, vegetations were found underneath the prosthetic valve leaflets. The valve had migrated distally from the aortic annulus, but no paravalvular leak was found. The aortic valve ring and periaortic area were thoroughly cleaned. The valve was replaced by a bioprosthetic valve. An Enterococcus species was isolated from the excised aortic valve. The sensitivity of the enterococcus for ciprofloxacine has not been determined. MRI findings Four months after surgery an MRI examination of the heart was performed with the aforementioned bioprosthetic valve in aortic position. This posed no contraindication for MRI. No more abscess collection was seen in the myocardium nor perivalvulary. Wall motion was reduced in the basal and midventricular segment of the anterolateral wall, expanding to inferolateral in the apical segment. In this area a large, anterolateral subepicardial rest perfusion defect and a small akinetic segment in the lateral wall were noted. Delayed enhancement imaging revealed a linear subepicardial zone of myocardial fibrosis.

B Fig 2. — A. The multiloculated mass touches the aortic valve ring, and surrounds the extensively calcified left anterior descending coronary artery. B. Coronal reformatting shows the aortic valve prosthesis and the multiloculated mass in the left ventricular wall.

Overall examination showed normal ejection fraction. Discussion Cardiac abscess is an uncommon and life-threatening disease. It has been described in various anatomic locations of the heart including the atrial auricle (1), the ventricular free wall (2-4), the interventricular septum (3) or perivalvular (5-8). The most common situation in which a myocardial abscess will develop is infective endocarditis. The aortic valve region – native and prosthetic valve – is usually involved (9). Rarely, a metastatic myocardial abscess, remote from the main focus, results from coronary embolization of septic material (4). An abscess can also be found in the setting of septicaemia, without infective endocarditis (8, 9). Occasionally myocardial abscess can

occur at the site of a myocardial infarction (8, 9). There is a wide variety of clinical conditions in which an abscess of the myocardium can occur as a complication, including trauma and penetrating injuries, following invasive cardiac procedures, infection of a (pseudo-) aneurysm, cardiac tamponade, infected transplanted heart following a sternotomy abscess and HIV associated myocarditis (6, 9). The clinical picture of a myocardial abscess can range from an asymptomatic state to myocardial wall rupture (8). A rapid clinical deterioration will often lead to further diagnostic evaluation and recognition of a myocardial abscess, with symptoms including protracted fever despite adequate antibiotics, development of pericarditis, congestive heart failure or new onset arrhythmias in the context of infective endocarditis (6, 9). A few rare

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C Fig. 3. â&#x20AC;&#x201D; A. On the balanced Fast Field Echo Cine sequence there is a subtle increase in signal intensity in the anterolateral wall (midventricular segment). This segment is hypokinetic. B. Gradient Echo perfusion examination shows a defect anterolaterally in the midventricular segment. C. Inversion recovery 2d gradient echo imaging for delayed enhancement in end diastole shows irregular, linear, nearly transmural subepicardial enhancement in the anterior and anterolateral wall.

B cases of intermittent compression of a coronary artery by a paravalvular pseudoaneurysm or aortic valve abscess have been described (10, 11). Intracardiac fistulas are also a rare complication of infective endocarditis (12). Echocardiography is accepted as the non-invasive gold standard in the detection of myocardial abscesses (9). The trans-oesophageal approach has an improved sensitivity (80-88%) in comparison with the trans-thoracic echocardiography (2536%), providing better detection of paravalvular abscesses, associated vegetations, valvular perforations, fistulas and rupture of chordae

tendineae (13). Due to artifacts caused by valve prostheses or vascular calcifications, the echocardiographic diagnosis of an abscess remains difficult. These two echocardiographic approaches should therefore be considered as complementary techniques. CT is the appropriate technique for the extensive evaluation of thorax and mediastinum in a context of septicaemia. Computed Tomography can depict lesions that are not accessible by transoesophageal echocardiography (13). Cardiac MRI has a high temporal and spatial resolution. A few case reports and studies suggest its useful diagnostic value in the setting of compli-

cated endocarditis, especially in diagnosing annular abscess, subvalvular abscess and pseudoaneurysm (14). Exact morphologic evaluation including volume and extent of the abscess, and relation with the coronary arteries is mandatory in the pre-operative management (13). Patients with infective endocarditis, complicated by abscesses require aggressive antibiotic treatment and urgent surgical intervention (15, 16). Anderson D.J. et al. (2005) found that mortality tended to be higher in patients with nonenterococcal prosthetic valve endocarditis, compared to enterococcal prosthetic valve endocarditis; however there was no statistically significant relation (p = 0,08). Mortality and outcome of enterococcal endocarditis are similar in patients with either native or prosthetic valve endocarditis. Intracardiac abscesses are more likely to be found in patients with enterococcal prosthetic valve endocarditis, while patients with enterococcal native valve endocarditis are more likely to have detectable valve vegetations or new valvular regurgitation (17).

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In conclusion, myocardial abscess is a rare but life-threatening disease with various clinical presentations. It occurs most frequently in infective endocarditis, but several other causes have been described. Early detection and urgent aggressive intervention are essential. We report an unusual intramural location of a large, late post-surgical, paravalvular abscess. References 1. Lee J.R., Kim J.S., Lee C., Han K.N., Chang J.M.: Successful treatment of left atrial auricular abscess. J Korean Med Sci, 2003, 18: 441-443. 2. Shackcloth M.J., Dihmis W.C.: Contained rupture of a myocardial abscess in the free wall of the left ventricle. Ann Thorac Surg, 2001, 72: 617-619. 3. Lembcke A., Rogalla P., Dohmen P.M.: Images in cardiology: Coronary artery stenosis caused by an aortic root abscess. Heart, 2005, 91: 1302. 4. Iqbal J., Ahmed I., Baig W.: Metastatic myocardial abscess on the posterior wall of the left ventricle: a case report. J Med Case Reports, 2008, 2: 258. 5. Arnett E.N, Roberts W.C.: Valve ring abscess in active infective endocardi-

8. 9.

10.

11.

tis. Frequency, location, and clues to clinical diagnosis from the study of 95 necropsy patients. Circulation, 1976, 54: 140-145. Ashdot A., Neuman Y., Berner Y., Zissin R.: Mitral valve abscess due to infective endocarditis detected by computed tomography. Isr Med Assoc J, 2010, 12: 383-385. Saxena P., Boyt A., Newman M.A.: Mitral valve leaflet abscess complicating infective endocarditis. Heart Lung Circ, 2009, 18: 133-162. Ryon D.S., Pastor B.H., Myerson R.M.: Abscess of the myocardium. Am J Med Sci, 1966, 251: 698-705. Chakrabarti J.: Diagnostic evaluation of myocardial abscesses. A new look at an old problem. Int J Cardiol, 1995, 52: 189-196. Lembcke A., Hein P.A., Enzweiler C.N., Hoffmann U., Klessen C., Dohmen P.M.: Acute myocardial ischemia after aortic valve replacement: a comprehensive diagnostic evaluation using dynamic multislice spiral computed tomography. Eur J Radiol, 2006, 57: 351-355. Pothula V.R., Waked A., Sadel S.M., McGinn J.T. Jr., Cai J., Baldari D.: Prosthetic aortic valve abscess producing intermittent right coronary artery compression. Ann Thorac Surg, 2009, 87: 963.

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12. Gasparovic H., Smalcelj A., Brida M.: Left ventricle to left atrium shunt via a paravalvular abscess. Thorac Cardiovasc Surg, 2009, 57: 421-422. 13. Reynier C.h., Garcier J.M., Legault B., Motreff P., Ponsonnaille J., Ravel A., et al.: Imagerie en coupes et abcès myocardiques paravalvulaires sur mitrale native au décours d’endocardites infectieuses: 4 cas. J Radiol, 2001, 82: 665-669. 14. Iqbal J., Ahmed I., Baig W.: Metastatic myocardial abscess on the posterior wall of the left ventricle: a case report. J Med Case Reports. 2008, 2: 258. 15. David T.E., Regesta T., Gavra G., Armstrong S., Maganti M.D.: Surgical treatment of paravalvular abscess: long-term results. Eur J Cardiothorac Surg, 2007, 31: 43-48. 16. Arnoni A.S., Arnoni R.T., Paulista P.P., Martinez V.E., Almeida A.F., Abdulmassih Neto C., et al.: Surgery for aortic valve endocarditis: treatment options for aortic abscess. Arq Bras Cardiol, 2008, 91: 65-69. D.J., Olaison L., 17. Anderson McDonald J.R., Miro J.M., Hoen B., Selton-Suty C., et al.: Enterococcal prosthetic valve infective endocarditis: report of 45 episodes from the International Collaboration on Endocarditis-merged database. Eur J Clin Microbiol Infect Dis, 2005, 24: 665-670.

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LEFT VEIN OF LABBÉ THROMBOSIS ASSOCIATED WITH IPSILATERAL DURAL SINUS THROMBOSIS: NON-ENHANCED CT AND CONTRASTENHANCED CT (CTV) FINDINGS D.I. Stýblo-Šramek1, G. De Temmerman1,2, B.M. Verbist1 A rare case of aseptic thrombosis of the left vein of Labbé in a young woman is reported. Cerebral venous thrombosis was suggested by computed tomography and confirmed after intravenous administration of contrast by computed tomography venography. The combination of the clinical setting with the findings on the non-enhanced CT may favour the diagnosis of vein of Labbé thrombosis. The diagnosis can be confirmed on computed tomography venography. Key-word: Cerebral blood vessels, thrombosis.

Cerebral venous and sinus thrombosis accounts for less than 1% of all strokes and the estimated annual incidence is 3 to 4 cases per 1 million (1). Isolated involvement of superficial cortical veins is very unusual; involvement of an anastomotic vein like the vein of Labbé is extremely rare (2). Labbé’s vein (the inferior anastomotic vein) connects the superficial middle cerebral vein posteriorly over the lateral aspect of the temporal lobe to the transverse sinus. Its calibre shows an inverse relationship with that of Trolard’s vein (the superior anastomotic vein connecting the superficial middle cerebral vein to the superior sagittal sinus) (3). We report a case of aseptic thrombosis of the left vein of Labbé associated with an ipsilateral dural sinus thrombosis, suspected on nonenhanced CT and confirmed on CT venography (CTV).

Case report A 32-year-old woman was admitted to the psychiatry department after a suicide attempt following one week of severe headache she developed shortly after delivering her first child. The pregnancy had been uncomplicated. There was no relevant medical history. Neurologic examination on admission revealed no abnormalities. Routine laboratory findings were normal. The patient was evaluated with a non-enhanced CT followed by CT venography with use of a GE 16-MDCT scanner with a 3-D workstation. Non-enhanced CT was obtained with 2,5 mm-thick continuous axial sections through the

D Fig. 1. — Non-enhanced CT with axial reformatted images. Note the venous infarct in the left temporal lobe (white arrowheads) (A) and the hyperdense overlying vein of Labbé and transverse sinus on the same side (white arrows)- “the cord sign” (B, C). The left sigmoid sinus (black arrow) is hyperdense compared to the right side (black arrowhead) indicating a fresh thrombus on the left side (D).

posterior fossa followed by 5,0 mmthick contiguous axial sections to the vertex. Non-enhanced computed tomography demonstrated an area of gyral swelling with effacement of

From: 1. Department of Radiology, Leiden University Medical Center (LUMC),Leiden, the Netherlands, 2. Department of Radiology, AZ KLINA, Brasschaat, Belgium. Address for correspondence: Dr D.I. Stýblo-Šramek, Heidezegge 8, 2318 ZE Leiden, The Netherlands. E-mail: gunther.de.temmerman@telenet.be

the sulci along with subcortical hypodensity in the posterior part of the temporal lobe on the left side (Fig. 1 and 2). A dense tubular structure (cord sign) was seen overlying the occipitotemporal convexity in close proximity to the abnormal temporal area. In this location also considering the size of the structure, it had to be a vein travelling in the subarachnoid space. A meticulous look to the ipsilateral transverse and

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Fig. 2. — Non-enhanced CT: coronal multiplanar reconstructions. Note the hypodense area in the left temporal lobe (C) and the hyperdense overlying vein of Labbé (black arrowhead) (C). The transverse sinus is also hyperdense due to fresh thrombus (white arrow) (A, B).

Fig. 3. — CT venography with coronal reconstructions. Note the enhancement of the Labbé ‘s vein (white arrow) and the transverse and sigmoid sinus (white arrowhead) on the right side as compared to the filling defect on the left side due to fresh thombus (black arrow and arrowhead). Also compare figure 3 to figure 2 and note that the fresh thombus is mildly hyperdense and does not enhance. Note collateral veins in the ipsilateral medial occipital area (small black arrows) (1).

sigmoid sinuses showed a subtle hyperdensity compared to the right side. The diagnosis of cerebral venous and dural sinus thrombosis was considered and contrastenhanced CT or CT venography was performed to confirm or exclude the assumed diagnosis. CT venography was performed with a minimum section thickness of 0,625 mm and a pitch of 1 scanning caudally from the calvarial vertex to the skull base. The obtained images were reformatted retrospectively to images with 1-mm collimation and 1-mm spacing for 3D reconstructions. 80 mL nonionic contast material was administered at a rate of 3 mL/sec by means of a power injector and a 20-gauge catheter in an antecubital vein with a 80-second prescanning delay. CT

venography showed no enhancement of the left vein of Labbé and the ipsilateral transverse and sigmoid sinus (Fig. 3). Dilated tortuous collateral venous pathways were noted on the left side in comparison to the right side. Anticoagulant therapy was started and the patient recovered completely. She had no clinical sequelae, although follow-up CT-scan after 6 and 14 months demonstrated some tissue loss due to venous infarction within the left temporal lobe where we saw gyral swelling and subcortical oedema (images not shown). Discussion The vein of Labbé is known to collect blood from the cortical veins of

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the lateral temporal lobe and drains into the transverse sinus. The lower cerebral veins drain the temporal and posterolateral occipital lobes. They may either drain into the vein of Labbé or terminate separately in the transverse sinus (3). There are ten reports of thrombosis of the left vein of Labbé in the radiological literature. There is no description of thrombosis of the right vein of Labbé. Clinical signs of cerebral venous thrombosis in patients with an isolated occlusion of the Labbé’s vein described in the literature are receptive aphasia, motor aphasia, amnestic aphasia, alexia and agraphia. In our case, the symptom was non-specific but in combination with the clinical setting (young woman, post-partum period) was suggestive of cerebral venous and or sinus thrombosis. CT scanning is a useful screening technique for a quick evaluation of acute neurologic signs, to rule out cerebral disorders like haemorrhage, hydrocephalus and space-occupying lesions. In the appropriate setting one should always look for signs of cerebral venous and dural sinus thrombosis. Signs on non-enhanced CT are a dense delineation of a cortical vein known as the ‘cord sign’ and a hyperattenuating dural sinus known as the ‘dense triangle sign’. These signs are usually subtle and easily overlooked. Changes in the brain parenchyma drained by thrombosed veins or sinuses are not obligatory and dependent on collateral venous capabilities. Changes can be vasogenic (congestive) or cytotoxic (ischemic) oedema in the cortices and subcortical white matter or frank haemorrhagic transformation. CT venography with multiplanar reformatted (MPR) images has proved to be a reliable method to investigate the cerebral veins, with a reported sensitivity of 95% compared with digital subtraction angiography as the standard reference (4). Absence of enhancement of cerebral veins and dural sinus is the key to the diagnosis. The filling defect in a dural sinus is better known as the ‘empty delta sign’. Other clues can be an asymmetrical distribution of superficial veins with so-called ‘cork-screw collaterals’ ipsilateral to the thrombosed veins or sinuses. CT venography is superior to MR venography in the identification of cerebral veins and dural sinuses and is at least equivalent in establishing the diagnosis of dural sinus thrombosis (5-7). Advantages of CT venography as compared with

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MR venography are that it can be instantly performed as an adjunct to an unenhanced CT scan in patients undergoing the initial workup, easier patient monitoring and shorter examination time in critically ill patients, further its overall availability and last but not least it’s lower cost (4). Owing to its vascular detail and ease of interpretation, CT venography can provide a rapid and reliable diagnosis or exclusion of cerebral venous and dural sinus thrombosis as is demonstrated in our case. We are the first to report the findings of thrombosis of the left vein of Labbé on reformatted CT venography.

Conclusion Thrombosis of Labbé’s vein associated with ipsilateral dural sinus thrombosis is rare. Findings on non-

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enhanced CT in favour of the diagnosis are the ‘cord sign’ overlying the posterior aspect of the temporal lobe, the ‘dens triangle sign’ within the ipsilateral transverse and sigmoid sinus, gyral swelling with subcortical edema with or without hemorrhagic transformation. Diagnostic findings on multi-planar reformatted CT venography are the absence of enhancement of the Labbé’s vein and ipsilateral transverse and sigmoid sinuses (‘empty delta sign’) and ipsilateral collateral veins. References 1.

Linn J., Brückmann H.: Cerebral Venous and Dural Sinus Thrombosis. Clin Neuroradiol, 2010, 20: 25-37. 2. Boukobza M., Crassard I., Bousser M.G., Chabriat H.: MR Imaging Features of Isolated Cortical Vein Thrombosis: Diagnosis and Follow-Up. Am J Neuroradiol, 2008, 30: 344-348.

3. Schaller B.: Physiology of cerebral venous blood flow: from experimental data in animals to normal function in humans. Brain Research Reviews, 2004, 46: 243-260. 4. Wetzel S.G., Kirsch E., Stock K.W., Kolbe M., Kaim A., Radue E.W.: Cerebral veins: comparative study of CT venography with intraarterial digital subtraction angiography. AJNR Am J Neuroradiol. 1999, 20: 249-255. 5. Renowden S.: Cerebral venous sinus thrombosis. Eur Radiol, 2004, 14: 215226. 6. Ozsvath R.R., Casey S.O., Lustrin E.S., Alberico R.A., Hassankhani A., Patel M.: Cerebral venography: comparison of CT and MR projection venography. AJR, 1997, 169: 16991707. 7. Linn J., Ertl-Wagner B., Seelos K.C., Strupp M., Reiser M., Brückmann H. et al.: Diagnostic value of multidetector-row CT angiography in the evaluation of thrombosis of the cerebral venous sinuses. AJNR Am J Neuroradiol, 2007, 28: 946-952.

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THE ASSOCIATION OF INTRAMAMMARIAN ARTERIAL CALCIFICATIONS DETECTED ON MAMMOGRAPHY WITH CORONARY ARTERY DISEASE AND ITS RISK FACTORS B. Hekimog˘lu1, B. Demirler S¸ims¸ir1, E. Öztürk1, C. Yücesoy1, R. Akdemir2 Aim of the study: To evaluate the association of intramammarian arterial calcifications seen on mammography with coronary artery disease and its risk factors and to discuss intramammarian arterial calcifications value as a predictor of coronary artery disease. Material and methods: Mammography was performed on 55 women over 40 years of age who have undergone coronary angiography and have not had a mammography in the past year. Coronary angiography results, coronary artery disease risk factors and intramammarian arterial calcifications are evaluated. Results: The prevalance of intramammarian arterial calcifications was 41.8%. A significant relationship between intramammarian arterial calcifications and coronary artery disease was indicated (OR 10,8, 95% CI 3,02-38,59). The positive predictive value and negative predictive value of intramammarian arterial calcifications for coronary artery disease was 78.3% and 75% respectively. Also advancing age was found relevant with these calcifications (OR 1,15, 95% CI 1,05-1,25). Conclusion: The results support the present literature and suggest that mammography, already widely in use as a screening tool among women over 40, may be used simultaneously in coronary artery disease risk assessment. These results should be confirmed by further larger group controlled studies. Key-words: Breast radiography – Breast neoplasms, calcification – Coronary vessels, diseases.

Coronary artery disease (CAD) and cancer are the leading causes of female mortality and morbidity, especially in western countries (1, 2). Breast cancer is among the most common deaths caused by cancer. It is known that with early detection it is possible to lower the mortality rate (3). Currently, mammography is used as a screening tool for breast cancer and it is recommended yearly for women over the age 40 (4). Intramammarian arterial calcifications (IMAC) are defined as medial arterial sclerosis or Mönckeberg’s medial sclerosis and its prevalence varies from less than 1% to more than 50% on mammograms (5-7). These calcifications are unrelated to cancer and therefore, usually not mentioned in the final reports (5). There is a growing body of literature investigating the relationship of IMAC with cardiovascular diseases, diabetes and hypertension. It is suggested that IMAC can be used as a predictor of cardiovascular diseases (6, 8-11). CAD is the result of systemic arterial disease (12). Early detection of CAD is important because first cardiovascular events are often fatal in women (13). Currently there are no

widespread inexpensive suitable screening tests available for CAD (2). Detection of coronary artery calcifications with Electron Beam Tomography and ultrasound measurement of carotid intima-media thickness techniques could be used for risk assessment whereas there are large group studies showing these methods do not provide additional information to the traditional Framingham risk assessment in predicting future coronary events in high-risk individuals (14). Other drawbacks of these tests are not being always readily available for a large group of population, higher costs and possible difficulties in being accepted as a screening tool by patients. However mammography is a widely accepted, low cost screening tool for breast cancer and if IMAC is proved to be relevant to CAD, mammography could be simultaneously used to predict CAD risk without any additional health care costs. The purpose of the study was to evaluate the association of IMAC with CAD and its risk factors and to discuss intramammarian arterial calcifications value as a predictor of CAD.

From: Department of 1. Radiology, 2. Cardiology, S.B. Ankara Diskapi YB Training and Research Hospital, Ankara, Turkey. Address for correspondence: Dr B. Demirler S¸ims¸ir, M.D., Turan Gunes Bulvarı Korman Sitesi 4. Blok 51 D Daire:18 Yıldız/Ankara Turkey. E-mail: bdemirler@yahoo.com

Material and methods During a one-year period (November 2008 and October 2009) mammography was performed on 55 women over the age 40 who had undergone coronary angiography and have not had a mammography in the past year [age range 40-79 (mean age 63)]. All coronary angiographies were planned due to angina pectoris or exertional dyspnea. At least 50% lumen narrowing at least in one coronary artery is regarded as positive for CAD. This criteria was used in previous studies and relies on the fact that significant decrease of blood flow occurs with ≥ 50% stenosis (9, 15, 16). Patients hospital records were examined to evaluate CAD risk factors; hypertension, diabetes mellitus (DM), dyslipidemia and obesity. Hypertension is defined as systolic blood pressures 140 mmHg and higher, diastolic blood pressures 90 mmHg and higher or prescribed antihypertensive agents (17). Diabetes is regarded as positive when the patient is on antidiabetic treatment or fasting blood glucose levels are 126 mg/dl and higher or a random glucose level of 200 mg/dl. Dyslipidemia is regarded as positive if total cholesterol levels are 200 mg/dl and higher, LDL cholesterol levels are 130 mg/dl and higher, HDL cholesterol levels are 35 mg/dl and lower or if anti lipidemic agents are being used (18). The standard BRFSS (Behavioral Risk Factor Surveillance System) definition for obesity (body

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mass index [BMI] ≥ 30.0 kg/m2, calculated by using self-reported height and weight) was used. All patients underwent mammography 7-14 days after coronary angiography. For all patients standard views (craniocaudal and mediolateral-oblique) were obtained by Fischer HF-X Plus (Denver, CO) conventional mammography unit. Further views such as spot compression, and magnification were obtained when necessary. Two radiologists who have more than 6 years of experience in breast imaging, who were blind to coronary angiography results, clinical data and patients’ hospital records analysed the mammograms according to BIRADS (breast imaging and reporting data system) classification, also presence of IMAC was noted in the final reports. Parallel, linear calcifica-

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tions and amorphic calcifications in between along the course of a vessel in one or both breasts, at least on one mammographic view was defined as positive for IMAC (19). IMAC severity was not graded by any scoring system. Statistical analysis Data analysis was performed by using Statistical Package for Social Sciences (SPSS) version 11.5 software (SPSS Inc., Chicago, IL, United States). Whether the metric discrete variables were shown as mean ± standard deviation, otherwise, percentages were used for categorical variables. The mean differences between groups were evaluated by Student’s t test. Categorical date was analyzed by Pearson Chi-square or Fisher’s exact test, where appropriate. Multiple Logistic Regression

Analyses (Backward method) were used to control for potential confounding effects. Any variable whose univariable test had a p value less than 0.25 was accepted as a candidate for the multivariable model along with all variables of known clinical importance. Odds ratio (OR) and 95% confidence intervals (CI) for all independent variables were also calculated. A p value less than 0.05 was considered statistically significant. Results Coronary angiography results of 55 patients were evaluated; 26 of them (47.3%) had significant CAD, whereas 29 of them (52.7%) had no significant coronary artery stenosis (Table I). The prevalence for IMAC was calculated as 41.8%.

Fig. 1. — 72-year-old patient. A. Bilateral MLO and B. Bilateral CC mammogram views showing IMAC. Significant stenosis of coronary arteries detected on coronary angiography. The patient also had hypertension and dyslipidemia.

Fig. 2. — A. Bilateral MLO and B. bilateral CC mammogram views showing IMAC. Significant stenosis of coronary arteries detected on coronary angiography. The patient did not have hypertension, dyslipidemia or obesity.

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The mean age of CAD positive patients (67.3 ± 7.5) was higher than CAD negative group (59.1 ± 8.5) (p < 0.001). It is shown that advancing age was associated with significant increased risk of CAD (p < 0.001, OR 1.1). Among patients with positive findings for CAD, 18 (69.2%) patients also had IMAC on their mammograms (Fig. 1,2). Only 5 (17.2%) of the patients with negative CAD findings had IMAC on their mammograms It is calculated that recognition of IMAC on mammography increased the detection of the significant coronary artery stenosis (p < 0.001, OR 10.8). Hypertension was found to be a risk factor which increased the development of CAD (p < 0.05, OR 5.4). In the CAD positive group 92.3% of the patients were hypertensive compared with 69% hypertensive patients in the CAD negative group. The patients were also evaluated in terms of DM, dyslipidemia and obesity. DM and dyslipidemia prevalence was found higher in CAD positive group whereas the difference between CAD positive and negative groups was not statistically significant. All results regarding these issues are summarized in Table II. When multivariate logistic regression analyses were performed for risk factors, strong correlation was found between CAD and IMAC (OR: 5.4, p < 0.05). This correlation was even stronger after adjustment for risk factors (OO: 6.3, p < 0.05). Hypertension was not a significant factor for CAD on multivariate analyses (Table III). The correlation between IMAC and CAD and its risk factors is shown at table IV. Advancing age (OR 1.1), hypertension (OR 10) and positive CAD on angiography (OR 10.8) was found significantly associated with

Table I. — Patients distribution of CAD and IMAC. IMAC (-) (n)

IMAC (+) (n)

Total (n)

CAD (-)

CAD (+)

Total

IMAC. DM and dyslipidemia prevalence was also higher in IMAC positive group but the difference between two groups did not a reach statistically significant level. The sensitivity, specificity, and positive and negative predictive value of IMAC detected on mammograms for predicting prevalent CAD were 69.2%, 82.8%, 78.3% and 75%, respectively.

12 761 women over the age 40 who attended multiphasic health check ups that included mammography (8). IMAC prevalence was low (3%) compared with other studies (2, 6, 10, 21). This could be explained by low prevalence of CAD and its risk factors among the study population which consisted of generally healthy check up patients. Besides, the radiologists also might have overlooked IMAC as the tests were run for screening purposes. Iribarren et al. found significant positive correlation between IMAC and DM, increasing age and parity. After adjustment for other variants (age, education level, race, cigarette smoking, alcohol use, BMI, serum total cholesterol, hypertension, DM, parental history of myocardial infarction (MI), parity, and hormone replacement therapy), IMAC was associated with a 1.32-fold increased risk of CAD (8). Another study by Von Noord et al. reported a 9.1% IMAC prevalence among a 12.239-patient group which consisted of women over the age 50 who participated in a population-based breast cancer screening project. IMAC was found significantly related with hypertension, stroke and MI (6). In the present study, similar to Irribaren and Von Noord’s large group studies, significant relation was found between IMAC and CAD. On the other hand IMAC prevalence was 41.8 % which is a high value compared with mentioned other two studies. This is could be due to

Discussion IMAC is the result of calcium deposition in the media layer of arteries and it has a characteristic appearance on mammograms. These calcifications are rare under the age 50 and seen as railroad track pattern or ring-like on ‘en face’ images. Their mechanism is not clearly known (20). Calcium deposits were considered as a natural part of aging and were thought to have no clinical significance but recent studies show correlation between IMAC and CAD and cardiovascular mortality (6, 8, 9). The prevalence of IMAC varies from less than 1% to more than 50% in previous studies (7). The possible reasons for this wide range are the differences in baseline risks of study groups, increase in detection of calcification with advancing imaging technology and IMAC not being mentioned in the final reports because it is not relevant to malignity. Iribarren et al performed a large group cohort study among

Table II. — Comparison of IMAC and CAD risk factors prevalence between positive and negative CAD patients. Variants Age IMAC

CAD negative (n = 29) (%)

CAD positive (n = 26) (%)

OR* (%95 CI**)

59,1 ± 8,5

67,3 ± 7,5

< 0,001

1,136 (1,049-1,231)

5 (17,2%)

18 (69,2%)

< 0,001

10,800 (3,022-38,594)

20 (69,0%)

24 (92,3%)

0,031

5,400 (1,044-27,924)

10 (34,5%)

13 (50,0%)

0,244

1,900 (0,642-5,623)

Dyslipidemia

18 (62,1%)

17 (65,4%)

0,799

1,154 (0,383-3,476)

Obesity

9 (31,0%)

3 (11,5%)

0,081

0,290 (0,069-1,220)

Hypertension

* Odds Ratio ** Confidence Interval.

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Table III. — Correlation of positive CAD with IMAC after adjustment for risk factors. Variants

Odds Ratio

Wald

%95 Confident Interval

Age

1,095

3,781

0,052

0,999-1,201

Hypertension

1,979

0,529

0,467

0,315-12,451

2,870

2,064

0,151

0,681-12,093

Obesity

0,574

0,369

0,543

0,096-3,435

IMAC

5,415

5,083

0,024

1,247-23,512

Age

1,098

4,070

0,044

1,003-1,203

Hypertension

2,077

0,616

0,432

0,335-12,877

2,757

1,955

0,162

0,665-11,428

IMAC

5,796

5,602

0,018

1,353-24,838

Age

1,102

4,425

0,035

1,007-1,207

2,784

2,026

0,155

0,680-11,402

IMAC

6,652

6,971

0,008

1,629-27,156

Age

1,091

3,906

0,048

1,001-1,190

IMAC

6,315

6,976

0,008

1,609-24,789

Model I

Model 2*

Model 3**

Model 4***

* adjustment for obesity ** adjustment for obesity and hypertension *** adjustment for obesity, hypertension and DM.

Table IV. — Correlation between IMAC and CAD and its risk factors. Variants Age

IMAC Negative (n = 32)

IMAC positive (n = 23)

OR*(%95 CI**)

59,4 ± 8,9

68,0 ± 6,5

< 0,001

1,152 (1,056-1,256)

CAD (+) Angiography

8 (25,0%)

18 (78,3%)

< 0,001

10,800 (3,022-38,594)

Hypertension

22 (68,8%)

22 (95,7%)

0,017

10,000 (1,178-84,900)

13 (40,6%)

10 (43,5%)

0,832

1,124 (0,380-3,327)

Dyslipidemia

19 (59,4%)

16 (69,6%)

0,438

1,564 (0,503-4,862)

Obesity

10 (31,3%)

2 (8,7%)

0,046

0,210 (0,041-1,071)

* Odds Ratio ** Confidence Interval.

increased CAD risk in the present study population, also attention was paid to mention the presence of IMAC on mammography reports as a part of study design. Henkin et al. reported IMAC prevalence as 41% among 319 patients (187 patients with severe CAD and 132 patients with negative CAD on coronary angiography) (21). The study population was parallel with the present study and consisted of patients who had undergone

coronary angiography with suspicion of CAD. Although the IMAC prevalence of the two studies show noteworthy similarity, Henkin et al. did not find significant relation between IMAC and CAD. The authors reported that regarding only severe stenosis as CAD positive might have a role in this result. They found significant relation between IMAC and increasing age, hypertension and DM. In our study IMAC and hypertension was found correlated on uni-

variate analyses whereas on multivariate analyses the correlation was not found significant. This result might have been due to our limited study population. IMAC detected on mammography might point to CAD and increasing age seems an important risk factor for CAD and IMAC. Dale et al. found significant relation between IMAC and CAD, between IMAC and increasing age (2). The present study also supports their result showing

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significant relation between IMAC and CAD, and also between IMAC and increasing age. Another study by Moshyedi et al. evaluated the relation between IMAC and CAD in a 182-patient study and they divided the patients into two age-groups; aged below 59 and aged above 59. All patients had undergone coronary angiography and mammography, similar to the present study. In the age-below-59 group IMAC’s positive predictive value and negative predictive value for CAD was found 88% and 65% respectively which is a statistically significant result. On the other hand they did not find a strong correlation in the aged above 59 group and stated that the correlation decreased with increasing age (9). In the present study, the patients were not classified according to age and IMAC’s positive predictive value and negative predictive value for CAD is 78.3% and 75% respectively. Oliveira et al. evaluated CAD and its risk factors relation in their study and on multivariate analyses, they found hypertension, family history and IMAC associated with CAD (22). In the present study, in addition to increasing age and IMAC, hypertension was also found to be associated with CAD on univariate analyses. Hypertension is a well known risk factor for CAD, whereas on multivariate analyses it was not found to be significant for CAD. This could be due to small population of the present study as previously mentioned. There are several studies showing significant association between DM and IMAC and suggesting IMAC as an additional risk factor for diabetic women (7, 23, 24). On the contrary, there are other authors claiming IMAC and DM are not related (25, 26). Sickles and Galvin’s study showed IMAC to be related to increasing age rather than DM (25). Similarly in the present study, IMAC and increasing age showed correlation (p < 0,001) although IMAC and DM did not have a significant relation (p > 0.05). Although the present study supports significant association between IMAC and CAD, a limitation of the study is that the number of cases is too limited for broad generalizations. Before IMAC could be considered a clue for CAD, confirmation by further large group controlled studies is necessary. Conclusion CAD is a leading cause of death and it may present as a fatal cardio-

vascular event. Early detection is highly important whereas there are no current widespread suitable screening tests for CAD and the patients are evaluated for risk factors. Mammography is a widely used, well accepted screening tool for another leading cause of death among women, breast cancer. If IMAC is proved to be an independent risk factor for CAD, mammograms could be simultaneously used to predict CAD risk. The results of the present study support the present literature, indicating a significant relationship between IMAC and CAD. After adjustment for well known risk factors, increasing age and IMAC are found to be independently and significantly important to predict CAD. This study suggests that mammography, already widely in use as a screening tool among women over 40, may be used simultaneously in coronary artery disease risk assessment without any additional health costs. Indicating IMAC in the final mammography reports is important as it could alert the clinician to evaluate the previously unsuspected patient for CAD with further tests. However it has to be emphasized that the results of the study are based on a relatively low number of patients and they should be supported with larger group controlled studies before IMAC could be considered an indicator of CAD, grading of IMAC and CAD could also be useful.

10.

11.

12.

13.

14.

15.

References 1. National Heart, Lung, and Blood Institute Web site. Morbidity and mortality: 2004 chartbook on cardiovascular, lung and blood diseases [chartbook online]. Bethesda, MD: National Institutes of Health, 2004: 59. 2. Dale P.S., Mascarhenas C., Richards M., Mackie G.: Mammography as a screening tool for coronary artery disease. J Surg Res, 2008, 148: 1-6. 3. Topuz E., Aydıner A.: Meme Kanseri, Biyoloji, Tanı, Evreleme, Tedavi. 1.basım, Istanbul, Nobel kitabevi, 2000, pp 136-138. 4. Dale P.S., Graham J., Nichols K.W., Catchings T., Richards M.: Mammography as a screening tool for peripheral vascular disease. Am J Surg, 2006, 192: 488-491. 5. Kim H., Greenberg J.S., Javitt M.C.: Breast calcifications due to Mönckeberg medial calcific sclerosis. RadioGraphics, 1999, 19: 1401-1403. 6. van Noord P.A., Beijerinck D., Kemmeren J.M., van der Graaf Y.:

16.

17.

18.

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Mammograms may convey more than breast cancer risk: breast arterial calcification and arterio-sclerotic related diseases in women of the DOM cohort. Eur J Cancer Prev, 1996, 5: 483-487. Leinster S.J., Whitehouse G.H.: Factors which influence the occurrence of vascular calcification in the breast. Br J Radiol, 1987, 60: 457-458. Iribarren C., Go A.S., Tolstykh I., Sidney S., Johnston S.C., Spring D.B.: Breast vascular calcification and risk of coronary heart disease, stroke, and heart failure. J Womens Health (Larchmt), 2004, 13: 381-389. Moshyedi A.C., Puthawala A.H., Kurland R.J., O’Leary D.H.: Breast arterial calcification: association with coronary artery disease. Work in progress. Radiology, 1995, 194: 181183. Cetin M., Cetin R., Tamer N.: Prevalence of breast arterial calcification in hypertensive patients. Clin Radiol, 2004, 59: 92-95. Crystal P., Crystal E., Leor J., Friger M., Katzinovitch G., Strano S.: Breast artery calcium on routine mammography as a potential marker for increased risk of CVD. Am J Cardiol, 2000, 86: 216-217. Schoepf U.J., Becker C.R., Ohnesorge B.M., Yucel E.K.: CT of coronary artery disease. Radiology, 2004, 232: 18-37. Mosca L., Grundy S., Judelson J., et al.: AHA/ACC Consensus Panel Statement: A guide to preventive cardiology for women. Circulation, 1999, 99: 2480-2484. Pearson T.: New tools for coronary risk assessment: What are their advantages and limitations?. Circulation, 2002, 105: 886-892. Breen J.F., Sheedy P.F. II., Schwartz R.S., et al.: Coronary artery calcification detected with ultrafast CT as an indication of coronary artery disease. Radiology, 1992, 185: 435-439. Gould K.L., Lipscomb K., Hamilton G.W.: Physiologic basis for assessing critical coronary stenosis: instantaneous flow response and regional distribution during coronary hyperemia as measures of coronary flow reserve. Am J Cardiol, 1974, 33: 8794. Chobanian A.V., Bakris G.L., Black H.R., et al.: National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA, 2003, 42: 1206-1252. National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Circulation, 2002 17, 106: 3143-421.

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234 19. Sickles E.A.: Breast calcifications: mammographic evaluation. Radiology, 1986, 160: 289-293. 20. Kumar V., Abbas A.K., Fausto N.: Robbins Basic Pathology. 8th ed. Philadelphia, Pa: Saunders Elsevier, 2007, pp 343-344. 21. Henkin Y., Abu-Ful A., Shai I., Crystal P.: Lack of association between breast artery calcification seen on mammography and coronary artery disease on angiography. J Med Screen, 2003, 10: 139-142. 22. Oliveira E.L.C., Freitas-Junior R., Afiune-Neto A., Murta E.F.C.,

JBRâ&#x20AC;&#x201C;BTR, 2012, 95 (4) Ferro J.E., Melo A.F.B.: Vascular calcifications seen on mammography: an independent factor indicating coronary artery disease. Clinics, 2009, 64: 763-767. 23. Pecchi A., Rossi R., Coppi F., et al.: Association of breast arterial calcifications detected by mammography and coronary artery calcifications quantified by multislice CT in a population of post-menopausal women. Radiol Med, 2003, 106: 305-312. 24. Maas A.H., van der Schouw Y.T., Mali W.P., et al.: Prevalence and determinants of breast arterial calcium in

women at high risk of cardiovascular disease. Am J Cardiol, 2004, 94: 655659. 25. Sickles E.A., Galvin H.B.: Breast arterial calcification in association with diabetes mellitus: too weak a correlation to have clinical utility. Radiology, 1985, 155: 577-579. 26. Schmitt E.L., Threatt B.A.: Relationship of mammographic intra-arterial calcifications and diabetes. South Med J, 1984, 77: 988-989.

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GRANULAR CELL TUMOR OF THE BREAST A.S. Celebi1, G. Toksoy1, A. Ozel1, K.C. Caliskan1, F. Kabukcuoglu2 Granular cell tumor is a rare benign soft-tissue neoplasm, usually appearing in the tongue, the oral cavity and subcutaneous tissue. Examples of granular cell tumor of breast are encountered in 30-50-year-old women. Herein, we report ultrasonographic and mammographic imaging findings of a 59 years old woman presented with a painless palpable mass, which was diagnosed as granular cell tumor on histopathological analysis. Key-word: Breast neoplasms.

Granular cell tumor (GCT) was first described as a separate clinicopathologic entity in 1926 by Abrikossoff (1) and was originally given the name granular cell myoblastoma. Granular cell tumor, an almost always benign neoplasm of putative Schwann cell origin, occurs in a wide variety of visceral and cutaneous sites. When it occurs in the breast , this uncommon lesion must be differentiated from primary breast carcinoma. Clinically, GCTs can

mimic carcinoma because of their fibrous consistency and hence their hardness, thus presenting as a palpable mass. Here in this report we are presenting the mammographic and ultrasound findings of GCT of breast in a 59 year old woman. Case report A 59-year-old woman presented to our radiology department with a palpable mass in her upper outer

quadrant of the right breast. At physical examination, a hard, painless mass without skin fixation was found in the upper outer quadrant of the right breast, at the axillary tail. Standard mammography, including mediolateral oblique view showed a 2 cm sized hyperdense mass with spiculated margins (Fig. 1). The lesion was not visible on craniocaudal view. There was no paranchymal distortion, associated microcalcifications or skin thickening. At ultrasound

Fig. 1. — MLO view of the right breast shows a hyperdense mass with spiculated margins at the axillary tail.

From: Department of 1. Radiology, 2. Pathology, Sisli Etfal Training and Research Hospital, Istanbul, Turkey. Address for correspondence: Dr A. Ozel, M.D., Department of Radiology, Sisli Etfal Training and Research Hospital, 34377 Istanbul, Turkey. E-mail: dralperozel@gmail.com

Fig. 2. — A: Gray scale ultrasound image of the lesion demonstrates a hypoechoic mass with strong acoustic shadowing. B: Power Doppler ultrasound image of the lesion.

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Fig. 3. — A: Granular cell tumor composed of cells with dark small nuclei and granular eosinophilic cytoplasm (H&E × 400). B: S100 protein immunoreactivity in granular cell tumor (×400).

examination, there was a round, hypoechoic solid mass with angular margins, associated with marked acoustic shadowing. The ultrasonographic and mammographic findings were assumed as compatible with breast carcinoma (Fig. 2). Ultrasound guided core biopsy was performed for histological diagnosis and histological assessment revealed infiltration of large rounded or polygonal cells with small, dark nuclei and coarsely granular eosinophilic cytoplasm and it was diagnosed as granular cell tumor. Immunohistochemical study showed positive staining for S100 and CD68 (Fig. 3A,B). Discussion GCT of the breast is rare, with an incidence of 5-8%, and occurs in approximately 1 in every 1,000 breast cancers (2). Patients with GCT of the breast are usually middle-aged, premenopausal women, although rare examples have been reported in males (3). The lesion usually presented as a painless, firm, mobile mass in the upper inner quadrant of the breast, corresponding to the cutaneous sensory territory of the supraclavicular nerve, which thought to derive from Schwann cells (2). When there is fixation to the pectoral fascia, chest wall or skin, there can be dimpling, retraction or edema which can simulate cancer that originated from breast or ectopic gland (4). Mammographic appearance of GCT ranges from a round, well-circumscribed mass to a distinct or spiculated lesion. Micro-

calcifications are not usually a feature of GCTs . At ultrasound, GCT may manifest as a solid, poorly marginated mass with marked posterior acoustic shadowing (4), alternatively it may have a benign appearance as a well-circumscribed solid mass (5, 6). MRI could be performed to evaluate the extent of the disease and the presence/absence of aggressive features seen in other breast malignancies. The MRI findings of GCT of the breast reported in the literature include isointensity on T1 and T2 weighted images and nonhomogeneous rim enhancement after gadolinium injection (7). It is not possible to establish a definitive diagnosis of GCT of the breast clinically or radiologically, without a biopsy. At pathological analysis, GCT manifests as a pattern of closely packed nests of cells with abundant cytoplasm containing numerous fine eosinophilic granules (6). The neoplastic cells of the tumor typically express S100 and CD68 (KP-1), the latter as a result of cytoplasmic lysosome content. However, the exact histogenesis of this tumor is still unknown (8). Wide local excision is curative for GCT, but local recurrence has been reported after incomplete excision. In addition, malignant GCT with metastases has been described in the literature (2). In conclusion, GCT of the breast is a rare benign neoplasm that bears similar mammographic and ultrasound appearances with breast cancer. The definite diagnosis can usually be achieved with histopathological assessment. The treatment of GCT is wide local excision and it

should be kept in the differential diagnosis list of breast masses. References 1.

Abrikossoff A.: Uber myome, ausgehend von der quergestreiften, wilkurlichen Muskulatur. Virchows Arch Pathol Anat, 1926, 260: 215. Adeniran A., Al-Ahmadie H., Mahoney M.C., Robinson-Smith T.M.: Granular cell tumor of the breast: a series of 17 cases and review of the literature. Breast J, 2004, 10: 528-531. Lauwers K., Bestman T.J., Bergmans G., Molderez C.: Granular cell tumour of the male breast. Acta Chir Belg, 2008, 108: 112-114. Scatarige J.C., Hsiu J.G., de la Torre R., et al.: Acoustic shadowing in benign granular cell tumor (myoblastoma) of the breast. J Ultrasound Med, 1987, 6: 545. Yang W.T., Edeiken-Monroe B., Sneige N., Fornage B.D.: Sonographic and mammographic appearances of granular cell tumors of the breast with pathological correlation. J Clin Ultrasound, 2006, 34: 153-160. Miller J.A., Karcnik T.J., Karimi S.: Granular cell tumor of the breast: definitive diagnosis by sonographically guided percutaneous biopsy. J Clin Ultrasound, 2000, 28: 89-93. Scaranelo A.M., Bukhanov K., Crystal P., Mulligan A.M., O'Malley F.P.: Granular cell tumour of the breast: MRI findings and review of the literature. Br J Radiol, 2007, 80 (960): 970974. Le B.H., Boyer P.J., Lewis J.E., Kapadia S.B. : Granular cell tumor: immunohistochemical assessment of inhibin-alpha, protein gene product 9.5, S100 protein, CD68, and Ki-67 proliferative index with clinical correlation. Arch Pathol Lab Med, 2004, 128: 771-775.

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GASTROINTESTINAL TRACT WALL VISUALIZATION AND DISTENTION DURING ABDOMINAL AND PELVIC MULTIDETECTOR CT WITH A NEUTRAL BARIUM SULPHATE SUSPENSION: COMPARISON WITH POSITIVE BARIUM SULPHATE SUSPENSION AND WITH WATER M.R. Oliva, S.M. Erturk, T. Ichikawa, T. Rocha, P.R. Ros, S.G. Silverman, K.J. Mortele Objective: When examining patients with contrast-enhanced multidetector-row CT, we determined if the stomach and small bowel were visualized and distended better with a neutral barium sulphate suspension than with positive barium sulphate suspension or water. Materials and methods: After obtaining approval from our institutional review board, 156 patients (women: 84; mean age: 54 yrs) with no history of gastrointestinal tract disease were randomized prospectively to receive orally either 900 ml of neutral (0.1%w/v) barium sulphate suspension (n = 53), 900 ml of positive (2.1%w/v) barium sulphate suspension (n = 53), or 900 ml of water (n = 50), prior to undergoing contrast-enhanced abdominal and pelvic multidetector-row CT. Two independent radiologists evaluated the stomach, and small bowel, for luminal distension and wall visualization, using a five point scale. Results were compared using Kruskal-Wallis and Mann-Whitney U tests. Results: The walls of the stomach, and small bowel were visualized better in patients who were administered neutral barium sulphate suspension than those who were administered either positive barium sulphate suspension (p < 0.01) or water (p < 0.01). In patients who received neutral barium sulphate suspension, the stomach and small bowel were distended better compared to patients administered water (p < 0.01); the stomach, duodenum, and ileum were distended better compared to patients administered positive barium sulphate suspension (p < 0.05). Conclusions: When examining patients with intravenous contrast-enhanced abdominal and pelvic multidetector-row CT, orally administered neutral barium sulphate suspension allows the gastrointestinal tract to be visualized and distended better than either positive barium sulphate suspension, or water. Key-words: Abdomen, CT – Pelvis, CT – Barium.

The stomach and small bowel are two of the most challenging organs to be assessed radiologically. The stomach is variable in shape and is often not distended. The small bowel is a long, tortuous, and tubular organ whose loops often overlap and are variable in their position (1). With the introduction of multidetector-row CT (MDCT), the entire abdomen and pelvis can be scanned during a short breathhold such that blurring due to motion is minimized. Furthermore, spatial resolution is improved and isotropic with the use of thin collimation (2). However, regardless of the technique used, the stomach and small bowel need to be distended for their lumen and walls to be evaluated (1, 3). The stomach can be examined fluoroscopically; and the small bowel with enteroclysis, a relatively invasive method using fluoroscopy or CT, that requires infusing contrast medium directly into the small bowel via a nasojejunal tube (4).

Positive oral contrast material is currently used for abdominal and pelvic CT scans, typically barium sulphate suspension (2.1%w/v). However, it often obscures the bowel wall and does not allow the enhanced bowel wall to be discriminated from dense luminal fluid. Also, positive oral contrast material may obscure other dense structures of interest, such as blood vessels and the urinary tract (2, 5-8). As a result, positive oral contrast material is typically not used during CT angiography and CT urography (9, 10). However, when oral contrast agent is not used, the small bowel is often collapsed and, therefore, the small bowel cannot be evaluated for masses and other abnormalities. At times, collapsed small bowel may mimic or obscure an abdominal mass or an abscess (11). Water has been used as a neutral oral contrast agent for abdominal and pelvic CT (2, 12, 13) . It is safe

From: Division of Abdominal Imaging and Intervention, Department of Radiology, Brigham and Women’s Hospital – Harvard Medical School Boston, MA, USA. Address for correspondence: Dr M.R. Oliva, M.D., Division of Abdominal Imaging and Intervention, Department of Radiology, Brigham and Women’s Hospital, 75 Francis St., Boston, MA, 02115. E-mail: maria_oliva@hms.harvard.edu This study was supported, in part, by a grant from EZEM Inc, Lake Success, NY. Both readers were not funded by the grant. The authors had control of the data and information submitted for publication. This study was compliant with the Health Insurance Portability and Accountability Act and was approved by our institutional review board.

and acceptable to patients (2, 10). Because the luminal fluid is hypodense, the enhancing wall can be visualized (2). However, water is absorbed rapidly by the stomach and proximal small bowel; as a result, the distal small bowel is rarely distended (2). A neutral barium sulphate suspension (0.1% w/v BaSO4- VoLumen®, EZEM, Lake Success, NY) has been developed for abdominal and pelvic CT with the purpose of providing a solution that results in luminal fluid attenuation that is close to water. Initial study with this agent showed good distention in patients with known or suspected pancreatic or biliary tract disease (14). The purpose of this study was to determine if, when examining patients with abdominal and pelvic contrast-enhanced multidetectorrow CT, the stomach and small bowel are visualized and distended better with a neutral barium sulphate suspension than with positive barium sulphate suspension or water. Materials and methods Patients and oral contrast media From September 2004 to September 2005, outpatients scheduled for intravenous contrastenhanced abdominal and pelvic MDCT were asked to participate in

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this study. Written informed consent was obtained from each enrolled patient. Inclusion criteria included patients who were 18 years of age or older, and without a history of gastrointestinal tract disease. The exclusion criteria included women known to be pregnant or lactating, patients known to be allergic to barium sulphate suspension, or patients on a restricted fluid diet or unable to drink fluid. One hundred and fifty six consecutive patients who met the eligibility criteria were randomized prospectively to drink either 900 ml of low attenuation barium sulphate suspension (VoLumen®, EZEM, Lake Success, NY) (n = 53), 900 ml of high attenuation barium sulphate suspension (ReadCat®, EZEM, Lake Success, NY) (n = 53), or 900 ml of filtered tap water (n = 50) over approximately one-hour time period, prior to the multidetector-row CT scan. The initial randomization list included a larger number of patients to be examined. However, due to significant results on our periodic assessment the study was terminated earlier. At this time there was a smaller number of patients in the water group, which explains the small discrepancy between the 3 groups. Both barium sulphate suspensions were fully prepared by the manufacturer in advance of the day of the scan, this including dilution with citric acid, natural gum, benzoic acid, sodium citrate, artificial blueberry flavor, potassium sorbate, purified water, saccharin sodium, simethicone emulsion, sodium benzoate, and sorbitol. Patients who received neutral barium sulphate solution included 28 women and 25 men; 45 patients were white, 5 were black, and 3 were from other racial backgrounds. Indications for the MDCT scan included: staging cancer (n = 42), suspected liver lesion (n = 6), abdominal pain (n = 2), and 3 were performed for other indications (suspected pancreatic lesion, gluteal mass, and trauma). Mean age was 53 years (range: 21-80 years); mean weight was 78 kg (range: 43-127 kg, standard deviation: 19 kg); and mean height was 171 cm (range: 150191 cm, standard deviation: 9 cm). Patients who received high-density barium sulphate suspension included 31 women and 22 men; of whom 46 were white, 3 were black, and 4 were from other racial backgrounds. Indications for the study included: staging cancer (n = 36),

JBR–BTR, 2012, 95 (4)

suspected liver lesion (n = 4), abdominal pain (n = 10), and 3 were performed for other indications (suspected pancreatic lesion, pancreatitis, and follow-up of enlarged perihepatic lymph nodes). Mean age was 53 years (range: 27-77 years); mean weight was 78 kg (range: 41147 kg, standard deviation: 21 kg); and mean height was 169 cm (range: 150-191 cm, standard deviation: 11 cm). Patients who received water included 25 women and 25 men; 43 of whom were white, 5 were black, and 2 were from other racial backgrounds. Indications for the study included: staging cancer (n = 37), abdominal pain (n = 4), hematuria (n = 3), follow-up of renal mass (n = 2), suspected liver lesion (n = 1), and in 3 patients there were other indications (suspected pancreatic lesion, splenic lesion, and lymphadenopathy). Mean age was 57 years (range: 28-78 years); mean weight was 78 kg (range: 39-125 kg, standard deviation: 19 kg); and mean height was 172 cm (range: 157198 cm, standard deviation: 11 cm). Adverse reactions to one of the 3 oral contrast agents used were documented if reported by the patients.

with the readers was conducted by the study coordinator to review classification criteria and practice reading 10 cases that were not used for the study. Anatomic landmarks were used to define stomach, duodenum, and small bowel. Bowel wall visualization and bowel distention were estimated. Bowel wall visualization (identification of bowel wall as a separate structure from the lumen content and adjacent structures) was graded as: 1.0 = not identified; 1.5 = identified in < 30% of the assessed segment; 2.0 = identified in 30-60% of the segment; 2.5 = identified in 6180% of the segment; 3.0 = identified in > 80% of the segment. Distension was defined as separation of the lumen and was graded based on an estimate of both the amount of distention and the length of the distended segment. Bowel distention was graded as: 1.0 = no distention (lumen not visible in any portion of the segment); 1.5 = distended lumen identified in < 30% of the segment; 2.0 = distended lumen identified in 3060% of the segment; 2.5 = distended lumen identified in 61-80% of the segment; 3.0 = distended lumen identified in > 80% of the segment.

Abdominal and pelvic MDCT scan technique

Statistical analysis

Patients underwent MDCT scans of the abdomen and pelvis with commercially available multidetector-row CT scanners (Sensation 4 and Sensation 16; Siemens Medical Solutions, Erlangen, Germany). All scans were performed 70 seconds after the IV administration of 100 ml of iopromide 300 mg I/mL (Ultravist 300®, Berlex, Wayne, NJ), at a flow rate of 2-3 ml/sec using a mechanical power injector. Images were reconstructed as five mm axial sections with no overlap. Image analysis Images were evaluated independently by two radiologists with 18 and 7 years of experience in reading abdominal and pelvic CT scans, respectively; they were not informed about the type of oral contrast agent administered. Using a picture archiving and communication system (PACS) workstation (AGFA-Gevaert AG, Belgium) with monitor’ resolution of 1280 × 1024 pixels, wall visualization and distension of the stomach, duodenum, jejunum and ileum, were assessed using a qualitative five point scoring scale. Prior to the image analysis, a test session

Differences in demographic information between the groups were evaluated with chi-square test (gender and race) and ANOVA (age, weight, and height). Differences were considered statistically significant if p < 0.05. ANOVA was also employed to analyze differences in mean time interval between the MDCT scan and the start of ingestion. For each reader, statistical analyses of the differences in mean scores for wall visualization and distention were performed using KruskalWallis and Mann-Whitney U tests for each segment. Differences were considered significant if p < 0.05. Interobserver agreement for wall visualization and distention of each segment was evaluated using linearweighted kappa statistics. Kappa statistics results were classified as: less than chance agreement (< 0), slight agreement (0.01-0.20), fair agreement (0.21-0.40), moderate agreement (0.41-0.60), substantial agreement (0.61-0.80), and almost perfect agreement (0.81-0.99) (15). Results There were no significant differences among the three groups

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Fig. 1. — 22-year-old man with prior history of testicular cancer. Intravenous contrast-enhanced transverse CT scans of the abdomen and pelvis after oral administration of neutral barium sulphate suspension. Both readers graded the stomach (A) wall visualization and distention as 3.0. Jejunal (B) wall visualization was graded as 2.5, and distention as 2.5 and 2.0. Ileal (C) wall visualization was graded as 2.5, and distention as 2.5 and 2.0.

Fig. 2. — 51-year-old woman with prior history of lymphoma. Intravenous contrast-enhanced transverse CT scans of the abdomen and pelvis after oral administration of positive barium sulphate suspension. Both readers graded the stomach (A) wall visualization as 1.5, and distention as 2.0. Jejunal (B) wall visualization was graded as 1.5, and distention as 2.0. Ileal (C) wall visualization was graded as 1.0, and distention as 1.5.

Fig. 3. — 48-year-old woman for follow-up of suspected splenic lesion. Intravenous contrast-enhanced transverse CT scans of the abdomen and pelvis after oral administration of water. Both readers graded the stomach (A) wall visualization and distention as 2.0 and 1.5. Jejunal (B) wall visualization was graded as 2.0 and 1.5, and distention as 1.5. Ileal (C) wall visualization and distention were graded as 1.0.

regarding patients’ gender and race, mean age, weight, and height. Using ANOVA, mean time interval between the MDCT scan and the start of ingestion of neutral barium sulphate (81 min), positive barium sulphate (91 min), and water (84 min) were not significantly different. None of the patients reported adverse reaction to the oral contrast media administered.

The walls of the stomach, duodenum, jejunum, and ileum were visualized better in patients who were administered neutral barium sulphate suspension than in patients who were administered either positive barium sulphate suspension or water (Fig. 1-3). Stomach and small bowel were also distended better in patients who were administered neutral barium sulphate suspension

compared to patients administered water; stomach, duodenum, and ileum were distended better compared to patients administered positive barium sulphate suspension (Tables I and II). For reader 1, when comparing patients who were administered neutral barium sulphate suspension with those who were administered positive barium sulphate suspen-

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Table I. â&#x20AC;&#x201D; Comparison of mean scores for wall visualization and distention of anatomic segments assessed with contrast enhanced MDCT for reader 1. CT Images Assessment

Barium Sulphate Suspensions 0.1%

2.1%

Water

p value #

Wall visualization

Stomach Duodenum Jejunum Ileum

2.60 2.31 2.36 2.46

1.99 1.87 2.05 2.07

1.98 1.85 1.92 1.96

< 0.01 < 0.01 < 0.01 < 0.01

0.88 0.83 0.07 0.21

Distention

Stomach Duodenum Jejunum Ileum

2.48 2.22 2.25 2.32

2.10 1.97 2.07 2.15

1.95 1.87 1.84 1.87

< 0.01 0.01 0.09 0.03

< 0.01 < 0.01 < 0.01 < 0.01

0.24 0.39 0.01 0.01

Note. - Mean values of a 5-point scoring scale (1.0 = not identified; 1.5 = < 30%; 2.0 = 30-60%; 2.5 = 61-80%; 3.0 = > 80%) # p values comparing neutral 0.1% barium sulphate suspension with positive 2.1% barium sulphate suspension; neutral 0.1% barium sulphate suspension with water; and positive 2.1% barium sulphate suspension with water, respectively.

Table II. â&#x20AC;&#x201D; Comparison of mean scores for wall visualization and distention of anatomic segments assessed with contrast enhanced MDCT by reader 2. CT Images Assessment

Barium Sulphate Suspensions

Water

p value

0.1%

2.1%

Wall visualization

Stomach Duodenum Jejunum Ileum

2.57 2.36 2.33 2.38

1.89 1.89 2.00 1.94

1.94 1.80 1.93 1.90

< 0.01 < 0.01 < 0.01 < 0.01

0.76 0.32 0.23 0.42

Distention

Stomach Duodenum Jejunum Ileum

2.56 2.36 2.35 2.41

2.05 2.02 2.17 2.11

1.91 1.86 1.93 1.91

< 0.01 < 0.01 0.47 < 0.01

< 0.01 < 0.01 < 0.01 < 0.01

0.31 0.16 < 0.01 0.01

sion, the wall of all segments (stomach, duodenum, jejunum, and ileum) were visualized better, and the stomach, duodenum and ileum distention were superior in patients who were administered neutral barium sulphate suspension. When comparing patients who were administered neutral barium sulphate suspension with those who were administered water, the walls of the stomach, duodenum, jejunum and ileum were visualized better, and there was improved distention of the stomach, duodenum, jejunum and ileum with neutral barium sulphate suspension. There were no differences for jejunal

distention between patients administered neutral and positive barium sulphate suspensions. When comparing patients who were administered positive barium sulphate suspension with those who were administered water, jejunal and ileal distention were better in patients who received positive barium sulphate suspension; and no differences were demonstrated in stomach and duodenum distention, and in wall visualization of all segments assessed. For reader 2, when comparing patients who received neutral barium sulphate suspension with

patients who were administered positive barium sulphate suspension, the walls of the stomach, duodenum, jejunum, and ileum were visualized better; moreover there was improved distention of the stomach, duodenum, and ileum in patients who received neutral barium sulphate suspension. When comparing patients who were administered neutral barium sulphate suspension with those who received water, the wall of all segments (stomach, duodenum, jejunum, and ileum) were visualized better, and there was improved stomach, duodenal, jejunal and ileal distention

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with neutral barium sulphate suspension. When compared to patients who received water, those administered positive barium sulphate suspension showed better jejunal, and ileal distention. No differences were demonstrated between patients administered positive barium sulphate suspension and water for stomach and duodenum distention, as well as for wall visualization of the stomach, duodenum, jejunum, and ileum. Interobserver agreement for distention and wall visualization ranged from substantial to almost perfect between both readers (kappa = 0.63 to 0.83). Discussion Our results show that the walls of the stomach and small bowel were visualized better in patients who were administered neutral barium sulphate suspension than those who were administered either positive barium sulphate suspension or water. The results of our study are in accordance with previous investigators who demonstrated that bowel wall was visualized better with other neutral oral contrast agents, such as lactulose (16), mannitol (17, 18), cellulose (19), methylcellulose (20), mucofalk diluted in water (Falk, Feiburg, Germany) (1, 21), and polyethylene glycol (2, 22). Some of these solutions are widely used, particularly in Europe. However, unlike the neutral barium sulphate suspension used on our study, these agents caused either side effects such as abdominal cramping, gas and diarrhea, or tasted poorly (2). Our results showed that the stomach, duodenum, and ileum were distended better in patients who received neutral barium sulphate suspension, compared to patients administered positive barium sulphate suspension. Similar results were found in a recent study of patients with known or suspected pancreatic or biliary tract disease, in which patients received neutral barium sulphate suspension, water with methylcellulose and positive barium sulphate suspension (14). However, this study had some important limitations. First, patients who received positive barium sulphate suspension were not enrolled in a randomized fashion at the time the other two groups were enrolled. Furthermore, patients who ingested positive barium sulphate ingested the contrast material over a longer period of time, and received water in addition

to the oral contrast media; both factors may have interfered with gastrointestinal tract distention and wall visualization in the positive barium sulphate group. In our study, all patients were randomized, and all patients received the same amount of oral contrast material over the same period of time prior to scanning. Our results therefore validate that neutral barium sulphate suspension improves bowel distention. Our results also demonstrated that barium sulphate suspensions (neutral and positive) are better than water in distending the small bowel. Stabilizing agents within the barium sulphate suspensions improve transit and limit absorption across the intestinal wall (14), leaving more contrast material to distend the distal small bowel. The stomach and small bowel walls were visualized poorly with positive barium sulphate suspension and water. Positive barium sulphate suspension does not allow the enhanced bowel wall to be discriminated from dense luminal fluid. The stomach and small bowel walls were not visualized well with water because of the lack of distention. Our study was limited because the readers could not be blinded to all types of contrast agents used; the positive barium sulphate suspension could be identified by its appearance. However, the readers were not able to differentiate neutral barium sulphate suspension from water. Furthermore, our assessment was semi-quantitative. However, our study included 2 blinded independent readers and interobsever agreement was substantial to almost perfect. Also, bowel diameters typically vary in each patient due to peristalsis making a quantitative analysis inaccurate to some degree too. In summary, when examining patients with intravenous contrastenhanced abdominal and pelvic multidetector-row CT, orally administered neutral barium sulphate suspension allows the gastrointestinal tract to be visualized and distended better than either water, or positive barium sulphate suspension.

10.

11. 12.

13.

References 1. Doerfler O.C., Ruppert-Kohlmayr A.J., Reittner P., Hinterleitner T., Petritsch W., Szolar D.H.: Helical CT of the small bowel with an alternative oral contrast material in patients with Crohn disease. Abdom Imaging, 2003, 28: 313-318. 2. Hebert J.J., Taylor A.J., Winter T.C., Reichelderfer M., Weichert J.P.: Low-

14.

15.

241

attenuation oral GI contrast agents in abdominal-pelvic computed tomography. Abdom Imaging, 2006, 31: 4853. Ajaj W., Goehde S.C., Schneemann H., Ruehm S.G., Debatin J.F., Lauenstein T.C.: Oral contrast agents for small bowel MRI: comparison of different additives to optimize bowel distension. Eur Radiol, 2004, 14: 458-464. Rajesh A., Maglinte D.D.: Multislice CT enteroclysis: technique and clinical applications. Clin Radiol, 2006, 61: 31-39. Stehling M.K., Lawrence J.A., Weintraub J.L., Raptopoulos V.: CT angiography: expanded clinical applications. AJR, 1994, 163: 947955. Raptopoulos V., Steer M.L., Sheiman R.G., Vrachliotis T.G., Gougoutas C.A., Movson J.S.: The use of helical CT and CT angiography to predict vascular involvement from pancreatic cancer: correlation with findings at surgery. AJR, 1997, 168: 971-977. McNicholas M.M., Raptopoulos V.D., Schwartz R.K., et al.: Excretory phase CT urography for opacification of the urinary collecting system. AJR, 1998, 170: 1261-1267. Raptopoulos V., Prassopoulos P., Chuttani R., McNicholas M.M., McKee J.D., Kressel H.Y.: Multiplanar CT pancreatography and distal cholangiography with minimum intensity projections. Radiology, 1998, 207: 317-324. Akbar S.A., Mortele K.J., Baeyens K., Kekelidze M., Silverman S.G.: Multidetector CT urography: techniques, clinical applications, and pitfalls. Semin Ultrasound CT MR, 2004, 25: 41-54. Kawamoto S., Horton K.M., Fishman E.K.: Opacification of the collecting system and ureters on excretory-phase CT using oral water as contrast medium. AJR, 2006, 186: 136-140. Shirkhoda A.: Diagnostic pitfalls in abdominal CT. Radiographics, 1991, 11: 969-1002. Winter T.C., Ager J.D., Nghiem H.V., Hill R.S., Harrison S.D., Freeny P.C.: Upper gastrointestinal tract and abdomen: water as an orally administered contrast agent for helical CT. Radiology, 1996, 201: 365-370. Gossios K.J., Tsianos E.V., Demou L.L., et al.: Use of water or air as oral contrast media for computed tomographic study of the gastric wall: comparison of the two techniques. Gastrointest Radiol, 1991, 16: 293297. Megibow A.J., Babb J.S., Hecht E.M., et al.: Evaluation of bowel distention and bowel wall appearance by using neutral oral contrast agent for multidetector row CT. Radiology, 2006, 238: 87-95. Viera A.J., Garrett J.M.: Under standing interobserver agreement: the kappa statistic. Fam Med, 2005, 37: 360-363.

oliva-_Opmaak 1 6/08/12 11:32 Pagina 242

242 16. Arslan H., Etlik O., Kayan M., Harman M., Tuncer Y., Temizoz O. Peroral CT enterography with lactulose solution: preliminary observations. AJR, 2005, 185: 1173-1179. 17. Zhang L.H., Zhang S.Z., Hu H.J., et al.: Multi-detector CT enterography with iso-osmotic mannitol as oral contrast for detecting small bowel disease. World J Gastroenterol, 2005, 11: 23242329. 18. Berther R., Patak M.A., Eckhardt B., Erturk S.M., Zollikofer C.L.: Comparison of neutral oral contrast versus positive oral contrast medium in

JBRâ&#x20AC;&#x201C;BTR, 2012, 95 (4) abdominal multidetector CT. Eur Radiol, 2008, 18:, 1902-1909. 19. Sahani D.V., Jhaveri K.S., D'Souza R.V., et al.: Evaluation of simethicone-coated cellulose as a negative oral contrast agent for abdominal CT. Acad Radiol, 2003, 10: 491-496. 20. Minordi L.M., Vecchioli A., Guidi L., Mirk P., Fiorentini L., Bonomo L.: Multidetector CT enteroclysis versus barium enteroclysis with methylcellulose in patients with suspected small bowel disease. Eur Radiol, 2006, 16: 1527-1536.

21. Reittner P., Goritschnig T., Petritsch W., et al.: Multiplanar spiral CT enterography in patients with Crohn's disease using a negative oral contrast material: initial results of a noninvasive imaging approach. Eur Radiol, 2002, 12: 2253-2257. 22. Minordi L.M., Vecchioli A., Mirk P., Bonomo L.: CT enterography with polyethylene glycol solution vs CT enteroclysis in small bowel disease. Br J Radiol, 2011, 84 (998): 112119.

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MILWAUKEE SHOULDER SYNDROME L. Dewachter, P. Aerts, I. Crevits, R. De Man1 Milwaukee shoulder syndrome or rapid destructive arthropathy of the shoulder is a rare form of arthropathy that mainly affects elderly women. It is characterized by a rapid destruction of the glenohumeral joint and the rotator cuff and by an important noninflammatory joint effusion containing hydroxyapatite crystals. Radiography plays an important role in the evaluation of patients with articular disease. However, magnetic resonance imaging is the method of choice for assessing the full extent of osseous, chondral, and soft-tissue involvement. Key-words: Shoulder, arthritis.

Case report An 84-year-old woman presented to her physician with right shoulder pain and a restricted active and passive range of motion of the affected shoulder. Swelling of the shoulder was absent and there was no history of recent trauma. Her medical history was unremarkable. Radiography of the right shoulder (Fig. 1) showed a destruction and cranial subluxation of the humeral head with intra-articular calcifications. A chest radiograph taken six months earlier (Fig. 2) showed none of these findings. CT scan (Fig. 3A, B) revealed a deformed humeral head with intraarticular and peri-articular calcifications and a large joint effusion. MRI (Fig. 4 A,B) also demonstrated an effusion, destruction and subluxation of the humeral head, thinning and destruction of the cartilage and subchondral bone. There was some synovial thickening and abnormal bone marrow signal (arrow). A partial undersurface tear of the supraspinatus tendon was demonstrated. Synovial fluid contained no leucocytes and culture was negative. Based on these imaging findings and the rapid destruction of the glenohumeral joint over a short period of the time, the diagnosis of Milwaukee shoulder or rapid destructive arthropathy of the shoulder was made. Discussion Milwaukee shoulder syndrome is a relatively uncommon entity first described by McCarty et al. in 1981 in Milwaukee, Wisconsin.

Fig. 1. — Radiograph of the right shoulder. Partial destruction of the humeral head with cranial subluxation and intraarticular calcifications (arrow).

Fig. 2. — Normal glenohumeral joint on a spot film of the right shoulder taken six months earlier.

Rapid destructive arthropathy mainly affects elderly woman with an age ranging from 50 to 90 years old. Both shoulders are affected in 64% with preferential involvement of the dominant side (1). The knees are affected in 50% (2). Symptoms include joint pain and tenderness, restricted range of motion or less frequently excessively mobile glenohumeral joints. Swelling due to an effusion is seen in most of the cases. Analysis of the synovial fluid reveals a high number of erythrocytes, a low leukocyte count and large concentrations of

calcium hydroxyapatite. In 10% admixture of calcium pyrophosphate crystals can occur (2). It is believed that calcium hydroxyapatite andcalcium pyrophosphate crystals develop in degenerative cartilage and in altered synovium and are released into the joint. These crystals, phagocytosed by synovial cells , then stimulate the release of collagenase and active protease. The release of these proteolytic enzymes results in joint and rotator cuff destruction with further release of additional crystals into the joint and thereby creating a vicious cycle and aggravating the destructive process (3). Predisposing factors are recent trauma (most often fall on an outstretched hand) or joint overuse, associated pyrophosphate deposition, neuroarthropathy, dialysis and hyperparathyroidism (1, 4).

From: 1. Department of Radiology, Heilig Hart hospital, Roeselare, Belgium. Address for correspondence: Dr L. Dewachter, Department of Radiology, Heilig Hart hospital, Wilgenstraat 2, B-8800 Roeselare, Belgium. E-mail: laura.dewachter@student.kuleuven.be

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Fig. 3. — Coronal (A) and axial (B) CT image. Deformity and subluxation of the humeral head with intra-articular effusion, calcifications (arrow) and subchondral sclerosis.

glenohumeral joint, thinning of the cartilage and destruction of the subchondral bone (5). Ultrasound may show calcific foci, joint effusion and an absent rotator cuff but it has no added diagnostic value. In the differential diagnosis we must consider neuropathic arthropathy of the shoulder (frequently associated with syringomyelia), avascular necrosis, dialysis arthropathy, rheumatoid arthritis and septic arthritis (2). Treatment is symptomatic and includes physical therapy, nonsteroidal anti-inflammatory drugs and intra-articular injection of steroids. Joint replacement by a shoulder prosthesis is a theoretical option but is technically challenging without the stabilizing effect of the rotator cuff. Tidal irrigation followed by intraarticular injection of steroids and tranexamic acid could affect the long term outcome of some patients with mild Milwaukee shoulder syndrome but is still controversial (6). References 1.

Fig. 4. — Coronal (A) and axial (B) STIR MRI image. Deformity of the humeral head with cartilage destruction. Intra-articular effusion and a partial tear of the rotator cuff.

Radiography and MR imaging play a major role in evaluation and differential diagnosis of suspected arthropathy. However, due to its superior soft-tissue contrast resolution and nonreformatted multiplanar imaging capability, MR imaging has become the imaging modality of choice. On plain radiographs, Milwaukee shoulder manifests as glenohumeral joint space narrowing with little or no osteophytosis, cranial subluxation of the humeral head with often

formation of a pseudoarthrosis with the acromion and distal clavicle, subchondral sclerosis with cyst formation in the humeral head, destruction of subchondral bone with partial bony collapse of the head, intra- and peri-articular calcifications and soft tissue swelling and intra-articular loose bodies. CT findings are similar to the radiographic characteristics. MR findings consist of a large joint effusion, a (large) tear of the rotator cuff, narrowing of the

McCarty D.J.: Milwaukee shoulder syndrome. Trans Am Clin Climatol Assoc, 1991, 102: 271-284. Nguyen V.D.: Rapid destructive arthritis of the shoulder. Skeletal Radiol, 1996, 25: 107-112. Farid N., Bruce D., Chung C.B., et al.: Miscellaneous conditions of the shoulder: anatomical, clinical, and pictorial review emphasizing potential pitfalls in imaging diagnosis. Eur J Radiol, 2008, 68: 88-105. Rood M., van Laar J., de Schepper A., Huizinga T.: The Milwaukee Shoulder/ Knee Syndrome. J Clin Rheumatol, 2008, 14: 249-250. Llauger J., Palmer J., Rosón N., Bagué S., Camins A., Cremades R.: Nonsepticmonoarthritis: imaging features with clinical and histopathologic correlation. Radiographics, 2000, 20: 263-278. Halverson P., Ryan L.: Tidal lavage in Milwaukee shoulder syndrome: do crystals make the difference? J Rheumatol, 2007, 34: 1446-1447.

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ERDHEIM-CHESTER DISEASE DETECTED WITH 99MTC MDP BONE SPECT/CT G. Ceulemans1, M. Keyaerts1, L. Verbruggen2, A. Hoorens3, C. Boulet4, D. Verdries4, M. De Maeseneer4, B. Ilsen4, H. Everaert1 Erdheim-Chester disease (ECD) is a rare non-Langerhans’ cell histiocytosis. Mild but permanent juxta-articular bone pain in mainly knees and ankles is the most frequent associated symptom. Despite the pathognomonic radiographic findings, most cases are still diagnosed by the pathologist. The lesions consist of lipid-storing CD 68 +/ CD 1a – nonLangerhans’ cell histiocytes, most frequently localized in bone but also involving multiple organ systems in the body. We present a case report in which the diagnosis of ECD was established with 99mTc MDP bone SPECT/CT. Key-word: Lipogranulomatosis.

Erdheim-Chester disease (ECD) or polyostotic sclerosing histiocytosis is a rare histiocytic disorder, which leads to xantogranulomatous infiltration by lipid-laden histiocytes of multiple organ systems (skin, lung, bone, heart, central nervous system, pituitary, retroperitoneum, (retro-) orbital tissue) (1). The pathologist Jakob Erdheim and physician William Chester reported the first cases in 1930. They described the clinical and pathologic findings of 2 patients with distinctive lipoid granulomatosis and associated bone changes (2). ECD remains sporadic with about 100 well-documented cases in literature (2). Case report A 51-year old woman with a 4year history of intermittent joint

Fig. 1. — A.

pains, primarily in ankles and knees, presented at rheumatology with fever and swelling of the right elbow. Blood sample result included an abnormal lipid metabolism with hypercholesterolemia (total cholesterol 248 mg/dl, nl range < 190 mg/dl; LDL 136 mg/dl, nl range < 115 mg/dl; triglycerides 335 mg/dl, nl range 150 mg/dl), elevated C-reactive protein (14,9 mg/l, nl range < 5 mg/l), elevated white blood cell count (13,8 × 103/mm3, nl range 3,6-9,6 × 103/mm3), slightly elevated sedimentation rate (25 mm/h, nl range 020 mm/h), nl kidney function (creatinine 0,74 mg/dl, normal range 0,401,20 mg/dl), nl red blood cell count (4,5 × 106, nl range 3,9-5,0 × 106). X-ray of forearms and knees showed heterogeneous osteosclerosis, suggesting metastatic disease. 99m Tc MDP bone scan revealed intense osteoblastic activity in the

right maxilla, distal femora, proximal tibiae, ankles and tarsal bones. Additional SPECT-CT of the knees revealed heterogeneous sclerotic bone marrow lesions with epiphyseal sparing, corresponding with the areas of osteoblastic activity (Fig. 1). MRI of the knee showed diffuse hyperintense lesions on the T1 sequence after the intravenous injection of Gadolium in femora, tibiae and fibulae, confirming the heterogeneous active detriment of the normal bone marrow (Fig. 2). Based on the symptoms and characteristic imaging, ECD was suspected. Bone biopsy of the distal femur revealed an infiltration of lipidstoring macrophages with nonLangerhans’ features (CD 68 +/CD1a –/S100 –), which is consistent with ECD (Fig. 3). 18 F-FDG-PET-CT was performed to detect visceral manifestation. Mild

Tc MDP bone total body scan demonstrated intense osteoblastic activity in the right maxilla, distal femora, proximal tibiae, ankles and tarsal bones. B. (transverse slices) and C. (sagittal From: 1. Department of Nuclear Medicine, 2. Department of Rheumatology, slices). Additional SPECT/CT revealed 3. Department of Pathology, 4. Department of Radiology, UZ Brussel, Brussels, corresponding sclerotic bone marrow Belgium. lesions with epiphyseal sparing. Address for correspondence: Dr G. Ceulemans, Dpt of Nuclear Medicine, UZ Brussels, Laarbeeklaan 101, B-1090 Brussels, Belgium. 99m

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Fig. 2. — A. MRI of the knee shows irregular zones with low signal on the T1 non-contrast enhanced image, sparing the epiphysis. B. These lesions had contrast enhancement on the T1 sequence after intravenous injection of Gadolinium.

Fig. 3. — A. Bone biopsy demonstrated a diffuse infiltration of the normal bone marrow by lipid-laden histiocytes. B. These histiocytes were identified as macrophages as they were CD 68-positive on immunohistochemistry.

involvement of the lungs included a thickening of the interlobular septa; in the abdomen perinephric stranding, an atypical sign of retroperitoneal fibrosis, was present (Fig. 4). All visceral and skeletal lesions were hypermetabolic (Fig. 5). Discussion ECD is a rare form of nonLangerhans’ cell histiocytosis affecting middle-aged adults (mean age of

53 years) without gender predisposition (3). The condition seems nonfamilial and no predisposing factors are defined (2). The precise origin of this disease is not yet fully understood; currently it has not been classified as cancer, neither as an infectious or autoimmune disease. Diagnosis of ECD remains challenging. Mild permanent juxtaarticular bone pain is the most frequent symptom and mainly affects the lower limbs. Other symp-

toms depend on the type of affected extra-skeletal tissue. In order of frequency of occurrence these comprehend retroperitoneal fibrosis, diabetes insipidus, exophalmia, xanthomas, neurologic signs (ataxia), dyspnea, kidney failure, hypopituitarism, liver failure. Of all cases 70-80% have skeletal involvement and more than 50% have visceral involvement (4). Radiological hallmarks (X-ray/CT) include symmetric heterogeneous

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Fig. 4. — A. (supine position) B. (prone position) HRCT of the lung showed mild involvement of the lungs: thickening of the interlobular septa.

B Fig. 5. — A. 18 F FDG PET/CT revealed metabolic active perinephric stranding, an atypical sign of retroperitoneal fibrosis. B. All visceral and skeletal lesions were hypermetabolic.

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osteosclerosis of the diaphysis and metaphysis of the long bones with epiphyseal sparing (4, 5). Bone scintigraphy shows a corresponding symmetric increased tracer uptake in the diaphysis and metaphysis of primarily the long bones (6, 7). MRI depicts a replacement of the normal fatty bone marrow by a heterogeneous high intensity signal infiltrate on T1 sequence after intravenous injection of gadolinium, sparing the epiphysis (5). Biopsy reveals a diffuse infiltration of bone and soft tissues by foamy histiocytes, further characterized by immunohistochemistry as non-Langerhans’ cell (S 100 – and CD 1a –) macrophages (CD 68 +) (3). As seen in our patient, blood samples often disclose an abnormal lipid metabolism, a moderate anaemia (related to the severity of the destruction of normal bone marrow, chronic inflammation and renal insufficiency), an increased sedimentation rate and C-reactive protein (signs of active inflammation). Because of the rarity of this disease, no clinical trials have been conducted and treatment plans are mainly based on anecdotal experience. Treatment options are not curative but attempt to control the disease extension and include chirurgi-

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cal debulking, systemic steroids, interferon alpha, various cytotoxic agents, radiation therapy and stem cell transplantation. 18F FDG PET/CT not only allows accurate staging of the disease (visceral and skeletal involvement), it is also an extremely useful tool to monitor treatment efficiency (8). The prognosis of patients with ECD is related to the extent of disease at presentation and especially the severity of visceral involvement. Most patients with extra-skeletal disease die within 3 years after diagnosis due to congestive heart failure, lung fibrosis or renal insufficiency (4).

Conclusion ECD is a rare form of nonLangerhans’ cell histiocytosis, which still remains frequently unrecognized. The typical symmetric long bone involvement and the FDGavidity of these osteoblastic lesions should however lead to the correct diagnosis in the era of hybrid imaging with 99m Tc MDP bone SPECT/CT or 18 F FDG PET/CT. References 1.

Shamburek R.D., Brewer H.B. Jr., Gochuico B.R.: Erdheim-Chester

disease: a rare multisystem histiocytic disorder associated with interstitial lung disease. Am J Med Sci, 2001, 321: 66. Rush W., Andriko J., Galateau-Salle F., et al.: Pulmonary pathology of Erdheim-Chester Disease. Mod Pathol, 2000, 13: 747-754. Al-Quran S., Reith J., Bradley J., et al.: Erdheim-Chester Disease: case report, PCR-based analysis of clonality and review of literature. Mod Pathol, 2002, 15: 666-672. Spyridonidis T., Giannakenas C., Barla P., Apostolopoulos D.: ErdheimChester disease: a rare syndrome with a characteristic bone scintigraphy pattern. Ann Nucl Med, 2008, 22: 323-326. Versini M., Jeandel P.Y., Fuzibet J.G., Ianessi A., Hauger O., Amoretti N.: Erdheim-Chester disease: radiological findings. Presse Med, 2010, 39: e233-237. Canbaz F., Dabak N., Baris S., Selcuk M.: Erdheim-Chester disease: 99m Tc-MDP bone scan provides the diagnosis. Eur J Nucl Med Mol Imaging, 2005, 32: 998. Nunez R., Tronco G., Hofman J., Amoashiy M., Bhuiya T., Palestro C.: Radionuclide bone imaging in Erdheim-Chester disease. Clin Nucl Med, 2005, 30: 32-34. Stenova E., Steno B., Povinec P., Ondrias F., Ramplalova J.: FDG-PET in the Erdheim-Chester disease: its diagnostic and follow-up role. Rheumatol Int, 2010 (epub ahead on print).

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SINGLE LEFT CORONARY ARTERY WITH THE RIGHT CORONARY ARTERY ARISING FROM THE MID-PORTION OF THE LEFT ANTERIOR DESCENDING ARTERY. DIAGNOSIS WITH MDCT P. Mailleux1, Th. Muller2 Single coronary artery is a very rare entity.We describe a very unusual subtype of this anomaly in which the right coronary artery arises from the mid-portion of the left anterior descending artery. MDCT allowed diagnosis of this non pathogenic variant and excluded any significant coronary stenosis. Key-word: Coronary vessels, anormalities.

Single coronary artery without congenital cardiac defect is very rare, with a prevalence of 0.024 to 0.06% in the general population. We describe a very unusual subtype of this anomaly, in which the right coronary artery arises from the midportion of the left ascending artery (LAD). MDCT allowed diagnosis and excluded any significant coronary stenosis. Case report The patient is a 62 year-old male with atypical chest pain, a metabolic syndrome and family risk factors. A complete right bundle branch block did not allow stress test and a gated MDCT of the coronary arteries was performed. It showed no artery arising from the right sinus of Valsalva and a very large (7 mm wide) left main coronary artery originating from the left sinus of Valsalva (Fig. 1, 2, 3). There was a normal dominant circumflex artery and a small calcified non stenosing plaques on the proximal LAD (Fig. 2). The RCA (right coronary artery) arised from the midportion of the LAD (Fig. 2, 3), joining the right atrioventricular groove after a course in front of the pulmonary outflow tract at the level of the valve. No significant stenosis on any of the arteries was noted.

Fig 1. — MDCT with intravenous injection of non ionic iodinated contrast (iopromide with 370 mg of iodine/cc, injection rate 4 cc/sec, total bolus of 90 cc. CT acquisition parameters with were 100 kV, modulated mAs, with a finale dose of 10.19 CTD/vol of mGy, DLP 525 mGy-cm and 9 mSev. Volume rendering image: upper view showing the left main coronary artery (broad arrow) giving the CX and the LAD (curved arrow) wich gives the RCA (small arrows) that crosses to the right in front of the pulmonary outflow tract, not seen on this volume rendering image.

Discussion As gated multidetector CT of the coronary arteries is being used more and more often to exclude stenosing disease in the coronary arteries, many variants are encountered. Some are incidental, some potentially serious when the artery passes between the aorta and pulmonary

artery before reaching the other side or when there is an ectopic coronary origin from the pulmonary artery (1). Single coronary artery without congenital cardiac defects is very rare, with an incidence of 0.024 to 0.06% in the general population. In a series of 125.596 patients undergo-

From: 1. Dept of Imaging, Clinique St Luc, Bouge Belgium, 2. Dept of Cardiology, St Luc Catholic University Hospital, Brussels, Belgium. Address for correspondence: Dr P. Mailleux, M.D., Clinique St Luc, rue St Luc 8, B-5004 Belgium. E-mail: p.mailleux@skynet.be

ing coronarography, it was noted in 0.040% (1). The Lipton classification scheme (2) can be used to classify the anomalies. The anomalous coronary artery is first designated with “R” or “L” depending upon whether the ostium is located in the right or left sinus of Valsalva. Our patient has a LI type anomaly, with the main coronary artery arising on the left. Many L1 type patients just have a huge distal circumflex artery giving the distal RCA (3). A double supply of the RCA was also described (4),

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Fig. 2. — Curved oblique reconstruction following the LAD (small arrows) in front of the pulmonary outflow tract (black star). Non stenosing small calcified plaques are seen in the proximal LAD. Curved arrows point to the distal LAD and the broad arrow to the left main coronary artery.

from the distal CX and from a RCA arising from the LAD. Just a few cases of isolated supply from the mid-LAD, as in our patient, have been described, the first one in 1998 (5). As the vessel crosses in front of the pulmonary outflow tract and not between aorta and pulmonary artery, it can be considered a non toxic variant. Conclusion MDCT is a useful tool to exclude coronary stenosis in low to middlerisk patients. Congenital anomalies of the origin of the coronary are

Fig. 3. — Oblique 4 mm thickness MIP slice (nearly axial) at the level of the left main coronary (broad arrow), showing the LAD (curved arrow) and the RCA (small arrows), which crosses to the right in front of the pulmonary outflow track (black star) in direction of the right atrioventricular groove.

encountered in about 1%. It must be recognized and analyzed to differentiate dangerous from anecdotal variants as in this case. Bibliography 1.

Yamanaka O., Hobbs R.E.: Coronary artery anomalies in 126,595 patients undergoing coronary arteriography. Catheter Cardiovasc Diagnosis, 1990, 21: 28-40. 2. Lipton M.J., Barry W. H., Obrez O. Silverman J.F., Wexler L.: Isolated Single Coronary Artery: Diagnosis, Angiographic Classification, and Clinical Significance1, Radiology, 1979, 130: 39-47.

3. Tanawuttiwat T., Harindhanavudhi T., Trivedi D.: Anomalous single coronary artery with absent right coronary artery diagnosed with the aid of 64slice multidetector computed tomographic angiography. Tex Heart Inst J, 2009, 36: 362-363. 4. Kaul P., Javangula K.: Single left coronary artery with separate origins of proximal and distal right coronary arteries from left anterior descending and circumflex arteries – a previously undescribed coronary circulation J Cardiothoracic Surg, 2007, 2: 20. 5. Rath S., Battler A.: Anomalous Origin of the Right Coronary Artery From the Left Anterior Descending Coronary Artery. Catheter Cardiovasc Diagnosis, 1998, 44: 328-329.

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DOUBLE CONTRAST PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHIC CT IN PATIENTS WITH OBSTRUCTIVE JAUNDICE: AN INITIAL EXPERIENCE OF SEVEN CASES C.-L. Wang1, Q. Shi1, X.-J. Xiang1, Z.-Z. Chen1, Z.-D. Yuan1, Q.-H. Deng1, H.-Y. Zhou1, X.-X. Ren1, L. Cheng1, Y.-X. J. Wang2 Purpose: To explore the technical feasibility of double contrast percutaneous transhepatic cholangiographic CT (DCPCT-CT) in patients with bile duct obstruction. Methods: Seven patients with bile duct obstructive diseases were studied, including 5 males and 3 females, ranging in age from 24 yrs to 74 yrs (average: 47.7 yrs). There were 5 cases of hilar cholangiocarcinoma, 1 case of sclerosing cholangitis, and 1 case of malignant transformation of adenoma at the distal end of the common bile duct. PTC was carried out initially, involving injection of 30ml 4.5-6.0mgI iohexol. After the bile duct system was filled, CT scan was performed, and further followed by enhanced CT with intravenous injection of 300mgI/ml contrast agent. Arterial phase, venous phase, and parenchymal phase acquisitions were obtained. Raw CT images were viewed and multiplanar reconstruction (MPR), maximum intensity projection (MIP), and volume rendering (VR) image post-processing were performed. Results: DC-PCT-CT was performed successfully and bile duct drainage was carried out. Mild lesion enhancement was demonstrated in three cases in arterial phase, while all seven cases demonstrated enhancement of various degrees in venous phase. The lesions lead to track-like, asymmetrical or irregular bile duct obstructive narrowing, and in one case intra-luminal filling defect. Reliable diagnosis was suggested in all cases. MPR, MIP and VR images were useful in demonstrating precise lesion location and for surgical planning. Conclusion: In patients with bile duct obstruction, DC-PTC-CT is a feasible technique offering both important diagnostic value and drainage application. Key-words: Bile ducts, stenosis or obstruction â&#x20AC;&#x201C; Jaundice.

Jaundice caused by bile duct obstruction is common clinically. Its diagnosis and further surgical planning depends on imaging investigation. A number of noninvasive or invasive modalities are available for imaging of the biliary tract. Ultrasound is commonly used for assessing biliary duct diseases (1-3). It is, however, user-dependent and the captured images are not easily understood by clinicians. Endoscopic retrograde cholangiopancreatography (ERCP) is often regarded as the gold standard for visualizing biliary duct diseases. However this modality is invasive, user-dependent and may induce pancreatitis. It should therefore not be performed in patients where intervention is not certain (4, 5). Used widely prior to 1980s, percutaneous transhepatic cholangiographic (PTC) was an established technique for diagnosis of bile duct obstructive diseases (6, 7). With the introduction of advanced CT and MRI technologies, particularly with the application of MR cholangiography (MRC), ERCP and PTC are used

less frequently for diagnostic purpose. MRC does not require any contrast agent to visualise the bile ducts, and dilatation and gallstones in the common bile duct are easily detected, the images are appreciated by the surgeons for surgical planning (8-11). Unfortunately, MRC cannot be performed in all patients and hospitals due to limited availability of MRI or due to contraindications. MRC is also often inconclusive in patients with air in the biliary system, e.g. after papillotomy or liver surgery with entero-hepatic anastomoses. Surgical clips after cholecystectomy may also give artefacts. 3D imaging is useful for assessing the complex structure of the biliary tree. The normal-sized biliary tract can be adequately depicted during 3D spiral CT cholangiography, facilitating the detection of biliary variations that might increase the risk of duct injury during cholecystectomy, particularly laparoscopic cholecystectomy (12). The use of a cholangiographic contrast agent increases the contrast between bile ducts and

From: 1. Department of Medical Imaging, Peking University Shenzhen Hospital, Shenzhen 518026, Guangdong Province, China, 2. Department of Imaging and Interventional Radiology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China. Address for correspondence: Dr Y.-X. J. Wang, M.D., Department of Imaging and Interventional Radiology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China. E-mail: yixiang_wang@cuhk.edu.hk

surrounding structures and between bile and most hypodense stones (12). CT cholangiography has not been commonly used due to the low resolution of single detector CT in the past and reports of adverse events after injection of biliary contrast agent (13, 14). The introduction of helical CT and multi-detector CT has renewed the interest for CT cholangiography because of the ability to obtain thin slices without misregistration and high-resolution reconstructions of the biliary tree (15). The number of adverse reactions with biliary contrast media has been reduced by drip infusing the contrast media instead of injecting. Drip infusion with an infusion rate of the biliary contrast agent adjusted according to the serum bilirubin value has been reported to be safe in patients with and without impaired biliary excretion (16). It was concluded that drip infusion CT cholangiography is a fast and widely available alternative technique to visualise hepatobiliary disease in patients with an inconclusive ultrasound and when MRI cannot be performed (16-19). It is less expensive and quicker than MRC. Nowadays, with the advances in CT technology such as thin-section, single-breathhold helical CT and three-dimensional and multiplanar reformation reconstruction techniques, the resolution of CT cholangiography tends to exceed that of MR. It has been

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reported that the main advantage of CT cholangiography to MRI and MRC was the superior mapping of the biliary tree (20), in other respects the two modalities were considered equivalent for the therapeutic planning (21). Gaining access to the biliary tract by minimal invasive image-guided techniques is one of the most used procedures for interventional radiologists to manage biliary bile duct obstructive diseases. For patients with obstructive jaundice requiring bile duct decompression and drainage, we explored the diagnostic value of double contrast CT with percutaneous transhepatic cholangiography together with intravenous contrast agent injection. We termed this technique double contrast percutaneous transhepatic cholangiographic CT (DC-PTC-CT). Our initial clinical experience with DC-PTC-CT is reported in this paper. Materials and methods DC-PTC-CT was carried out in seven cases, composed of five males and two females, aged 24-74 yrs (mean: 47.7). These seven cases included 5 cases of hilar cholangiocarcinoma, one case of sclerosing cholangitis, and one case of malig-

nant transformation of adenoma at the distal end of the bile duct. The patients had highly elevated serum bilirubin. The detailed information of these 7 cases is listed in table I. Before procedures, prothrombin time and platelet count were checked to be in competent range. All patients received broad-spectrum antibiotics. PTC was performed with the guidance of an X-ray DSA unit. The puncture site was right mid-axillary 8th-9th rib space. Under local anaesthesia, a small cut was made to the skin. Then the puncture needle was introduced horizontally toward vertebrae 11 and 12, and stopped when the needle tip reached a distance of 2 cm to the right border of vertebrae. Diluted contrast material was gently infiltrated while retracting the needle until a bile duct was opacified. A micro-guidewire was introduced via the puncture needle to one of the major intra-hepatic biliary duct or the common biliary duct, and a catheter was introduced for contrast agent injection and the micro-guidewire was removed. When the bile duct system was filled with contrast agent satisfactorily under DSA fluoroscopy, the catheter position was fixed, and the patient underwent CT exanimations. The contrast agent for PTC was iohexol

["Ominipaque 300", GE]) diluted with normal saline to 4.5-6.0 mgI/ml (density: 200 Hu) in six cases. In one initial case (case 1), a higher concentration (30 mgI/ml) was used resulting in beam hardening CT artefact. After the filling of contrast agent in the bile duct system, CT was performed before and after intravenous contrast agent administration. For intravenously contrast enhanced CT, Iohexol (300 mgI/ml) of 1.5 ml/kg body weight was used. The total contrast volume was 70-120 ml, injected at the rate of 3-5 ml/sec. The completion of contrast agent injection was followed by a flush with 30-50 ml normal saline at the same rate. Bolus tracking technique was used for arterial phase acquisition, a region-ofinterest (ROI) was placed on the aorta just above the diaphragm. Acquisition was started 6 sec later than the threshold reached 120 Hu. Venous phase was performed 15 sec after the arterial phase. Delayed phase acquisition was obtained 35 min later. CT was performed with a Toshiba Aquilion 16 slices scanner, using a standard abdominal protocol with FOV of 40 cm*40 cm, collimation of 1-mm, and a pitch of 0.9. CT image post-processing was performed with Vitrea 2 Imaging Software (Vital Images, Minneapolis,

Table I. — General information of the seven patients who underwent double contrast percutaneous transhepatic cholangiographic CT. sex

age

Symptoms

Serum total bilirubin*

Final diagnosis

Case 1

Cutaneous and sclera jaundice, yellow urine for two weeks

176.5 µmol/L

Hilar cholangiocarcinoma

Case 2

Cutaneous and sclera jaundice, yellow urine for 10 days

52.4 µmol/L

Hilar cholangiocarcinoma

Case 3

Recurrent upper abdominal discomfit with sclera jaundice and yellow urine for 1 month

21.2 µmol/L

sclerosing cholangitis

Case 4

Recurrent upper abdominal pain for 1 month Progressive jaundice 9 days.

52.4 µmol/L

Hilar cholangiocarcinoma

Case 5

Progressive jaundice for > one month

315.7 µmol/L

Hilar cholangiocarcinoma

Case 6

Recurrent fever, with progressive sclera jaundice and yellow urine for > one month

100.9 µmol/L

Malignant transformation of adenoma at the distal end of the common bile duct

Case 7

Two years post colon cancer surgery. Progressive jaundice for two weeks

18.2 µmol/L

Hilar cholangiocarcinoma

* reference value in authors’ institution < 9 µmol/L.

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Fig. 1. â&#x20AC;&#x201D; Case 4. 48-year-old female. Hilar cholangiocarcinoma involving left and right hepatic duct. (A). Percutaneous transhepatic cholangiographic CT demonstrates blockage of hilar hepatic duct. (B). Contrast CT arterial phase demonstrates mild enhancement of thickened hilar common hepatic duct wall. (C). Venous phase demonstrate marked enhancement of thickened hilar common hepatic duct wall and irregular lumen narrowing. (D). Volume rendering image demonstrates the hilar common bile duct blockage (arrow) and involvement of right and left hepatic ducts (arrow heads).

MN, USA). The reconstructed images had a slice thickness of 1 mm. Maximum intensity projection (MIP), multi-planar reconstruction (MPR), and volume rendering (VR) images were reviewed in additional to source images. All the seven cases had percutaneous transhepatic cholangiographic drainage treatment. For this, a standard guidewire was introduced through the cholangiographic catheter. The cholangiographic catheter was removed and a biliary drainage catheter drainage catheter

was introduced through the guidewire. The guidewire was removed. The drainage catheter was fixed for external drainage. In our series, in one case with severe jaundice, DC-PTC-CT was performed three days after the initial drainage, and surgery was performed one week later. Results In the first case of our series, as PTC catheter was introduced too deeply to superior segment of right

posterior hepatic duct, and too high concentration of contrast agent was used, the cholangiographic results were not optimal, However, the lesion location and lesion diagnosis were still being able to be made. The remaining six cases had satisfactory double contrast PTC-CT. PTC-CT demonstrated dilated intra-hepatic bile duct for all seven cases, the lesion cannot be clearly shown (Fig. 1A, 2A). With DC-PTC-CT, the lesion locations can be demonstrated precisely i.e. 5 cases in the bile duct at hepatic hilum level,

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Fig. 2. â&#x20AC;&#x201D; Case 6. 61-year-old female. Malignant transformation of adenoma at the distal end of the common bile duct. (A): Percutaneous transhepatic cholangiographic CT demonstrates distal common bile duct oval filling defect and dilatation of pancreas duct (arrow). (B): Double contrast CT arterial phase demonstrates mild enhancement of the lesion (arrow), with Hounsfield value increased by 15 Hu compared with pre-enhancement image. (C) Double contrast CT venous phase demonstrates marked enhancement of the lesion (arrow), with Hounsfield value increased by 28 Hu compared with pre-enhancement image. (D) Volume rendering image demonstrates blockage of the distal common bile duct (arrow) and upstream symmetrical dilation of the bile duct system. (E): Surgical specimen shows the small mass lesion (arrow). (F): Microscopic photograph of the resected specimen shows hyperplasia of mucous membrane in a villous adenoma shape, blockage of glandular tube, and infiltration of interstitial lymphocytes. (G): Zoomed-in image of G, Hyperplasia of local mucous membrane in a villous adenoma shape.

1 case involve both intra-and extrahepatic bile duct (case 3), and 1 case at the distal end of the common bile duct (case 6).

In 3 cases, arterial phase contrast CT showed lesion mild enhancement (Fig. 1B, Fig. 2B). In the other 4 cases, there was no apparent

enhancement in arterial phase. Venous phase contrast CT demonstrated enhancement of lesion with various degrees for all the seven

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cases (Fig. 1C, 2C). DC-PTC-CT, demonstrated track-like bile duct wall thickening with lumen narrowing in 3 cases (case 1, 5, 7), epicentral or irregular bile duct wall thickening with lumen narrowing in 2 cases (case 2, 4), symmetrical bile duct wall thickening with lumen narrowing in 1 case (case 3), and intralumenal filling defect in one case (case 6). There was no apparent enhancement for all the 7 cases in parenchymal phase. With three cases of hilar cholangiocarcinoma, tumour infiltration of the surrounding liver was observed. In all cases, MPR and MIP images helped demonstrate the lesion and precise locations of these lesions. While VR was able to demonstrate the location of the lesion, it could not demonstrate the bile duct wall and extra-mural lesion, nor the lesion within the lumen. On the other hand, although the bile duct system and remnant anatomy could be easily deduced on the transverse source and MPR and MIP images, they were it depicted in its entirety most clearly on the VR images (Fig. 1D, 2D). In all seven cases, clinical symptom improved with the drainage, and in all cases, correct diagnosis was suggested and later confirmed with later surgery or follow-up. No case had adverse reactions during the DC-PTC-CT procedure. Discussion Bile duct system is small in size with high tortuosity in its course. Although there are a number of techniques to demonstrate the bile duct, most are good at demonstrating the location of obstruction and the changes within the lumen while cannot demonstrate the bile duct wall itself well. Some techniques suffer from sub-optimal spatial resolution. Ultrasound can demonstrate dilatation of the bile duct system, but it is can be of limited value in lesion diagnosis and differential diagnosis, and often is inconclusive for hilar lesions. Of the 7 cases in this study, all underwent ultrasound test initially. However, none of the cases ultrasound was able to diagnose the nature of lesion. X-ray PTC and ERCP demonstrate the bile duct system proximal or distal to the obstruction and intra-lumenal changes, however, they cannot demonstrate the changes in the wall and extra-mural changes. In some cases due to suboptimal spatial resolution and respiration artifacts, MRI/MRC may not

demonstrate periductal-infiltrating lesions well. With DC-PTC-CT, high resolution CT image can demonstrate the bile duct wall and extra-lumenal changes including the changes in the surrounding liver parenchyma. Intravenously enhanced CT can demonstrate the blood supply status of the lesion. After filling of contrast agent in the bile duct, MPR and MIP can demonstrate symmetrical or asymmetrical track-like, tapering narrowing, or abrupt narrowing of the bile duct wall and lumen. When lesion infiltrate extra-murally or infiltrate surrounding liver parenchyma, extra-mural lesion enhancement can be observed. DC-PTC-CT can be helpful in lesion differential diagnosis. There are many causes with bile duct obstruction, with the common ones being stone, cholangiocarcinoma, and cholangitis. When stones contain sufficient calcium, CT is also able to make the diagnosis. However, CT has difficulties in demonstrating negative biliary stone. Concentrated biliary fluid may also demonstrate stone-like appearance. With stones of mixed components and irregular shapes, particularly with surrounding secondary inflammation, it is difficult for MRC or CT to make correct diagnosis. Combined with 3D image post-processing techniques, DC-PTC-CT is able to provide information of lesion’s blood supply, growth pattern and lesion extent, and is able to make a more accurate differential diagnosis. Lesion enhancement excludes bile duct stone. In case 6 in this series, PCT CT demonstrated filling defect within bile duct lumen, and diagnosis was not able to be made. Double contrast CT indicated there was lesion enhancement. A diagnosis of adenoma or adenocarcinoma was reached. Through the experience of this series, we found that the success and quality of DC-PTC-CT depend on successful catheter induction, proper concentration of contrast agent, and skilled image reconstruction. The concentration of contrast agent for PTC is important for quality demonstration of bile duct system in CT. Too high concentration can lead to artefact, while too low concentration does not fulfil the purpose of contrast. The experience gained from this series is 4.5-6.0 mgI/ml solution is suitable for CT contrast. DC-PTC-CT also offers the drainage treatment for jaundice. Patients with obstructive jaundice

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tend to have various degrees of liver function compromise. In addition to fulfill the purpose of diagnosis, particularly for the patients with selective surgery plan, drainage treatment for jaundice can help improve liver function, and lead to lower mobility or mortality (22, 23). In all our cases, clinical symptom improved with the drainage after DCPTC-CT procedure. There are a few limitations with DC-PTC-CT technique. PTC-CT is an invasive technique also involving radiation. In our institution, PTC under the guidance of DSA and CT scans were performed in the separate units of radiology department. To move the patient from DSA unit and CT unit is not convenient. This difficulty can be overcome with an interventional CT unit where a CT scanner and a radiofluoroscopic system are combined together. In conclusion, the technical feasibility and clinical application of DCPCT-CT in bile duct obstruction patients was explored in this study. DC-PTC-CT can provide mapping of the biliary tree and a reliable diagnosis. Particularly, DC-PTC-CT is suitable for patients with severe jaundice and bile duct drainage is part of the therapeutic plan. In terms of diagnostic performance, further head-to-head comparison with other techniques such as MRI/MRC remained to be carried out. Acknowledgement This study was supported by Shenzhen Science and Technology Planning Projects (Ref No. 201102003). References 1. Dietrich C.F., Braden B.: Sonographic assessments of gastrointestinal and biliary functions. Best Pract Res Clin Gastroenterol, 2009, 23: 353-367. 2. Foley W.D., Quiroz F.A.: The role of sonography in imaging of the biliary tract. Ultrasound Q, 2007, 23: 123-35. 3. Benson M.D., Gandhi M.R.: Ultrasound of the hepatobiliarypancreatic system. World J Surg, 2000, 24: 166-170. 4. Woods K.E., Willingham F.F.: Endoscopic retrograde cholangiopancreatography associated pancreatitis: A 15-year review. World J Gastrointest Endosc, 2010, 2: 165178. 5. Coté G.A., Sherman S.: Advances in pancreatobiliary endoscopy. Curr Opin Gastroenterol, 2010, 26: 429-435. 6. Weber A., Schmid R.M., Prinz C.: Diagnostic approaches for cholangiocarcinoma. World J Gastroenterol, 2008, 14: 4131-4136.

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256 7. Siegel J.H., Yatto R.P.: Approach to cholestasis: an update. Arch Intern Med, 1982, 142: 1877-1879. 8. Kanzer G.K., Weinreb J.C.: Magnetic resonance imaging of diseases of the liver and biliary system. Radiol Clin North Am, 1991, 29: 1259-1284. 9. Zidi Z.H., Prat F., Le Guen O., Rondeau Y., Pelletier G.: Performance characteristics of magnetic resonance cholangiography in the staging of malignant hilar strictures. Gut, 2000, 46: 103-106. 10. Vaishali M.D., Agarwal A.K., Upadhyaya D.N., Chauhan V.S.: Magnetic resonance cholangiopancreatography in obstructive jaundice. Clin Gastroenterol, 2004, 38: 887-890. 11. Masselli G., Gualdi G.: Hilar cholangiocarcinoma: MRI/MRCP in staging and treatment planning. Abdom Imaging, 2008, 33: 444-451. 12. Van Beers B.E., Lacrosse M., Trigaux J.P., de Cannière L., De Ronde T., Pringot J.: Noninvasive imaging of the biliary tree before or after laparoscopic cholecystectomy: use of three-dimensional spiral CT cholangiography. AJR, 1994, 162: 1331-1335. 13. Nilsson U.: Adverse reactions to iotroxate at intravenous cholangiography. A prospective clinical investigation and review of the literature.

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14.

15. 16.

17.

18.

Acta Radiologica, 1987, 28: 571575. Okada M., Fukada J., Toya K., Ito R., Ohashi T., Yorozu A.: The value of drip infusion cholangiography using multidetector-row helical CT in patients with choledocholithiasis. Eur Radiol, 2005, 15: 2140-2145. Van Beers B.E., Pringot J.H.: Imaging of cholelithiasis: helical CT. Abdom Imaging, 2001, 26: 15-20. Persson A., Dahlström N., Smedby O., Brismar T.B.: Three-dimensional drip infusion CT cholangiography in patients with suspected obstructive biliary disease: a retrospective analysis of feasibility and adverse reaction to contrast material. BMC Med Imaging, 2006, 6: 1. Miyoshi H., Hattori T., Kou K., Katayama M., Arakawa A., Taki T., Inui K., Yoshino J., Nakazawa S., Naitoh Y.: Usefulness of DIC-CT in choledocholithiasis. Nippon Shokakibyo Gakkai Zasshi, 1999, 96: 644-51. Kitami M., Murakami G., Ko S., Takase K., Tuboi M., Saito H., Nakajima Y., Takahashi S.: Spiegel's lobe bile ducts often drain into the right hepatic duct or its branches: study using drip-infusion cholangiography-computed tomography in 179 consecutive patients. World J Surg, 2004, 28: 1001-1006.

19. Persson A., Dahlström N., Smedby O., Brismar T.B.: Volume rendering of three-dimensional drip infusion CT cholangiography in patients with suspected obstructive biliary disease: a retrospective study. Br J Radiol, 2005, 78: 1078-1085. 20. Yeh B.M., Breiman R.S., Taouli B., Qayyum A., Roberts J.P., Coakley F.V.: Biliary tract depiction in living potential liver donors: comparison of conventional MR, mangafodipir trisodium-enhanced excretory MR, and multi-detector row CT cholangiography – initial experience. Radiology, 2004, 230: 645-51. 21. Schroeder T., Malago M., Debatin J.F., Goyen M., Nadalin S., Ruehm S.G.: "All-in-one" imaging protocols for the evaluation of potential living liver donors: comparison of magnetic resonance imaging and multidetector computed tomography. Liver Transpl, 2005, 11: 776-787. 22. Koyama K., Takagi Y., Ito K., Sato T.: Experimental and clinical studies on the effect of biliary drainage in obstructive jaundice. Am J Surg, 1981, 142: 293-299. 23. Kawarada Y., Higashiguchi T., Yokoi H., Vaidya P., Mizumoto R.: Preoperative biliary drainage in obstructive jaundice. Hepatogastroenterology, 1995, 42: 300-307.

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COMBINATION OF PARTIAL SITUS INVERSUS, POLYSPLENIA AND ANNULAR PANCREAS WITH DUODENAL OBSTRUCTION AND INTESTINAL MALROTATION Y. Ben Ahmed1, S. Ghorbel1, T. Chouikh1, F. Nouira1, H. Louati2, A. Charieg1, B. Chaouachi1 Situs inversus is a challenge to the physician, both for the diagnostic and for the therapeutic. A combination of partial situs inversus, annular pancreas and polysplenia with bowel malrotation has been reported in a newborn who presented as duodenal obstruction. Situs inversus is rare especially without heart malformation. All the abnormalities in this combination can be explained on the basis of multiple organ malrotation. It also demonstrates the necessity of meticulous investigation and precise description of the anomaly as far as the management of this case is concerned. Key-word: Infants, newborn.

Situs inversus is a lateralization anomaly that can be associated to other malformations that alter prognosis: isolated cardiac malformations, cardiosplenic syndromes, or Kartagener’s syndrome (1). The location of the thoracic and abdominal viscera in cases with situs inversus has been determined to be everywhere between the normal and the mirror image place. The pathogenesis of heterotaxia has not been clarified yet. Genetic and environmental factors have been reported as possible causes. We report the case of partial situs inversus, polysplenia and annular pancreas with duodenal obstruction and malrotation. We tried to explain the probable embryogenesis and give detailed description of the anatomy and clinical features of the syndrome. Case report An 18-day-old girl, who weighed 2.800 kg at birth, was admitted for non bilious vomiting since the age of 8 days. Parents report a rarefaction of stool. No Antenatal Ultrasounds were available. Physical examination revealed a normally placed apex beat on the left side of the chest but the liver was palpated in the left upper abdominal quadrant. The blood tests were normal. Investigation included a plain radiograph of the abdomen, which shows deviation of the nasogastric tube to the right (Fig. 1). That raised the question of inversion of the abdominal viscera. The investigation was com-

Fig. 1. — Abdominal X-Ray shows deviation to the right of the nasogastric tube.

pleted by upper abdominal opacification (Fig. 2), abdominal ultrasonography and echocardiogram.

From: Department of 1. Paediatric Surgery B, and 2. Paediatric Radiology, Children Hospital of Tunis, Tunis, Tunisia. Address for correspondence: Dr T. Chouikh, M.D., Department of Paediatric Surgery B, Children Hospital of Tunis, Place Bab Saadoun Jabary 1007 Tunis, Tunisia.

Abdominal ultrasound was not able to visualize the inferior vena cava that is why a CT scan was performed (Fig. 3). Unfortunately MRI was not available in our center. The results of the examinations supported the preoperative diagnosis of levocardia associated with inversion of the abdominal viscera

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Fig. 2. — Upper abdominal opacification shows stomach in the right area of the abdomen.

with right polysplenia and annular pancreas. Situs inversus was associated to a stenosis of the second portion of duodenum. This part of the duodedum was encircled by the annular pancreas. The inferior cave vein wasn’t visible neither on ultrasonography nor on CT, it was interrupted at the retrohepatic portion to be continued into the azygos vein. The hepatic vein formed a suprahepatic duct that drained into the systemic venous atrium. A bilateral superior vena cava was noticed. The echocardiogram demonstrated that there was a muscular ventricular septal defect and a little mitral insufficiency. The baby was operated 6 days later, after adequate reanimation. The intraoperative findings consisted of duodenal obstruction due to an incomplete intraluminal diaphragm of the second duodenum; left-sided liver, right-sided polysplenia and stomach. Multiple spleens were found along the greater curvature of the stomach in the right upper quadrant varying in size from 0.5 to 1.5 cm;

B Fig. 3. — A. Abdominal CT: Situs inversus, stenosis of the second portion of duodenum (2) annular pancreas (1). B: Abdominal CT: interruption of the inferior cave vein in the retrohepatic portion. 1. Aorta, 2. Interrupted inferior vena cava, 3. Liver, 4. Kidney.

Totally right-sided located colon in position like a mirror image of nonrotation with congenital bands on small bowel; Abnormal position of the inferior vena cava to the left side was also noted. After the investigation a longitudinal duodenotomy with diaphragm resection was performed then we close the duodenotomy with a continuous suture helped by a transanastomic gastric tube. LADD’s

procedure was performed, including division of peritoneal bands and placement of bowel in a state of nonrotation. Immediately postoperative course was uneventful; the patient tolerated a regular diet on the fifth day and was discharged nine days after surgery. The echocardiogram done at the age of 6 months was normal. The patient was hospitalized at the age of 7 months for bowel occlusion due to intestinal adhesion.

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She underwent surgery after failure of gastric aspiration. There was no need for intestinal resection, Follow-up after this second surgery was normal. The infant is doing well at age 12 months. She is regularly seen in consultation with a good weight intake and no alimentary or transit problems. Discussion Situs inversus viscerum, also termed heterotaxia, is a condition where the position of the organs is a perfect mirror image of their normal physiological position (1). It is divided into total and partial. In total situs inversus the heart is to the right of the midline, the cardiac chamber position is reversed, the aorta courses to the right, there are three left and two right lung lobes, the thoracic duct is on the right, the liver and stomach are transposed, the colon flexures are reversed, and the spleen is on the right. In partial situs inversus, there may be thoracic inversion only, cardiac chamber reversal or abdominal inversion only, and there are frequently syndromes associated with splenic anomalies, annular pancreas, horseshoe kidney, diaphragmatic hernia, or a number of other developmental abnormalities (2). The true incidence of situs abnormalities is unknown. Some estimates suggest that situs inversus occurs in approximately 1 per 8000 to 25,000 live births (2). The reported sex distribution of the disease is equal for males and females; when there are associated anomalies of the spleen, boys predominate. The pathogenesis of heterotaxia has not been clarified yet. Genetic and environmental factors have been reported as possible causes. Von Woelworth reported that some cases could be attributed to early embryonic factors (3). Situs inversus is generally an autosomal recessive genetic condition, although it can be X-linked or found in identical "mirror" twins. The partial situs inversus being described is probably caused by reversal of location in terms of left and right, of the duodenum, pancreas, liver, stomach, and spleen, as a consequence of disturbances of rotation early in embryonic life (4), precisely between the fifth and sixth gestational week. It is conceivable that a single, or less likely, more than one event occurring at this period

can interfere with these rotational activities and cause an absence of rotation of an organ or an incomplete rotation, or perhaps to rotate in the opposite direction. So, anomalies of gut fixation and rotation are not difficult to understand. Various theories have been advanced to explain the formation of the annular pancreas. Perhaps the most popular is that advanced by Lecco, which suggests fixation of the tip of the ventral pancreatic primordium to the duodenum during the 180Â° rotation of its base to fuse with the dorsal pancreatic bud. Diversity of structural lesions, and the absence of congenital cardiac malformations suggest a less specific timing of the teratogenic insult than has been postulated in the past, Campbell and Deuchar have suggested that the initial abnormality may be situs inversus which leads to and is responsible for the other malformations (5). Situs inversus occurs more commonly with dextrocardia. A 3-5% incidence of congenital heart disease is observed in situs inversus with dextrocardia, usually with transposition of the great vessels. Situs inversus with levocardia is rare, and it is almost always associated with congenital heart disease (6). In the absence of congenital heart defects, individuals with situs inversus can lead normal healthy lives. The functional malformations associated with situs inversus are primarily cardiovascular with severe cardiac malformations such single ventricle, single atrium, pulmonary atresia, ventricular septal defect, transposition of great arteries, truncus arteriosus, mitral stenosis, complete heart block, tricuspid astresia, atrioventricular canal, anomalous pulmonary venous drainage. Although significant visceral or structural deformities can occur, a review of all cases reported in the literature confirms the presence of significant gastrointestinal pathologies, mainly annular pancreas but also congenital obstruction of the gastrointestinal tract secondary to stenosis or atresia of the duodenum or jejunum or incomplete fixation of the bowel mesentery that can be complicated by a midgut volvulus (7). Preduodenal portal vein which is a rare cause of duodenal obstruction should be borne in mind to avoid inadvertent damage during surgery (8). The majority of the cases are associated to splenic defect. Polysplenia syndrome is usually

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characterized by one multilobulated or a number of individual splenules. The most common sites in which extra splenic tissue has been found are the splenic hilum, the splenic pedicle, the peritoneal ligaments and in the tail or head of the pancreas (9). Venous malformations like bilateral superior venae cavae, the absence of a segment of the inferior vena cava were described. Anomalous of hepatic venous drainage is a frequent finding in cases of levocardia. It has been suggested that the abnormal hepatic veins represent persistent omphalomesenteric veins (10). So, the combination of annular pancreas and partial situs inversus associated with duodenal obstruction nonrotation is rare. The originality of this case is also due to absence of major cardiac anomalies and the presence of hepatic venous drainage. Clinical manifestations depend on the individualâ&#x20AC;&#x2122;s specific anatomical anomalies. Severe and complex cardiac abnormalities are likely to be apparent at birth or soon afterward. Individuals without congenital heart disease may present later with conditions such as biliary atresia or volvolus. In persons without clinically morbid abnormalities, these conditions may be discovered during an evaluation for an unrelated problem or complaint when they are adults (2). Diagnosis of a situs inversus abdominus by physical examination is difficult. Transposition of visceral organs is more difficult to detect on physical examination than dextrocardia, by palpating the liver on the left and the spleen on the right. In patients with situs inversus viscerum presenting with an acute illness, localization of the abdominal pain can be confusing. Organ reversal can occur without concomitant reversal of the sensory nerve pathway. Non reversal of the pain pathways would explain the occasional case in which symptoms of cholecystitis become manifest in the right upper quadrant or those of appendicitis in the right lower quadrant even though the involved organ is located on the opposite side (11). Situs abnormalities may be recognized first by using radiography or ultrasonography. The interruption of the inferior vena cava with azygos or hemiazygos continuation may be suggested after the evaluation of plain chest radiographs showing an absence of an inferior vena cava on the lateral projection and a widening of the

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paravertebral pleural reflection in the right or left paravertebral area because of a dilated azygos or hemiazygos vein. A plain radiograph of the abdomen showing a reversed double bubble confirms the diagnosis. Ultrasound and CT scans are the most accurate noninvasive means of diagnosing the abnormal (12). However, computed tomography (CT) scanning is preferred for the definitive diagnosis of situs inversus. It provides good anatomic details of organ position, cardiac apical position, and great vessel branching and precise the localization of splenules in order to avoid hemorrhage during surgery. Magnetic resonance imaging (MRI) is usually reserved for difficult cases or for patients with associated cardiac anomalies (13). Moreover prenatal diagnosis of situs anomalies by obstetric ultrasonography was mostly reported in conjunction with congenital heart disease: location of the stomach; liver lateralization; interruption of the Vena Cava associated to abnormal azygos return and visualization of the spleen (14). The rational approach to a patient with situs inversus abdominus includes the collection of as much preoperative information as possible using sonography and computerized scanning. To prevent incorrect preoperative diagnoses and inappropriate incision placement, such studies are critical to delineate intra-abdominal pathology; but in addition, such information might also provide important data relative to life-threatening associated cardiac disease (1).

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Detection of a malformation must lead to search for other associated anomalies. We consider that any situs anomaly should warrant bowel malrotation exclusion shortly after birth because of their potential association and risk of midgut volvolus.We should also be attentive to an eventual duodenal or jejuna obstruction in case of situs inversus. Conclusion Situs inversus is a rare malformation; however it should be suspected and searched through clinical and radiological signs in case of intestinal obstruction. Ultrasound exam and CT are of great help for meticulous investigation and detailed description of the anatomic futures in all the cases of situs inversus. This is of great importance for the management of the patient and useful in case of surgery. References 1. Cheikhelard A., De Lagausie P., et al.: Situs Inversus and Bowel Malrotation: Contribution of Prenatal Diagnosis and Laparoscopy. J Pediatr Surg, 2000, 35: 1217-1219. 2. Winer-Muram H.T.: Adult presentation of heterotaxic syndromes and related complexes. J Thorac Imaging, 1995, 10: 43-57. 3. Seung E.L., Hyun-Young K.: Situs anomalies and gastrointestinal abnormalities. J Pediatr Surg, 2006, 41: 1237-1242.

4. Tryfonas G.I., Chaidos C., Avtzoglou P.P.: Partial Situs Inversus: Duodenal Obstruction in a Neonate with Isolated Levocardia. J Pediatr Surg, 1992, 27: 1584-l586. 5. Debo Adeyemi S.: Combination of Annular Pancreas and Partial Situs Inversus: A Multiple Organ Malrotation Syndrome Associated With Duodenal Obstruction J Pediatr Surg, 1988, 23: 188-191. 6. Maldjian P.D., Saric M.: Approach to dextrocardia in adults. AJR, 2007, 188: S39-49; quiz S35-38. 7. Mordehai J., Cohen Z.: Preduodenal Portal Vein Causing Duodenal Obstruction Associated With Situs Inversus, Intestinal Malrotation, and Polysplenia: A Case Report. J Pediatr Surg, 2002, 37 (4): E5. 8. Koonosuke N., Fumio K.: Digestive Tract Disorders Associated With Asplenia/Polysplenia Syndrome. J Pediatr Surg, 1997, 32: 91-99. 9. William J., Futrell S.: Cecal Volvulus Associated with Incomplete Situs lnversus and Splenic Dysgenesis. Am J Surg, 1874, 128: 421-426. 10. Paddock R.J., Arensman R.M.: Polysplenia Syndrome: Spectrum of Gastrointestinal Congenital Anomalies. J Pediatr Surg, 1982, 17: 563-566. 11. Shlomo S., Egon R., et al.: Levocardia with partial situs inversus, an incidental finding in a 15 year-old boy. Am Heart J, 1962, 699-704. 12. Applegate K.E., Goske M.J.: Situs revisited: imaging of the heterotaxy syndrome. Radiographics, 1999, 19: 837-852. 13. Silverman N.H.: An ultrasonic approach to the diagnosis of cardiac situs, connections, and malpositions. Cardiol Clin, 1983, 1: 473-486. 14. Tonkin I.L., Tonkin A.K.: Visceroatrial situs abnormalities: sonographic and computed tomographic appearance. AJR, 1982, 138: 509-515.

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MANAGING CORONARY ARTERY VEIN BYPASS GRAFT STUMP PSEUDOANEURYSM: A NOVEL APPROACH V. Rachapalli, R. Evans, D. Roberts1 We present a case of a pseudoaneurysm of the saphenous vein graft stump, which was managed with percutaneous thrombin injection. Aneurysms of a saphenous vein coronary bypass graft are rare and aneurysms of a bypass graft stump are even rarer. To our knowledge this is the first reported case of a pseudoaneurysm of a graft stump with the use of thrombin to treat a saphenous vein graft pseudoaneurysm. Key-word: Aneurysm, coronary.

Case report An 85-year-old man, with a background cardiac history of myocardial infarction and aortic stenosis, presented with a shortness of breath and central chest pain, radiating to the right arm and back. A coronary angiogram demonstrated a narrowing of the proximal right coronary artery (RCA), mid left anterior descending artery (LAD) and proximal first diagonal (D1) branch. He underwent an aortic valve replacement and three vessel bypass. The left internal mammary artery was anastomosed to the LAD, venous grafts (VG) to the D1 and RCA. He underwent emergency sternotomy 10 days later, for pericardial tamponade, which demonstrated bleeding from two sites: a slit in the VG to the D1 which was 2 cm from the aortic end and from the lateral angle of the aortotomy. The VG slit was thought to be secondary to trauma from the emergency bedside sternotomy. Post-operatively patient developed respiratory compromise, renal impairment and a sternal wound infection. Eight days later, he became hypotensive, with oozing from the sternal wound. A further sternotomy identified the source of bleeding to be from the previous site of injury to the VG. It was elected to resect the VG, as repairing it would have severely compromised the luminal diameter. Further sternal bleeding occurred 25 days after the third operation, but was haemodynamically stable. A computer tomography (CT) of the chest demonstrated a pseudoaneurysm from the aortic stump of the VG to D1 (Fig. 1A,B). Under CT guidance a spinal needle was inserted into the pseudoaneurysm sac parasternally. 1.2 mls of thrombin

Fig. 1. — Pseudoaneurysm in the anterior mediastinum lying anterior to the ascending aorta (A, arrow). The graft stump (arrow) is seen in relation to the pseudoaneurysm on the sagittal reformats (B).

Fig. 2. — Panel A demonstrates the spinal needle with its tip placed in the position of the pseudoaneurysmal sac. Panel B shows occlusion of the pseudoaneurysm on the post contrast scan.

was injected (Fig. 2A). Post procedure CT scan showed that the pseudoaneurysm had thrombosed

From: Department of Radiology, Morriston Hospital, Swansea, UK. Address for correspondence: Dr V. Rachapalli, FRCR., 8 Ffordd Ty Unnos, Cardiff CF14 4NJ, UK.

(Fig. 2B). Ten days after the thrombin injection, the patient developed further bleeding from the sternal wound. CT of the chest demonstrated that the pseudoaneurysm had recurred. A repeat thrombin injection was undertaken. A spinal needle was placed into the sac of the pseudo-

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pressure which exists in the ascending thoracic aorta. We would suggest that these patients are kept under review and at the earliest sign of a bleed be re-imaged. To the best of our knowledge, this is the first case where a pseudoaneurysm was associated with a coronary artery bypass graft stump and CT guided percutaneous thrombin has been successfully used to treat this complication. Conclusion

Fig. 3. â&#x20AC;&#x201D; A demonstrates the tip of the needle in the pseudoaneurysm. Upon contrast injection through the needle, contrast is seen to enter the aorta (arrow) and pseudoaneurysmal sac (B, arrow). Post contrast CT after thrombin injection demonstrates occlusion of the pseudoaneurysmal sac (C).

Though pseudo aneurysms of a SVCBG are rare, their presence requires urgent treatment as the potential for rupture is high. Though surgery is the main stay of treatment; endovascular therapy can be a viable option, particularly if the patient is not suitable for surgery. This case demonstrates that CT guided percutaneous thrombin injection can be further option for successful treatment. References

aneurysm and contrast injected via the spinal needle demonstrating the recurrent pseudoaneurysm and patency of the graft stump (Fig. 3A,B). 1.5 ml of thrombin was injected, with the immediate post procedure CT showing complete thrombosis of the pseudoaneurysm (Fig. 3C). The patient had an uneventful recovery and a repeat CT prior to discharge showed no recurrence of the pseudoaneurysm. Discussion Aneurysmal dilatation of a coronary bypass graft is a rare. True aneurysms are more common and involve the mid portion of the graft. Pseudoaneurysms tend to occur at anastomotic sites (1). The first case of an aneurysm of a saphenous vein coronary bypass graft (SVCBG) was reported in 1972 and of a pseudoaneurysm in 1975 by Riahl et al. (2, 3). Trauma to the vein at the time of harvest, inherent areas of weakness (valve site and branch points), atherosclerotic degeneration of the vessel wall and wall necrosis are some of the possible explanations for their formation (4). Infection at

insertion site and wound dehiscence also play a contributory role (1). Most aneurysms are detected incidentally. The can present as myocardial ischaemia or infarction, fistula formation into the cardiac chambers and rupture (5). Graft stump aneurysms which arise, from the proximal aspect of the graft (1 to 2 cm length extending from the aortic attachment left after a redo surgery) are rare (6). Given the increased risk of rupture and associated morbidity and mortality, surgical management is recommended; especially if it is a pseudo-aneurysm (1). To date there has been only one other report of an aneurysm related to a stump of a previously ligated SVCBG. This was proven histologically to be a true aneurysm and was managed surgically (6). But an endovascular approach could be considered particularly if the patient is not medically fit to undergo surgery. Tamirisa et al successfully managed a patient with a pseudoaneurysm of the internal mammary artery graft by local thrombin injection (7). In the current case the original pseudoaneurysm probably recurred due to the high arterial

Memon A.Q., Huang R.I., Marcus F., Xavier L., Alpert J.: Sapehnous vein graft aneurysm: case report and review. Cardiol Rev, 2003, 11: 26-34. Carrasquilla C., Weaver A.W.: Aneurysm of a saphenous vein graft to the common carotid artery. Vasc Surg, 1972, 6: 66-69. Riahi M., Vasu C.M., Tomatis L.A., Schlosser R.J., Zimmerman G.: Aneurysm of a saphenous vein bypass graft to coronary artery. J Thorac Cardiovasc Surg, 1975, 70: 358-359. Benchimol A., Harris C.L., Desser K.B.: Aneurysms of an aorto-coronary artery saphenous vein bypass graft-a case report. Vasc Surg, 1975, 9: 261-264. Trop I., Samson L., Cordeau MP., Leblanc P., Therasse E.: Anterior mediastinal mass in a patient with prior saphenous vein coronary artery bypass grafting. Chest, 1999, 115: 572576. Baldwin RT., Klima T., Frazier OH., Lonquist J., Radovancevic B.: True aneurysn of the saphenous vein graft stump associated with CABG in a cardiac transplant patient. Ann Thorac Surg, 1992, 54: 978-979. Tamirisa PK., Rinder M., Singh J., Lonquist J., Radovancevic B.: Thrombin injection to treat pseudoaneurysm of internal mammary artery bypass graft: a case report. Catheter Cardiovasc Interv, 2002, 57: 548-551.

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CHRONIC RECURRENT MULTIFOCAL OSTEOMYELITIS MIMICKING OSTEOID OSTEOMA Z. Jibri, M. Sah, R. Mansour1 In this article we illustrate an unusual case of chronic recurrent multifocal osteomyelitis (CRMO) in a 9 year old girl who presented with right thigh pain. The initial plain radiographs were normal. The white cell count was normal and there was a mild rise in C-reactive protein. Cross sectional imaging of the right femur showed a lesion with features suggestive of osteoid osteoma. However, when the lesion was excised, the appearances on histopathological examination were non-specific showing chronic inflammatory cells and the microbiological testing revealed no organisms. Six months later, this child presented with right shoulder pain and the subsequent imaging demonstrated bilateral clavicular lesions. At this stage, the diagnosis of CRMO was made based on the combination of the clinical, radiological, histopathological and microbiological features. This case demonstrates that the cross sectional imaging features of the bony lesion in CRMO can mimic osteoid osteoma. Key-word: Bones, infection.

CRMO is an idiopathic inflammation of the bone that was first described by Giedion et al in 1972 as “sub-acute and chronic symmetrical osteomyelitis” (1). It has nonspecific clinical, radiological and histopathological features (2). Therefore, it is a diagnosis of exclusion. The cause of CRMO remains unclear. The typical imaging findings of CRMO include lytic and sclerotic lesions in the metaphyses of long bones and the medial clavicles (3). In this article, we illustrate a case of CRMO in which the presenting bony lesion had imaging features which are characteristic of an osteoid osteoma. Case report A 9-year-old girl presented to her family physician with right thigh pain. The clinical examination was unremarkable. The plain radiographs of the hip and pelvis were normal. As the symptoms persisted, the patient was referred to the Orthopaedic team when laboratory investigations, MRI and CT of the right femur were performed. The blood tests showed normal white cell count and a mild rise in C-reactive protein. MRI of the right femur demonstrated a focus of high signal intensity related to the posterior cortex of the proximal femoral diaphysis on the STIR sequences which was surrounded by bone marrow oedema

Fig. 1. — A. Axial STIR- MR image of the right thigh demonstrating a focus of high signal intensity within the posterior cortex of the femur (arrow) with bone marrow oedema and also high signal intensity (oedema) in the adjacent soft tissues (open arrows). B. Coronal STIR- MRI of the right thigh illustrating the extensive bone marrow oedema involving the proximal femur (arrow) and also the oedema in the surrounding soft tissues (arrowheads).

(Fig. 1). There was also a slight high signal change in the adjacent soft tissue of the thigh on the fluid sensitive sequences. CT was also performed for further characterisation. This showed a 10 mm radiolucent focus associated with cortical thickening in the same area of the proximal femur (Fig. 2). The appearances were reported as suggestive of osteoid osteoma.

From: 1. Department of Radiology, University Hospital of Wales, Cardiff, United Kingdom. Address for correspondence: Dr Z. Jibri, M.D., Department of Radiology, University Hospital of Wales, Cardiff, CF 14 4XW, United Kingdom. E-mail: zjibri@doctors.org.uk

Surgical excision of the right proximal femoral lesion was undertaken. However, the appearances on the histopathological examination were non-specific showing chronic inflammatory cells with no tumour cells identified. The microbiological testing revealed no organisms. Six months later, the patient presented with right shoulder pain with swelling over the right clavicle. The plain radiograph demonstrated expansion of the medial end of the right clavicle which appeared sclerotic with small focal areas of radiolucency. The medial end of the left clavicle had a similar but less extensive appearance (Fig. 3). MRI scan was performed and demonstrated bone marrow oedema with

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Fig. 4. — Coronal STIR- MRI sequences of the clavicles demonstrating bone marrow oedema and periosteal reaction with expansion of the medial end of the right clavicle and to a lesser extent the left clavicle which is associated with high signal within the surrounding soft tissues (arrows). Fig. 2. — Axial CT image of the right thigh demonstrating a small lucent focus related to the posterior cortex of the proximal femoral diaphysis mimicking osteoid osteoma (arrow).

on the excised femoral lesion. The presenting right femoral lesion was in fact part of the CRMO disease entity and not an osteoid osteoma. Discussion

Fig. 3. — Plain radiograph of the right clavicle which also includes the medial end of the left clavicle. This shows expansion of the medial ends of both clavicles (arrows), more so on the right side, which appear sclerotic with foci of radiolucency. These appearances are typical of CRMO.

periosteal reaction and expansion of the medial end of the right clavicle and to a lesser extent the left clavicle which was associated with high signal within the surrounding soft tissues on the STIR sequences (Fig. 4). A whole body radionuclide bone scan was obtained to search for other bony lesions. In addition to showing areas of high tracer uptake at the medial ends of both clavicles, the bone scan has revealed a focus of high uptake in the upper thoracic spine (Fig. 5). MRI scan of the thoracic spine was performed at a later stage and it demonstrated increased

signal intensity at T4 and T6 vertebral bodies on the STIR images with anterior wedging and collapse of T6 vertebral body resulting in kyphosis (Fig. 6). At the stage when the right clavicular lesion was imaged, the diagnosis of chronic recurrent multifocal osteomyelitis was made. This was based on the multifocality of the disease process which involved the medial ends of both clavicles, the absence of abscess formation, the lack of a causative organism on microbiological testing and the nonspecific histopathological findings

CRMO is characterised by multifocal non-pyogenic inflammatory bone lesions and a course of exacerbations and remissions (3). The disease predominantly affects children and adolescents. It usually occurs in the latter half of the first decade and the first half of the second decade of life (mean age of 10.5 year) (4). It affects females more than males (5). The aetiopathogenesis of CRMO remains unclear and it is currently regarded as an auto-inflammatory syndrome (6). Reaching the diagnosis is important in avoiding unnecessary diagnostic procedures and to initiate appropriate therapy (7). The clinical presentation is non-specific with insidious onset of fever, local swelling and pain in affected bones. The laboratory findings are also nonspecific often demonstrating raised ESR and CRP with a normal white cell count (5, 8). It has been reported that CRMO can be associated with skin lesions including palmoplantar pustulosis, psoriasis vulgaris, Sweet syndrome, and pyoderma gangrenosum (3, 9). CRMO predominantly affects the metaphysis of long bones and the clavicles. The lesions can occur in

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Fig. 5. — Whole body radionuclide bone scan showing high tracer uptake at the medial ends of both clavicles and at the 4th thoracic vertebra. There is also a subtle tracer uptake at the proximal part of the right femur, at the site of the surgically excised lesion.

other areas throughout the skeleton including the spine, pelvis, sacroiliac joints, ribs, sternum, scapulae, metatarsals, metacarpals, tarsal bones, phalanges and mandible (2). Radiologists can be the first to suggest this diagnosis. Plain radiography typically demonstrates lytic lesions usually at the metaphysis of the tubular bone at the early stages of the disease. With healing, progressive sclerosis is usually seen around the lytic lesion with associated hyperostosis (3). During relapses, new lytic lesions appear with periosteal reaction resulting in bone thickening (2, 3). Spinal lesions are characterised by erosion of the vertebral end plate with adjacent sclerosis. CRMO lesion can lead also to vertebral collapse and subsequent kyphosis (2, 10). The MRI appearances of the affected areas are non-specific showing abnormal hyperintensity on STIR images and contrast enhancement on T1-weighted images, which are features of oedema like lesions (11). MRI can also demonstrate periosteal reaction and soft tissue oedema (7, 12). Therefore, MRI is useful in monitoring disease activity (5). With healing, these MR features gradually disappear with

regeneration of normal marrow signal (5). MRI can also help in differentiating CRMO from infective osteomyelitis. This is particularly helpful in characterising the spinal CRMO lesion. This appears as irregular vertebral endplate with adjacent bone marrow oedema. The adjacent disc may become involved showing altered signal intensity but, unlike infectious osteomyelitis, the lesion does not cross the intervertebral disc and there is no abscess formation (3, 5). Given the multifocality of the disease and the lack of ionizing radiation with MRI, whole body MRI can have a role in establishing the diagnosis of this disease entity which predominantly affects the paediatric population (11). CRMO lesions can also be detected using radionuclide bone scan which can help in making the diagnosis and in showing the extent of the disease by identifying the multiple osseous involvement (4). The histopathological findings in CRMO usually include non-specific subacute or chronic inflammation with intertrabecular spaces filled with fibrovascular material and inflammatory cells mainly lymphocytes (5, 8). Because the histopathologic features are non-specific, the

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Fig. 6. — STIR sagittal MRI of the thoracic and cervical spine showing high signal intensity and collapse at T6 vertebral body (arrow) and also increased signal intensity at the superior end plate of T4 vertebral body (open arrow).

definite diagnosis should be made by combining the clinical picture, imaging studies, bacterial culture, and histopathologic analysis in a multidisciplinary approach (13). The differential diagnosis includes multifocal bacterial osteomyelitis, multifocal trauma, stress fracture, juvenile idiopathic arthritis, histiocytosis, Scheuermann disease (the spinal lesion), leukemia, lymphoma, primary neoplasms (Ewing's sarcoma or osteosarcoma) and metastatic secondary malignancies (sarcoma, neuroblastoma) (2, 4, 5). This case has illustrated that osteoid osteoma is also part of the differential diagnosis. In this case of CRMO, the right femoral lesion had a radiolucent cortically based focus that was associated with cortical thickening on the CT images. This focus had high signal intensity on the corresponding STIRMR images. These features are uncharacteristic of CRMO. At the same time these appearances, and also the location of the lesion, are more typical of osteoid osteoma (14). Infective osteomyelitis in the form of intracortical abscess can mimic osteoid osteoma but it is not typical of CRMO to produce these features (14). In conclusion, CRMO can create a diagnostic challenge due its nonspecific manifestations and it is a diagnosis of exclusion. This case

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illustrates that the cross sectional imaging features of the bony lesion in CRMO can mimic osteoid osteoma. References 1. Giedion A., Holthusen W., Masel L.F., Vischer D.: Subacute and chronic “symmetrical” osteomyelitis. Ann Radiol, 1972, 15: 329-342. 2. Jurriaans E., Singh N.P., Finlay K., Friedman L.: Imaging of chronic recurrent multifocal osteomyelitis. Radiol Clin North Am, 2001, 39: 305-327. 3. Khanna G., Sato T.S.P., Ferguson P.: Imaging of chronic recurrent multifocal osteomyelitis. RadioGraphics, 2009, 29: 1159-1177. 4. Mandell G.A., Contreras S.J., Conard K., Harcke H.T., Maas K.W.: Bone scintigraphy in the detection of chronic recurrent multifocal osteomyelitis. J Nucl Med, 1998, 39: 1778-1783.

JBR–BTR, 2012, 95 (4) 5. Jurik A.G.: Chronic recurrent multifocal osteomyelitis. Semin Musculoskelet Radiol, 2004, 8: 243-253. 6. Eleftheriou D., Gerschman T., Sebire N., Woo P., Pilkington C.A., Brogan P.A.: Biologic therapy in refractory chronic non-bacterial osteomyelitis of childhood. Rheumatology (Oxford), 2010, 49: 1505-1512. 7. Jurik A.G., Egund N.: MRI in chronic recurrent multifocal osteomyelitis. Skeletal Radiol, 1997, 26: 230-238. 8. Bjorkstén B., Boquist L.: Histopathological aspects of chronic recurrent multifocal osteomyelitis. J Bone Joint Surg Br, 1980, 62: 376-380. 9. Vanhoenacker F.M., Baekelandt J., Vanwambeke K., Willemen D., De Schepper A.M.: Chronic recurrent multifocal osteomyelitis. JBR-BTR, 1998, 81: 84-86. 10. Snoeckx A., Vanhoenacker F.M., Mulier E., De Schepper A.: Chronic recurrent multifocal osteomyelitis with primary spinal involvement. JBR-BTR, 2008, 91: 114-115.

11. Fritz J., Tzaribatchev N., Claussen C.D., Carrino J.A., Horger M.S.: 2.: Chronic recurrent multifocal osteomyelitis: comparison of whole-body MR imaging with radiography and correlation with clinical and laboratory data. Radiology, 2009, 252: 842-851. 12. Sundaram M., McDonald D., Engel E., Rotman M., Siegfried E.C.: Chronic recurrent multifocal osteomyelitis: an evolving clinical and radiological spectrum. Skeletal Radiol, 1996, 25: 333-336. 13. Girschick H.J., Huppertz H.I., Harmsen D., Krauspe R., MullerHermelink H.K., Papadopoulos T.: Chronic recurrent multifocal osteomyelitis in children: diagnostic value of histopathology and microbial testing. Hum Pathol, 1999, 30: 59-65. 14. Chai J.W., Hong S.H., Choi J.Y., et al.: Radiologic diagnosis of osteoid osteoma: from simple to challenging findings. Radiographics, 2010, 30: 737-749.

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INFLAMMATORY MYOFIBROBLASTIC TUMOR OF THE PANCREATIC HEAD L. Lacoste, Ch. Galant2, J.-F. Gigot3, B. Lacoste1, L. Annet1 Inflammatory myofibroblastic tumors are rare, especially in the pancreas. It is sometimes difficult to obtain a definitive diagnosis with radiological imaging and there is not yet consensus about treatment. We report a case of a 56year-old man with recurrent abdominal pain particularly in the right upper quadrant without other symptoms. The imaging results showed a pancreatic hypovascularized mass with stenosis of the main pancreatic duct and the common bile duct without metastasis. The FDG PET scanner showed two hypermetabolic foci in the head of the pancreas. The biopsies of the mass were not diagnostic. The therapy adopted was Whipple’s pancreaticoduodenectomy with a histological diagnosis of the inflammatory myofibroblastic tumor. Key-word: Pancreas, neoplasms.

Inflammatory myofibroblastic tumors (IMT), previously known as inflammatory pseudotumors, are rare lesions of the soft tissue, appearing most frequently in the young and for which the origin is unknown (1). They were initially observed in the lungs but they can also be found in the mesentery, the omentum, the abdominal organs, the bladder or the orbit. Today, only 28 cases of pancreatic IMT have been reported in the literature (2). This pathology resembles both clinically and radiologically an adenocarcinoma of the pancreas which causes real problems in reaching a differential diagnosis. We present a new case of inflammatory myofibroblastic tumor of the pancreas covering all aspects from diagnosis to treatment.

Fig. 1. — Axial T1-weighted gadolinium contrast-enhanced MR image shows a hypovascularized mass in the head of the pancreas (arrow).

Case report A 56-year-old man was hospitalized several times in the gastroenterology department for recurrent localized abdominal pain particularly in the right upper quadrant, sometimes accompanied by nausea. There were no other symptoms and the clinical exam showed no particularities. Blood tests revealed an increase in transaminases, lipases, amylases and CA 19.9. CT and MRI showed a heterogeneous solid hypervascularized mass that was slightly hypointense on T2, hypointense on T1, hypovascularized, in the head of the pancreas with stenosis of the cephalic Wirsung duct and of the intra-pancreatic portion of the common bile duct with upstream dilatation (Double Duct Sign) and visibility of the secondary

Fig. 2. — MR cholangiopancreaticography shows a stenosis of the main pancreatic duct and the common bile duct (thick arrows) «Double Duct Sign» with an upstream dilatation and visible secondary pancreatics ducts (thin arrow).

From: 1. Department of Medical Imaging, 2. Department of Anatomopathology, 3. Department of Surgery, UCL Saint Luc, Catholic University of Louvain, Brussels, Belgium. Address for correspondence: Dr L. Lacoste, Department of Medical Imaging, UCL Saint Luc, Catholic University of Louvain, Avenue Hippocrate 10, B-1200 Brussels, Belgium.

pancreatic ducts (Fig. 1, 2). There was no local adenopathy and no lesion of the liver to suggest metastasis. The endoscopic ultrasonography showed a chronic pancreatopathy of the complete pancreas and con-

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Fig. 3. — Axial FDG PET image shows a heterogeneous pancreatic head with two hypermetabolic foci (arrows).

Fig. 5. — Strong immunoreactivity of most of the spindle cells for alpha smooth muscle actin (original magnification × 40).

Fig. 4. — Tumor of the pancreatic head. Spindle cell proliferation made of myofibroblasts accompanied by a prominent inflammatory infiltrate consisting of plasma cells, lymphocytes, and eosinophils (original magnification × 20). Fig. 6. — Strong immunoreactivity of some myofibroblasts for desmin (original magnification × 40).

firmed the presence of an expansive mass in the cephalic region of the pancreas. Biopsies were realized at the same time but were non conclusive. A FDG PET scan was realized, showing a heterogeneous cephalic pancreatic region similar to what can be observed in chronic pancreatitis, but with the presence of two distinct foci of which the metabolic rates were comparable with active tumorous phenomena but also with acute inflammatory pathologies (Fig. 3). Due to the difficulty in making an accurate diagnosis and eliminating a malignant tumor, it was decided in the multidisciplinary meeting to

undertake Whipple’s pancreaticoduodenectomy. The operation went ahead without complications. The macroscopic analysis of the specimen revealed a white solid mass with stenosis of the Wirsung duct. Histopathological analysis showed a proliferation of myofibroblasts accompanied by an important infiltration of chronic inflammatory cells (Fig. 4). The immunohistochemical analysis was positive for alpha smooth muscle actin (Fig. 5) and for desmin (Fig. 6).

The surgical follow-up was uneventful and now the patient is doing well. Discussion The terminology of inflammatory myofibroblastic tumor is now generally accepted for the majority of lesions formerly named: inflammatory pseudotumor, plasma cell granuloma, omental-mesenteric myxoid hamartoma, and inflammatory fibrosarcoma (3, 4).

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The inflammatory myofibroblastic tumors, often considered as a neoplastic entity, are part of the group of solid mesenchymal tumors characterized by the proliferation of myofibroblasts associated with a variety of inflammatory cells such as plasma cells, lymphocytes and eosinophils (3, 5). They are rare tumors that can appear at any age but more frequently in the first two decades of life (1, 3-5) and in women (3). They were initially observed in the lungs and can also be found in the mesentery, the omentum and in some rare cases in the abdominal organs, the bladder, the orbit, the head, the cervical region and the salivary glands (4-6). The origin is still undetermined. Considered historically as reactionary inflammatory lesions following a trauma, a surgery, or an infection or considered as a paraneoplastic lesion, recent molecular and chromosomal studies lean more towards a neoplastic lesion rather than a reactionary lesion (1, 4). IMTs of the pancreas are often incidentally diagnosed (5). When the tumors are symptomatic, one observes, as shown by Surakit et al. (1, 7), mainly abdominal pain (64%), weight loss (44%), jaundice (40%), a palpable mass (28%) and in rare cases, anemia, fatigue or sudden diabetes. Imaging findings highlight a solid well-defined pancreatic mass, which can be multilobular or infiltrative, vascularized or not (5), of which the size is usually between five and ten centimeters (3). Radiology also allows one to identify local complications and enables staging. However, imaging does not always allow to make a differential diagnosis with adenocarcinoma of the pancreas, endocrine tumors of the pancreas, auto-immune pancreatitis, metastasis and lymphoma. Histologically, IMTs are essentially cellular, composed of an important

proliferation of fascicular myofibroblasts accompanied by a voluminous infiltration of chronic inflammatory cells particularly lymphoplasmocytary. The mitotic rates are variable and sometimes calcifications or necrosis can be found (3). On immunohistochemistry, these lesions are generally positive for alpha smooth muscle actin as well as desmin and keratin. In 30 to 40% of the cases, and especially in the child, molecular genetic and cytogenetic analysis has revealed ALK gene rearrangements/translocations causing an overexpression of ALK protein which can be detected by specific immunohistochemistry (3). Although, the risk of malignant transformation or metastasis has been described by certain teams, it remains low (< 5%) (1, 3, 5). Given the difficulty in obtaining a definitive diagnosis based on biopsies and radiological exams, surgery with complete excision of the lesion associated with a clinical follow-up remains the primary therapeutic option (4, 5, 8), despite there being no real consensus regarding the treatment of IMT of the pancreas (1, 4). When the lesion cannot be excised, the patient can be treated with chemotherapy or radiotherapy and/or with medication but the latter is not clearly defined (1, 2). Some authors obtain results either with corticoid medication or with an anti-inflammatory medical treatment, with or without radiotherapy (2, 4, 8). The prognosis for this tumor is generally favorable (1, 6). There is a risk of up to 25% of recurrence post surgery, namely when the excision is incomplete (5). Conclusion Inflammatory myofibroblastic tumors of the pancreas are rare. The prognosis is usually favorable. However, there are currently no criteria for predicting the evolution.

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Therefore, treatment must be decided case by case in function of the surgical risks. References 1.

Diffaa A., Samlani Z., El bahlouli A., et al.: Le pancréas: localisation rare des tumeurs myofibroblastiques inflammatoires. J Afr Hépatol Gastroentérol, 2011, 5: 163-167. Schütte K., Kandulski A., Kuester D., et al.: Inflammatory Myofibroblastic Tumor of the Pancreatic Head: An Unusual Cause of Recurrent Acute Pancreatitis – Case Presentation of a Palliative Approach after Failed Resection and Review of the Literature. Case Rep Gastroenterol, 2010, 4: 443-451. Christopher D.M. Fletcher, Soft tissue tumors, Diagnostic Histopathology of tumors, Christopher D.M. Fletcher, Churchill Livingstone Elsevier, Third edition, 2007, Volume 2: 1553-1554. Fragoso A.C., Eloy C., EstevaoCosta J., Campos M., Farinha N., Lopes J.M.: Abdominal inflammatory myofibroblastic tumor: a clinicopathologic study with reappraisal of biologic behavior. J Pediatr Surg, 2011, 46: 2076-2082. Yamamoto H., Watanabe K., Nagata M., et al.: Inflammatory myofibroblastic tumor (IMT) of the pancreas. J Hepatobiliary Pancreat Surg, 2002, 9: 116-119. Wreesmann V., Van Eijck C.H.J., Naus D.C.W.H., Van Velthuysen M. L.F., Jeekel J., Mooi W.J.: Inflammatory pseudotumour (inflammatory myofibroblastic tumour) of the pancreas: a report of six cases associated with obliterative phlebitis. Histopathology, 2001, 38: 105-110. Pungpapong S., Geiger X.J., Raimondo M.: Inflammatory Myofibroblastic Tumor Presenting as a Pancreatic Mass: A Case Report and Review of the Literature. JOP. J Pancreas, 2004, 5: 360-367. Colangelo M., Di Renzo D., Persico A., Lelli Chiesa P.: Case report: Inflammatory myofibroblastic tumor of pancreatic origin in a patient with Down syndrome: The role of diagnostic ultrasound. J Ultrasound, 2011, 14: 7-9.

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CONTINUING EDUCATION MRI OF MYELITIS* J. Hodel1,2, O. Outteryck3, P. Jissendi1, M. Zins2, X. Leclerc1, J.-P. Pruvo1

MRI of myelitis The diagnosis of myelitis relies on MRI. The purpose of this review is to describe the imaging findings in patients with myelitis through clinical cases. MR findings in Multiple Sclerosis, Neuromyelitis Optica and others Transverse Myelitis are highlighted. Multiple sclerosis The spinal cord is frequently involved in Multiple Sclerosis (MS) (1). The MS spinal cord lesions are typically small, peripherally located, involving less than two vertebral segments in length and less than half the cross-sectional area of the cord (Fig. 1) (1, 2). On axial MR images, the MS lesions have a wedge shape with the basis at the cord surface (Fig. 1). Concomittant intracranial lesions are a key concept in differentiating MS from other myelitis (3). Enhancement of the spinal cord MS lesions is less frequent than in the brain lesions (Fig. 2). MS may rarely presents as transverse myelitis but follow-up imaging will demonstrate new lesions occurring in cord and brain. Patients with MS may also exhibit spinal cord atrophy mainly related to axonal degeneration. The spinal cord atrophy correlates with clinical disability (4).

Fig. 1. — Patient with Multiple Sclerosis. Hyperintense, wedge-shaped, peripherally located lesions (arrow) were observed on axial T2-weighted MR image at the C4 level. These cord lesions occupyied less than half the crosssectional area of the cord.

Transverse myelitis Transverse myelitis (TM) is an acute inflammatory condition characterized by rapid onset of bilateral motor, sensory, and autonomic dysfunction (5). TM is mainly observed in the second and fourth decades and the thoracic spine is most commonly involved (6). Diagnostic criteria of TM were previously defined by the «Transverse Myelitis Consortium Working Group» and include: 1) clin-

Fig. 2. — Patient with MS and active spinal cord lesions. Sagittal T2-weighted MR image (A) of the cervical spinal cord showed several focal hyperintense spinal cord lesions (arrows). On sagittal postFrom: 1. Service de Neuroradiologie, CHRU Lille, France, 2. Service de Radiologie, contrast T1-weighted MR image (B), Hôpital Saint Joseph, Paris, France, 3. Service de Neurologie, CHRU Lille, France. nodular enhancement of the MS lesions Address for correspondence: Pr Jean-Pierre Pruvo, Service de Neuroradiologie, CHRU was observed consistent with active Salengro, Lille, France. inflammatory lesions (arrows). * Paper presented at the 2011 RBRS Annual Symposium.

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D C

Fig. 3. — Patients with Devic disease. Sagittal T2-weighted MR image (A) showing hyperintense, confluent lesions extending across multiple vertebral segments (arrows) with swelling involving the dorsal cord. The lesion was centrally located (arrow) on axial T2 weighted image (B) Patchy enhancement was observed on a postcontrast T1-Weighted MR image (C). In this patient, involvement of optic nerves (arrows) was well demonstrated on STIR FLAIR images (D) consistent with an associated optic neuritis.

Fig. 4. — Patient with Sarcoidosis. (A) On the sagittal T2-Weighted MR images, intramedullary high-signal-intensity lesion was detected at the conus medullaris with a mild increase in signal intensity (arrow). (B) On the STIR MR sequence, the lesion showed a marked increase in signal intensity and is more easily appreciated (arrow). Note the combination of leptomeningeal and peripheral intramedullary enhancement (arrows) using sagittal (C) and axial (D) T1 weighted sequence.

ical symptoms referable to the spinal cord, 2) progression to clinical nadir between 4 hours and 21 days 3) confirmation of an active inflammatory process by MR examination or CSF examination 4) exclusion of extraaxial compressive etiology. The prognosis is variable. Idiopathic is distinguished from disease-associated TM. Disease-

associated transverse myelitis may be related to neuromyelitis optica, autoimmune conditions, sarcoidosis or para-infectious conditions. In patients with TM, MRI typically demonstrates a thoracic cord T2hyperintense lesion centrally located, extending over more than three vertebral segments, and involving all or most of the cross section of the

cord (7, 8). On post contrast T1 weighted images, gadolinium enhancement can be observed, with a peripheral enhancement of the central lesion (9). Devic disease Devic disease or neuromyelitis optica (NMO) is a demyelinating dis-

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Fig. 5. — Patient with a Spinal Vascular Malformation. Sagittal T2 weigted images showed T2 hyperintensity of the spinal cord with vascular flow voids (arrows) around the cord suggesting the diagnosis of arteriovenous malformation.

ease characterized by visual disturbance and transverse myelopathy. The 2006 revised diagnostic criteria for NMO (10) include: NMO IgG positivity, longitudinally extensive cord lesion, or onset MR imaging of the brain which is nondiagnostic for multiple sclerosis. MRI typically demonstrates a longitudinally extensive transverse myelitis with T2hyperintense dorsal cord lesions, centrally located, spanning more than three vertebral segments (Fig. 3) (11). Enhancement and cord swelling are common in such patients (12). The myelitis can extend cranially involving the brainstem. MRI is also of use to depict the associated neuromyelitis optica (Fig. 3).

meningeal enhancement commonly observed in such patients (11, 13) (Fig. 4).

Autoimmune conditions

Vascular malformations

TM has also been described in various autoimmune conditions without specific MR findings (11). Several NMO patients have a coexistent autoimmune disorder such as Systemic Lupus Erythematosus (SLE), Sjögren syndrome, myasthenia gravis or Neuro-Behcet’s disease (11).

Patients with spinal arteriovenous malformation may exhibit sudden onset or progressive myelopathy (17). MRI typically demonstrates a transverse myelitis associated with vascular flow voids around the cord (Fig. 5). MRI may also reveal spinal cord hematoma, siderosis or subarachnoid hemorrhage. The diagnosis still relies on conventional angiography.

Sarcoidosis Sarcoidosis is a noncaseating granulomatous disease that may involve central nervous system. MRI typically demonstrates intramedullary lesions with enhancement extending more than three levels. A keypoint is the associated lepto-

Infectious Transverse myelitis may be associated with a history of infectious syndrome or vaccination preceding clinical onset. In such cases, MR findings are usually nonspecific but a leptomeningeal and/or nerve root enhancement can be observed. In AIDS patients, HIV myelitis must be distinguished from vacuolar myelopathy (14, 15). In patients with vacuolar Myelopathy, MRI typically reveals nonenhancing symmetric dorsolateral T2-signal hyperintensity of the thoracic cord (15, 16).

Differential diagnosis of transverse myelitis Cord ischemia Patient with cord infarction exhibit a sudden onset motor, sensory,

Fig. 6. — Patient with Cord Ischemia. Sagittal T2-Weighted (A) and STIR (B) demonstrated abnormal T2 hyperintensities involving the anterior columns of the spinal cord with a “snake-eyes” appearance (arrows) on axial T2 images (C). Note the increase signal on diffusion images (D) related to a restricted diffusion.

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and autonomic disturbance. The anterior spinal artery that supplies the corticospinal tracts and most of gray matter is frequently involved. MRI typically demonstrates abnormal T2 hyperintensities of the anterior columns with a “snake-eyes” appearance (Fig. 6) (18). The whole central cord may be invloved with a rim of spared peripheral white matter (19). MR conventional sequences may show negative results in the acute phase. Diffusion-weighted imaging (DWI) of the spinal cord may show signal abnormalities in such cases due to a restriction of diffusion related to the infarction (Fig. 6). Tumors Cavernomas appear as a cord lesion with a hypointense related to susceptibility artifacts from hemosiderin deposits (20). Spinal cord metastasis can be observed with edema and mass effect mimicking a longitudinal transverse myelitis (Fig. 7).

Fig. 7. — Patient with spinal cord metastases. Sagittal T2 weigted images (A) showed an extensive hyperintensity of the spinal cord with nodular enhancement (arrows) on postcontrast T1-Weighted MR images (B) related to metastases of a lung cancer.

Delayed radiation myelopathy In such patients MRI reveals increased T2 signal of the cord with swelling corresponding to the irradi-

Fig. 8. — Patient with Cobalamin Deficiency. Sagittal T2-Weighted images (A) demonstrated a longitudinal hyperintensity of the dorsal columns of the cervical cord with an “inverted V” appearance (arrows) on the axial T2 images (B). Note the increased signal on diffusion images (C).

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Fig. 9. — Patient with Syringohydromyelia. Sagittal T2 and T1Weighted images (A) revealed a central cystic lesion of the spinal cord with CSF intensity and flow related artifacts. Through Plane - Cine Phase Contrast Imaging (B) confirmed the diagnosis of syringohydromyelia showing a pulsatile CSF flow (black: systolic CSF flow; white: diastolic CSF flow) within the cavity.

Fig. 10. — Patient with MS explored with Diffusion Tensor Imaging. Sagittal T2 weigted images (A) showed an extensive myelitis with atrophy. DTI parametric maps (B) and tractography images (C) revealed a marked increase in diffusivity values with reduced FA values.

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Fig. 11. — Schematic drawing of the diagnostic work-up in patients with myelitis.

ation port. Signal abnormalities may occur several months after the irradiation. Enhancement can be observed.

ing a pulsatile flow within the cavity (22). MR protocol

Cobalamin Deficiency MRI demonstrates symmetric T2 hyperintensities of the dorsal columns, with an “inverted V” appearance on axial images (Fig. 8) (21). Increased signal on diffusion images can also be observed in such patients. Signal abnormalities may decrease after treatment. Syringohydromyelia In patients with syringohydromyelia, MRI reveals a central cystic lesion of the spinal cord with CSF intensity in all sequences (Fig. 9). This must be distinguished from a cystic central canal of the spinal cord. Cerebrospinal fluid flow related artefacts can be observed in the cavity on T2 weighted images. Cine Phase Contrast Imaging may be of use to confirm the diagnosis show-

The entire spinal cord should be imaged in patients who have spinal symptoms and who have a known or presumptive diagnosis of MS. Slice thickness should not exceed 3 mm, with a maximum interslice gap of 10% (23). The imaging protocol should include the following sequences: sagittal T2-WI, T1-WI, axial T2-WI for exact anatomic location of the lesion, and contrastenhanced T1-WI. Studies have shown the superiority of short-time inversion-recovery sequences to Fast Spin Echo sequences in the detection of lesions in the spinal cord (24, 25). Recently the value of the PSIR sequence was reported for the detection of spinal cord lesions (26). Diffusion Tensor Imaging (DTI) is a promising technique for the imaging

of myelitis (Fig. 10). Indeed this technique provides information about the tissue microstructure. DTI parameters such as Fractional Anisotropy (FA), Mean Diffusivity (MD) may help to distinguish myelin repair from axonal loss or improve the detection of occult spinal cord pathology (27-29). Diagnostic work-up The presence of hyperintense T2 lesions in the spinal cord remains a nonspecific finding. The first step of the diagnostic work-up is to rule out spinal cord compression, a surgical emergency. Clinical data and NMO IgG are very useful in the work-up of transverse myelitis. MR findings may help to differentiate inflammatory myelitis from mimics according to T2-hyperintensities and gadolinium enhancement on post contrast T1 weighted images. A schematic drawing summarizing these findings is shown in Fig. 11.

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References 1. Filippi M., Rocca M.A.: MR imaging of multiple sclerosis. Radiology, 2011, 259 (3): 659-81. 2. Tartaglino L.M., et al.: Multiple sclerosis in the spinal cord: MR appearance and correlation with clinical parameters. Radiology, 1995, 195 (3): 725-32. 3. Pretorius P.M., Quaghebeur G.: The role of MRI in the diagnosis of MS. Clin Radiol, 2003, 58 (6): 434-48. 4. Evangelou N., et al.: Pathological study of spinal cord atrophy in multiple sclerosis suggests limited role of local lesions. Brain, 2005, 128 (Pt 1): 29-34. 5. Krishnan C., et al.: Demyelinating disorders: update on transverse myelitis. Curr Neurol Neurosci Rep, 2006, 6 (3): 236-43. 6. Transverse Myelitis Consortium Working Group, Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology, 2002, 59 (4): 499-505. 7. Alper G., et al.: Idiopathic acute transverse myelitis in children: an analysis and discussion of MRI findings. Mult Scler, 2011, 17 (1): 74-80. 8. Choi K.H., et al.: Idiopathic transverse myelitis: MR characteristics. AJNR Am J Neuroradiol, 1996, 17 (6): 115160. 9. de Seze J., et al.: Idiopathic acute transverse myelitis: application of the recent diagnostic criteria. Neurology, 2005, 65 (12): 1950-3. 10. Wingerchuk D.M., et al.: Revised diagnostic criteria for neuromyelitis optica. Neurology, 2006, 66 (10): 1485-9.

JBRâ&#x20AC;&#x201C;BTR, 2012, 95 (4) 11. Goh C., Phal P.M., Desmond P.M.: Neuroimaging in acute transverse myelitis. Neuroimaging Clin N Am, 2011, 21 (4): 951-73, x. 12. Collongues N., et al.: Neuromyelitis optica in France: a multicenter study of 125 patients. Neurology, 2010, 74 (9): 736-42. 13. Smith J.K., Matheus M.G., Castillo M.: Imaging manifestations of neurosarcoidosis. AJR Am J Roentgenol, 2004, 182 (2): 289-95. 14. DeSanto J., Ross J.S.: Spine infection/inflammation. Radiol Clin North Am, 2011, 49 (1): 105-27. 15. Thurnher M.M., Cartes-Zumelzu F., Mueller-Mang C.: Demyelinating and infectious diseases of the spinal cord. Neuroimaging Clin N Am, 2007, 17 (1): 37-55. 16. Santosh C.G., Bell J.E., Best J.J.: Spinal tract pathology in AIDS: postmortem MRI correlation with neuropathology. Neuroradiology, 1995, 37 (2): 134-8. 17. Krings T., et al.: Imaging in spinal vascular disease. Neuroimaging Clin N Am, 2007, 17 (1): 57-72. 18. Weidauer S., et al.: Spinal cord infarction: MR imaging and clinical features in 16 cases. Neuroradiology, 2002, 44 (10): 851-7. 19. Mawad M.E., et al.: Spinal cord ischemia after resection of thoracoabdominal aortic aneurysms: MR findings in 24 patients. AJNR Am J Neuroradiol, 1990, 11 (5): 987-91. 20. Weinzierl M.R., et al.: MRI and intraoperative findings in cavernous haemangiomas of the spinal cord. Neuroradiology, 2004, 46 (1): 6571.

21. Larner A.J., et al.: MRI appearances in subacute combined degeneration of the spinal cord due to vitamin B12 deficiency. J Neurol Neurosurg Psychiatry, 1997, 62 (1): 99-100. 22. Heiss J.D., et al.: Elucidating the pathophysiology of syringomyelia. J Neurosurg, 1999, 91 (4): 553-62. 23. Fazekas F., et al.: The contribution of magnetic resonance imaging to the diagnosis of multiple sclerosis. Neurology, 1999, 53 (3): 448-56. 24. Hittmair K., et al.: Spinal cord lesions in patients with multiple sclerosis: comparison of MR pulse sequences. AJNR Am J Neuroradiol, 1996, 17 (8): 1555-65. 25. Rocca M.A., et al.: Comparison of three MR sequences for the detection of cervical cord lesions in patients with multiple sclerosis. AJNR Am J Neuroradiol, 1999, 20 (9): 1710-6. 26. Poonawalla A.H., et al.: Cervical Spinal Cord Lesions in Multiple Sclerosis: T1-weighted InversionRecovery MR Imaging with PhaseSensitive Reconstruction. Radiology, 2008, 246 (1): 258-264. 27. Hesseltine S.M., et al.: Diffusion tensor imaging in multiple sclerosis: assessment of regional differences in the axial plane within normal appearing cervical spinal cord. AJNR Am J Neuroradiol, 2006, 27 (6): 1189-93. 28. Klawiter E.C., et al.: Radial diffusivity predicts demyelination in ex vivo multiple sclerosis spinal cords. Neuroimage, 2011, 55 (4): 1454-60. 29. Fox R.J., et al.: Measuring myelin repair and axonal loss with diffusion tensor imaging. AJNR Am J Neuroradiol, 2011, 32 (1): 85-91.

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IN MEMORIAM Professor emeritus Pierre Bodart 1923-2012

“Un grand maître, un grand patron nous quitte…”1 Professor Bodart passed away unexpectedly in the evening of June, 27th 2012 after a peaceful day spent with his wife, Edith. Pierre Bodart was a master radiologist with great professional skills, a brilliant teacher, a charismatic and passionate leader, and an idealist. Over four decades in the second half of the last century he was highly instrumental in the exponential development of Radiology in the hospitals, clinics, and medical faculty of the Université Catholique de Louvain² and developed a great influence in the radiological community of his country. Internationally, he made major contributions to the development of gastrointestinal and abdominal radiology. During his career he remained committed to solid principles: deep respect of the patient and pursuit of excellence. He was a great defender of radiology as a specialty, and fought to prevent it from becoming a technical commodity. He did so by promoting the clinical dimension of his field, and by promoting the development of radiological subspecialties. As a professor emeritus he remained involved in the social events of his department and faculty and devoted the rest of his time to his wife, family, friends, and to playing the piano. Pierre was born in December 1923 in Temploux, North of Namur, where he was educated at Collège Notre Dame de la Paix. In 1951, he brilliantly graduated in medicine, surgery and obstetrics from the Université Catholique de Louvain and specialized first in Internal Medicine before engaging in the field of Radiology at the same university. After his accreditation as a radiologist in 1959, he started in Namur a joint private practice with Charles Dive, his friend and colleague gastroenterologist. In 1960 he became head of the radiological department of the Clinique Universitaire St Joseph in Herent and consultant at the Universitaire Kliniek Sint-Barbara in Pellenberg. In a favorable medical environment he acquired a renowned experience in gastrointestinal radiology, particularly in Crohn’s disease, with many publications in international journals, such as Archives des Maladies de l’Appareil Digestif and American Journal of Digestive Diseases. In Herent he started to organize his department with a team of subspecialized radiologists and was subsequently promoted lecturer at the UCLouvain in 1964 and associate professor in 1966. At the time, he was also very involved in a mixed group of gastroenterologists, digestive surgeons and fellow radiologists, which met on Sunday mornings at the Maison des Médecins in Brussels. Promoted Professor of Radiology and Chairman of the department of Radiology of Hôpital Saint Pierre in Leuven in 1968, he further developed subspecialties in his department, notably in gastrointestinal, bone and joints, urogenital, pediatric as well as vascular radiology. 1. J.J. Haxhe in “Si Saint Luc m’était conté…” p. 239, 2001, Editions Racine, Bruxelles. 2. P. Bodart, “De la radiologie d’hier (1950) à l’imagerie médicale d’aujourd’hui“ in “50 ans de médecine à l’UCL, 1950 – 2000”, pp 435465, 2002. Edited by J.J. Haxhe. Editions Racine, Bruxelles.

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Subsequently in 1977, after the medical staff and faculty of UCLouvain moved to the Cliniques Universitaires St Luc in Brussels, he centralized all of the radiological activities in one single department and secured the acquisition of a broad range of new technical equipment including US and CT imagers. This new department later obtained the status of an academic and clinical department of Radiology and Medical Imaging. Pierre Bodart provided his undergraduate students with remarkable teaching based on correlations with anatomy and pathology. His brilliant communication skills and charisma inspired many of those who attended his lectures to specialize in Radiology. The postgraduate training programme provided by his staff under his supervision gave his residents the opportunity to acquire a robust practical and theoretical expertise in the field of Radiology. Since 1960 Pierre Bodart has been a regular member of the Royal Belgian Society of Radiology. He was elected member of the Board from 1977 to 1979 and served as president in 1978, organizing a very successful annual General Assembly on bone pathology. He was made honorary member of the RBRS in 1981. From 1974 until his retirement, he sustained the Belgian Journal of Radiology (JBR-BTR) by hosting the editorial office in his department. Between 1983 and 2000, he was president of the French-speaking accreditation board in radiodiagnosis. He received the Paul de Backer 1979-1981 prize of the Royal Belgian Academy of Medicine for his coauthorship in the reference textbook “Alimentary Tract Radiology” for a chapter on Inflammatory Diseases of the Small Bowel. In 1995, Professor Bodart delivered an invited lecture before the two Royal Belgian Academies for the commemoration of the centenary of the discovery of X-Rays by W.C. Röntgen. He was also a regular member of the Royal Belgian Society of Gastroenterology, which he presided in 1980. He was a member of the association of the Belgian Museum of Radiology. He sustained the foundation and the activities of alumni of the department of Radiology at UCLouvain, of which he was nominated the honorary president. During his career, Professor Bodart gained respect and admiration from his many fellow radiologists and colleagues. After becoming Professor emeritus in 1989, he maintained and even developed his charming, friendly and witty character. His many jokes, which he told with boisterous humor, often made his friends and the teller himself laugh uncontrollably. President De Wispelaere and the members of the Board of the RBRS join the numerous friends and colleagues, former students and residents, as well as acquaintances in presenting deep condolences to his wife Edith, his sons Alain et Patrick, and the other members of his family. We will all miss this great radiologist and great personality, but his legacy remains and will be remembered. Jacques Pringot and Baudouin Maldague, Professors emeriti of Radiology, UCLouvain

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