JBR 2014-1 by office

WETTEREN 1

P 702083

Volume 97 Page 1-56

January-February

Bimonthly

–

2014

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

ORGANE DE LA SOCIETE BELGE DE RADIOLOGIE (SBR) ORGAAN VAN DE BELGISCHE VERENIGING VOOR RADIOLOGIE (BVR) 00a-Couv-2014.indd 1

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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 Single issue Belgium 150 € 38 € Other Countries 175 € 44 € All amounts are net and include postal and handling charges. You are kindly invited to address all your correspondence to Mrs A. Hirsch and execute all payments to ARSMBKVBMG (see below).

Instructions aux abonnés Le JBR-BTR publie 6 fascicules par an. Les tarifs sont susceptibles de modifications sans préavis, en fonction de l’évolution des prix du marché du papier et des travaux d’impression. Le prix de l’abonnement des membres de la Société Royale de Radiologie est inclus dans le montant de la cotisation. L’abonnement d’un non-membre est à souscrire auprès de l’ARSMB. La souscription d’abonnement ou la commande de numéro isolé doit être exécutée rapidement, l’éditeur ne pouvant pas garantir la livraison d’éditions passées. Les changements d’adresse doivent être signalés 60 jours à l’avance. TARIF: Annuel Fascicule Belgique 175 € 42 € Autres pays 200 € 49 € Envoi et port inclus. Nous vous prions d’adresser toute correspondance à Mme A. Hirsch et d’effectuer tout paiement au compte de l’ARSMB-KVBMG (voir ci-dessous).

Instructies voor abonnees Het JBR-BTR geeft 6 nummers uit per jaar. Het tarief is vatbaar voor wijzigingen zonder voorafgaand bericht, in verhouding tot de evolutie van de papierprijzen en loonkosten in de grafische nijverheid. Het abonnement van de leden van de Koninklijke Vereniging voor Radiologie is begrepen in de bijdrage van het lidgeld. De abonnementen van niet-leden zijn te onderschrijven bij de KVBMG. Jaarabonnementen of bestellingen van losse nummers moet zo snel mogelijk gebeuren, de uitgever waarborgt de levering van de vorige nummers niet voor de abonnementen die te laat werden onderschreven. De adresveranderingen moeten 60 dagen te voren gemeld worden. TARIEF: Jaarlijks Aflevering Belgie 175 € 42 € Andere landen 200 € 49 € Verzendingskosten zijn inbegrepen. U wordt vriendelijk verzocht alle briefwisseling te richten aan Mevr. A. Hirsch en alle betalingen te verrichten op het banknummer van ARSMB-KVBMG (zie hieronder).

Association Royale des Sociétés Scientifiques Médicales Belges – (ARSMB), asbl avenue W. Churchill 11/30, B-1180 Bruxelles, Belgique tél.: (02) 374 25 55 fax: (02) 374 96 28

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Koninklijke Vereniging van de Belgische Medische Wetenschappelijke Genootschappen – (KVBMG), vzw W. Churchill-laan 11/30, B-1180 Brussel, België tel.: (02) 374 25 55 fax: (02) 374 96 28

Webaddress: http://www.ulb.ac.be/medecine/loce/amb.htm E-mail: jbr-btr@skynet.be Bank Account: Post Office Account Fortis: 210-0251210-32 Giro: 000-0273502-59 IBAN: BE 90210025121032 IBAN: BE 84000027350259 BIC: GE BABEBB36A BIC: BPOTBEB1

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Editor-in-Chief: J. Pringot

Board of the Belgian Society of Radiology:

Consulting Co-Editor: Ph. Grenier (Paris)

President: G. Villeirs

Managing Editors: P. Seynaeve

Vice-President: D. Henroteaux

Editorial Board: F. Avni, L. Breysem, N. Buls, 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, P. Simoni, S. Sintzoff Jr, A. Snoeckx, J. Struyven, H. Thierens, P. Van Dyck, F. Vanhoenacker, Ph. Van Hover, J. Verschakelen, K. Verstraete.

Secretary: Ch. Delcour Treasurer: P. Vanhoenacker BVAS/ABSYM-Representative: O. Ghekiere Board Members: P. Aerts, B. De Foer, J.-F. De Wispelaere, M. Grieten, H. Jaspers, J.-P. Joris, R. Oyen, P. Seynaeve, G. Souverijns, D. Tack, B. Vandeberg, G. Vandenbosch, Ch. Van de Velde

Scientific Committee Members: R. Achten, D. Bielen, B. De Foer, Y. Lefebvre, M. Lemort, J. Pringot, R. Salgado, D. Tack, J. Ver schakelen

President: R. Oyen Secretaries: J. de Mey, B. Vande Berg

Sections of the Belgian Radiological Society (BSR): Abdominal and digestive imaging Bone and joints Breast imaging Cardiac imaging Cardiovascular and interventional radiology Chest radiology Head and neck radiology Neuroradiology Pediatric radiology

B. Op de Beeck, E. Danse J.F. Nisolle, M. Shahabpour M. Mortier, S. Murgo N. Mollet, A. Nchimi S. Heye, D. Henroteaux B. Ghaye, W. De Wever J. Widelec, R. Hermans M. Lemmerling, L. Tshibanda B. Desprechins, L. Breysem

For addresses and particulars, see website at http://www.rbrs.org Instructions to authors The purpose of The Belgian Journal of Radio logy is the publication of articles dealing with diagnostic radiology and related imag ing techniques, therapeutic radiology, allied sciencesand continuing education. All — new and revised — manuscripts and correspond ence should be addressed to JBR-BTR Edito rialOffice, 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 Jour nals” 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 fol lowing 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 accord ingly. All articles must contain substantive and specific scientific material. – Original articles are articles dealing with one specific area of Radiology or allied sciencerelated through the personal expe rience of the author. – Review articles are special articles reporting the experience of the author considered in

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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 individual 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 diagno sis. References should be present, though limited in number. Tables and acknowl edgements are usually omitted. – Pictorial essays are articles presenting information through illustrations and leg ends. 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 introduc tion, material and methods, results, discus sion, 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 back ground information useful to understand why the topic is relevant, and describing the subtopics covered by the study), refer ences, 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 enti ty. 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 radi ologists. 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 accompa nied 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 illus trations (when available), and price. The author should specify to whom the book is intended and give a personal apprecia tion. They will be published with the initial lettersof the signature. (continued on p. 56)

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JBR-BTR  97/1  2014 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 Editorial: The consulting co-sditor in 2014: Prof. Ph. Grenier J. Pringot. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Review article: Myocardial dynamic contrast-enhanced MR : vascular diseases and beyond A. Nchimi, J. Djekic, B. Raskinet, A. Morar, I. Mancini, Th. Broussaud, O. Ghekiere . . . . . . . . . . . . . . . . . . . . . . 3 Correlation of MRI T2 mapping sequence with knee pain location in young patients with normal standard MRI R. Dautry, V. Bousson, J. Manelfe, A. Perozziello, P. Boyer, Ph. Loriaut, P. Koch, A. Silvestre, E. Schouman-Claeys, J.D. Laredo, B. Dallaudière. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Developmental venous anomaly : MR and angiographic features M. Faure, M. Voormolen, T. Van der Zijden, P.M. Parizel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Spinal chondrosarcoma arising from a solitary lumbar osteochondroma C. Ruivo, M.A. Hopper. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 CT features of small bowel obstruction sur to mesodiverticular band O. Tutar, M. Velidedeoglu, I. Yanik, B. Kocak, A. Bas, B. Tutar, F. Kantarci. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Arteries get confused: an arch variation M. Velioglu, S. Kaya, E.E. Ertugrul. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Incidentally detected congenital giant left atrial appendage aneurysm in a child: MRI findings A. Oz, B. Oguz, M. Karcaaltincaba, M. Yilmaz, M. Haliloglu. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 US diagnosis of acute pancreatitis caused by ruptured hydatid disease to the biliary system O. Ozcaglayan, A.M. Halefoglu, T. Ozcaglayan, H.A. Sumbul. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 Ileocolic intussusception due to lipomatosis of the ileum: a common complication of a rare clinical entity M. Eyselberghs, L.C. Ceulemans, S. De Bontridder, F. Vanhoenacker, L. Van Overbeke, I. Quanten, G. Jacomen, A. Snoeckx. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 The case of HNF-1ß mutation with medullary cysts A. Bensouda Mourri, M. Cassart, M. Hall, F.E. Avni. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 A rare case of diffuse alveolar hemorrhage following oral amphetamine intake N.F. Peters, R. Gosselin, K.L. Verstraete. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

IMAGES IN CLINICAL RADIOLOGY Drink responsibly – rapid regression of fatty liver disease on enhanced CT after alcohol withdrawal T. Kirchgesner, E. Danse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 Bilateral elastofibroma dorsi: typical CT and MRI features G. Clinckemaille, A. Larbi, P. Omoumi, J. Manelfe, B. Dallaudière . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 Intraparenchymal meningioma in a child C. Werbrouck, D. Florin, B. Van Holsbeeck, E. Laridon, M. De Weweire, J. Marrannes. . . . . . . . . . . . . . . . . . . . 46 Toothpick perforation of the caecum D. Niciforovic, A. Spasic, I. Turkalj, F.M. Vanhoenacker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Epiphyseal “systemic” osteonecrosis of humeral head M. Kahloune, B. Dallaudière, P. Omoumi, B. Vande Berg, F. Lecouvet, A. Larbi . . . . . . . . . . . . . . . . . . . . . . . . . 48 Abstracts of papers for full RBRS membership. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 Forthcoming Courses and Meetings. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Grants of the BSR. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 Clasified services. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi News from the Museum. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . viii Instructions to Authors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . i Subscribers information. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . cii Advertising index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . viii u 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. uu Indexed in Index Medicus and in Zentralblatt Radiologie. Evaluated for Medline User, EMBASE and CANCERNET. Abstracted in Excerpta Medica Journals.

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SCK-CEN - Prof Roger Van Geen award Objective The Belgian Nuclear Research Centre (SCK•CEN) attaches great importance to the promotion of research in the field of nuclear energy. With the patronage of the SCK•CEN, the FWO awards every two years a scientific prize to a postdoctoral researcher. This scientific prize should also stimulate collaboration between the Belgian universities, research institutes and the SCK•CEN. Features • Prize in the amount of €12,000 • in recognition of original research in the field of nuclear energy or radiation. Both technical/ scientific disciplines and socio-economically oriented research on nuclear energy are eligiblefor this prize. The submitted work must be in the domain of, or have a potential connection with, the research areas of the Belgian Nuclear Research Centre (SCK•CEN). Refer to the list of eligible research areas. • This Prize is awarded every two years. Profile and conditions • You are a postdoctoral researcher affiliated to a Belgian university or research institute. • You have the nationality of a member state of the European Union • You are not older than 40 years • You are not employed by the SCK•CEN. • You have not previously received a prize for the submitted work. Procedure • The submitted work consists of max. 30 pages (Dutch or English). • The work must include an English abstract. • Your candidacy is submitted to a jury. • The jury selects the winner of each prize. • The Board of Trustees decides on the allocation.

www.fwo.be

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CENTRE HOSPITALIER DE LUXEMBOURG

Le Centre Hospitalier de Luxembourg, Hôpital de 600 lits avec mission d’enseignement et de recherche recrute

DES MEDECINS SPECIALISTES EN RADIODIAGNOSTIC M/F sous contrat à durée indéterminée à temps plein ou à temps partiel (50%)

Votre mission En collaboration avec 6 radiologues exerçant dans un service disposant d’un plateau technique moderne (dont 2 IRM), vous assurez les examens d’imagerie médicale prescrits par les cliniciens de l’hôpital et les cliniciens externes.

Votre proﬁl •

Diplôme de médecin spécialiste en imagerie médicale et autorisation d’exercer la médecine au Grand Duché de Luxembourg délivrée par le Ministère de la Santé.

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Connaissance des langues luxembourgeoise et française ou engagement à les apprendre.

Notre oﬀre •

Développement de l’activité dans les secteurs thoraco-abdominal et écho-Doppler.

•

Epanouissement personnel par la participation aux réunions cliniques pluridisciplinaires et à la formation des médecins en voie de spécialisation.

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Statut de médecin salarié.

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Contexte de modernisation et d’innovation favorisant l’initiative personnelle.

Pour plus d’information n’hésitez pas à visiter notre site www.chl.lu ou à contacter le Directeur médical par mail à direction.medicale@chl.lu. Merci d’envoyer votre Curriculum Vitae accompagné d’une lettre de motivation à la Direction médicale du Centre Hospitalier de Luxembourg, 4 rue Barblé, L-1210 Luxembourg. WWW.CHL.LU

HÔPITAL MUNICIPAL

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CLINIQUE D’EICH

CLINIQUE PÉDIATRIQUE

MATERNITÉ

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News from the Belgian museum of Radiology The Radiology marches up to the front lines: from 1914 to 2014 Why this exhibit? On the occasion of the remembrance of the Great War, the Belgian Museum of Radiology hosts an exhibit that retraces a century of armed conflicts, which will be displayed in the Military Hospital Reine Astrid, rue Bruyn 200, 1120 Brussels. This event is sponsored by the Central Office for Social and C ultural Action of the Belgian Army.Four distinct periods are illustrated with large photographs. On large mural panels the visitor will also discover the most important steps of the technical development of the medical radiology. At the beginning of the first world war the radiology is just a19 years young specialty. At the end of this war of the trenches it has acquired its true credentials. From 1918, all hospitals, clinics and sanatoriums are equipped with at least one X-ray room. After this first conflict, numerous technical improvements become general features and are applied worldwide. But, it is during the Second World War, and the Korean War, that we observe the apparatuses grow more robust. The period called Cold War, sees conflicts sprout somewhat all over the globe. To be able to deploy the military radiology service close to the fields of operation, the new technologies are combined with the most adequate means of transportation. Thus one sees the CT scanner appear integrated in a container, deployed in the field on the grounds in Iraq. Instead of the ultrasound, which does not need employ the ionizing radiation, the magnetic resonance completes from 1990 on the diagnostic arsenal. These technologies are utilized in the hospital units in Afghanistan. At a time of remembrance, like now, it is good to direct the spotlights onto the selfless commitment of the researchers. Their work has resulted into innovating medical technologies which are indispensable for the military medical actors in the country at war. This brief historical overview is equally a testimony of gratitude to our elders who, with rudimentary apparatus, have been the pioneers in the radiology. Their labours d eserve our total admiration and respect.

PROJECTION OF THE FILM “Marie CURIE, A WOMAN ON THE FRONT” On this occasion, the preview of the documentary-fiction “Marie Curie, a Woman on the Front” will be projected. This film is a co-production of the French company CAPA DRAMA and the Belgian one Be-FILMS, for France Televisions and the RTBF. The private viewing of the film and the exhibition, to both of which you are invited, will take place the Friday 14th March. The meeting will close with a friendship’s drink! Further information about these events can be found on the following website: info@radiology-museum.be

René Van Tiggelen Curator Belgian Museum for Radiology

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JBR–BTR, 2014, 97: 1.

EDITORIAL THE CONSULTING CO-EDITOR IN 2014: PROFESSOR PHILIPPE GRENIER 2013 was a year of pioneering the consulting editorship of JBR-BTR by an international expert in a radiological subspecialty. Professor Mauricio Castillo, the editor-in-chief of the American Journal of Neuroradiology made it with great success by contributing as the author of an important review paper on Acute Stroke1 and accrediting in some way the role of JBR-BTR for diffusing information of general interest to the Belgian radiological community. We are immensely grateful to Prof. Castillo for his enthusiastic involvement which we hope to benefit from in a less official way in the future. 2013 has seen the transformation of the RBRS, a mainly scientific society, into a new organization having both scientific and professional missions. JBR-BTR will remain the organ of the new Belgian Society of Radiology (BSR) and will be regulated by the board and the scientific committee of the BSR. Professor Philippe Grenier is presently full professor of Radiology at the University Pierre and Marie Curie in Paris and chairman of the Department of Radiology and Head of the medical board at Pitié-Salpêtrière Hospital. He was nominated honorary member of the RBRS at the annual general assembly meeting in January 2013 by the then president De Wispelaere and accepted enthusiastically to serve as consulting co-editor of JBR-BTR in 2014. His outstanding career as researcher and teacher was summarized in JBR-BTR 2013, 96: 98. Let me emphasize that he was a pioneer in the diagnosis of chronic airway and diffuse lung diseases using first standard CT and later HRCT and is an internationally acclaimed expert in this field. Personally, I remember well one of his first very original contribution to the CT diagnosis of bronchiectasis and the first step in the impressive development of modern bronchial imaging. I am convinced that Philippe Grenier will be very influential in fostering chest imaging in JBR-BTR during the coming year, particularly in the category Continuing Education and I am excited by the prospect of publishing about. I hope very much, dear Readers, that it will be of benefit to you and that you will enjoy reading the JBR-BTR issues especially focused on chest imaging during the coming year. Jacques Pringot Editor-in-Chief

1. Acute stroke: basic concepts and use of imaging for clinicians. M. Castillo, H. Alvarez, JBR-BTR, 2013, 96: 3-9

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JBR–BTR, 2014, 97: 3-10.

REVIEW ARTICLE MYOCARDIAL DYNAMIC CONTRAST-ENHANCED MR: VASCULAR DISEASES AND BEYOND A. Nchimi1, J. Djekic², B. Raskinet³, A. Morar³, I. Mancini², Th.K.Y. Broussaud², O. Ghekiere² Contrast-enhanced cardiac magnetic resonance imaging allows the evaluation of both myocardial perfusion and myocardial tissue characteristics. This paper reviews different microvascular and non-vascular conditions that can cause abnormal findings on contrast-enhanced myocardial magnetic resonance imaging. Knowledge of their characteristics can avoid misinterpretation and avoid inappropriate referral for further invasive imaging in patients suspected of myocardial vascular disease. Key-word: Myocardium, MR.

Due to an unprecedented combination of spatial resolution, temporal resolution and tissue contrast differentiating properties, unenhanced magnetic resonance imaging (MRI) is in many instances considered a reference standard for assessment of cardiac morphology, function and mass. Using dynamic and delayed contrast-enhancement techniques after intravenous injection of a T1shortening contrast agent allows further evaluation of myocardial signal intensity changes, additionally helping to assess myocardial vascular supply and tissue composition. Cardiac dynamic contrast-enhanced magnetic resonance (DCEMR) imaging is as such increasingly used as an alternative technique to nuclear isotope studies in the evaluation of myocardial perfusion (1-3), while late contrast-enhanced MR (LCEMR) imaging has been established as a reference standard in the assessment of myocardial viability (4). Nevertheless, a large number of microvascular and non-vascular diseases are important to recognize, as their may both clinically and on imaging studies mimic vascular diseases that require revascularization. The purpose of this paper is to describe these abnormal myocardial findings on DCEMR, correctly assess their sig nificance, and consequently avoid misinterpretation and incorrect referral for further diagnostic procedures.

Imaging principles and analysis Electrocardiographically-triggered T1-weighted images are acquired across the heart during the circulation of a bolus of a contrast agent at typical doses of 0.025-0.2 mmol of gadolinium/kg of body weight, injected intravenously at a rate of 2-3 ml/sec. At least three slice positions should be acquired in the leftventricle’s short axis (5). Several saturation recovery images can be obtained within a single heartbeat using fast low-angle spin echo, echoplanar or steady-state free precession acquisition protocols, hereby aided by technical advances such as parallel imaging (6). To lower the threshold for vascular disease detection, data should be acquired after adenosine or dipirydamole administration (stress-DCEMR), with territories supplied by diseased arteries failing to display blood flow increase (the so-called perfusion reserve) under vasodilatation (7). On DCEMR, normal myocardial enhancement is homogenous and occurs nearly simultaneously with contrast arrival in the epicardial arteries (Fig. 1). Time-resolved signal intensity curves in any region of interest can be extracted from these frames, allowing a semi-quantitative or a quantitative assessment of myocardial blood flow. A relatively hypointense myocardial area during DCEMR is the ele-

From: 1. Department of Medical Imaging, University Hospital Liège (CHU), Domaine Universitaire du Sart Tilman, Liège, 2. Department of Medical Imaging, Centre Hospitalier Chrétien (CHC), Liège, 3. Department of Cardiology, Centre Hospitalier Chrétien (CHC), Liège, Belgium. Address for correspondence: Dr A. Nchimi, M.D., Department of Cardiovascular and Thoracic Imaging, University Hospital ULg, Rue de l’Hôpital, 1, 4000 Liège, Belgium. E-mail: anchimi@chu.ulg.ac.be

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mentary abnormal finding, which can be detected either visually or by a observing a defect in the ascending portion of the time-signal intensity curve. Across the literature, these hypo intensities are better specified as: – Showing no spatial variation with time (8, 9); – Involving the subendocardium, with a variable extent; as coronary obstruction initially decreases blood flow to the subendocardial circulation, only afterwards extending deeper towards the epicardial circulation (10); – Showing temporal persistence (9, 11-13). The diagnostic accuracies using these criteria for the diagnosis of significant coronary disease were all above 88% (8-13). Their importance was further stressed by Lubbers et al. (14) who observed a decrease of the interobserver variability with the use of these criteria for the diagnosis of myocardial perfusion abnormalities. Finally, delayed-enhancement techniques are used for a comprehensive assessment of myocardial vascular disease. Through an inversion pulse, the normal myocardial signal on a T1-weighted sequence is nulled in order to better detect pathological areas where the contrast agent accumulates in excess. Abnormalities on DCEMR are artefactual until proven otherwise Meta-analyses have shown variations in sensitivity and specificity of DCEMR in the detection of coronary artery disease requiring revascularization, in the ranges of 88-94%, and 77-85% respectively (15, 16), showing that myocardial revascularization

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Fig. 1. — Normal findings on DCEMR. On short-axis DCEMR in normal subjects, the contrast agent bolus first arrives into the right ventricle (RV), with a strong enhancement (A). Shortly after, the pulmonary vasculature also becomes enhanced (arrow, B). Then the contrast agent bolus returns to the heart and starts to enhance the left ventricle (LV) chamber (C), with the RV enhancement being progressively washed by the saline flush (D). At this time, the myocardium also begins to enhance progressively, while epicardial vessels may appear in both interventicular grooves and on the posterior and lateral faces of the LV (D, E, arrows). Epicardial vessels visualization is an inconsistent figure, but these vessels appear nearly simultaneously at all locations. The myocardium reaches homogenous enhancement shortly after the LV’s peak. Thereafter, all cardiac chambers appear fugaciously at equilibrium enhancement, before the contrast recirculation occurs (F).

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solely based on DCEMR findings may actually lack accuracy in some cases. The main pitfalls of DCEMR are artefacts caused by the technical constraints to produce several images in less than a second. Among these, the so-called “dark-rim artifact” (DRA) or banding artifact is the most challenging. DRA is a generic name for a myocardial rim-like hypointensity that may occur with a subendocardial predominance as a result of multiple causes, leading in some cases to major challenges in differentiating it from a true perfusion abnormality. Susceptibility effects may cause DRA as a result of field distortion (B0) during the first-pass of a contrast agent leading to dephasing of individual voxels around boundaries (17, 18). Partial volume effects causes DRA by contribution of different compartments (blood pool versus myocardium) within voxels of interest; similar to k-space weighting heterogeneity by distortion of the point spread function (16). These effects are enhanced by cardiac motion, causing oscillations in the voxel values along the borders of different tissues with different signal intensities (19). Lastly, the finite nature of the spatial resolution causes DRA due to Gibbs ringing artifacts or truncation of the high k-space frequencies (20). DRAs are commonly perpendicular to the phase-encoding direction and are transient, lasting a few heartbeats and displaying little spatial persistence (18). Although the criteria of temporal and spatial persistence may allow in most cases to distinguish DRA from a true perfusion abnormality, the presence of a strong enhancement and challenging technical demands – leading to a compromised image quality caused by e.g. respiratory motion, poor electrocardiographic synchronization, tachycardia or delayed intracardiac conduction – can further trigger or enhance these artifacts to a point where they may be undistinguishable from true perfusion defects. In such circumstances, evaluating to which extend the myocardial hypointensities actually don’t correspond to an artery distribution territory may provide a clue to differentiation, since the segmental perfusion abnormalities can be anticipated a (21, 22) priori for a given artery (Fig. 2). Strategies for DRA reduction include: (i) administration of a lower dose of contrast agent (0.025-0.05 instead of 0.1 mmol of gadolinium per

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kg of body weight) to decrease the level of enhancement, (ii) oxygen administration to decrease respiratory motion, and (iii) repetition time reduction to shorten image acquisition time. Other strategies are more controversial and require trade-offs. For example, Gibbs ringing and partial volume artifacts may be reduced by increasing image resolution, although at the cost of longer acquisition times that may conversely increase motion artifacts (18). Other technical artifacts may cause false low signal intensity on DCEMR. They pose less serious interpretation challenges, as they are easily recognizable, distorting the normal anatomy or extending into tissues surrounding the heart. These artifacts include off-resonance ghosting, chemical shift and aliasing artifacts.

Always confront DCEMR to LCEMR Klem et al and Cury et al (9, 23) have proposed to compare stressand rest-DCEMR to differentiate “reversible” from “fixed” abnormalities that respectively represent true perfusion deficits versus changes in tissueproperties (scars) or artifacts. They subsequently identify artifacts as abnormalities which are further unmatched to findings on LCEMR. Nevertheless, caution is advised when applying this approach. First, it is debatable whether only “reversible” hypointensities should be considered perfusion abnormalities, since severe vascular lesions may cause perfusion alterations even at rest. Second, myocardial signal intensities on rest-DCEMR may be different than expected in some instances. Indeed, differences in heart rate induced by refractory tachycardia to pharmacological vasodilatation makes the exact duplication of a given heart rate unpredictable, leading to a different amount of heartrate related DRA during stress- and rest-DCEMR. Moreover, in clinical protocols rest-DCEMR is usually performed after vasodilatation-DCEMR. In such instances, the expected hypointensity of altered tissues on rest-DCEMR may be overshadowed by contrast staining. Furthermore, given the small risk of nephrogenic systemic fibrosis, the additional dose of contrast agent administered for rest-DCEMR may come under debate, especially in patients with altered or unknown renal function. Finally, some DCEMR hypointensities may match imperfectly with scars detected on LCEMR, since myocar-

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Fig. 2. — An asymptomatic 51-year-old man with diabetes mellitus. Post-adenosine apex- (A, B), mid- (C, D) and basal- left ventricle (E, F) short-axis slices 10’’ and 20’’ after contrast agent injection to exclude silent myocardial ischemia showed a subendocardial hypointensity involving the interventricular septum (arrows). These findings are suggestive of a dark-rim artifact (DRA), since an epicardial coronary artery stenosis causing such a large perfusion deficit is likely to involve either the anterior or the inferior wall, respectively in case of obstruction of left anterior descending artery or posterior descending artery.

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– Insufficient spatial resolution may be cause for false-positive DCEMR in myocardial thinning. Indeed, the presence of a subendocardial DRA may actually involve a much larger proportion of the myocardial thickness. Conversely, unmatched demands in coverage caused by increased heart volume may result into failed depiction of small vascular territories, especially when the number of frames is reduced. – Decrease in blood flow demand is proportional to the alteration of systolic function. This phenomenon is common during the course of several cardiomyopathies and may cause diffusely prolonged DCEMR hypointensities. – Myocardial tissue alterations are common in inflammatory, infiltrative and scar processes that cause changes in the microvasculature (Fig. 5) and replacement by abnormal extracellular matrix (Fig. 6). These processes may cause hypointensities on DCEMR, but are depicted on LCEMR. Left ventricular pressure overload

Fig. 3. — A 68-year old male with epigastralgia and normal gastrointestinal endoscopy. Peak enhancement post-adenosine basal left ventricle short-axis view (A) showed inferior myocardial hypointensity (arrows), with normal LCEMR (B) and rest DCEMR (C), consistent with reversible abnormalities, suggesting a right coronary artery stenosis that was evidenced on catheter coronary angiography (D, circled area).

dial scars may be surrounded to a variable extent by tissues with impairedmicrovasculature (24, 25). There is, to the best of our knowledge, no available data in the literature evaluating specifically how to differentiate microvascular from macrovascular obstruction in a LCEMR-DCEMR mismatch, resulting into systematic and potentially excessive referrals to catheter coronary angiography. In our experience, macrovascular obstruction causes larger mismatches than microvascular obstruction, the latter typically procuding rim-like, sharp and strong hypointensities on DCEMR. In summary, in order to correctly characterize abnormal findings on vasodilatation-DCEMR we recommend additionally performing only LCEMR. It may help to report myocardial appearances requiring no revascularization, ie: (i) matching and (ii) rim-mismatching LCEMR abnormalities; and those potentially requiring revascularization ie: (iii) largely mismatching LCEMR abnormalities (Fig. 3 and 4).

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Beware of other special conditions Other vascular conditions and myocardial diseases that cause morphologic and functional altera tions to the vessels or myocardial tissue are important to recognize, as they all impact DCEMR interpretation. Cardiomyopathies The total prevalence of cardiomyopathies is unknown; they include a wide range of diseases, from primary cardiomyopathies (ie: genetic, mixed, and acquired cardiomyopathies) to cardiomyopathies caused by either another organ or a systemic disease (26). Although overlaps are common, it is important to understand that cardiomyopathies can be the cause for one of the following: – Microvascular obstruction occuring either in acute primary cardiac syndromes like cardiac syndrome X and Takotsubo disease (27-29), or in vasculitis involving small vessels, like Kawasaki disease (30).

Increased left ventricle diastolic pressure overload, such as in aortic valve stenosis or systemic hypertension, potentially decreases the subendocardial myocardial perfusion, resulting into diffuse subendocardial hypointensities on DCEMR, even with normal epicardial vasculature. Flow competition Left main coronary artery and multiple vessel disease cause challenges to DCEMR, although the latter has a higher accuracy than single photon emission computed tomography (31, 32). Indeed, when a single epicardial artery disease is narrowed, the imaging contrast between normal and underperfused myocardium is caused by the differences in perfusion reserve. Unfortunately, this contrast is decreased to a variable extent – with regard to the level of collateral flow compensation – when multiple epicardial arteries are occluded. On the other hand, a vessel obstruction with excellent collateral flow may exhibit normal DCEMR findings. In some cases, only a delayed epicardial vessel enhancement may help suspecting multiple vessel or collateralized vessel obstruction (Fig. 7). When applicable, flow competition between coronary bypass grafts and native coronary vessels may oc-

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Fig. 4. — A 65-year old male with clinical suspicion of coronary vascular disease. Post-adenosine mid- ventricle short-axis DCEMR (A) showed both anterior and inferior transmural hypointensities (arrows). LCEMR (B) showed hyperenhancement in these segments (asterisks), consistent with matching DCEMR abnormalities caused by myocardial scars.

Fig. 5. — A 49-year-old heavy smoker female was evaluated for atypical chest pain and left ventricle outflow tract obstruction caused by myocardial hypertrophy at echocardiography (not shown). Diastolic (A) and systolic (B) LV outflow tract outflow views showed a localized anteroseptal myocardial hypertrophy (asterisk) causing flow acceleration signal voids (arrowheads), consistent with obstructive hypertrophic cardiomyopathy. Post-adenosine basal- (C) and mid-left ventricle (D) short-axis DCEMR showed anterior and inferoseptal segmental hypointensities (arrows). LCEMR was unremarkable, as catheter coronary angiograms of both the left (E) and right (F) coronary arteries.

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Fig. 6. — A 35-year-old male with a recently diagnosed pulmonary sarcoidosis experienced an episode of malignant tachyarrhythmia. Left ventricle basal short-axis DCEMR (A) showed persistent patchy hypointensities (arrows), involving intramyocardial subendocardial and subpericardial areas, caused by inflammation and/or necrosis, as demonstrated by hyperenhancement on LCEMR (B, arrows).

Fig. 7. — A 63-year old male with thoracic angina underwent post-adenosine DCEMR (A-C). On left ventricle basal slices, the myocardial enhancement was homogenous. The anterior interventricular groove vasculature enhancement coincides with the peak left ventricle cavity enhancement (arrows), while the posterior interventricular groove vasculature started to enhance only at the end of the myocardial first-pass (C, arrowheads). The patient remained symptomatic and underwent eventually a catheter coronary angiography few weeks later, where a low-grade stenosis of the left circumflex artery and high-grade stenoses of both the right coronary (D, circled area) and left anterior descending (E, circled area) arteries were found.

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Fig. 8. — An 83-year old male experiencing an increasing chest pain was evaluated by DCEMR. His medical records were positive for aortic valve replacement and coronary grafts to the distal left anterior descending and circumflex arteries to bypass stenosis of the left main coronary artery, 11 years earlier. Post-adenosine mid-LV short-axis DCEMR images showed transient anteroseptal and lateral segmental myocardial hypointensities (A, arrows). Catheter coronary angiography was performed to exclude grafts stenosis, since LCEMR was normal (B). It actually showed a narrowed but still-patent left main artery (C, circled area), and no stenosis of both the venous (D) and left internal mammary artery (E) bypass grafts. DCEMR hypointensities were therefore attributable to blood flow competition between the grafts and the native arteries.

cur. It results into transient myocardial hypointensities on DCEMR, potentially leading to inappropriate referrals to diagnostic catheter coronary angiography (Fig. 8). Conclusion Signal distortions and a large variety of pathological conditions may either mimic or overshadow treatable myocardial vascular disease on DCEMR. Nevertheless, knowledge of both the origins of technical pitfalls and the presence of particular patient conditions can in many instances strongly help to provide appropriate recommendation and a correct stratification of patients for catheter coronary angiography.

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References 1. Al-Saadi N., et al.: Noninvasive detection of myocardial ischemia from perfusion reserve based on cardiovascular magnetic resonance. Circulation, 2000, 101: 1379-1383. 2. Schwitter J., et al.: Assessment of myocardial perfusion in coronary artery disease by magnetic resonance: a comparison with positron emission tomography and coronary angiography. Circulation, 2001, 103: 2230-2235. 3. Ishida M., et al.: Cardiac MRI in ischemic heart disease. Circ J, 2009, 73: 1577-1588. 4. Kim R.J., et al.: Assessment of Myo cardial Viability by Contrast Enhance ment. In: A HCadR, editor. MRI and CT of the cardiovascular system. (2006). 5. Hundley W.G., et al.: ACCF/ACR/AHA/ NASCI/SCMR 2010 expert consensus

document on cardiovascular magnetic resonance: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents. J Am Coll Cardiol, 2010, 55: 2614-2662. 6. Kellman P., et al.: Imaging sequences for first pass perfusion – a review. J Cardiovasc Magn Reson, 2007, 9: 525537. 7. Gould K.L.: Does coronary flow trump coronary anatomy? JACC Cardiovasc Imaging, 2009, 2: 1009-1023. 8. Pilz G., et al.: Negative predictive value of normal adenosine-stress cardiac MRI in the assessment of coronary artery disease and correlation with semiquantitative perfusion analysis. J Magn Reson Imaging, 2010, 32: 615621. 9. Cury R.C., et al.: Diagnostic performance of stress perfusion and de-

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10 layed-enhancement MR imaging in patients with coronary artery disease. Radiology, 2006, 240: 39-45. 10. Kloner R.A., et al.: Consequences of brief ischemia: stunning, preconditioning, and their clinical implications: part 1. Circulation, 2001, 104: 2981-2989. 11. Bernhardt P., et al.: Prediction of necessity for coronary artery revascularization by adenosine contrast-enhanced magnetic resonance imaging. Int J Cardiol, 2006, 112: 184-190. 12. Ingkanisorn W.P., et al.: Prognosis of negative adenosine stress magnetic resonance in patients presenting to an emergency department with chest pain. J Am Coll Cardiol, 2006, 47: 1427-3142. 13. Kwong R.Y., et al.: Detecting acute coronary syndrome in the emergency department with cardiac magnetic resonance imaging. Circulation, 2003, 107: 531-537. 14. Lubbers DD., et al.: Inter-observer variability of visual analysis of “stress”-only adenosine first-pass myocardial perfusion imaging in relation to clinical experience and reading criteria. Int J Cardiovasc Imaging, 2011, 27: 557-562. 15. Nandalur K.R., et al.: Diagnostic performance of stress cardiac magnetic resonance imaging in the detection of coronary artery disease: a meta-analysis. J Am Coll Cardiol, 2007, 50: 1343-1353. 16. Hamon M., et al.: Meta-analysis of the diagnostic performance of stress perfusion cardiovascular magnetic resonance for detection of coronary artery disease. J Cardiovasc Magn Reson, 2010, 12: 29. 17. Ferreira P., et al.: Variability of myocardial perfusion dark rim Gibbs artifacts due to sub-pixel shifts. J Cardio vasc Magn Reson, 2009, 11: 17.

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JBR–BTR, 2014, 97 (1) 18. Ferreira P., et al.: Measurement of myocardial frequency offsets during first pass of a gadolinium-based contrast agent in perfusion studies. Magn Reson Med, 2008, 60: 860-870. 19. Storey P., et al.: Band artifacts due to bulk motion. Magn Reson Med, 2002, 48: 1028-1036. 20. Di Bella E.V., et al.: On the dark rim artifact in dynamic contrast-enhanced MRI myocardial perfusion studies. Magn Reson Med, 2005, 54: 12951299. 21. Cerqueira M.D., et al.: Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation, 2002, 105: 539-542. 22. Yao J., et al.: Bulls-eye display and quantitation of myocardial perfusion defects using three-dimensional contrast echocardiography. Echocardio graphy, 2001, 18: 581-588. 23. Klem I., et al.: Improved detection of coronary artery disease by stress perfusion cardiovascular magnetic resonance with the use of delayed enhancement infarction imaging. J Am Coll Cardiol, 2006, 47: 16301638. 24. Cochet A.A., et al.: Major prognostic impact of persistent microvascular obstruction as assessed by contrastenhanced cardiac magnetic resonance in reperfused acute myocardial infarction. Eur Radiol, 2009, 19: 2117-2126. 25. Mather A.N., et al.: Appearance of microvascular obstruction on high resolution first-pass perfusion, early and late gadolinium enhancement CMR in patients with acute myocardal infarction. J Cardiovasc Magn Reson, 2009, 11: 33.

26. Maron BJ., et al.: from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee, Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisplinary Working Groups, and Council on Epidemiology and Prevention. Circulation, 2006, 113: 1087-1816. 27. Lanza G.A., et al.: Relation between stress-induced myocardial perfusion defects on cardiovascular magnetic resonance and coronary microvascular dysfunction in patients with cardiac syndrome X. J Am Coll Cardiol, 2008, 51: 466-472. 28. Kaski J.C., et al.: Cardiac syndrome X: clinical characteristics and left ventricular function. Long-term follow-up study. J Am Coll Cardiol, 1995, 25: 807-814. 29. Abdelmoneim S.S., et al.: Microvascular function in Takotsubo cardiomyopathy with contrast echocardio graphy: prospective evaluation and review of literature. J Am Soc Echo cardiogr, 2009, 22: 1249-1255. 30. Kashyap R., et al.: Exercise myocardial perfusion imaging to evaluate inducible ischaemia in children with Kawasaki disease. Nucl Med Commun, 2011, 32: 137-141. 31. Ishida N., et al.: Noninfarcted myocardium: correlation between dynamic first-pass contrast-enhanced myocardial MR imaging and quantitative coronary angiography. Radiology, 2003, 229: 209-216. 32. Schwitter J., et al.: MR-IMPACT: comparison of perfusion-cardiac magnetic resonance with single-photon emission computed tomography for the detection of coronary artery disease in a multicentre, multivendor, randomized trial. Eur Heart J, 2008, 29: 480-489.

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Correlation of MRI T2 mapping sequence with knee pain location in young patients with normal standard MRI R. Dautry1, V. Bousson2,3, J. Manelfe1,3, A. Perozziello4, P. Boyer5, Ph. Loriaut5, P. Koch¹, A. Silvestre6, E. SchoumanClaeys1,3, J.D. Laredo2,3, B. Dallaudière1,3,7 Objective: To assess the correlation of T2 mapping abnormalities to knee pain location, in young adults with normal standard knee MRI at 3.0 Tesla. Subjects and methods: Twenty-three consecutive patients were included prospectively from September 2011 to April 2012. Inclusion criteria were age under 50 years old, knee pain without surgical history, and normal knee MRI at 3.0 Tesla (sagittal T1-weighted images, and sagittal, axial and coronal proton-density-weighted images with saturation of fat signal). Ten asymptomatic volunteers were also included as a control group. Patients and controls had a cartilage T2 mapping MRI sequence in addition to the standard MRI protocol. Two musculoskeletal radiologists, blinded to the patient/control condition and pain location, independently reviewed the T2 mapping images. T2 values below 40 ms were considered normal. They rated the number of hyaline cartilage lesions and their grade according to an ICRS-like score (inspired by the International Cartilage Research Society score) in each anatomical compartment (medial and lateral femoro-tibial and anterior patello-femoral joints). In addition, the T2 value of the largest lesion was measured. Patient’s pain location was classified in the following categories: anterior, lateral, medial and global. T2 mapping findings were compared to pain location, and retrospectively to the initial standard sequences. Sensitivity and specificity were calculated for MRI with T2 mapping according to pain location for each reader. Kappa coefficient was calculated for inter-reader agreement. We used variance analysis in a linear regression to compare T2 values and ICRS-like classification in each compartment. Results: Sensitivity of MRI with T2 mapping, according to the symptomatic compartment, was respectively: 78% and 87% for Reader 1 and Reader 2 and specificity was 70% for both readers. Kappa coefficient for T2 mapping abnormalities location and pain location was good, with a calculated value of 0.64. There was no significant correlation between ICRS-like classification and T2 values of lesions (p = 0.18). Conclusion: Our results suggest that T2 mapping is an interesting MRI sequence for the exploration of young patients knee pain in case of normal MRI with a standard protocol, with a good correlation between pain location and focal prolongations of the cartilage T2 relaxation time. Key-words: Knee, MR – Knee, ligaments, menisci, and cartilage.

Isolated focal cartilaginous knee lesions are a frequent condition in young patients (1), can cause both pain (2) and functional impairment, and may lead to osteoarthritis. MRI is the gold standard imaging technique for knee pain in young patients with normal radiographs, with high sensitivity and specificity for the detection of meniscal lesions, anterior cruciate ligament disrup tion, lesions of the tendons and bone marrow abnormalities. On the con trary its use for detection of chondral lesion is less widely accepted; although it is very accurate for deep chondral defects (accuracy superior to 90% for the grades III and IV of the ICRS classification (3)), it is much less sensitive for ICRS grades I and II lesions (4). This means that morpho logical MRI shows chondral damage

at a stage when cartilage is already irreversibly lost. CT-arthrography and MR-arthro graphy display better sensitivity and specificity than standard MRI for the detection and classification of low-grade chondral lesions (5), with the downside of intra-articular injection. MRI T2 mapping of the cartilage is a non-invasive functional imaging technique delivering cartography of the T2 relaxation time of the carti lage without any contrast injection. It is sensitive to tissue anisotropy, and provides compositional information on the cartilage collagen network, water content and proteoglycans concentration (6). T2 mapping has been studied in both animal (7, 8) and human knee cartilage models, especially in the femoro-patellar

From: 1. Service de Radiologie, Hôpital Bichat - Claude Bernard, Paris, France, 2. Service de Radiologie Ostéo-articulaire, Hôpital Lariboisière, 3. Université Paris Diderot Paris - 7, 4. Unité de Recherche Clinique Hôpital Bichat - Claude Bernard, 5. Service de Chirurgie Orthopédique Hôpital Bichat - Claude Bernard, 6. Centre d’Imagerie Ostéo-articulaire, Clinique du Sport, Bordeaux-Mérignac, France, 7. Hôpital Bichat - Claude Bernard, Inserm U698, Paris, France. Address for correspondence: Dr B. Dallaudière, M.D., Ph.D., Service de Radiologie, Bichat-Claude Bernard Hospital, 46, rue Henri Huchard, F-75018, Paris, France. E-mail: benjamindallaudiere@gmail.com

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joint (9). For knee osteoarthritis, it has been shown that T2 mapping is sensitive to T2 prolongation induced by cartilage degeneration (10), and that the cartilage T2 value increases with the severity of osteoarthritis (11). However, some results indicate that T2 values are not correlated with late, radiographic stages of osteo arthritis (12). In the early phase of osteoarthritis, elevated cartilage T2 values as well as cartilage damage have been shown to be associated with findings of pain (13). It has also been hypothesized that a focal prolongation of the cartilage T2 value could be linked to focal cartilage damage, as foci of increased T2-weighted signal intensity are visible in such lesions on conven tional T2 sequences (14). To our knowledge, the value of T2 mapping for the detection of focal chondral lesions not visible on morphological MRI sequences has not yet been confirmed, and has neither been correlated with unex plained clinical symptoms. The aim of our study was to assess the correlation of T2 mapping to knee pain location in young patients with a normal baseline standard knee MRI at 3.0 Tesla.

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Material and methods Patients All patients and controls were in formed of the study procedure and gave their informed consent. We conducted this prospective monocentric observational study from September 2011 to April 2012. Twenty-three consecutive ambulato ry patients referred for an MRI ex amination at our institution were se lected if they fulfilled the following criteria: – Age over 20 years and below 50, in order to increase the probability of normal X-ray and normal knee MRI, – Knee pain of at least one-month duration, without surgical knee history, – Normal radiographs (standing antero-posterior view, Lyon schuss view and femoro-patellar view). – Normal conventional 3.0 Tesla MRI of the knee with sagittal T1weighted images, and sagittal, axial and coronal proton-densityweighted (PDW) images with sat uration of fat signal. All MRI were reviewed for ligaments, meniscus, enthesis, Hoffa fat, spongious bone and cartilage lesions. Carti lage lesion was defined either as a morphological irregularity of the cartilage, or as a signal abnormal ity on PDW images. Exclusion criteria were abnormal radiographs, prior history of knee trauma or surgery, contra-indication to MRI. Pain characteristics were recorded (duration of symptoms and location in medial, lateral or anterior com partment) at the time of the MRI ex amination. The control group consisted of ten healthy volunteers (radiology tech nologists), selected using the same exclusion criteria. All MRI in the control group were performed with the same protocol as for the symp tomatic group, and were normal. Immediately following the acqui sition of the conventional MRI sequences, patients and controls had a cartilage T2 mapping sequence on the patello-femoral and femorotibial joints. Knee MRI technique All MRI examinations were per formed on a 3-Tesla MR scanner (GE® Healthcare MR 750) with a knee coil (8 elements, 8 channels). All exams were performed between

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3.00 pm and 5.00 pm, with identical room temperature (18°C) to over come diurnal and temperature linked variations of the cartilage T2 (15). All patients rested for 40 minutes in supine position prior to MRI, to overcome variation linked to weightloading of the knee (16). During the MR-scan, patients were in supine position, feet first with full limb extension. The conven tional MRI protocol included the fol lowing sequences: – Sagittal T1- WI: TR = 588 ms, TE minimum, Nex = 1, FOV 16 cm, thickness 3 mm, spacing 0.5 mm; 24 slices, antero-posterior direc tion, duration 2 min 17 s – Sagittal, coronal, and axial PDW sequences with fat-saturation: – Sagittal PDW sequences: TR/TE: 2362/45 ms, Nex = 2, FOV 16 cm, 3 mm-thickness, 0.5 spacing, 24 slices, duration 3 min 14 s – Coronal PDW sequences: TR/TE: 2000/45 ms, Nex = 2, FOV 16 cm, 3 mm-thickness, 0.5 spacing, 20 slices, duration 2 min 44 s ms, – Axial PDW: TR/TE: 2257/45 Nex = 2, FOV 16 cm, 3 mm-thick ness, 0.5 spacing, 24 slices, dura tion 3 min 05 s A commercially available sagittal T2 mapping sequence (Cartigram, GE Healthcare, Waukeshaw, WI) was performed with the following para meters: – Axial sequence for the patellofemoral joint: TR = 1000 ms, TE of 6.1, 14.1, 22.1, 30.1, 38.1, 46.1, 54.1 and 62.1 ms, Nex = 2, FOV 16 cm, 256 x 192 matrix, Slices = 9, thick ness = 3 mm with 0.6 mm spacing, duration 5 min 09 s. – Coronal sequence for the femorotibial joints: TR = 1000 ms, TE of 6.1, 14.1, 22.1, 30.1, 38.1, 46.1, 54.1 and 62.1 ms, Nex = 2, FOV 16 cm, 256 x 192 matrix, Slic es = 9, thickness = 3 mm with 0.6 mm spacing, duration 5 min 09 s. Image interpretation T2 mapping sequences were qual itatively and quantitatively assessed on an ADW workstation with the “functool” software. All MRI images were anonymized. Two musculoskeletal radiologists (BD with a 3 year experience and JM with a 2 year experience) analyzed the T2 mapping images indepen dently, in random patient/control order, blinded to clinical data, and reported their results using a prewritten reading grid. In accordance

with the literature (16, 17) and GE® healthcare engineer, and consider ing the clinical settings, the thresh old for the normal T2 value was set at 40 ms. T2 mapping was consid ered positive for the presence of a chondral lesion when a prolongation of the T2 above 40 ms was demon strated on at least two consecutive slices. T2 mapping images were viewed at two different windowing settings using color coding scales; the first with T2 values ranging from 0 to 39 ms, the second with values ranging from 40 to 160 ms. In each joint compartment, radiologists re corded the number of chondral le sions and T2-value of the largest chondral lesion using regions of interest having an area of at least pixels. The largest lesion was 4 graded according the depth of the T2 abnormality, using an ICRS-like classification (Grade 1: superficial lesions; Grade 2: lesions extending down to < 50% of cartilage depth; Grade 3: cartilage defects extending down > 50% of cartilage depth and down but not to the subchondral bone; Grade 4: lesions extending to the subchondral bone). Once a T2 prolongation was detected, a comparison with the con ventional MRI images (sagittal T1weighted images and PDW with saturation of fat signal images) was performed by the 2 radiologists to retrospectively determine if T2 pro longations were linked to initially overlooked lesions in conventional MRI sequences. Statistical methods Statistical analysis was performed using the SAS/STAT® 9.2 software. Sensitivity and specificity for the presence of chondral lesions were calculated for T2 mapping, accord ing to pain location for each reader. The kappa coefficient was used to estimate the inter-reader agreement according to pain location. A Wilcox on test was also used to compare le sions distribution in each joint com partment for the MRI findings of each reader. The association between the ICRS-like classification of lesions and the T2 value was tested using a re gression model (linear regression). A p value < 0.05 was considered as significant. Results Population Twenty-three consecutive patients (symptomatic group: 16 men and

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7 women), and 10 healthy volunteers (asymptomatic group 6 men and 4 women) were included in this study. The mean and median ages were 36.5 and 34 years (SD was 12.8 years). Eleven patients had an terior knee pain, 6 had medial pain, 1 had lateral pain and 5 had global knee pain. In patients with global knee pain, the three joint compart ments were considered as symptom atic. The mean duration of knee pain was 39 days (SD 6.1 days). In the 10 volunteers of the nonsymptomatic control group, the mean and median ages were 33 and 34.5 years (SD was 10.1 years). Lesion detection using T2 mapping and standard images In the patient group, Reader 1 found T2 mapping focal abnormali ties in the symptomatic compart

ments of 18 out 23 patients (13 out of 16 symptomatic anterior compart ments, 8 out of 11 symptomatic me dial compartments and 1 out of 6 symptomatic lateral compartment). Reader 2 found T2 mapping focal abnormalities in the symptomatic compartments of 20 out 23 patients (16 out of 16 symptomatic anterior compartments, 8 out of 11 symptom atic medial compartments and 3 out of 6 symptomatic lateral compart ments). Figures 1 and 2 illustrate the as pect of the T2 mapping abnormali ties in the patient group. Table I sum marizes the T2 mapping findings in the symptomatic joint compartments of the patient group. In the 10 volunteers of the control group, the two readers found the same T2 mapping focal abnormali ties in 2 anterior compartments and 1 medial compartment. No T2

apping abnormality was found in m the lateral compartment. Table II summarizes the T2 mapping find ings in the control group. T2 mapping abnormalities and pain location For Reader 1, sensitivity of the T2 mapping sequence in the patient group was 78%. For Reader 2 sensi tivity of the T2 mapping sequence in the patient group was 87%. For both readers, specificity of T2 mapping in the control group was 70%. Five T2 mapping lesions in 5 pa tients were retrospectively seen on conventional MR images. Figure 3 il lustrates such a lesion on a patellar cartilage. There were differences of inter pretation between the two readers concerning the lateral and anterior compartment. This discrepancy may

Fig. 1. — Medial cartilage abnormality (blue arrows) in a symptomatic medial compartment, visible as a focal prolongation of the T2 value on the coronal T2 maps (A: 0 ms ≤ T2 ≤ 39 ms; B: 40 ms ≤ T2) compared to the normal coronal PDW image (C).

Fig. 2. — Anterior cartilage abnormality (blue arrows) in a symptomatic anterior compartment, visible as a focal prolongation of the T2 value on the axial T2 maps (A: 0 ms ≤ T2 ≤ 39 ms; B: 40 ms ≤ T2) compared to the normal axial PDW image (C).

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Table I. — T2 mapping findings for Reader 1 (R1) and Reader 2 (R2) in the symptomatic joint compartments. No T2 mapping abnormality was found in the only patient with a lateral knee pain (not shown). 11 patients with 6 patients with 5 patients with global knee pain pain in anterior pain in medial compartment compartment Reader Number of symptomatic compartments with T2 mapping lesions Number of T2 mapping lesions

R1 9

R2 11

R1 5

R2 4

ICRS-like classification range

1-4

2-3

44-70

42-54

T2 value range (ms)

4 Anterior

R1 3 Medial

1 Lateral

5 Anterior

R2 4 Medial

3 Lateral

3-4

1-3

2-3

42-66

48-59

43-63

54-68

42-52

46-51

46-49

be explained by the frequent finding of an increased T2 value in the trochlear groove, and at the medial aspect of the lateral femoral condyle, that was sometime considered as a lesion. This was also found in some of our controls (Figure 4) and may be explained by a “magic angle” effect (18). Inter-reader agreement Common agreement for patholo gic compartments in T2 mapping according to pain location was 0.64 (Kappa coefficient). The Wilcoxon test for lesions dis tribution in knee joint compartments did not reveal a significant difference of lesions cartography for Reader 1 and 2 (p = 0.37). T2 values and ICRS-like classification There was no correlation between the T2 value and the ICRS-like clas sification of the lesions in all three joint compartments: medial (p = 0.41

for Reader 1, p = 0.69 for Reader 2), lateral (p = 0.56 for Reader 1, p = 0.83 for Reader 2) and anterior zone (p = 0.11 for Reader 1, p = 0.19 for Reader 2). Discussion Sensitivity and specificity of T2 mapping for the detection of focal T2 prolongations in the cartilage of the symptomatic compartments of the patients were excellent (sensitivity 78% and 87%, specificity 70% for both readers), with a substantial in ter-reader agreement (kappa = 0.64). However, no significant correlation was found between the ICRS-like classification and T2 values of the lesions. To our knowledge, this is the first study that prospectively analyzed the correlation between knee pain location and T2 mapping abnormali ties at 3.0 Tesla in young adults with a normal conventional MRI.

T2 mapping is one of several MRI cartilage imaging techniques cur rently investigated, including T2* mapping, T1 rho mapping, dGEMRIC, sodium imaging and diffusionweighted imaging (19). None of these techniques is used on a daily basis in clinical practice. In our experience and according to the literature (10-12,19), T2 map ping is a sensitive technique for chondral lesions. However, it has several limitations. T2-value of the cartilage is dependent on field strength (17), moderately dependent on temperature (15) and more nota bly dependent on physical activity, weight-loading of the knee (16) and age (14). For these reasons, in the present study, MRI exams were per formed on the same MRI device, dur ing the same period of the day and after a 40 minutes resting time, while room temperature was kept constant at 18°C. Another limitation of the technique is that the T2 of the carti lage depends on the orientation of

Table II. — T2 mapping findings for Reader 1 (R1) and Reader 2 (R2) in the control group. Reader Number of compartments with T2 mapping lesions Number of T2 mapping lesions ICRS-like classification range T 2 value range (ms)

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Anterior compartment R1 R2 2 2

Medial compartment R1 R2 1 1

Lateral compartment R1 R2 0 0

1 to 2

2 to 3

…

42-46

41-47

42-44

43-49

…

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Fig. 3. — Anterior cartilage abnormality (blue arrows) in a symptomatic anterior compartment, visible as a focal prolongation of the T2 value on the axial T2 maps (A: 0 ms ≤ T2 ≤ 39 ms; B: 40 ms ≤ T2), and retrospectively visible on the axial PDW image (C) as an inconspicuous hypersignal.

Fig. 4. — Superficial linear prolongation of the T2 value of the medial femoral cartilage (blue arrow) on the coronal T2 maps of an asymptomatic patient from the control group, interpretated as a “magic angle” effect (A: 0 ms ≤ T2 ≤ 39 ms; B: 40 ms ≤ T2) compared to the normal PDW image (C).

the collagen fibers. This “magic ngle” effect, described by Mosher a et al. (18), is at its maximum when the cartilage is oriented 55° to B0, accounting for an increased T2 value in the trochlear groove, and at the medial aspect of the lateral femoral condyle, found in some patients as well as controls. Our main results show that, as suggested by the literature (19), T2 mapping imaging may potentialize MRI ability to detect focal chondral lesions in the knee, when T2 map ping abnormalities are correlated to pain location. Although non-full thickness chondral defects are asso ciated with knee pain (2) the mecanism is indirect and probably implies the release of cytokines and other signaling molecules from the cartilage (20). However, it has not been proven yet that isolated T2

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mapping focal abnormalities without visible lesion on anatomical MRI are bound to turn into more severe chondral lesions. At the minimum, the presence of a T2 mapping focal chondral abnor mality, linked to pain location, should support a more precocious indica tion to CT-arthrography or MR- arthrography. An interesting secondary result in the present study is that, in five patients, a lesion visible on the T2 mapping images in a painful joint compartment was retrospectively visible on the proton-density-weight ed images with saturation of fat signal. These lesions were initially overlooked as they displayed incon spicuous hyper signal on protondensity weighted images. In these cases, T2 mapping improved the diagnostic performances of MRI.

Our study has some limitations. The number of patients included in our study is small, but it is to our best knowledge the only series correlating MRI T2 mapping to pain in patients with a normal conven tional MRI protocol. It lacks the arthroscopic proof for the chondral defects. The body mass index of the patients and controls were not recorded, and cannot be matched. Location of the T2 prolongation was correlated to patient pain location, but we didn’t study whether it was correlated to pain intensity and dura tion, or to knee articular function. In conclusion, our results suggest that T2 mapping is an interesting MRI sequence for the exploration of young patients knee pain in case of normal MRI with a standard proto col, with a good correlation between pain location and focal prolongations

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of the cartilage T2 relaxation time. It may improve the diagnostic accura cy of MRI for focal chondral lesions, and should help decide whether and MR-arthrography or CT-arthrography is necessary. References 1. Widuchowski W., Widuchowski J., Trzaska T.: Articular cartilage defects: study of 25,124 knee arthroscopies. Knee, 2007, 14: 177-812. 2. Zhai G., Cicuttini F., Ding C., et al.: Correlates of knee pain in younger subjects. Clin Rheumatol, 2007; 26: 75-80. 3. Galea A., Giuffre B., Dimmick S., Coolican M.R.J., Parker D.A.: The accuracy of magnetic resonance imaging scanning and its influence on management decisions in knee surgery. Arthroscopy, 2009, 25: 473480. 4. Figueroa D., Calvo R., Vaisman A., et al.: Knee Chondral Lesions: Incidence and Correlation Between Arthroscop ic and Magnetic Resonance Findings. Arthroscopy, 2007, 23: 312-315. 5. Smith T.O., Drew B.T., Toms A.P., Donell S.T., Hing C.B.: Accuracy of magnetic resonance imaging, mag netic resonance arthrography and computed tomography for the detec tion of chondral lesions of the knee. Knee Surg Sports Traumatol Arthrosc 2012, 20: 2367-2379. 6. Watrin-Pinzano A., Ruaud J.-P., Olivier P., et al.: Effect of proteogly

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JBR–BTR, 2014, 97 (1) can depletion on T2 mapping in rat patellar cartilage. Radiology, 2005, 234: 162-170. 7. Watrin A., Ruaud J.P.B., Olivier P.T.A., et al.: T2 Mapping of Rat Patellar Cartilage. Radiology, 2001, 219: 395402. 8. Kim D.J., Suh J.-S., Jeong E.-K., Shin K.-H., Yang W.I. Correlation of laminated MR appearance of articular cartilage with histology, ascertained by artificial landmarks on the carti lage. J Magn Reson Imaging, 1999, 10: 57-64. 9. Frank L.R., Wong E.C., Luh W.-M., Ahn J.M., Resnick D.: Articular Carti lage in the Knee: Mapping of the Physiologic Parameters at MR Imag ing with a Local Gradient Coil – Pre liminary Results. Radiology, 1999, 210: 241-246. 10. Li X., Benjamin Ma C., Link T.M., et al.: In vivo T1 [rho] and T2 mapping of articular cartilage in osteoarthritis of the knee using 3 T MRI. Osteoarthritis Cartilage, 2007, 15: 789-797. 11. Dunn T.C., Lu Y., Jin H., Ries M.D., Majumdar S.: T2 Relaxation Time of Cartilage at MR Imaging: Compari son with Severity of Knee Osteo arthritis. Radiology, 2004, 232: 592598. 12. Koff M.F., Amrami K.K., Kaufman K.R.: Clinical evaluation of T2 values of pa tellar cartilage in patients with osteo arthritis. Osteoarthritis Cartilage, 2007, 15: 198-204. 13. Baum T., Joseph G.B., Arulanandan A., et al.: Association of magnetic reso nance imaging-based knee cartilage

T2 measurements and focal knee lesions with knee pain: data from the Osteoarthritis Initiative. Arthritis Care Res, 2012, 64: 248-255. 14. Mosher T.J., Dardzinski B.J., Smith M.B.: Human articular cartilage: influence of aging and early symp tomatic degeneration on the spatial variation of T2-preliminary findings at 3 T. Radiology, 2000, 214: 259-66. 15. Nelson T.R., Tung S.M.: Temperature dependence of proton relaxation times in vitro. Magn Reson Imaging, 1987, 5: 189-199. 16. Apprich S., Mamisch T.C., Welsch G.H., et al.: Quantitative T2 mapping of the patella at 3.0T is sen sitive to early cartilage degeneration, but also to loading of the knee. Eur J Radiol, 2012, 81: 438-443. 17. Gold G.E., Han E., Stainsby J., et al.: Musculoskeletal MRI at 3.0 T: relax ation times and image contrast. AJR, 2004, 183: 343-351. 18. Mosher T.J., Smith H., Dardzinski B.J., Schmithorst V.J., Smith M.B.: MR imaging and T2 mapping of femoral cartilage: in vivo determination of the magic angle effect. AJR Am J Roentgenol, 2001, 177: 665-669. 19. Crema M.D., Roemer F.W., Marra M.D., et al.: Articular Cartilage in the Knee: Current MR Imaging Techniques and Applications in Clini cal Practice and Research. Radiographics, 2011, 31: 37-61. 20. Dieppe P.A., Lohmander L.S.: Patho genesis and management of pain in osteoarthritis. The Lancet, 2005, 365: 965-973.

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JBR–BTR, 2014, 97: 17-20.

Developmental Venous anomaly: MR and angiographic features M. Faure1, M. Voormolen1, T. Van der Zijden1, P.M. Parizel1 Developmental venous anomaly (DVA) is probably the most common anomaly of the intracranial vasculature. DVAs consist of multiple, radially oriented dilated medullary veins that converge into a transcerebral vein. We describe the imaging findings of this vascular anomaly in different patients and the role of different imaging modalities. Key-words: Cerebral blood vessels, abnormalities – Cerebral blood vessels, MR – Cerebral angiography.

Developmental venous anomaly (DVA) was first considered a rare vascular malformation (1, 2). Nowadays, with the advent of Computed Tomography (CT) and especially Magnetic Resonance Imaging (MRI), DVAs are seen every week to month by radiologists (3, 4). Most DVAs are solitary, asymptomatic lesions and are discovered incidentally. They have a relatively benign nature with a low incidence of hemorrhage. When they do bleed, this is thought to be due to associated vascular malformations, like cavernous angiomas. The typical angiographic appearance of a DVA is a caput medusae appearance in the venous phase. MRI combined with MR angiography (MRA) replaces angiography in most uncomplicated cases as a non-invasive alternative (3, 5).

Case reports Case 1 A 32-year-old woman presented with headache, with no particular location and no neurological deficit. MRI of the brain was made in another hospital that showed a flow void running transcerebral, suggestive for a vascular malformation (Fig. 1A,B). Initially, there was no gadolinium contrast given and an arterial feeder could thus not be excluded with MRI. Patient was referred to our hospital to perform a cerebral angiography to further characterize the vascular malformation and to exclude an arteriovenous malformation (AVM). The angiography gives the definitive diagnosis of a DVA in the left parietal lobe by showing typical dilated medullary veins – caput medusae appearance –, without arterial feeders, that drain into a transcerebral vein. This vein drains into the superior sagittal sinus (Fig. 1C, D).

Fig. 1. — Axial T2-weighted MR-images showing a focus of abnormal signal in the left parietal lobe (A) with a flow void running transcerebral, suggestive for a vascular malformation (B). Anteroposterior (C) and lateral (D) cerebral angiography, venous phase, show the typical appearance of a DVA in the left parietal lobe with the caput medusae of dilated medullary veins (arrows), accompanied by a single, large draining vein that drains in the superior sagittal sinus (arrowhead).

Case 2 A 53-year-old man presented with acute headache in another hospital. MRI of the brain showed a lesion with heterogeneous signal intensity,

From: 1. Department of Radiology, UZ Antwerpen, Antwerp, Belgium. Address for correspondence: Dr. M. Faure, Department of Radiology, UZ Antwerpen, Wilrijkstraat 10, 2650 Edegem, Belgium. E-mail: marguerite_faure@hotmail.com

faure-.indd 17

hypointense rim in the left frontal white matter and is in close relationship with the frontal horn of the left lateral ventricle. This lesion represents a cavernous malformation. There are some additional vascular structures adjacent to the cavernoma. Cerebral angiography was performed to further characterize these structures and to exclude an AVM. The angiography showed the presence

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Fig. 2. — Axial T2-weighted MR-images through the brain (A) show a lesion with heterogeneous signal and hypointense rim in the left frontal white matter, in close relationship with the frontal horn of the left lateral ventricle, representing a cavernous malformation. Axial T1-weighted images post gadolinium obtained at the same level djacent to the cavernoma, representing an associated DVA. Susceptibility(B, C) reveal contrast-enhancing vascular structures a weighted imaging (SWI) (D) shows striking hypointense ‘blooming’ of the cavernous malformation. Cerebral angiography, venous phase, sagittal views (E, F) confirm the presence of a DVA in the right frontal white matter (arrows), draining into the thalamostriate vein (arrowhead), in turn draining to the great cerebral vein.

of a DVA in the right frontal white matter, draining into the thalamostriate vein, in turn draining to the great cerebral vein (Fig. 2). Discussion DVA is probably the most common anomaly of the intracranial vasculature. Usually, they are discovered as incidental lesion on imaging studies. DVA is about 3 to 4 times more prevalent than AVM. They represent 60% of the cranial vascular malformations found at autopsy and occur in up to 4% of the population (3, 6). Most DVAs are asymptomatic and solitary lesions.

faure-.indd 18

DVAs consist of multiple, radially oriented dilated medullary veins that drain normal cerebral nervous tissue and are located in the white matter. These medullar veins converge into a trancortical or subependymal draining vein. This vein drains into a superficial cortical vein or dural sinus or to a deep ependymal vein. The enlarged veins provide the main venous drainage for intervening normal brain. DVAs were previously known as venous angiomas, venous malformations or medullary venous malformations. This terminology is replaced by DVA because it represents an anatomical variant of venous

drainage of the white matter rather than a true vascular malformation (3, 4, 7). The etiology is unclear. DVAs are mostly found in the frontal and cerebellar white matter, respectively in 50 and 25% of cases (3, 8) DVAs are thought to be benign entities that are unlikely to become symptomatic, although headache and epilepsy are reported. Most DVAs are discovered incidentally at contrast-enhanced CT or MRI (9, 10). There is controversy about the hemorrhagic risk of a DVA. It remains unclear whether the hemorrhage is always caused by an associated occult cavernous malformation, or that it may be caused by the DVA itself.

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Fig. 3. — Susceptibility-weighted imaging (SWI) is very sensitive to venous blood and show the DVA as a hypo-intense lesion.

Possibly thrombosis or stenosis of the draining vein can cause a hemorrhagic event (9, 11, 12). There is a coexistence between DVAs and vascular malformations, especially cavernous malformations. Abe et al found a coexistence of 33% between DVA and cavernous malformations with a relative high prevalence of coexisting lesions in the (5). Although less posterior fossa commonly reported, DVAs may be associated with neuronal migration anomalies, such as cortical dysplasias (4). Multiple DVAs can be found in the blue rubber bleb nevus syndrome or in sinus pericranii. In contrast to other vascular malformations in the brain, DVA resection is not recommended. Because they drain normal brain tissue, resection of these venous pathways is associated with high morbidity and mortality and major neurologic complications (7, 12). Imaging DVAs were thought to be rare before the advent of CT and MRI imaging. Nowadays they are seen with high frequency as incidental finding at CT or MRI. Invasive imaging is nowadays mostly reserved for complicated cases or to exclude associated vascular lesions (4, 10, 13). At cerebral angiography the pathognomic appearance appears during the venous phase of the cerebral angiogram. This includes the caput medusae of deep medullary veins, accompanied by a single, large draining vein that drains in a super

faure-.indd 19

ficial cortical vein or dural sinus. The arterial phase of the cerebral angiogram is normal in most cases. Angio graphy is still the best technique to image DVA and to differentiate it from AVMs which have a different clinical significance. Cavernous malformations and capillary telangiectasias are angiographically occult. Unenhanced imaging studies are normal in approximately 50%. On unenhanced MR images DVAs typically show a transhemispheric flow void on the T1- and T2-weighted images with normal non-gliotic surrounding parenchyma. Enhanced CT and MRI have a sensitivity of over 85% for detection of DVAs. Enhanced CT and MRI can show the draining vein of the DVA as a linear area of enhancement, that courses from the deep white matter to a superficial or deep vein or to a dural sinus. 2D MRI (time-of-flight) angiography can show the pathognomic features of a DVA in more than 85% of cases (10, 13). 2D-MRA is superior to 3D methods for the imaging of slow flow vessels, like veins, because they have less saturation effects. The imaging plane is best chosen perpendicular to the direction of flow. CT and MRI have the advantage of showing hemorrhage, angiographically occult malformations and other pathology, that cannot be demonstrated with angiography. Contrast enhanced MR angiography is performed to exclude an arterial component – an indication for treatment- and to exclude focal stenosis of the draining vein – which is thought to be associated with

emorrhagic events. However, small h AVMs or micro AVMs cannot be shown by MRI/MRA. In some cases there is variable enhancement of the brain parenchyma at enhanced MRI. It is suggested that this enhancement indicates venous restrictive disease in association of the draining vein and thus possibly also associated with a higher risk of bleeding (4, 14). Susceptibility-weighted imaging (SWI) can also be used to image venous structures. SWI appears to have a better detectability of venous structures than conventional T2*weighted imaging (15). Therefore, SWI can be useful to detect DVA. They typically have a low signal intensity on SWI due to the blood oxygen level-dependent (BOLD) effect in the dilated medullary and draining veins (Fig. 3). Conclusion Developmental vascular anomaly (DVA, formerly known as venous angioma, venous malformation or medullary venous malformation) is probably the most common anomaly of the intracranial vasculature and represents an anatomical variant of venous drainage rather than a true malformation. They have a relatively benign nature with low incidence of hemorrhage. When bleeding is found, this is thought to be due to an associated vascular malformation, like a cavernous angioma. Alternatively, thrombosis or stenosis of the draining vein of a DVA is thought to give a hemorrhagic event. DVAs are often seen incidentally at CT or MRI. Although angiography still is the best technique to image DVA, with the typical caput medusae appearance in the venous phase, invasive imaging is nowadays mostly reserved for complicated cases and in case of acute hemorrhage to differentiate it from AVM. MR angiography can be an adequate non-invasive alternative to diagnose a DVA. References 1. Saito Y., Kobayashi N.: Cerebral venous angiomas. Radiology, 1981, 139: 87-94. 2. Olson E., Gilmor R.L., Richmond B.: Cerebral venous angiomas. Radiolo gy, 1984, 151: 97- 104. 3. Ostertun B., Solymosi L.: Magnetic resonance angiography of cerebral developmental anomalies: its role in differential diagnosis. Neuroradiolo gy, 1993, 35: 97-104. 4. Truwit C.L.: Venous angioma of the brain: history, significance, and imaging findings. AJR, 1992, 159: 12991307.

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20 5. Abe T. et al.: Coexistence of occult vascular malformations and developmental venous anomalies in the central nervous system: MR evaluation. AJNR, 1998, 19: 51-57. 6. Abdulrauf S.I., Kaynar M.Y., Awad I.A.: A comparison of the clinical profile of cavernous malformations with and without associated venous malformations. Neurosurgery, 1999, 44: 41-46. 7. Clatterbuck R.E., Elmaci I., Rigamonti D.: The juxtaposition of a capillary telangiectasia, cavernous malformation, and developmental venous anomaly in the brainstem of a single patient: case report. Neuro surgery, 2001, 49: 1246-1250. 8. Valavanis A., Wellauer J., Yasargil M.G.: The radiological diagnosis of cerebral venous angioma:

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JBR–BTR, 2014, 97 (1) cerebral angiography and CT. Neuro radiology, 1983, 24: 193-199. 9. Hammoud D., Beauchamp N., Wityk R., Yousem D.: Ischemic complication of a cerebral develop mental venous anomaly: case report and review of the literature. J Comput Assist Tomogr, 2002, 26: 633636. 10. Ostertun B., Solymosi L.: Magnetic resonance angiography of cerebral developmental venous anomalies: its role in differential diagnosis. Neuro radiology, 1993, 35: 97-104. 11. Field L., Russel E.: Spontanous hemorrhage from a cerebral venous malformation related to thrombosis of the central draining vein: demonstration with angiography and serial MR. Am J Neuroradiol, 1994, 16: 1885-1888.

12. Abe T. et al.: Coexistence of occult vascular malformations and developmental venous anomalies in the central nervous system: MR evaluation. Am J Neuroradiol ,1998, 19: 51-57. 13. Fok K.F. et al.: Spontanous intracerebral hemorrhage caused by an unusual association of developmental venous anomaly and arteriovenous malformation. Interventional neuro radiology, 2006, 12: 113-121. 14. Dillon W.P., Wilson C.B., Hieshima G.B., Roseenau W.: Hemorrhage venous malformations: the role of venous restriction. Presented at the 30th annual meeting of the American society of neuroradiology, St. Louis. June 1992. 15. Fushimi Y. et al.: a developmental venous anomaly presenting atypical findings on susceptibility-weighted imaging. AJNR, 2008, 29: 56.

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JBR–BTR, 2014, 97: 21-24.

Spinal chondrosarcoma arising from a solitary lumbar osteochondroma C. Ruivo1, M.A. Hopper2 Chondrosarcoma is a primary malignant neoplasm of cartilage-forming cells that rarely involves the axial skeleton, typically affecting skeletally mature patients. It may arise as a primary bone tumour or as a secondary lesion from a pre-existing benign cartilaginous neoplasm such as an osteochondroma or enchondroma. We report the case of a 68-year-old female who presented with a mildly painful paraspinal mass lesion as a result of malignant degeneration of a previously unknown solitary lumbar osteochondroma into a large chondrosarcoma. The characteristic imaging findings on cross-sectional imaging techniques are reviewed and illustrated, along with an outline of relevant clinical and therapeutic aspects. Key-word: Chondroma.

Spinal chondrosarcomas are rare lesions, representing less than 10% of all chondrosarcomas (1-4). Most occur in the thoracic spine, and patients typically present in middle-age with back pain and/or neurological symptoms. Men are affected more often than women (2-5). Secondary neoplasms arising from malignant transformation of previously existing cartilaginous lesions are seen more frequently in patients exostoses, with hereditary multiple and may be suspected when there is new onset pain, continued/rapid lesion growth, and a hyaline cartilage cap measuring more than 1.5 cm in thickness on MRI (6-8). Case report A 68-year-old female presented with a mildly painful paraspinal swelling that she had recently become aware of. Her past medical history and laboratorial findings were noncontributory. Physical examination revealed a large, firm, tender lump over the right thoracolumbar paraspinal region, but was otherwise normal; in particular the neurological assessment showed no sensorymotor deficits. Spinal radiographs centered on the thoracolumbar junction were obtained. On the lateral view, erosions of the spinous processes of T12-L2 and speckled soft-tissue calcifications were apparent (Fig. 1). CT of the spine disclosed a large lobulated soft tissue mass located in the right posterior paraspinal region,

Fig. 1. — Lateral radiograph of the spine, centered at the thoracolumbar junction, with manual optimisation of the image parameters. Cortical irregularity and erosions of the spinous processes of T12-L2 (arrowheads) and small areas of flocculent soft-tissue calcification (dotted arrows) are seen.

extending from the level of T9 to L3, measuring 14.5 cm in maximum craniocaudal length, with scarce areas of flocculent calcification within

From: 1. Medical Imaging Department and Faculty of Medicine, University Hospital of Coimbra, Portugal, 2. Department of Radiology, Addenbrooke’s Hospital, Cambridge, United Kingdom. Address for correspondence: Dr C. Ruivo, M.D., Medical Imaging Department, Hospitais da Universidade de Coimbra – Centro Hospitalar e Universitário de Coimbra, Bloco Central – Piso -1, Praceta Mota Pinto, 3000-075 Coimbra, Portugal. E-mail: ruivo.catarina@gmail.com

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it. The mass involved and disrupted the cortex of the spinous processes of T12-L3. At L1 a distinct exostosis with multiple osteolytic areas and cortical destruction was seen arising from the right aspect of the spinous process and ipsilateral lamina (Fig. 2). On MRI, the mass showed peri pheral and septal heterogeneous enhancement following gadolinium administration. At T12-L1 a lobule of the soft tissue mass extended into

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Fig. 2. — Axial non-contrast-enhanced CT scan image on bone window setting (A) shows a pedunculated osteochondroma with multiple osteolytic areas and cortical disruption arising from the right aspect of the spinous process and ipsilateral lamina of the L1 vertebra (arrow). The sagittal reformatted CT image (B) shows a large soft-tissue low-attenuating mass (dotted arrows) with scarce areas of speckled calcification (consistent with chondroid mineralisation – arrowheads).

the spinal canal, mildly indenting the dura (Fig. 3). The imaging findings were very suggestive of spinal chondrosarcoma arising from a lumbar osteochondroma. A CT-guided core biopsy of the paraspinal mass was performed, and the histopathological study revealed features consistent with a low-grade malignant cartilaginous neoplasm. The patient underwent tumour resection and right laminectomy of T11-L1. The histopathological examination of the surgical specimen confirmed the lesion to be a grade 1 chondrosarcoma. Follow-up MR imaging disclosed significant tumour debulking with removal of the intraspinal component but residual small tumour deposits were still seen, which increased in size in subsequent examinations. The patient was therefore reoperated on and received adjuvant radiotherapy to the tumour bed (T9-L3; 70.2 Gy in 39 sessions). She has had stable disease on 14-month follow-up. Discussion Although chondrosarcoma is the third most common primary malignant bone tumour (after osteosarcoma and myeloma), chondrosarcoma of the spine is a relatively uncom-

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mon neoplasm, representing 4-10% of all chondrosarcomas and 12% of all malignant tumours of the spine. Peak prevalence occurs between 30 and 70 years of age, and men are affected two to four times more frequently than women (1-5, 9, 10). It can be found within all regions of the spine but it occurs most frequently in the thoracic region (1-4, 10). Within the vertebra, lesions may arise in the posterior elements (40%), the vertebral body (5%), or both (45%), with lesions located in the posterior elements typically arising from an underlying benign chondral lesion, as in this case (2, 3, 10). Pain, swelling and sensory or motor deficits resulting from spinal cord compression are the main presenting symptoms, particularly when the neoplasm arises from the posterior arch (2-5, 9). Clinical symptoms sometimes develop over a long period of time (weeks to years), since most tumours are low-grade slowgrowing lesions (1, 2, 10). Plain radiographs demonstrate spinal chondrosarcoma as a bone destructive lesion or a well-defined mass with internal irregularly mottled calcifications (1-3). Cross-sectional imaging techniques are particularly helpful in depicting lesions in areas with complex anatomy, such as the spinal elements (3, 10). Spinal

chondrosarcomas usually manifest as large lobulated masses with bone destruction. Calcification or true ossification may occur, corresponding to residual underlying osteochondroma, in cases of secondary chondrosarcoma. CT demonstrates chondroid matrix mineralization to a better advantage than radiographs or MR, and the nonmineralized areas of the tumour show low attenuation (2, 3, 10). On MR, chondrosarcomas show a low-intermediate signal intensity on T1, and very hyperintense on T2-weighted images, due to the presence of high water content hyaline cartilage; calcified chondroid matrix is identified as areas of signal void in any sequence (2, 3, 5, 10). Following the administration of intravenous gadolinium, tumours typically show septal and peripheral rim-like enhancement – the “ringand-arc” pattern – corresponding to fibrovascular bundles surrounding lobules of hyaline cartilage. Highgrade chondrosarcomas usually display a more homogeneous pattern of enhancement (3, 7). Primary spinal tumours have a less favorable prognosis than lesions in the appendicular skeleton (1). Early and wide surgical tumour resection with tumour-free margins is the treatment of choice, providing the best chance of survival and the

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SOLITARY LUMBAR OSTEOCHONDROMA — RUIVO et al

Fig. 3. — Axial (A-C) and sagittal (D-E) MR images demonstrate a large lobulated heterogeneous mass predominantly intermediate in signal on T1-weighted (A and D) and high signal intensity on T2-weighted images (B and E). On contrast-enhanced T1-weighted images, the typical “ring-and-arc” pattern of enhancement is evident (C and F), reflecting the lobulated growth pattern of these cartilaginous tumours. Note the intra-spinal component at T12-L1 (arrowheads in A-C).

lowest local recurrence rate (1-4, 9, 10). It is fundamental that the biopsy path is also contained by the excision margins at the definite surgery to prevent seeding along the biopsy track (1, 3). However, total resection is not always feasible, due to lesion size and location, and risk of neurological deficits. Prognosis in this scenario is poor, since chondro sarcomas in the spine usually are not responsive to adjuvant measures such as chemotherapy or radiation. When complete en bloc resection is not possible, partial removal followed by radiotherapy may provide palliation of pain and improve eventual neurological deficits (4). Chondrosarcomas are locally aggressive tumours but have limited potential for metastases. When these

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occur, they usually appear late in the course of the disease, generally involving the lungs (2, 9). However, some authors have reported a higher rate of metastases in patients with spinal chondrosarcomas, even despite the fact that most lesions are low to intermediate grade, presumably due to incomplete resection (which is more frequent with lesions in this location) that leads to local recurrence and ultimately to pulmonary metastases (3, 4, 11). Spinal osteochondromas represent only 1-4% of all osteochondromas, with the majority found in the cervical and lower thoracic levels. Malignant degeneration is their most concerning complication, occurring in 1% of solitary lesions (versus 10% of patients with hereditary multiple

exostoses), and it is almost invariably due to chondrosarcoma, which develops in the cartilage cap of the osteochondroma (2, 6-8, 10). Centrally located lesions (pelvis, hips and shoulders) are particularly prone to undergo malignant transformation (8). Patients with malignancies arising in solitary lesions are typically older (average age: 50-55 years) than those with hereditary multiple exostoses (average age: 2530 years) (2, 8). Imaging findings that suggest malignancy arising in an osteochondroma include: (a) growth of an osteochondroma after skeletal maturity, (b) hyaline cartilage cap measuring more than 1.5 cm in thickness, (c) irregular or indistinct lesion cortical surface, (d) focal regions of radiolucency

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within the lesion, (e) erosion or destruction of the adjacent bone, and (f) a significant soft-tissue mass particularly containing scattered or irregular calcification (6, 8, 10). Conclusion Unlike chondrosarcomas of the appendicular skeleton, lesions arising in the elements of the spine may be particularly difficult to detect on plain films, and cross-sectional imaging is thus crucial to adequately evaluate them. Radiologically, these tumours appear as bone destructive lesions in the spine or as a para spinal mass with calcification. While CT is optimal to detect the matrix mineralization, MRI depicts the high water content of these lesions as very high signal intensity with T2weighting. Furthermore, both techniques are essential for purposes of staging and guiding surgical excision, which should be as wide as possible, in order to obtain tumourfree margins and thus prevent recurrent disease.

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References 1. Hermann G., Sacher M., Lanzieri C.F., Anderson P.J., Rabinowitz J.G.: Chondrosarcoma of the spine: An unusual radiographic presentation. Skeletal Radiol, 1985, 14: 178-183. 2. Murphey M.D., Andrews C.L., Flemming D.J., Temple H.T., Smith W.S., Smirniotopoulos J. G.: From the Archives of the AFIP – Primary Tumors of the Spine: Radiologic-Pathologic Correlation. Radiographics, 1996, 16: 1131-1158. 3. Murphey M.D., Walker E.A., Wilson A.J., Kransdorf M.J., Temple H.T., Gannon F.H.: From the Archives of the AFIP – Imaging of Primary Chondrosarcoma: Radiologic-Pathologic Correlation. Radiographics, 2003, 23: 1245-1278. 4. Strike S.A., McCarthy, E.F.: Chondrosarcoma of the spine: A series of 16 cases and a review of the literature. Iowa Orthop J, 2011, 31: 154-159. 5. Varma D.G., Ayala A.G., Carrasco C.H., Guo S.Q., Kumar R., Edeiken J.: Chondrosarcoma: MR Imaging with Pathologic Correlation. Radiographics, 1992, 12: 687-704. 6. Park Y.K., Yang M.H., Ryu K.N., Chung D.W.: Dedifferentiated chondro

sarcoma arising in an osteochondroma. Skeletal Radiol, 1995, 24: 617-619. 7. Strovski E., Ali R., Graeb D.A., Munk P.L., Chang S.D.: Malignant degeneration of a lumbar osteochondroma into a chondrosarcoma which mimicked a large retroperitoneal mass. Skeletal Radiol, 2012, 41: 13191322. 8. Murphey M.D., Choi J.J., K ransdorf M.J., Flemming D.J., Gannon F.H.: From the Archives of the AFIP – Imaging of Osteochondroma: Variants and Complications with Radiologic-Pathologic Correlation. Radiographics, 2000, 20: 1407-1434. 9. Panelos J., Voulgaris S., Michos E., Doukas M., Charalabopoulos K., Batistatou A.: Chondrosarcoma of the spine: a rare case with unusual presentation. Diagn Pathol, 2006, 1: 39. 10. Rodallec M.H., Feydy A., Larousserie F., Anract P., Campagna R., Babinet A., et al.: Diagnostic Imaging of Solitary Tumors of the Spine: What to Do and Say. Radiographics, 2008, 28: 10191041. 11. Rizzo M., Ghert M.A., Harrelson J.M., Scully S.P.: Chondrosarcoma of bone: Analysis of 108 cases and evaluation for predictors of outcome. Clin Orthop Relat Res, 2001, 391: 224-233.

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COMPUTED TOMOGRAPHY FEATURES OF SMALL BOWEL OBSTRUCTION DUE TO MESODIVERTICULAR BAND O. Tutar1, M. Velidedeoglu2, I. Yanik1, B. Kocak1, A. Bas1, B. Tutar3, F. Kantarci1 Meckel’s diverticulum is the most common congenital anomaly of the small intestine. Common complications related to a Meckel’s diverticulum include hemorrhage, intestinal obstruction, and inflammation. Small bowel obstruction due to mesodiverticular band of Meckel’s diverticulum is a rare complication. Herein, we report a case of small bowel obstruction occurring due to mesodiverticular band of a Meckel’s diverticulum. The important aspect of our case is clear demonstration of the mesodiverticular band adjacent to the Meckel’s diverticulum on pre-operative computed tomography (CT). Key-word: Intestines, stenosis or obstruction.

Meckel’s diverticulum is the most common congenital abnormality of the gastrointestinal tract, affecting 2% of the general population (1-3). Most of the Meckel’s diverticula are discovered incidentally during the surgical procedures performed for other reasons. Although it generally remains silent, life threatening complications may arise, making it an important structure for having a detailed knowledge of its anatomical and pathophysiological properties. Only 4% of patients with Meckel’s diverticulum develop complications that include bleeding, perforation, inflammation, or obstruction. On the other hand, a mesodiverticular band accompanying the Meckel’s diverticulum is an extremely rare congenital malformation (4). Radiological feature of such an anomaly has not been reported previously. In this paper, we report a case of adult intestinal obstruction due to a mesodiverticular band of Meckel’s diverticulum and describe its CT features. Case report A 36-year-old man admitted to the emergency department with an approximately 12 hours history of persistent abdominal pain about the umbilicus, accompanied by nausea and vomiting; no flatus had been passed. On examination his temperature was 36.3 C and pulse 84. Examination of the abdomen revealed some distension and generalized tenderness, most pronounced in the epigastric region, but no rigidity. Laboratory studies were all within normal limits.

Erect radiograph of the abdomen showed multiple air-fluid levels situated in the central abdomen. Ultrasonography (USG) of the abdomen revealed hyperperistaltic dilated small bowel loops with a small amount of free fluid in the abdomen. The patient previously (2 times during the last 5 years) admitted to the emergency unit with the same complaints that did not require any surgical operation. The patient reported that the pain he endured in the last incident was more severe. The patient was referred to the CT unit to investigate the etiology of the ileus. CT examination showed dilated jejunal and proximal ileal segments that were measured up to 4.5 cm with air-fluid levels. In addition, a diverticular formation of 4 cm in size at the anti-mesenteric side was recognized (Fig. 1). A linear structure (Fig. 2) adjacent to this diverticulum was noted that caused knotting of the ileum approximately 60-80 cm from the ileocecal valve which corresponds to the transition zone of the obstruction (Fig. 3). There were no findings suggestive of Meckel’s diverticulitis on CT examination. On laparoscopy, the distal part of the ileum was found to be markedly compressed by a linear fibrous structure, the mesodiverticular band, within an area 70 cm proximal to the end of the ileum. Ileal loops were dilated at the superior part of the mechanical obstruction. Obstruction was caused by trapping of a bowel loop by this mesodiverticular band (Fig. 4). After separating the mesodiverticular band from the mesentery,

From: Department of 1. Radiology, 2. Surgery, Istanbul University, Cerrahpasa Medical Faculty, Kocamustafapasa, Istanbul, Turkey, 3. MAMOMED Imaging Centre, SisliIstanbul, Turkey. Address for correspondence: Dr B. Kocak, M.D., Istanbul University, Cerrahpasa Medical Faculty, Department of Radiology, Kocamustafapasa, 34098 Istanbul, Turkey. E-mail: drburakkocak@gmail.com

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the ileal loop was released from the diverticulum. Resection of the Meckel’s diverticulum and then functional end-to-end ileoileal anastomosis of the bowel were performed. Histological examination showed a Meckel’s diverticulum with no pathological changes. Discussion Intestinal obstruction due to Meckel’s diverticulum is an infrequent cause, but is the most common presentation in adult, being the second most common in children (4, 5). Various mechanisms of small intestinal obstruction from Meckel’s diverticulum include diverticular intussusception, which is the most common mechanism, volvulus from persistent attachment to the umbilicus, Littre’s hernias, foreign body impaction, diverticulitis, and adhesions or neoplasms (6-9). Other very rare cause of obstruction from Meckel’s diverticulum include, as in our case, by trapping of a bowel loop by a mesodiverticular band. Mesodiverticular band embryology was described in detail by Johann Meckel in 1808. As the embryonic yolk sac enlarges, it develops a connection to the primitive gut via the vitelline duct (10). Typically, this duct obliterates in the embryo by the fifth to ninth week during the progression and rotation of the foregut and hindgut. As this occurs, the yolk sac also begins to atrophy (11). In 0.3% to 2.5% of the population, this vitelline duct persists to become a Meckel’s Diverticulum (1, 11). The yolk sac is supplied by 2 vitelline arteries, one of which degenerates as the yolk sac atrophies, while the remaining artery develops into the superior mesenteric artery (11). When one of the vitelline arteries fails to degenerate, it develops into a peritoneum covered fibrous band or a mesodiverticular band (11).

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Fig. 1. — Axial post-contrast CT showing the Meckel’s diverticula (asterisk).

Fig. 3. — Parasagittal reconstructed post-contrast CT image depicts the mesodiverticular band (between white arrows) trapping the small bowel. Note the dilated bowel loops before and collapsed bowel loops (asterisk) after the compression. The Meckel’s diverticulum (white arrowhead) is just adjacent to the mesodiverticular band. Fig. 2. — Axial post-contrast CT reveals the mesodiverticular band (white arrow) as a linear fibrotic structure adjacent to the Meckel’s diverticula (white arrowhead).

On CT, Meckel’s diverticulum is difficult to distinguish from normal small bowel in uncomplicated cases. However, a blind-ending fluid or gasfilled structure in continuity with small bowel may be revealed. Abdominal CT is used for complicated cases such as intussusceptions. CT can help to confirm the presence of intussusception and distinguish between lead point and non-lead point intussusceptions (12-14). In our case the problem was intestinal obstruction caused by a mesodiverticular band adjacent to the Meckel’s diverticula. The mesodiverticular band also caused compression to the Meckel’s diverticulum, but there were no radiological or histopathological signs of diverticulitis. The Meckel’s diverticulum itself did not exert any trapping to the transition zone; rather the linear fibrotic band (mesodiverticular band) was the cause of obstruction. Based on our literature review, the complicated mesodiverticular band as reported in our case is the first one shown clearly by a pre-operative CT study and one of the few that have been determined surgically.

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Fig. 4. — Laparoscopic view of the Meckel’s diverticulum (asterisk) and mesodiverticular band (white arrows).

Surgical treatment for Meckel’s diverticulum and mesodiverticular band may be by open or laparoscop(15). Surgical treatic procedures ment options include simple diverticulectomy or ileal resection. Associated bands should be removed. Laparoscopic resection of MD is feasible and ideal, especially when performed in specialized centers; techniques including intra-ab-

dominal wedge resection or extracorporeal or intra-corporeal bowel segment resection have been reported (3). Results of surgical excision are generally excellent. In conclusion trapping of a bowel loop by a mesodiverticular band as in our case is very rare cause of intestinal obstruction. The important aspect of our case is clear demonstration of the mesodiverticular band

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CT FEATURES OF MESODIVERTICULAR BAND — TUTAR et al

adjacent to the Meckel’s diverticulum on pre-operative CT. References 1. Altinli, E., Pekmezci S., Gorgun E, Sirin F.: Laparoscopy- assisted resection of complicated Meckel’s diverticulum in Adults. Surg Laparosc Endosc Percutan Tech, 2002, 3: 190-194. 2. Matthews P., Tredgett M.W., Balsitis M.: Small bowel strangula tion and infarction: an unusual complication of Meckel’s diverticulum. J R Coll Surg Edinb, 1996, 41: 54-56. 3. Yahchouchy E.K., Marano A.F., Etienne J.C., Fingerhut A.L.: Meckel’s diverticulum. J Am Coll Surg, 2001, 192: 658-662. 4. Prall R.T., Bannon M.P., Bharucha A.E.: Meckel’s diverticulum causing intestinal obstruction. Am J Gastroenterol, 2001, 96: 3426-3427. 5. Nath D.S., Morris T.A.: Small bowel obstruction in an adolescent: a case of Meckel’s diverticulum. Minn Med, 2004, 87: 46-48.

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6. Dumper J., Mackenzie S., Mitchell P., Sutherland F., Quan M.L., Mew D.: Complications of Meckel’s diverticula in adults. Can J Surg, 2006, 49: 353357. 7. Tomikawa M., Taomoto J., Saku M., Takeshita M., Yoshida K., Sugimachi K.: A loop formation of Meckel’s diverticulum: a case with obstruction of the ileum. Ulus Travma Acil Cerrahi Derg, 2003, 9: 134-136. 8. Karadeniz C.G., Emre A.U., Tascilar O., Bektaş S., Uçan B.H., Irkorucu O., et al.: Lipoma within inverted Meckel’s diverticulum as a cause of recurrent partial intestinal obstruction and hemorrhage: a case report and review of literature. World J Gastroenterol, 2007, 13: 1141-1143. 9. Coulier B., Sergeant L., Maldague P., Ramboux A., Broze B., Hamels J.: Complicated Meckel’s diverticulum diagnosed preoperatively in three cases by complementing CT with detailed us studies. JBR-BTR, 2003, 86: 65-71. 10. Vork J.C., Kristensen I.B.: Meckel’s diverticulum and intestinal obstruc

tion – report of a fatal case. Forensic Sci Int, 2003, 138: 114-115. 11. Yoo J.H., Cerqueira D.S., Rodrigues A.J. Jr., Nakagawa R.M., Rodrigues C.J.: Unusual case of small bowel obstruction: persistence of vitelline artery remnant. Clin Anat, 2003, 16: 173175. 12. Dutta G., Chowdhury A.S., Panda M.: Band of cacophony – abdominal catastrophe caused by the fibrous band of Meckel’s diverticulum: a case report. Cases J, 2009, 2: 7160. 13. Malik A.A.; Shams-ul-Bari, Wani K.A., Khaja A.R.: Meckel’s diverticulum- Revisited. Saudi J Gastroenterol, 2010, 16: 3-7. 14. Lee T.H., Kim J.O., Kim J.J., Hong S.S., Jin S.Y., Kim H.G., Cho J.Y., Lee J.S.: A case of intussuscepted Meckel’s diverticulum. World J Gastroenterol, 2009, 15: 5109-5111. 15. Sumer A., Kemik O., Olmez A., Dulger A.C., Hasirci I., Iliklerden U., et al.: Small bowel obstruction due to mesodiverticular band of meckel’s diverticulum: a case report. Case Report Med, 2010, 2010: 901456.

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Arteries get confused: an arch variation M. Velioglu1, S. Kaya2, E.E. Ertugrul3 We present a case of an arch anomaly in a 54-year-old female who was admitted to our hospital for magnetic resonance angiography (MRA) to evaluate her right-sided numbness. MRA revealed a truncus bicaroticus, right common carotid artery (CCA) originating right vertebral artery, right subclavian artery arising as the final branch of the descending aortic arch and arch originating left vertebral artery. The possible embryologic mechanism and clinical importance of this previously unreported variant are reviewed. Key-word: Arteries, abnormalities.

There are several types of aortic arch anomalies. They are mostly asymptomatic and incidental find ings of arteriograms or anatomic postmortem studies, but it is important to identify them especially before surgeries. In this case report we present unique arch variation with magnetic resonance angiography (MRA) and try to explain its potential embryological development. Case report A 54-year-old woman was referred to radiology department for

MRA for the evaluation of right-sided numbness. Patient stated that the numbness was increasing while she was elevating her arm. Her medical history was uneventful. On her physical examination right radial artery pulse was weaker than left and there was more than 30 mmHg discrepancies between her right and left upper extremity blood pressures. MRA revealed contour abnormalities and mild stenosis of right subclavian artery and an unique aortic arch variation; truncus bicaroticus, right common carotid artery (CCA) originating right vertebral artery (VA),

right subclavian artery arising as the final branch of the aortic arch and arch originating left vertebral artery (Fig. 1). No other abnormalities such as dissection, stenosis, or aneurysmal dilatations were detected on that variative arterial vasculature. We suggested a barium swallow chest x-ray and thorax computed tomography to further evaluate the course of the right subclavian artery, but the patient denied any further evaluation. We gave the patient 100 mg acetyl salicylic acid daily for mild stenosis of right subclavian a rtery and recommended follow up annually.

Fig. 1. — MRA of the aortic arch. A: truncus bicaroticus (thick long arrow), left vertebral artery (thin long arrow) originating directly from arch, aberrant right subclavian artery (thick short arrow), left subclavian From: 1. Girne Military Hospital, Department of Radiology, Girne, 2. GATA Department artery (short arrow). B: Aberrant right of Neurosurgery, Ankara, 3. Echomar Hospital, ENT Department, Ereg˘li Zonguldak, subclavian artery (thick arrow), right verTurkey. tebral artery (thin arrow) originating from Address for correspondence: Dr M. Velioglu, M.D., Soganlık Orta Mahalle, Yalnız Selci right CCA. Caddesi, Uplife Park Sites A Blok No=100, Kartal, Istanbul, Turkey. E-mail: muratvelix@yahoo.com

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Discussion Aortic arch anomalies are common congenital aberrations, which typically do not manifest any overt clinical symptoms. They are usually found incidentally during aortograms, workup for mediastinal diseases or autopsy. Among all the variants, the most frequent anomaly is the common origin of left common carotid artery and brachiocephalic truncus, which is also known as ‘Bovine arch’. An aberrant right subclavian artery as the most distal branch of the aortic arch is rare, representing approximately 1% of all arch vessel anomalies and can cause dysphagia associated with compression of the esophagus between the trachea and the artery, termed dysphagia lusoria (1). There are also several types of anomalous origin of the vertebral arteries. The most common form is the origin of the left vertebral artery directly from the aortic arch between the left common carotid artery and left subclavian artery with a prevalence of 2.4% to 5.8% (2). Also anomalous right vertebral artery origins are reported in literature (2-4). Our report represents an extremely rare combination of anomalies of the aortic arch: first, aberrant right subclavian artery; second, the left and right common carotid arteries share a common origin (truncus bicaroticus); third, the right vertebral artery originates from the right common carotid artery and fourth, left vertebral artery originates from arch directly. In the embryo, the right subclavian artery develops during the sixth to eighth week of gestation. The proximal part originates from the right fourth aortic arch artery, and the distal part from the right dorsal and right seventh intersegmental ar-

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ARTERIES GET CONFUSED — VELIOGLU et al

teries. If the right fourth aortic arch artery and/or the right dorsal aorta abnormally regress, the right subclavian artery develops from the right seventh intersegmental artery and the distal segment of the right dorsal aorta. This vessel usually originates dorsally and therefore has a retroesophageal course and may result in dysphagia due to compression of the esophagus (5). There are six pairs of primitive aortic arches, one for each brachial cleft. Among those, the third and fourth pairs are associated with the development of the aortic arch system. The third pair of cervical aortic arches gives rise to the left and right common carotid arteries. At seven weeks gestation, both common carotid arteries arise from a common vascular trunk. The persistence of this stage of development in the derivatives of the embryonic ventral aorta gives the vascular pattern called common origin of carotid arteries (truncus bicaroticus). The prevalence of this anomaly is less than 0.2% (6). Embryologically, the VA is formed by the development of longitudinal anastomoses that link the cervical intersegmental arteries. The inter segmental arteries eventually regress except for the seventh, which becomes the proximal subclavian artery and which includes the point of origin of the VA in adults. A separation of the right vertebral artery origin from the subclavian artery can be explained by migration of the vertebral artery onto the dorsal aorta or with a separate development of the vertebral artery from the C6 or C8 intercostal artery instead of the C7 intercostal artery (4). If the right vertebral artery arises from the C6 intercostal artery, with obliteration of the longitudinal anastomosis between the C6 and C7 intercostal

artery, and the obliteration of the right dorsal aorta occurs proximal to the C7 intercostal artery origin, the origin of the right subclavian artery is moved to the left (A. lusoria). The right vertebral artery, however, originates from the right common carotid artery. And in the left side if the sixth intersegmental artery persists instead of the seventh, the left vertebral artery has a single origin from the aortic arch, between the left common and subclavian arteries. As a conclusion, aortic arch anomalies are interesting anatomic variants which thoracic and vascular surgeons as well as interventional radiologists should be aware of especially prior to interventions. References 1. Asherson N., Bayford D.: His syndrome and sign of dysphagia lusoria. Ann R Coll Surg Engl, 1970, 61: 63-67. 2. Lemke A.J., Benndorf G., Liebig T., Felix R.: Anomalous origin of the right vertebral artery: review of the literature and case report of the right vertebral artery origin distal to the left subclavian artery. AJNR Am J Neuroradiol, 1999, 20: 1318-1321. 3. Karcaaltincaba M., Strottman J., Washington L.: Multidetector-row CT angiographic findings in the bilateral aortic arch origin of the vertebral arteries. AJNR Am J Neuroradiol, 2003, 24: 157. 4. Albayram S., Gailloud P., Wasserman B.A.: Bilateral arch origin of the vertebral arteries. AJNR Am J Neuroradiol, 2002, 23: 455-458. 5. Rogers A.D., Nel M., Eloff E.P., Naidoo N.G.: Dysphagia lusoria: a case of an aberrant right subclavian artery and a bicarotid trunk. ISRN Surg, 2011, doi: 10.5402/2011/819295. 6. Gluncic V., Marusic A.: Association of the truncus bicaroticus, common trunk of the left subsclavian and vertebral arteries, and retroesophageal right subclavian artery. Ann Anat, 2000, 182 : 281-283.

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Incidentally detected congenital giant left atrial appendage aneurysm IN a child: MRI findings A. Oz1, B. Oguz1, M. Karcaaltincaba1, M. Yilmaz2, M Haliloglu1 Left atrial appendage aneurysms are usually congenital and are very infrequent anomalies of the heart. They are very rarely diagnosed during childhood, with most cases symptomatic between the 2nd and 4th decades of life. Diagnosis is vitally important due to potential life-threatening complications. Surgical excision is the treatment of choice. Surgery reduces the risks of cardiac arrest, respiratory distress, arrhythmia, heart failure, thromboembolism, or rupture. We report the case of a 3-year-old boy with incidental diagnosis of a giant aneurysm of the left atrial appendage that was confirmed with magnetic resonance imaging and treated with surgery. Key-word: Cardiac anomalies, atrial appendage, aneurysm, MRI.

A left atrial aneurysm is a very rare cardiac anomaly. There are two types: intrapericardial and extrapericardial. In the intrapericardial type, the pericardium is intact, whereas the extrapericardial type is associated with pericardial defects. Intrapericardial type aneurysms are congenital, and they can bulge from the left atrial wall or from the left atrial appendage (1, 2). Although initially small, they are thought to grow over decades and cause symptoms when they reach a certain size (2). Patients are usually symptomatic after the 2nd decade, and the most frequent symptom is arryhythmia (1). Surgical excision is indicated even in asymptomatic patients because of potentially life-threatening complications, including arrhythmias, systemic thromboemboli, and congestive heart failure. There are only a few reports of this anomaly in children diagnosed by echocardiography. The aneurysm causes an abnormal cardiac border on routine chest radiography mimicking a tumor or a cyst. We report the case of a child with a giant left atrial appendage aneurysm (LAAA) suspected on chest radiography and detected and confirmed by cardiac magnetic resonance imaging (MRI) without the need for conventional angiography and treated with surgery. Case report A 3-year-old boy was admitted to the pediatrics department with coughing of 5 months’ duration. A cardiac murmur was not detected on physical examination. There was en-

Fig. 1. — Chest radiography shows enlargement of the left heart border at the level of the left atrial appendage segment (arrows).

largement of the left heart border at the level of the left atrial appendage segment on chest radiography (Fig. 1). No previous chest radiograph was available for comparison. An ECG showed a normal sinus rhythm. Echocardiography revealed a left atrial aneurysm. Cardiac MRI was performed with a 1.5T scanner (Symphony; Siemens, Erlangen, Germany). ECG gating was used to confirm the exact size of the aneurysm and to exclude the possibility

From: Department of 1. Radiology, 2. Thorax and Cardiovascular Surgery, Faculty of Medicine, Hacettepe University, Hacettepe Universitesi Tip Fakültesi Radyoloji Anabilim Dali Sihhiye Ankara, Turkey. Address for correspondence: Dr A. Oz, M.D., Department of Radiology, Faculty of Medicine, Hacettepe University, Hacettepe Universitesi Tip Fakültesi Radyoloji Anabilim Dali Sihhiye Ankara, Turkey. E-mail: aoz.ayseguloz@gmail.com

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of any associated cardiac lesions. Black blood HASTE sequences on 3 orthogonal planes, short axis 4-chamber cine images, and sagittal oblique MR angiography sequences were obtained before intravenous contrast media administration. Sagittal oblique MR angiography and transverse plane fat-suppressed T1weighted images were then obtained. The MRI revealed a 4.2 × 3 × 3.5 cm sized left atrial appendage dilatation compatible with an LAAA. The aneurysm was compressing the left ventricle wall (Fig. 2). The aneurysm was connected to the left atrium with a large opening. The aneurysm was larger than the left ventricle. There was no other cardiac anomaly. The patient was managed surgically with aneurysmectomy and

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INCIDENTALLY DETECTED CONGENITAL GIANT LEFT ATRIAL APPENDAGE ANEURYSM — OZ et al

C Fig. 2. — A: Axial cine image shows giant aneurysm (*) c ommunicating with left atrium (a), indenting left ventricule (v) lateral wall. Sagittal oblique MR angiography (B) and volume rendering technique (VRT) (C) images show giant left atrial appendage aneurysm (*).

B rimary repair. The surgical findings p revealed a 4 × 3 cm sized aneurysm at the left atrial appendage. Histopathologically, all 3 cardiac wall layers were intact. The postoperative course was uncomplicated, and the patient was discharged on the 7th postoperative day. At 6-month follow up, he was asymptomatic with no complications and with no evidence of recurrence. Discussion Intrapericardial LAAAs are congenital but usually asymptomatic. Asymptomatic patients are diagnosed during adulthood incidentally. In some cases, acute symptoms and complications may occur, such as supraventricular arrhythmia, pulmonary and systemic embolism, mitral regurgitation, cardiac arrest, respiratory distress, heart failure, and cardiac tamponade (1, 2). Compression of the left coronary artery or its branches causes supraventricular arrhythmias and atypical chest pain

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episodes (3). Left atrial dilatation with annular deformity of the mitral valve caused by the aneurysm leads to mitral regurgitation. The risk of possible complications rises with the increase in the size of the aneurysm (1, 2). When an enlarged abnormal upper left heart border is detected on a chest radiograph, a left atrial aneurysm should be considered in the differential diagnosis. Other condi tions that can cause a similar abnormality are a mediastinal mass, a pericardial cyst, a bronchogenic cyst, an epicardial lipoma, a cardiac or paracardiac tumor, a pericardial defect, or valvular heart disease. Fetal echocardiography, transthoracic echocardiography, transesophageal echocardio graphy, chest CT, nuclear molecular imaging, and CT and conventional angiography are other invasive and noninvasive methods useful for the diagnosis of left atrial aneurysms (1). Transthoracic echocardiography is the most useful noninvasive method because

it typically shows the cyst-like structure connected to the left atrium. Transesophageal echocardiography is a useful diagnostic tool for the detection of thrombi inside the left atrium or the aneurysm, but it is a more invasive technique. Angiography is also an invasive procedure, which should be reserved for patients with concomitant cardiac anomalies or for cases in which echocardiography or MRI are inconclusive. Cardiac multidetector CT is valuable for evaluating the anatomy of the coronary artery when compression of the left coronary artery or its branches is suspected (4, 5). MRI has the highest temporal resolution among the various diagnostic methods. This quality makes MRI the optimum approach for evaluating the surrounding structures, revealing the cardiac anatomy, and obtaining reproducible measurements of systolic and diastolic function. The absence of ionizing radiation also makes MRI superior in the evaluation of cardiac anomalies of (6). children and young patients Complications are more likely to occur with intrapericardial aneurysms than with extrapericardial aneurysms. Differentiation between an

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extrapericardial- and an intrapericardial-type aneurysm by echocardio graphy is usually not possible. Smaller aneurysms can mimic left pulmonary artery anomalies. In such cases, axial and coronal sections are recommended (7). Pericardial cysts show high signal intensity on T2-weighted images when the left atrial wall is not involved. Central bronchogenic cysts that have no contact with the pericardium have high signal intensity on T2-weighted images. The presence of air or fluid in these cysts may also be detected. Epicardial lipomas have typical high signal intensity on both T1- and T2-weighted MR images. Cardiac tumors can be differentiated by the presence of a flow signal (7). The goal of treating an LAAA is to prevent life-threatening complications, the likelihood of which increases with the size of the aneurysm. Particularly in children, aneurysmectomy through a median sternotomy with a cardiopulmonary bypass is a conventional and safe method (2). An anurysmal thrombus is detected in one-third of patients with a LAAA (1).

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On the MRI, signal voids can be seen within the sac, suggestive of thrombus. In this case, a thrombus was not observed on either the echocardio graphy, MRI, or during surgery. Moderate to severe mitral regurgitation is associated with the absence of thrombus (8). In conclusion, this rare cardiac pathology should be kept in mind in the differential diagnosis of lesions adjacent to the left heart. Both noninvasive and invasive diagnostic methods are useful for detecting a left atrial aneurysm (1). MRI can reveal morphological and functional para meters of the aneurysms while excluding other cardiac abnormalities without ionizing radiation (6). To prevent complications and high mortality and morbidity, early diagnosis and aneurysmectomy are mandatory. References 1. Park J.S., Lee D.H., Han S.S., Kim M.J., Shin D.G., Kim Y.J., Shim B.S.: Incidentally found, growing congenital aneurysm of the left atrium. J Korean Med Sci, 2003, 18: 262-266.

2. Cho M.J., Park J.A., Lee H.D., Choo K.S., Sung S.C.: Congenital left atrial appendage aneurysm diagnosed by fetal echocardiography. J Clin Ultrasound, 2010, 38: 94-96. 3. Gupta S., Agarwal S., Pratap H., Datt V., Banerjee A. Congenital aneurysm of left atrial appendage: a case report. J Card Surg, 2010: 25: 3740. 4. Plonska-Gosciniak E., Larysz B., Jurczyk K., Kasprzak J.D.: Five- chambered heart: a 20-year story of left atrial appendage aneurysm. Eur Heart J, 2009, 30: 1014. 5. Smeglin A., Merchan J., Maysky M., Johnstone M., Pastore J.O.: Images in cardiovascular medicine: giant left atrial appendage aneurysm. Circulation, 2008, 118: 2393-2394. 6. Kroft L.J., de Roos A.: MRI diagnosis of giant right atrial aneurysm. AJR Am J Roentgenol, 2007, 189: W94-95. 7. Hoffmann U., Hamed N., Herold C., Globits S.: Radiological signs of a left atrial aneurysm. Eur Radiol, 2000, 10: 1332-1334. 8. Bilge M., Yasar A.S., Bozkurt M., Karakas F., Bilen E., Yuksel I.O.: Left atrial appendage aneurysm secondary to eccentric severe ischemic mitral regurgitation. Echocardiograph, 2009, 26: 1225-1227.

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JBR–BTR, 2014, 97: 33-35.

ULTRASONOGRAPHIC DIAGNOSIS OF ACUTE PANCREATITIS CAUSED BY RUPTURED HYDATID DISEASE TO THE BILIARY SYSTEM O. Ozcaglayan1, A.M. Halefoglu2, T. Ozcaglayan1, H.A. Sumbul3 Acute pancreatitis is a rare complication of hydatic disease which occurs following the rupture of a cyst to the intrahepatic bile ducts. Herein, we report a case of a 34-year-old Turkish man, who presented with upper abdominal pain. In laboratory examination, amylase and lipase levels were elevated. Ultrasound examination showed a cystic hypoechoic mass lesion located in the right lobe of the liver with dilated intrahepatic bile ducts, and germinative membranes were detected originating from the ruptured hydatid cyst to the common bile duct. The pancreas was found to be diffusely hypoechoic, consistent with acute pancreatitis. Contrast enhanced CT and MRI were also performed for further evaluation of the primary lesion and its complications. Key-word: Echinococcosis.

Hydatidosis is a zoonosis caused by infestation of tapeworms named Echinococcus Granulosus and Echinococcus multilocularis. The liver is the most effected location in hydatic disease. Less frequently, cysts are found in the lungs and rarely in the spleen, kidneys, brain, muscles, bones and pancreas (1-3). Rupture of a hydatid cyst into the biliary tract is rare (2, 3). In the literature, only a few cases of acute pancreatitis manifested with the presence of hydatid membranes in the biliary tract have been described (4, 5). We are reporting a case of acute pancreatitis, occuring by a hydatic cyst of the liver that ruptured into the biliary tract and describing the main disease and its complications by using ultrasonography (US), computed tomography (CT) and magnetic resonance imaging (MRI).

Laboratory findings were presented as; leukocyte 12.5 x 109/L (normal: 4.0-10.0 x 109/L), neutrophils 6.1 x 109/L (normal: 2.10-6.13 x 109/L), eosinophils 1.8 x 109/L (normal: 0.04-0.45 x 109/L), total bilirubin 5.7 mg/dl (normal: 0.31.1 ml/dl), direct bilirubin 3,5 mg/dl (normal: 0.1-0.4 mg/dl), indirect bili-

rubin 2.2 mg/dl (normal: 0.1-0.9 mg/ dl), amylase 1466.1 IU/L (normal: 30110 IU/L), lipase 977.2 IU/L (normal: 0-60 IU/L), alanine aminotransferase (ALAT) 513 IU/L (normal: 10-45 IU/L), aspartate aminotransferase (ASAT) 388 IU/L (normal: 7-35 IU/L), lactate dehydrogenase 395 IU/L (normal 122-

Case report A 34-year-old Turkish man was admitted to the Emergency department complaining of an acute onset of epigastric pain. The pain was constant and radiating from the back. The patient also had nausea and vomiting. There was no history of drug or alcohol ingestion nor specific dietary history. Clinical examination described an acutely ill patient having mild jaundice and high fever (38,5°C) and also epigastric tenderness. Physical examination revealed an enlarged right liver lobe 3 cm below the right costal margin by palpation.

Fig. 1. — US reveals the multiloculated cystic mass lesion compatible with hydatid disease in the right lobe of the liver, with associated dilated intrabiliary bile ducts (white arrows).

From: Department of 1. Radiology and 3. General Surgery, Tokat State Hospital, Tokat, Turkey, 2. Department of Radiology, Sisli Etfal Training and Research Hospital, Istanbul, Turkey. Address for correspondence: Dr A.M. Halefoglu, M.D., Birlik sok. Parksaray ap. No: 17/4 34340 Levent, Istanbul, Turkey. E-mail: halefoglu@hotmail.com

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Fig. 2. — US shows dilated choledoc lumen (white arrows) containing echoic debris and membranes compatible with hydatic material, due to rupture into the biliary system (black arrow).

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phragma and thoracic cavity occurs in 0.6-16% of cases of hepatic hydatid disease (18). The various US appearances of hydatid cysts were originally classified by Gharbi et al in 1981 (19). They described five categories of hydatid cyst of the liver as below, which they believed corresponded to the evolutionary changes of the hydatid cyst.

Fig. 3. — US reveals hydatic material in the choledoc lumen, leading to partial obstruction (white arrow). Mildly enlarged diffuse hypoechoic pancreas is also seen (black arrow).

222 IU/L), gamma glutamyl transpeptidase 98 IU/L (normal: 0-60 IU/L), C-reactive protein 65 mg/dl (normal 0-10 mg/dl). The patient was referred to ultrasonograpic examination (US) with a suspicion of choledocholithiasis. US detected a multiloculated cystic lesion compatible with cyst hydatid located in the right lobe of the liver (Fig. 1) .The patient was living in the southern part of the Turkey where hydatid disease is endemic. Choledocal and intrahepatic bile ducts were found to be mildly dilated and containing echoic debris and membranes in their lumens. These materials were interpreted as germinative membranes that were originating from hydatid cyst lesion in the liver. Pancreatic parenchyma had a diffusely hypoechoic appearance, a finding that was suggestive of acute pancreatitis (Fig. 2, 3). The main cystic lesion and germinative membranes were also detected in CT and MRI examinations. The presence of these germinative membranes was also verified during the endoscopic retrograde cholangio pancreatography (ERCP) procedure. Discussion Hydatic disease is a zoonosis caused by a tapeworm of dogs named E. Granulosus and E. Multilocularis. Humanbeings are intermediate hosts of these parasites.The parasite eggs passes into body by ingestion of contaminated uncooked or unwashed vegetables or direct contact with dogs (6). Following the consumption of contaminated food,

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the embryo is released in the intestine and carried to the liver to compose the cystic lesion via portal venous system (7). The hydatic cyst has three layers: (i) the outer pericyst, composed of reactive host cells that form a dense and fibrous protective zone; (ii) the middle laminated membrane, which is acellular and supplies the passage of nutrients; and (iii) the inner germinal layer, where the scolices and the laminated membrane are produced (8, 9). The infestation of hydatic disease in the human body affects mostly the liver (75%), lungs (15%) and the other organs (10%) (10). The most frequent complication of hydatic disease is a spontaneous rupture into the intrabiliary tract (11). This complication is seen aproximately in 5-17% of cases (12, 13) . Acute pancreatitis is a quite rare complication that occurs after the intrabiliary rupture of echinococcal disease, by obstruction of ampulla vateri. Obstruction of intrabiliary tracts and choledoc by hydatic membrane fragments, scolices or secondary cysts may mimic choledocholithiasis (14) as seen in our case. Rupture into the peritoneum occurs less often (15) with reported rates ranging from 3.2% to 16% (16). Significant risk factors for hydatid cyst perforation include younger age, cyst diameter of > 10 cm, and superficial cyst location (17). Intraperitoneal rupture of a hydatid cyst is considered an urgent clinical event. The dissemination of the cyst contents poses 1-2.5% risk of severe, life threatening anaphylactic reaction (17). Involvement of the dia-

Type 1- Pure fluid collection - univesicular cyst, Type 2- Fluid collection with a split wall - detached laminated membrane - ‘water lily’ sign, Type 3- Fluid collection with septa - daughter cyst, Type 4- Heterogenous appearance - presence of matrix - mimics a solid mass, Type 5- Reflecting thick walls calcifications. The diagnosis can be made by demonstrating elevated amylase and lipase values with detecting presence of germinal membranes in the intrabiliary tract and choledoc by imaging modalities such as US, CT and MRI. US, CT, MRI and MRCP are useful imaging modalities in the diagnosis of the disease. Especially US is regarded as helpful in the differential diagnosis of stones and hydatic cyst materials in the lumen of biliary tracts (20, 21). In addition, these imaging modalities also provide differential diagnosis of pyogenic abscess, amebic abscess and hydatic disease. CT has a high sensitivity and specificity for hepatic hydatid disease. Although US examination is regarded as an initial diagnostic tool, CT is more useful in terms of revealing calcification and daughter cysts (22). Typical CT findings include sharply defined single or multiple, round or oval cystic masses with fluid attenuation values (3-30 HU) and a thin high-attenuation rim that usually does not enhance after the administration of contrast material (23). On MRI, hydatid cysts typically appear multiloculated or multicystic structures with a hypointense rim on T2 weighted images. This finding has been proposed to be a characteristic sign of hepatic hydatid disease. When present, daughter cysts are seen as cystic structures attached to the germinal layer that are hypointense relative to the intracystic fluid on T1 weighted images and hyper intense on T2 weighted images (24). Serology is very helpful for diagnosis but negative serologic findings will not exclude the diagnosis (25).

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US OF ACUTE PANCREATITIS DUE TO RUPTURED HYDATID CYST — OZCAGLAYAN et al

In treatment, endoscopic sphincterotomy and surgery are frequently used. Conclusion Acute pancreatitis is a very rare complication of ruptured hydatid disease into intrabiliary tract. US is a very useful imaging modality for the diagnosis of hydatid disease and its complications, such as rupturing into the intrabiliary ducts and choledoc. It demonstrates hydatid material in their lumens and also provides differentiation from stones. Additionally, CT and MRI modalities can be used to confirm the diagnosis. References 1. Bolognose A., Barborosos A., Muttillo I.A., Valabrega S., Bocchetti T.: Echinococcus cyst of the pancreas: description of a case and review of the literature. G Chir, 2000, 21: 389-393. 2. Ammann R.W., Eckert J.: Cestodes. Echinococcus. Gastroenterol Clin North Am. 1996, 25: 655-689. doi: 10.1016/ S0889-8553(05)70268-5. 3. Miguet J.P., Bresson-Hadni S., Vuitton D.: Echinococcosis of the liver. In: Rodes J., Benhamou J.P., Bircher J., McIntyre N., Rizzetto M., editors. Oxford Textbook of Clinical Hepatology. 2. Vol. 1. Barcelona, Ediciones Cientificas y Tecnicas, 1993, pp 839-849. 4. Mentes A., Batur Y., Ahmet E.: Pancreatitis as a complication of hydatid liver cyst. Jpn J Surg, 1990, 20: 356358. 5. Aydin A., Ersoz G., Tekesin O., Mentes A.: Hydatid acute pancreati

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tis: a rare complication of hydatid liver disease. Report of two cases. Eur J Gastroenterol Hepatol, 1997, 9: 211214. 6. Barros J.L.: Hydatid disease of the liver. Am J Surg, 1977, 182: 597-600. 7. von Sinner W.N.: New diagnostic sign in hydatid disease: radiography, ultra sound, CT and MRI correlated to pathology. Eur J Radiol, 1990, 12: 150159. 8. King C.H.: Cestodes (tapeworms). In: Mandell G.L., Bennett J.E., Dolin R., Principles and practice of infectious diseases. 4th ed. New York, NY, Churchill Livingstone, 1995, pp 25442553. 9. Lewall D.B.: Hydatid disease: biology, pathology, imaging and classification. Clin Radiol, 1998, 52: 863-874. 10. Pedrosa I., Saiz A., Arrazola J.: Hydatid Disease: Radiologic and Pathologic Features and Complications. RadioGraphics, 2000, 20: 795-817. 11. Manuoras A., Genetzakis M., Antonakis P.T.: Endoscopic management of a relapsing hepatic hydatic cyst with intrabiliary rupture: A case report and review of the literature. Can J Gastroenterol, 2007, 21: 249253. 12. Wong L.S., Braghirolli-Neto O., Xu M., Buckels J.A., Mirza D.F.: Hydatid liver disease as a cause of a recurrent pancreatitis. J R Coll Surg Edinb, 1999, 44: 407-409. 13. Becker K., Frieling T., Saleh A.: Resolution of hydatic liver cyst by spontaneous rupture into the biliary tract. J Hepatol, 1997, 26: 1408-1412. 14. Kattan Y.B.: Intrabiliary rupture of hydatic cyst of the liver. Br J Surg. 1975, 62: 885-890. 15. Lo Casto A., Salerno S., Grisanti M., Mastrandrea G.: Hydatid cyst of the liver communicating with the left

colon. Br J Radiol, 1997, 70: 650-651. 16. Prousalidis J., Tzardinoglou K., Sgouradis L., Katsohis C., Aletras H.: Uncommon sites of hydatid disease. World J Surg, 1998, 22: 17-22. 17. Akcan A., Akyildiz H., Artis T., et al.: Peritoneal perforation of liver hydatid cysts: clinical presentation, predisposing factors and surgical outcome. World J Surg, 2007, 31: 1284-1291. 18. Kilani T., El Hammami S., Horchani H., et al.: Hydatid disease of the liver with thoracic involvement. World J Surg, 2001, 25: 40-45. 19. Gharbi H.A., Hassine W., B rauner M.W, Dupuch K.: Ultrasound examination of the hydatid liver. Radiology, 1981, 139: 459-463. 20. Milichevic M.: Hydatid disease in surgery of the liver and biliary tract. edited by Blumgart L.H., Edinburg, Churchill Livingstone, 1994, pp 11211150. 21. Fernando C., Gonzalo S., Ricardo R.: Ultrasound diagnosis of ruptured hydatid cyst of the liver with biliary obstruction. Gastrointest Radiol, 1986, 11: 271-274. 22. Angulo J.C., Sanchez-Chapado M., Diego A., et al.: Renal echinococcosis: clinical study of 34 cases. J Urol, 1997, 157: 787-794. 23. Scherer V., Weinzieri M., Strum R., Schildberg F.W., Zrenner M., L issner J.: Computed tomography in hydatid disease of the liver: a report on 13 cases. J Comput Assist Tomogr, 1987, 2: 612-617. 24. Marani S.A., Canossi G.C., Nicoli F.A., Alberti G.P., Monni S.G., Casolo P.M.: Hydatid disease: MR imaging study. Radiology, 1990 , 175: 701-706. 25. Parija S.J.: A review of some simple immunassays in the serodiagnosis of hydatid disease. Acta Trop, 1998, 70: 17-24.

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ILEOCOLIC INTUSSUSCEPTION DUE TO LIPOMATOSIS OF THE ILEUM: A COMMON COMPLICATION OF A RARE CLINICAL ENTITY M. Eyselbergs1, L.J. Ceulemans,3,4, S. De Bontridder3, F. Vanhoenacker1,2,5, L. Van Overbeke6, I. Quanten3, G. Jacomen7, A. Snoeckx2 We report a case of intestinal ileal lipomatosis in a 56-year-old Caucasian male complicated with small bowel obstruction due to ileocolic intussusception with a lipoma serving as lead point. This rare disease is often only discovered incidentally as a consequence of mechanical complications and not well reported in the international literature, compared to intussusception due to an isolated lipoma. Computed tomography is the imaging modality of choice to depict complications of this distinct clinicopathological entity. Density measurements can confirm the fatty content and homogeneity analysis of the lesions can guide the radiologist in the differential diagnosis. Key-word: Lipoma and lipomatosis.

Case report A previously healthy 56-year-old male without significant medical history was referred by his general practitioner to the hospital with intermittent cramping abdominal pain and bloody stools. Apart from rebound tenderness in the right fossa the clinical examination was unremarkable. Inflammatory parameters were elevated. Colonoscopy was performed but interrupted because of intolerable pain. Additionally, Computed Tomography (CT) was carried out and revealed small bowel obstruction due to ileocolic intussusception with a low attenuating sharply demarcated mass as lead point (Fig. 1). Also, diffuse fatty infiltration of the submucosal layer and multiple other low attenuating submucosal masses protruding into the bowel lumen were seen scattered throughout the terminal ileum. The density varied between -80 and -120 Hounsfield units, in keeping with lipomatous tissue. Because of the small bowel obstruction, an urgent laparotomy was performed. Manual reduction was not possible and ileocaecal resection was performed. The post operative course was uneventful. Macroscopical (Fig. 2) and histopatho logical (Fig. 3) analysis of the resected specimen confirmed the presence of numerous tumors composed of mature adipose tissue interspersed with some fibrous tissue. The diagnosis of intestinal ileal lipomatosis

Fig. 1. — CT of the abdomen (A and B) coronal reformatted and (C and D) axial images show small bowel obstruction with dilated small bowel loops (asterisk) due to ileocolic intussusception (arrow in A and C) with infiltration of the mesenterial fat suggestive of ischemia (double arrowhead in A). A lead point could be identified (arrow in B). Also, multiple additional lipomas and diffuse submucosal fatty infiltration were seen throughout the terminal ileum (arrowheads).

From: 1. Department of Radiology, 3. Department of General Surgery, 6. Department of Internal Medicine, 7. Department of Surgical Pathology, AZ Sint Maarten DuffelMechelen, Duffel, Belgium, 2. Department of Radiology, Antwerp University Hospital, Edegem, Belgium, 4. Department of Abdominal Transplant Surgery, University Hospitals Leuven, Leuven, Belgium, 5. Faculty of Medicine and Health sciences, Ghent University, Ghent, Belgium. Address for correspondence: Dr F. Vanhoenacker, M.D., Ph.D., Department of R adiology, AZ Sint Maarten Duffel-Mechelen, Rooienberg 25, 2570 Duffel, Belgium. E-mail: filip.vanhoenacker@telenet.be

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complicated with ileocolic intussusception was made. Discussion Benign tumors of the small bowel are relatively rare with lipoma being the second most common type in

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ILEOCOLIC INTUSSUSCEPTION DUE TO LIPOMATOSIS OF THE ILEUM — EYSELBERGS et al

Fig. 2. — Macroscopic examination of the resected ileocaecal specimen shows intraluminal yellowish sharply delineated masses (arrows) in the terminal ileum and submucosal fatty infiltration (asterisk). Also note the ileocolic intussusception (arrowheads).

Fig. 3. — Histopathological examination of the resected s pecimen shows submucosal lipomatous tissue (asterisks) and muscularis propria (arrows) separated by lipocytes (arrowheads), in keeping with diffuse lipomatosis (magnification: 40x, H and E stain).

pproximately 25% of the cases, a only preceded by leiomyomas (1). Typical manifestations of lipomas on CT are symmetric, sharply delineated masses with a density ranging from -80 to -120 Hounsfield units compatible with fatty tissue. Solitary lipomas need to be differentiated from lipomatosis of the ileocaecal valve and intestinal lipomatosis. Lipo matosis of the ileocaecal valve involves a symmetrical fatty enlargement and is a very common finding (2). The term intestinal lipomatosis is currently used to describe diffuse infiltration and overgrowth of well differentiated fatty tissue in the submucosal layer. On histopathological examination, proliferation of adipose

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cells may extend to the s erosal layer or mesenteric fatty tissue (3). The ileum is the most common site involved. Intestinal lipomatosis was first described in 1906 by Hellström (4). The diagnostic criteria used nowadays are not clearly defined and range from a minimum of 4 to more than 100 lipomas (5). The etiology has not yet been elucidated. Some patients with intestinal lipomatosis have a family history, incriminating an inherited tendency. Association with hypercholesterolemia (1) or with macrodactylia fibrolipomatosis (6) has also been suggested. According to Climie et al, intestinal lipomatosis might be of hamartomatous origin

since neuronal bundles were observed in the lipomas of their series (7), although this was not the case in our patient. There seems to be no gender predilection. Less than 50% of the reported cases were symptomatic with symptoms attributed to obstruction, intussusception, volvulus or (occult) bleeding (8, 9). When encountered incidentally, no treatment is necessary (3, 10). This rare clinical entity is not well reported in the international literature (1113), compared to intussusception due to an isolated lipoma. Imaging modality of choice is CT since density measurements can confirm the lipomatous nature of the luminal masses. CT is also capable of differentiating lipoma from liposarcoma when evaluating the homogeneity of the fatty content and absence of increased density (3). In some cases – however – loss of fat density of lipomas may mimic malignancy (14). The differential diagnosis of multiple intestinal lipomas includes intestinal manifestations of Proteus syndrome, neurofibromatosis, lymphoma, mesenteric masses or metastases (3). Proteus syndrome is caused by a germline mutation of the tumor suppressor gene PTEN, and is characterized by vascular malformations, lipomas, hyperpigmentation and cutaneous nevi (15). Some specific histopathological features of the fatty masses discriminate these lesions from the lipomas encountered in intestinal lipomatosis (5). Neurofibromatosis, lymphoma and metastases often comprise other more specific clinical features that help in the differential diagnosis. Conclusion Intestinal lipomatosis is a rare clinicopathological condition in which multiple lipomas are seen in the bowel wall. This condition is often detected as a consequence of mechanical complications, such as obstruction, intussusception or volvulus, but can also be discovered incidentally. CT is the imaging modality of choice to depict the complications and may contribute to the differential diagnosis since density measurements of the masses can demonstrate their lipomatous origin. References 1. Yakabe S., Muranaka T., Sumii T., Takeshita M., Yamashita T., Tsuruta S., Saku M.,Yoshida K.: Jejunal lipomatosis with diverticulosis: report of a case. Surg Today, 1998, 28: 846-849.

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38 2. Hoeffel C., Crema M.D., Belkacem A., Azizi L., Lewin M., Arrive L., Tubiana J.M.: Multi-detector row CT: spectrum of diseases involving the ileocecal area. Radiographics, 2006, 26: 1373-1390. 3. Chen Y.L., Huang T.Y., Chang W.C.: Lipomatosis of the small intestine. Clin Res Hepatol Gastroenterol, 2012, May 1, [Epub ahead of print]. 4. Hellström N.: Kasuistische Beiträge zur Kenntnis des Intestinallipoms. Dtsch Z Chir, 1906, 84: 488-511. 5. Liu X., Wilcox C.M., Nodit L., Lazenby A.J.: Multiple gastrointesti nal stromal tumors and lipomatosis. Arch Pathol Lab Med, 2008, 132: 18251829. 6. Mazziotti S., Salamone I., Vinci S., Pandolfo A.: Macrodactylia fibrolipomatosis associated with multiple small-bowel lipomas. AJR Am J Roentgenol, 2006, 186: 1195-1196.

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JBR–BTR, 2014, 97 (1) 7. Climie A.R., Wylin R.F.: Small-intestinal lipomatosis. Arch Pathol Lab Med, 1981, 105: 40-42. 8. Purohit V., Joshi R., Kalla A.R., Purohit R.C.: Colo-colic intussuscep tion due to intestinal lipomatosis. Indian J Gastroenterol, 2003, 22: 151152. 9. Tani T., Abe H., Tsukada H., Kodama M.: Lipomatosis of the ileum with volvulus: report of a case. Surg Today, 1998, 28: 640-642. 10. Ormson M.J., Stephens D.H., Carlson H.C.: CT recognition of intestinal lipomatosis. AJR Am J Roentgenol, 1985, 144: 313-314. 11. Kalund Jensen H., Knudsen N.: [Jejuno-ileal invagination caused by multiple lipomas]. Ugeskr Laeger, 1966, 128: 1347-1348. 12. Rivera Irigoin R., Fernandez Moreno N., Funez Liebana R., Medina Cano F., Navarro Sanchis E., Moreno

Mejia P.P., Garcia Fernandez G., Navarro Jarabo J.M., de Sola Earle C.M., Fernandez Perez F.J., Moreno Platero J.J., Sanchez Cantos A.: [Ileo-ileal and ileocecal invagination due to intestinal lipomatosis]. Gastroenterol Hepatol, 2003, 26: 482484. 13. Scotti M., Castrati G., Arrigoni G., Fiorone E.: [Intestinal invagination caused by multiple lipomas of the small intestine]. Minerva Chir, 1989, 44: 1405-1407. 14. Thompson W.M.: Imaging and findings of lipomas of the gastrointestinal tract. AJR Am J Roentgenol, 2005, 184: 1163-1171. 15. Vanhoenacker F.M., De Beuckeleer L.H., Deprettere A., De Moor A., De Schepper A.M.: Proteus syndrome: MRI characteristics of plantar cerebriform hyperplasia. Skeletal Radiol, 2000, 29: 101-103.

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The case of HNF-1β mutation with medullary cysts A. Bensouda Mourri1, M. Cassart1, M. Hall2, F.E. Avni3 We describe one case of long term post-natal follow-up of hyperechoic fetal kidneys related to HNF-1β mutation with cystic changes over a 9-year period in a female patient. This diagnosis was suspected on the basis of the renal US findings and was confirmed by complementary genetic examination. After birth, cortical cysts were detected and at the age of 4, medullary cysts were found, that disappeared with time. Currently our patient displays hyperechoic kidneys with only cortical cysts. This case report highlights the variability of US appearances in relation with HNF-1β genetic mutation. Key-words: Kidneys, cysts – Kidney, US.

The hepatocyte nuclear factor (HNF-1β), encoded by the transcription factor 2 gene (TCF2) which maps to the short arm of human chromosome 17, plays a role in the specific regulation of gene expression in various tissues such as the liver, kidney, intestine, genital organs and pancreatic islets and is involved in the embryonic development of these organs. The heterozygous mutations of TCF2 are known to be responsible for Maturity-Onset Diabetes of the Young type 5 (MODY 5) (1). MODY is a monogenic form of diabetes mellitus that is inherited as an autosomal dominant trait. The diabetes typically presents before the age of 25 and is not associated with ketosis or obesity. The diagnosis of TCF2 mutations is based essentially on molecular genetic testing and radiological findings. The prevalent genetic anomaly is the complete heterozygous deletion of the TCF2 (83%) (2). A family screening revealed de novo TCF2 anomalies in more than half of the patients. The kidney is the organ most affected by the TCF2 mutation. In analyzing the renal sonographic signs (with TCF2 mutations), it was noted a bilateral hyperechoic kidneys in 80% and cortical microcysts in 84% of patients with HNF-1β mutation (2). The aim of the present case report is to provide the evolution of US patterns observed in one patient over a 9 year-period. Case report AB was a healthy 29 year-old woman in her second pregnancy. Her first child did not have any health problem. AB had no significant past

Fig. 1. — 32 weeks gestation. Coronal ultrasound scan of both kidneys shows hyperchogenicity of cortex and enlarged kidney. Renal length is 50 mm (+2 SD).

medical history, was not taking any medication and there was no history of consanguinity. Regarding her family history, her cousin has a urinary reflux and her uncle has an undetermined moderate renal failure. Her husband was healthy with no significant past medical or family history. There is neither diabetes nor hypertension in the family. She was referred to our center from her local hospital for a detailed obstetrical US scan held at 23 weeks because an obstetrical ultrasonographic examination had shown some anomalies. When scanned in our center at a postmenstrual age of 32 weeks, the head and abdominal circumference and femur length measurements were appropriate for estimated gestational age. The kidneys are hyper-

From: 1. Department of Radiology, Université Libre de Bruxelles (ULB), Brussels, Belgium, 2. Department of Nephrology, Université Libre de Bruxelles (ULB), Brussels, Belgium, 3. Department of Radiology, Centre Hospitalier Régional Universitaire de Lille (CHRU-Lille), Lille, France. Address for correspondence: Dr A. Bensouda Mourri, M.D., Dept of Radiology, Institut Bordet (Université Libre de Bruxelles). Boulevard Waterloo 121, 1000 Brussels, Belgium. E-mail: abensoud@ulb.ac.be

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echoic and enlarged (the left kidney measured 50 mm and the right one with 52 mm, +2 standard deviations) and associated with a large bladder (Fig. 1). The amniotic fluid volume was within normal limits. No other fetal abnormalities were detected. Following these results, an MRI imaging examination was performed at 33 weeks for depicting small cystic lesions. No cysts were visualized. No specific diagnosis was proposed at this stage. Delivery occurred at term and the weight and size of the baby girl were normal. At birth, her Apgar score was 10/10/10, she had neither renal insufficiency nor hypertension. A renal ultrasound scan performed on day 7 and confirmed the prenatal findings of bilaterally enlarged (the left kidney with 52 mm and the right one with 58 mm, +2 standard deviations) hyperechoic kidneys but with small cysts were detected in the peripheral cortex of both kidneys (Fig. 2). A renal US scan at 2 months showed again enlarged kidneys measuring 56 mm for the left kidney and 58 for the right kidney in long

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Fig. 2. — 7-day-old. Transverse (A) and coronal (B) ultrasound scan show right kidney with cysts (arrows) in the peripheral cortex.

axis with cortical hyperechogenicity and increasing cortico-medullary differentiation. It also showed 2-3 small peripheral cortical cysts of 3 to 4 mm of diameter in both kidneys. There was no dilatation of pelvicalyceal system. Up to the age of 4 years, controls US were made during regular followup examinations. Ultrasound results were similar. The last US performed at age of 4 years revealed this time the cysts to be predominant by the medullary areas (Fig. 3). Throughout this period, she was healthy. The patient was further examined at the age of 9 years. The Biology and urinalysis were normal. Renal sonography revealed echogenic parenchyma and renal cysts of maximum 3 mm diameter within the cortex, the medullary cysts disappeared (Fig. 4). The bipolar diameter of the kidneys was 70 mm (normal for age). Genetic evaluation, performed at this time, showed the presence of a heterozygous deletion carrying the entire gene HNF-1β (exons 1-9).

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Fig. 3. — 4-year-old. Transverse ultrasound scans (A and B) show multiple cysts in the medullary areas (arrows).

Fig. 4. — 9-year old. Ultrasound scan in partial sagittal view shows two small cysts (arrows) in the cortex. No medullary cysts are found.

urther investigation is now being F carried among the rest of the family. Discussion Our case represents an example of hyperechoic fetal kidneys related to

HNF-1β mutation and the evolution of the US patterns over a 9 year period. Various types of renal cystic diseases are encountered in case of HNF-1β mutation; they include bilateral renal cysts, mainly detected after birth (which was the case of our

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patient), multicystic dysplastic kidney (MCDK), and glomerulocystic kidney disease under its hypoplastic form. In addition to the formation of cysts, other congenital renal anomalies have been described in association with HNF-1β mutation including oligomeganephronia, solitary kidney, renal hypoplasia/dysplasia, and horseshoe kidney (3). At histology the predominant cystic lesions are glomerular cysts, more rarely oligomeganephronia, associated with interstitial fibrosis. Recently, mutations of HNF-1β have been reported as the most frequent genetic abnormality detected in fetuses with bilateral hyperechoic kidneys (2). The mechanism by which HNF-1β might be involved in the development of hyperechoic kidneys is most probably related to the type of cysts associated with the mutation. Gresh et al. have shown in animal studies that HNF-1β controlled the expression of 3 genes expressed in tubular epithelial cells whose mutations resulted in cystic renal diseases: UMOD (leading to medullary cystic kidney diseases (MCKD)), PKHD-1 (autosomal recessive polycystic kidney diseases (ARPKD)), PKD-2 (autosomal dominant polycystic kidney diseases (ADPKD)) (4, 5). These genes all play a crucial role in cilium formation. Inactivation of HNF-1β leads to a decreased expression of these genes, thus reducing the number of proteins encoded, which normally inhibits growth through a calcium-dependent mechanism (6, 7), and thus leads to a malfunction of the primary ciliary structure leading to the formation of cysts. The multiplicity of cysts creates numerous interfaces leading to hyperechoic kidney. These results obtained on animal models suggest

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MEDULLARY CYSTS — MOURRI et al

that HNF-1β might be a major actor in kystogenesis. The present case gave us the opportunity to follow a HNF-1β case with cystic changes over a 9 year period. The US evolution of our case displays some typical as well as atypical features of HNF-1β mutation related cystic kidneys changes. The first stage in utero was the classical hyperechoic fetal kidney with normal cortico-medullary differentiation. The second stage after birth was the detection of cortical cysts. The third stage was the unusual detection of medullary cysts at age 4 that disappeared with time. These different patterns must be related to the anomalies induced by the mutation. In our clinical case, inactivation of HNF-1β could be responsible for a decrease in the expression of the gene UMOD and/ or PKD-2 and/or PKHD-1 which would then explain the presence of medullary cysts in addition to cortical cysts that were found in 84% of patients with HNF-1β mutation (2, 4, 5). Noteworthy, at each stage, there is a differential diagnosis. The most common differential diagnosis that might be suggested for the first stage is: autosomal recessive polycystic kidney diseases (ARPKD), autosomal dominant polycystic kidney diseases (ADPKD) and cystic dysplasia. With the emergence of cortical cysts, HNF1β mutation case must be included in the differential diagnosis of renal cysts in children as causes for glomerulocystic kidney disease (GCKD), autosomal dominant polycystic kidney diseases (ARPKD) and polymalformative syndrome (Zellweger syndrome). The unusual development of medullary cysts could raise the diagnosis ARPKD, nephronophtisis and medullary cystic dysplasia (8).

In conclusion, one US follow up highlights that different US patterns including medullary cysts can be present in a patient with a HNF-1β mutation. Therefore, it is very important to make a follow up to see the evolution of lesions and it is important to note that the presence of medullary cysts may occur at any time and should not exclude the diagnosis of HNF-1β mutation. References 1. Horikawa Y., Iwasaki N., Hara M., et al.: Mutation in hepatocyte nuclear factor-1 beta gene (TCF2) associated with MODY. Nat Genet, 1997, 17: 384385. 2. Decramer S., Parant O., Beaufils S., et al.: Anomalies of the TCF2 gene are the main cause of fetal bilateral hyperechogenic kidneys. J Am Soc Nephrol, 2007, 18: 923-933. 3. Bellanné-Chantelot C., Chauveau D., Gautier J.F., et al.: Clinical spectrum associated with hepatocyte nuclear factor-1 beta mutations. Ann Intern Med, 2004, 140: 510-7. 4. Gresh L., Fischer E., Reimann A., et al.: A transcriptional network in polycystic kidney disease. EMBO J, 2004, 23: 1657-1668. 5. Fischer E., Gresh L., Reimann A., Pontoglio M.: Cystic kidney diseases: learning from animal models. Nephrol Dial Transplant, 2004, 19: 2700-2702. 6. Watnick T., Germino G.: From cilia to cyst. Nat Genet, 2003, 34: 355-356. 7. Nauli S.M., Alenghat FJ., Luo Y., et al.: Polycystins 1 and 2 medaite mechanosensation in the primary cilium of kidney cells. Nat Genet, 2003, 33: 129-137. 8. Avni F.E., Garel G., Cassart M., D’Haene N., Hall M., Riccabona M.: Imaging and classification of congenital cystic renal diseases. AJR, 2012, 198: 1004-1013.

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JBR–BTR, 2014, 97: 42-43.

A rare case of diffuse alveolar hemorrhage following oral amphetamine intake N.F. Peters, R. Gosselin, K.L. Verstraete1 Diffuse alveolar hemorrhage (DAH) is a clinical syndrome, which refers to injury to the capillaries, arterioles and venules, leading to red blood cell accumulation in the distal air spaces. It is defined by the clinical triad of hemoptysis, anemia and progressive hypoxemia. Chest radiographs reveal non-specific patchy or diffuse bilateral pulmonary consolidation. Multiple conditions are associated with DAH, of which Wegener’s granulomatosis is the most frequent, and underlying disease determines the prognosis and treatment. This case describes DAH as a result of oral amphetamine abuse in a young patient of which the diagnosis was established by laboratory, clinical and radiologic findings. The patient experienced a rapid recovery without significant sequelae. Key-word: Drugs, abuse.

Case report A 20-year-old male patient was admitted to the emergency department because of aggressive behavior and respiratory depression with a short episode of apnea, after the administration of 20 mg of diazepam, during a Techno party. He reported the oral use of amphetamine (ecstasy). After admission there was an episode of hemoptysis and hema temesis. Arterial oxygen saturation dropped to 70%, without clinical repercussion. Clinical findings Lung auscultation showed discrete crepitation of the lower right lung. Laboratory findings were a mild leukocytosis and C-reactive protein increase. Chest radiograph (AP-view) (Fig. 1) shows a normal cardiac size and bilateral, predominantly perihilar, areas of increased opacity. High-resolution CT examination of the lungs (Fig. 2) revealed multi focal ground glass attenuation with areas of consolidation and discrete peribronchovascular thickening, here depicted on an axial image (A). A Reformatted image in the coronal plane (B) shows the diffuse extent in both lungs. There was a normal heart size and no presence of pleural effusion. Based on the clinical and CT findings the diagnosis of pulmonary hemorrhage was made. The presence of hemoptysis, hypoxemia, recent amphetamine use and rapid radiographic recovery supported the diagnosis.

Fig. 1. — Chest radiograph (AP-view) showing normal cardiac size and bilateral, predominantly perihilar, areas of increased opacity.

The patient was admitted and treated with oxygen administration and antibiotic therapy for the risk of aspiration pneumonia. The lung opacities cleared rapidly over the course of 48 h. Laboratory results tested positive on the use of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy). No other drug substances were found. Discussion Diffuse alveolar hemorrhage (DAH) is a clinicopathological syndrome describing the accumulation

From: 1. Department of Radiology, University Hospital Ghent, Ghent, Belgium. Address for correspondence: Dr N. Peters, M.D., Dienst Radiologies, UZ Gent, De Pintelaan 185, 9000 Gent, Belgium. E-mail : niels.peters@ugent.be

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of intra-alveolar red blood cells originating from the alveolar capillaries. The classical clinical triad includes hemoptysis, anemia and hypoxemia, which can be severe (1). On plain radiography DAH manifests as multifocal bilateral areas of increased opacity with a normal heart size. High-resolution CT shows multifocal ground-glass attenuation, which occasionally is centrilobular in distribution and associated with interlobular septal thickening. The differential diagnosis of these radiologic findings must be broad and include acute lung injury, diffuse infection, and noninfectious inflammatory conditions (e.g. pulmonary hemorrhage and acute hypersensitivity pneumonitis). Inhaled and intravenously abused drugs, including opiates and cocaine

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ORAL AMPHETAMINE INTAKE — PETERS et al

A Fig. 2. — High-resolution CT reveals multifocal ground glass attenuation with areas of consolidation and discrete peribronchovascular thickening (A). Reformatted image in the coronal plane (B) shows the diffuse extent in both lungs.

or crack, are known to cause acute lung injury (noncardiogenic pulmonary edema) and DAH. The mechanism by which the increased pulmonary capillary permeability occurs in acute lung injury is unclear, but is thought to be the consequence of a pulmonary endothelial abnormality (2). Diffuse alveolar hemorrhage and acute lung injury are radiographically indistinguishable. Because of this the development of respiratory failure with bilateral airspace consolidation that typically appear shortly after crack use and rapid recovery after the cessation of the responsible agent had been termed “crack lung”. Lung biopsy of this condition has revealed diffuse alveolar damage, alveolar hemorrhage, and interstitial and intra-alveolar inflammatory cell infiltration (3). During the past 2 decades, the acute toxic effects of MDMA have

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been widely investigated. Observational studies in humans and direct animal experiments had demonstrated typical acute toxic syndromes, including hyperthermia, hyponatremia, myocardial ischemia, intracerebral hemorrhage, acute hepatic failure and acute hallucinogenic psychosis (3). Although there are a few case reports of MDMA-related acute noncardiogenic pulmonary edema to be found in the literature (4), limited work has been done concerning the pulmonary toxic effects of MDMA. The mechanism causing noncardiogenic pulmonary edema due to abuse of amphetamines, a structurally similar material with MDMA, is still not clear but may be due to direct cellular toxicity as suggested by animal studies (4). To our knowledge there hasn’t been a single case report of MDMAinduced diffuse alveolar hemorrhage

after oral amphetamine intake published. Our patient provided us with an experience of uncomplicated DAH after the oral use of MDMA (ecstasy) that resolved under supportive care without significant sequelae. References 1. Lara A.R., Schwarz M.I.: Diffuse alveolar hemorrhage. Chest, 2010, 137: 1164-1171. 2. Gotway M.B., Marder S.R., Hank D.K., et al.: Thoracic complications of illicit drug use: an organ system approach. Radiographics, 2002, 22: S119S135. 3. Devlin R.J., Henry J.A.: Clinical review: major consequences of illicit drug consumption. Critical Care, 2008, 12: 202. 4. Chang S.H., Lai T.I., Chen W.J., et al.: MDMA-induced acute pulmonary edema in a patient without other organ dysfunction. Am J Emerg Med, 2006, 24: 734-736.

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IMAGES IN CLINICAL RADIOLOGY Drink responsibly! Rapid regression of fatty liver disease on enhanced CT after alcohol withdrawal T. Kirchgesner1, E. Danse1

A 50-year-old woman is admitted in Emergency Room for acute epigastric pain. She acknowledges the consumption of 6 to 7 beers per day last days before admission (8 to 10 alcohol units per day). Blood samples demonstrate inflammation (CRP: 5,2 mg/dL), hepatocytes cytolysis (AST 3 times higher than normal, ALT 2 times higher than normal and GGT 20 times higher than normal) and hyperlipasemia (15 times higher than normal). Diagnosis is obvious based on clinic and biology, which is confirmed the same day by an enhanced CT at portal venous phase demonstrating an acute pancreatitis graded D according to Balthazar scoring (Fig. A). After 9 days of hospitalization a follow up CT is performed in the exact same conditions (Fig. B). Comment

Admission CT shows deep fatty liver disease (FLD) characterized by a «dark liver» aspect because of fat infiltration. Follow up CT performed in the same conditions after 9 days of complete alcohol withdrawal demonstrates significative regression of FLD with liver density approaching spleen density and tending to normal. Liver densities are respectively 31 Hounsfield Units (HU) and 105 HU on B first and second CT while differences between liver and spleen densities are respectively -84 HU and -24 HU. Liver biopsy is the gold-standard exam for FLD diagnosis and quantification, but this technique is invasive with a morbidity rate of 1-3% and a mortality rate of 0,01-0,03%, so that medical imaging is in the front line to identify patients with steatosis and orientate them toward biopsy if necessary (1). On CT FLD is responsible of a “dark liver” aspect: without contrast liver density 10 HU lower than spleen density is highly suggestive of fatty infiltration (sensitivity of 84% and specificity of 99%) whereas at portal venous phase liver density 20 HU lower than spleen density has a sensitivity of 86-87% and a specificity of 75-87% for FLD diagnosis. At portal venous phase liver density inferior to 40 HU is also a good indicator of FLD. MRI is considered as the most performant imaging method to assess and quantify fatty liver infiltration: several protocols including in-phase/out-of-phase imaging, fat saturation imaging and magnetic resonance spectroscopy (MRS) are currently in use for both detection and quantification of FLD. Recently MRS that directly measures proton signals from the acyl groups in hepatocyte triglyceride stores has shown accuracy for diagnosing and quantifying FLD and may be replacing liver biopsy as the new gold standard (1). Ultrasonography is non irradiant, available and low cost compared to MRI. Whereas FLD is characterized by a «dark liver» aspect in CT, US demonstrates a «bright liver» with increased echogenicity compared to right kidney cortex. Recent studies demonstrated the possibility to quantify FLD with B-mode ultrasound and computer analysis, while others demonstrated the efficiency of methods based on transient elastography (Fibrosan®) to evaluate steatosis as fibrosis (1). ther hand This case demonstrates on one hand the reversibility of FLD if underlying cause is treated and on the o the possible rapidity of the regression process in less than ten days. We sincerely hope this report will encourage physicians to support abusive drinker patients to lower their alcoholic beverages c onsumption before irreversible damages occur. Reference 1. Machado M.V., Cortez-Pinto H.: Non-Invasive Diagnosis of Non-Alcoholic Fatty Liver Disease – A Critical Appraisal. J Hepatol, 2013, 58 (5): 1007-1019.

1. Department of Radiology, Cliniques Universitaires Saint-Luc, Brussels, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Bilateral elastofibroma dorsi: typical CT and MRI features G. Clinckemaillie1, A. Larbi2, P. Omoumi2, J. Manelfe3, B. Dallaudière2,4 An asymptomatic 57-year-old patient with a history of COPD was referred for a routine CT-scan of the chest. In addition to the changes caused by COPD, a bilateral soft-tissue lesion was observed deep to the inferior pole of both scapulas, just over the rib cage. The borders of the lesions were indistinct but the adjacent fat planes and bones were preserved. The lesions were heterogeneous presenting predominant areas of density similar to that of the adjacent muscles alternating with streaks of tissue with a fat density (Figure A). MRI better depicted these findings showing clearly an alternating pattern of fibrous tissue (arrows Figures B & C, respectively T1- and T2-Fat Sat) and fatty tissue (arrowheads Figure B). These observations are typical of an elastofibroma dorsi. Comment

Elastofibroma dorsi is a slow-growing, benign soft tissue lesion that nearly always occurs at the inferior pole of the scapula. Other sites have been described but are rare. It is considered a pseudotumor or a tumor-like lesion, with no malignant transformation, occurring after the 5th decade. Less than half of patients present with symptoms, which are usually mild and consist of physical discomfort when moving the shoulder. MRI is the imaging modality of choice as it beautifully shows the characteristic alternating pattern of fibrous and fatty tissue. The fibrous tissue is isointense relative to skeletal muscle on T1- and T2-weighted images, whereas the interspersed scattered or striated streaks of fatty tissue have a high signal intensity on T1-weighted images (arrowheads figure B). The margins may be sharp or indistinct. Size is variable with diameters that can exceed 5 cm. Post gadolinium enhancement is noncontributory, ranging from subtle to marked. In up to 60%, it is bilateral. In the right clinical setting, these findings are sufficient to make the diagnosis of an elasto fibroma dorsi without confirmation by biopsy. Excision may be offered to symptomatic patients, with curative marginal resection. A wait-and-see approach is appropriate in asymptomatic patients, as was the case in this patient. Reference 1. Malghem J., Baudrez V., Lecouvet F., et al.: Imaging study findings in elastofibroma dorsi. Joint Bone Spine, 2004, 71: 536-541.

image-clinckemaillie-.indd 1

1. Department of Radiology, Universitaire Ziekenhuizen Leuven, Leuven, Belgium, 2. Department of Radiology, Cliniques Universitaires St-Luc, Brussels, Belgium, 3. Department of Radiology, Hôpital Bichat – ClaudeBernard, Paris, France, 4. Université Paris Diderot, Paris, France.

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IMAGES IN CLINICAL RADIOLOGY Intraparenchymal meningioma in a child C. Werbrouck1, D. Florin2, B. Van Holsbeeck1, E. Laridon1, M. De Weweire3, J. Marrannes1

A 13-year old boy presented with loss of consciousness, and 2 episodes of generalized convulsions on a short period of 2 days. CT scan without intravenous contrast revealed a mild hyperdense lesion in the right temporal lobe. Intralesional calcifications and perilesional edema with a mass-effect on the right lateral ventricle were seen (Fig. A). MRI identified a heterogeneously hypointense mass on T2 weighted images (WI) and FLAIR in the right temporal lobe (Fig. B). The mass was well circumscribed, measuring approximately 15 x 18 x 34 mm in its greatest craniocaudal, transverse, and anteroposterior dimensions respectively. An edematous rim surrounded the lesion. Following intravenous contrast administration, vivid and homogeneous enhancement of the lesion was shown on T1 WI with fat suppression (Fig. C). Coronal and axial MR imaging revealed no dural attachment, the mass appeared to be located intraaxial (Fig. C). The mass showed no restriction on diffusion WI. Multiple susceptibility artefacts were identified on gradient echo WI, compatible with the calcifications seen on CT. Our differential diagnosis of this intraparenchymal temporal lobe mass with intralesional calcifications existed of ganglioglioma, gangliocytoma, or an atypical presentation of another tumor. The mass was resected and pathological examination revealed, to our surprise, a fibrous meningioma grade I. No other treatment was necessary. Comment

Meningiomas arise from meningiothelial cells that line the arachnoid membrane. The vast majority of the meningiomas are dural-based. These typical meningiomas are typical slightly hyperdense and may show calcifications on CT. MRI typically identifies a vivid and homogeneous enhancement, and an edematous rim. These classic findings were also seen in our patient, but on a very unusual location. In rare cases, meningiomas occur without dural attachment, arising from ectopic meningiothelial cells within the stroma of the choroid plexus, tela choroidea or the pia mater. Meningiomas without dural attachment can be classified into 5 types: intraventricular meningioma, pineal meningioma, deep sylvian meningioma, intra parenchymal or subcortical meningioma, and others. C Meningiomas of the pia-arachnoid arise from the stromal cells that surround the perforating blood vessels as they enter the surface of the brain. They will appear either within the Sylvian cistern or within the brain parenchyma. Meningiomas are uncommon in childhood, but intraparenchymal meningiomas occur more frequently in children than in adults. Preoperative diagnosis is difficult, considering the rarity and the similarity of imaging findings to other, more common intra-axial lesions. Total removal and a long follow up are necessary. Reference 1. Tekkök I.H., Cinel L., Zorludemir S.: Intraparenchymal meningioma. J Clin Neurosci, 2005, 12: 605-608.

1. Department of Radiology, Stedelijk Ziekenhuis Roeselare, Roeselare, Belgium, 2. Medical student, Catholic University Leuven, Leuven. 3. Department of Neurology, Stedelijk Ziekenhuis Roeselare, Roeselare, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Toothpick perforation of the caecum D. Nic´iforovic1,2, A. Spasic1, I. Turkalj1, F.M. Vanhoenacker3,4,5

A 61-year-old male was admitted to the Emergency department with a history of increasing abdominal pain for 7 days. On physical exam pain and tenderness in the right lower quadrant were evident while laboratory examination revealed slightly elevated neutrophil count. Abdominal ultrasound was unremarkable probably due to artifacts induced by gas in caecum. Subsequent CT showed a thin and pointy, foreign body in the caecum near the ileocaecal valve, which had perforated lateral wall of caecum and had thrusted into transverse abdominal muscle (Fig. A and B, arrow). The foreign body was 65 mm long, 2 mm thick, and its density was 100 HU. The lateral wall of caecum was thickened and there was edema of the transverse abdominal and internal oblique muscle and along with fatty peritoneal tissue on the trajectory of the foreign body (Fig. A and B, arrowheads). No signs of ascites and pneumoperitoneum were present. Surgery revealed a toothpick, which was pointed at both ends, traversing from caecal lumen through lateral caecal wall and peritoneum and thrusting into abdominal wall muscles. Right hemicolectomy with ileotransverse anastomosis was performed due to longstanding ischemic changes of the caecal wall. Comment

Usual places of a foreign body (FB) delay and obstruction are junction of second and third part of duodenum, ileocaecal region, vermiform appendix, the junction of caecum and ascending colon and flexures and haustrae of large intestine including rectal ampulla. Protective reaction of the small intestine to FB impaction is due to contractions of muscularis mucosa which form small concavity and firmness of intestinal wall on a place of contact with sharp end of the FB. This phenomenon along with peristaltic movements of the intestine and propulsion of its content enables FB to change angulations and start advancing through the intestine with the other end ahead. This protective contractile reaction is less constant in the large intestine. Angular insertion of ileum into the caecum and lower protective contractility compared to the small intestine make the caecum B prone to perforation caused by sharp objects, such as ingested toothpicks. A perforation of the gastrointestinal tract occurs in less than 1% of ingested FB. Toothpicks are involved in less than 0.1%. On ultrasound toothpick can be seen as hyperechoic formation, without reverberation artifact, usually with shadow artifact. CT is more sensitive than plain radiography in depicting of toothpicks. The most common signs of an ingested FB are segmental bowel wall thickening adjacent to localized extraluminal gas bubbles, infiltrated fatty tissue near thickened bowel wall and direct demonstration of FB. Toothpicks can be either hyper- or hypodense on CT, as they are usually made up of wood. Dry wood has high air content and therefore is hypodense, whereas fresh wood has higher water content and higher density. Free intra peritonal air is less common since the FB is gradually impacted and the perforation is locally covered with fibrin. Reference 1. Zissin R., Osadchy A., Gayer G.: Abdominal CT findings in small bowel perforation. Br J Radiol, 2009, 82: 162-171.

1. Centre of Radiology, Clinical Centre of Vojvodina, Novi Sad, Serbia, 2. University of Novi Sad, Medical Faculty, Novi Sad, Serbia, 3. Department of Radiology, AZ Sint-Maarten DuffelMechelen, Mechelen, 4. Department of Radiology, Antwerp University Hospital, Edegem, 5. University of Ghent, Faculty of medicine and Health sciences, Ghent.

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JBR–BTR, 2014, 97: 48.

IMAGES IN CLINICAL RADIOLOGY Epiphyseal «systemic» osteonecrosis of humeral head M. Kahloune, B. Dallaudière, P. Omoumi, B. Vande Berg, F. Lecouvet, A. Larbi1

A 47-year-old man presented to the Emergency department for a strong right shoulder pain with functional disability. This pain had evolved for a few weeks, without traumatic notion and in clear worsening in spite of regular taking of antalgics. The shoulder stump palpation woke the pain. The patient’s medical history included non-insulin-dependent diabetes, osteoporosis, and stomach ulcer. We also noted an important ethylic and smoking intoxication. A right shoulder radiography was performed (Fig. A) that showed osteonecrosis of the humeral head associating a wide heterogeneous change centered on the epiphysis encircled by a border sclera with an irregular aspect of subchondral bone and collapse of the head. The patient was sent to orthopaedic surgery consultation. CT-arthrography (Fig. B, C) showed a subchondral dissection with an osteo cartilaginous fragment (arrows) of practically 2 cms in the upper joint recessus but rest exceptionally attached to the humeral head. Comment

Avascular osteonecrosis (AVO) presents two variants: local or systemic. Local AVO is epiphyseal, usually caused by traumas or repeated microtraumas (as in the medial femoral condyle osteonecrosis and in vertebral osteonecrosis). Systemic AVO manifests as epiphyseal necrosis or a bone infarct (affecting B metaphysis and diaphysis; epiphyseal necrosis can be associated); the origin is multifactorial. The advanced mechanism is a vascular obliteration by microscopic emboli. Several etiologies were described in the systemic AVO : glucocorticoid therapy with high dose (> 0.5 mg/kg), alcohol abuse, organ transplantation, systemic lupus erythematosus, dyslipemia, decompression sickness, sickle cell anemia, antiphospholipid antibodies, Gaucher disease, HIV infection, and idiopathic shape (25% affecting especially males). Systemic osteonecrosis is generally detected 1-6 months after exposure to a risk factor. The starting point in epiphyseal necrosis is subchondral fracture outcome secondarily to collapse of necrotic fragment and mostly affects the femoral head, medial femoral condyle and humeral head. MRI is the most sensitive imaging technique for its early detection. MRI allows diagnosis a few days or few weeks after the beginning of the disorder. In epiphyseal necrosis, the interface between normal and necrotic bone is early and easily seen as an hypointense band in T1 weighted sequence corresponding to granulation tissue. MRI signal of necrotic bone is initially normal. At this stage, radiography or CT are often normal. At a more advanced C stage, the interface undergoes calcification and a sclerosis band is visible on radiography or CT. These two examinations present an undeniable diagnostic delay compared to MRI and radionuclide bone scan even if this last technique is non specific. At a later stage, necrosed fragment will be hypointense on all MRI sequences without enhancement and denser than normal bone in radiography or CT. Because of low biomechanical properties of necrotic fragment, it will present stress fractures with irreversible epiphyseal deformations. In our case, radiography allowed to establish e asily the diagnosis because of the late stage of AVO. This technique remains essential and allows to assess the sphericity of the humeral head and to look for arthritis. CT is a more sensitive technique than radiography to detect bone sclerosis and loss of trabecular pattern. By using multiplanar reconstructions, it also allows to look for a subchondral fracture or a flattening of the humeral head, sometimes difficult to see in radiography. Arthrography can be associated to CT to analyze the cartilaginous damage as in this case. It is necessary to underline the superiority of CT compared to MRI in bone subchondral dissection analysis. The main factors of bad prognosis are presence of radiography anomalies and a necrotic fragment size superior to 25% of humeral head (a size < 10% being considered as a factor of good prognosis). Our patient currently benefits from a conservative management. However, evolution of the AVO of proximal humeral epiphysis is known as very pejorative, mostly requiring a prosthetic replacement after several years of evolution, adapted to the degree of clinical tolerance, the evolution capacities and the possible necessity of an important use of the shoulder in everyday life. Reference 1. Lafforgue P.: Pathophysiology and natural history of avascular necrosis of bone. Joint Bone Spine, 2006, 73: 500-507.

1. Department of Radiology, Cliniques Universitaires St-Luc, Brussels, Belgium.

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ABSTRACTS OF PAPERS FOR FULL MEMBERSHIP BONE AND JOINTS MR imaging of the spine and sacroiliac joints in spondylarthropathy: tips, tricks and pitfalls M. Van Borsel, L. Jans, K. Verstraete1 Purpose: To translate the existing knowledge of MR imaging in spondylarthropathy into easy-to-use recommendations concerning imaging technique and image interpretation, applicable in daily clinical practice. Approach: A concise review of the current literature is presented, illustrated by images obtained from our own database. The results of a comprehensive retrospective study that was performed at our own institution is discussed, and the practical implications of these results are highlighted. Findings: According to the new classification criteria for axial spondylarthropathy developed by the “Assessment of SpondyloArthritis international Society (ASAS)”, MR imaging of the sacroiliac joints plays a huge role in the early diagnosis of spondylarthropathy. MRI may show active and structural lesions. Active changes include bone marrow oedema, enthesitis, synovitis and capsulitis. Structural changes include fat deposition, sclerosis, erosions and ankylosis. The presence of bone marrow oedema is a key feature for the diagnosis of sacroillitis at MR imaging. Other active changes and structural changes are suggestive but do not suffice for the definition of a positive MRI. MRI findings in sacroillitis have to be differentiated from findings that can have similar appearance but are non pathologic in nature. Coil artefacts can enhance the signal intensity at the posterior parts of the sacroiliac joints. Normal variants of the anatomy of the sacroiliac joint should not be confused with pathology. Normal vasculature in the sacroiliac joint has to be differentiated from small but relevant minimal bone marrow oedema. Non-inflammatory disease can mimic the inflammatory type back pain in patients suspected of spondylarthropathy. These entities have to be actively looked for on MRI of the sacroiliac joints and reported if present. A dedicated imaging protocol is mandatory to allow correct interpretation and diagnosis. For the spine, sagittal T1 and STIR images are the key sequences. For the sacroiliac joints, semicoronal T1 and STIR imaging is generally accepted as optimal imaging technique, but additional axial images of the pelvis are highly recommended, as they may demonstrate some anatomic variants and non-inflammatory changes that remain undetected if only semicoronal images are obtained. Conclusion: Imaging plays a key role for the diagnosis of spondylarthropathy. It is very important not to overdiagnose

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spondylarthropathy as its treatment may be potentially harmful. Therefore a dedicated imaging technique is necessary and radiologists should be familiar with the findings in spondylarthropathy, the differential diagnosis and pitfalls of findings both in the spine and the sacroiliac joints. Reference 1. Jans L., Van Praet L., Elewaut D., Van den Bosch F., Carron P., Jaremko J.L., Behaeghe M., Denis A., Huysse W., Lambrecht V., Verstraete K.: MRI of the SI joints commonly shows noninflammatory disease in patients clinically suspected of sacroiliitis. Eur J Radiol, 2013, Oct 16. pii: S0720048X(13)00530-5. doi: 10.1016/j. ejrad.2013.10.001. [Epub ahead of print] 1. Department of Radiology, University Hospital Gent, Ghent. Cone Beam Computed Tomography: technical aspects and clinical applications in musculoskeletal imaging E. De Smet1,2, G. De Praeter1, K. Verstraete3, F.M. Vanhoenacker1,2,3 Learning objectives: In the past decade, Cone Beam Computed Tomography (CBCT) has become the standard imaging modality in dental radiology due to its high spatial resolution and low radiation dose. On the contrary, musculoskeletal applications of CBCT are only scarcely reported, despite the major advantage of high spatial resolution when imaging small osseous structures. The purpose of this pictorial review is twofold: (1) to give a short review of technical aspects of CBCT (including radiation dose), and (2) to illustrate the additional value of CBCT in frequently encountered musculoskeletal pathologies. Materials and methods: The material is mainly culled from an ongoing comparative study between direct digital radiography of peripheral joints (elbow, wrist, hand-fingers, ankle, feet-toes and knees) and CBCT of patients referred for acute trauma. In addition, CBCT was done for patients presenting with non acute pain as additional method to plain films or MRI in order to obtain a more specific diagnosis. In all cases, informed consent was given by the patient and the study was approved by the ethical committee of our institution. During the period June 1, 2013-November 15, 2013, a total number of 289 musculoskeletal CBCT examinations were performed. Discussion: Technical aspects of CBCT: In CBCT, a cone-shaped ray beam makes a single

r otation around the patient and is projected on a flat panel detector (FPD), unlike conventional Multi Detector CT (MDCT) where a fan shaped beam and concave detector rotate in a helical fashion. The major advantage of CBCT is the high spatial resolution of the images, acquired at lower radiation doses than MDCT-studies. The disadvantages of CBCT include lower contrast resolution (i.e. soft tissue visualization) and a longer imaging time (susceptibility to movement artifacts). CBCT has also a limited field of view, allowing only small joints and bones to be examined. Clinical musculoskeletal applications: Because of its high spatial resolution, CBCT is a useful imaging modality for visualization of small osseous structures. In our series, CBCT adds valuable information in the diagnosis of acute and chronic (repetitive) trauma, inflammatory disease (e.g. gout, hydroxyapatite deposition, …), grading of osteoarthritis of small joints, detection and characterization of bone tumors in small bones, as well as the postoperative evaluation of osteosynthesis. Conclusions: CBCT provides high resolution images at a relative low radiation dose compared to conventional MDCT, and is therefore a useful modality to evaluate small bone and joint - pathology. Particularly, in the setting of acute trauma, CBCT may be useful to detect subtle or nondisplaced fractures, not visible on plain radiography. This may have important medico-legal implications, as it may have an impact on patient reassurance and management. 1. Department of Radiology, AZ SintMaarten Duffel-Mechelen, campus Duffel, Duffel, 2. Department of Radiology, University Hospital Antwerp, Edegem, 3. Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium. CHEST Dose is not only dose: understanding the consequences of decreasing radiation parameters F.C. Deprez1, A. Vlassenbroek², B. Ghaye1, Y. Nae, R. Raaijmakers, E. Coche1 The learning objectives of this presentation were to review the effects of lowering kVp and mA in MDCT acquisition on the x-rays attenuation of various materials and on patient dose, to understand the consequences of reducing radiation parameters on global image quality and worldwide-used abacus, i.e. the Agatston Calcium scoring method and to show alternative techniques of dose reduction in MDCT. To achieve this goal, we used an anthropomorphic cardio phantom (QRM, Germany), human cadavers and clinical data to demonstrate the effects of lowering

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50 the kVp or mAs, and iterative reconstructions on the measured CT Hounsfield unit (HU) numbers. As previously described, HU measurements of a structure are linked to the tube voltage (kVp), depending of atomic number (Z) of the structure. HU measurements are not linked to the tube current (mAs), but mAs will influence the noise value and the standard deviation (SD) of HU measurements. Consequently, CT examination with different kVp acquisitions should not be compared (e.g. bone metastasis comparison with different kVp protocols should not be misinterpreted as an evolving osteoblastic process) and a careful attention should be paid with universal protocol-independent density threshold (e.g. for urinary stone identification). For the same low-dose and in highly attenuating organs, the best image quality is obtained with the highest kVp acquisition, resulting in less noise, less photon starvation artifacts and less metallic artifacts (Fig. 1). Consequently, low-dose protocols should give priority to high kVp with ultra-low mAs (as far as possible) rather than low kVp. In practice, if the lowest tube current (mAs) that the CT scan can support is reached (i.e. 10 mAs on Brillance 256-Slice iCT), and if the dose can still be decreased with acceptable image quality (e.g. for pediatric examinations, thin patient or chest studies...), then tube voltage (kVp) can be decreased secondary. At present, limited ultra low mAs are available on modern MDCT units and the priority is given to perform low-kVp acquisition in order to reduce the radiation dose to the patient. In this way, CT manufacturers should be encouraged to develop ultra-low mAs (< 10 mAs) acquisition protocols. An interesting characteristic of lowkVp acquisition is to enhance iodine contrast compared with adjacent tissue (m =  80 kV(HU) /  140 kV (HU) → iodine: m = 1.9 > organic tissues: m ≈ 1) (Fig. 2). Modifying radiation parameters (kVp, mAs) may have consequences on automatic quantification software or worldwide-used abacus. For example, radiologists have to know that Agatston coronary calcium scoring (CCS) can only be performed with 120 kVp acquisition: whether it is correlated to CT density measurements, the Agatston CCS is a non linear function of the X-rays attenuation due to a multi-threshold measurement (with a step weighting function). Consequently the variation of the HU measured when lowering the kVp used during the CT acquisition could highly increase the CCS of a low density calcification, and in a practical way it cannot be corrected by the adaptation of Agatston thresholds as suggested by some authors. However, low-dose Agatston CCS can be obtained reducing tube current (mAs) with iterative reconstruction to reduce the noise. Indeed, noise level is an important parameter to obtain accurate automatic quantification. In this way, iterative reconstructions (IR) allow noise (SD) reduction and image quality improvement, without affecting HU measurement.

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JBR–BTR, 2014, 97 (1)

Fig. 1

Fig. 2 References 1. Deprez F.C., et al.: Dose is Not Only Dose: Understanding the Consequen ces of Decreasing Radiation Parameters. RSNA (2012) Education Exhibit, Physics Category. 2. Nagel H.D., et al.: Factors influencing patient dose in CT. In: Radiation Exposure in Computed Tomography. Fundamentals, Influencing Parameters, Dose Assessment, Optimisation, Scanner Data, Terminology. European Coordination Committee of the Radiological and Electromedical Industries. 3. Vlassenbroek A., et al.: CT radiation dose: Philips Perspective. In Tack D et al (2012) Radiation Dose from Multidetector CT, Medical Radiology. Diagnostic Imaging, Ed Springer, Verlag Berlin Heidelberg. DOI: 10.1007/174_ 2012_544. 1. Department of Medical Imaging, Cliniques Universitaires St-Luc, Brussels, Belgium, 2. CT Clinical Science, Philips HealthCare, Brussels, Belgium. PEDIATRIC RADIOLOGY Imaging in apophysitis and apophysiolysis L. De Clercq, C. Ernst, J. Demey1 Purpose: We reviewed the literature concerning the physiopathology and role of imaging in apophyseal lesions. We

present imaging cases with emphasis on ultrasound and MRI features of apophysitis of the lower limb. Results: Different sites of apophyses share the same physiopathology. During apophyseal maturation, the strong fibrous cartilage converts to a weaker columnar cartilage, responsible for apophyseal ossification. This makes the apophysis more prone to injury during maturation, especially in growth spurt. Apophysiolysis is an acute avulsion fracture of the apophysis due to a strong muscular contraction. Radiographic features are usually straight forward when ossification of the apophysis has already started. Apophysitis is an overuse injury or chronic inflammation of the apophysis and attached tendon, resulting from repetitive muscle contractions. Radiography in apophysitis is not specific and nonconclusive. The apophysis may appear normal, irregular, may show fragmentation, osteoporotic patches or sclerosis, with bony fragments in or near the attached tendon. However this can also be seen in asymptomatic children during normal apophyseal growth. Due to apophyseal enlargement, the ossified central part of an inflammed apophysis can mimick an avulsion fracture on radiographs. Ultrasound in apophysitis shows typical apophyseal cartilage swelling with hypervascularisation, tendon thickening or heterogeneity and ossification in or near the attached tendon.

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ABSTRACT OF PAPERS FOR FULL MEMBERSHIP

MRI in apophysitis shows morphologic and signal characteristics that allow precise and straightforward diagnosis. T1 sequences depict anatomical detail of the tendon and osseous fragments, apophysis enlargement at site of tendon insertion. Fluid sensitive sequences depict increased signal in the apophysis, periapophyseal bony and soft tissues. The apophysis and periapophyseal tissues enhance after IV contrast. Only discrete or absent physeal plate separation is seen in apophysitis. Most affected sites in the lower limb are the Achilles tendon on the calcaneum (Sever), distal patellar tendon on tibial tubercle (Osgood-Schlatter), proximal patellar tendon on inferior patellar pole (Sinding-Larsen-Johansson). In the pelvis overuse injuries of the the tendons at the iliac crest, anterior iliac spines, pubic ramus, ischial tubercle and trochanters give rise to apophyseal lesions. Less known is the apophysitis of the base of the 5th metatarsal or Iselin disease. Conclusion: Imaging in apophysitis, which is a chronic inflammation, is more complex than in apophysioloysis, which is an acute avulsion fracture. Imaging has

an important role in atypical clinical findings or abscence of recovery to guide proper management. In apophysitis radiographic imaging is nonspecific. Ultrasound and MRI are the best modalities to show apophyseal enlargement and inflammation of peri apophyseal bony and soft tissues. Ultrasound provides a more easy acces to evaluate the apophyses of the lower limb, even in the pelvis. It is important to become familiar with the normal and abnormal imaging features of apophyses in the growing child to recognize their pathology.

References 1. Arnaiz J.: Imaging findings of lower limb apophysitis. AJR, 2011, 196: W316-325. 2. Davis K.W.: Imaging pediatric sports injuries upper and lower extremity. Radiol Clin North Am, 2010, 48: 12131235. 3. Stevens M.A., El-Khoury G.Y., Kathol M.H., et al.: Imaging features

51 of avulsion injuries. Radiographics, 1999, 19: 655-672. Volpon J.B., et al.: Calcaneal apophysitis: a quantitative radiographic evaluation of the secondary ossification center. Arch Orthop Trauma Surg, 2002, 122: 338-341. Czyrny Z.: Osgood-Schlatter disease in ultrasound diagnostics – a pictorial essay. Med Ultrason, 2010, 4: 323335. Hirano A., et al.: Magnetic resonance imaging of Osgood-Schlatter disease: the course of the disease. Skeletal Radiol, 2002, 31: 334-342. Draghi F., et al.: Overload syndromes of the knee in adolescents: Sonographic findings. J Ultrasound, 2008, 11: 151-157. Vandervliet E.J., et al.: Sports-related acute and chronic avulsion injuries in children and adolescents with special emphasis on tennis. Br J Sports Med, 2007, 41: 827-831.

1. Department of Radiology, UZ Brussel, Brussels, Belgium.

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FORTHCOMING COURSES AND MEETINGS NATIONAL MEETINGS 14.03.14 BRS – Cardiovascular and Interventional Radiology Liège, CHR Citadelle Information: denis.henroteaux@chrcitadelle.be 25.03.14 BRS – Pediatric Radiology Brussels, HUDERF Information: catherine.christophe@huderf.be 10-11.05.14 6th SYMPOSIUM MAMMOGRAPHY Oostduinkerke Information: monika.philips@uzleuven.be

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ANNOUNCEMENT STUDY GRANTS OF THE BELGIAN SOCIETY OF RADIOLOGY

BOURSE DE LA SOCIETE ROYALE BELGE DE RADIOLOGIE

BEURS VAN DE KONINKLIJKE VERENIGING VOOR RADIOLOGIE

BELGISCHE

La Société Royale Belge de Radiologie met à la disposition de chacun des 7 centres universitaires de radiologie (KUL, RUG, UCL, VUB, UIA, UCL, ULB, ULg) une bourse d’un montant de 2975 €. Celle-ci est destinée à couvrir les frais de voyage d’étude d’un de ses membres ou à couvrir les frais d’un travail de recherche d’un de ses membres.

Door de BVR wordt een beurs ten bedrage van € 2975 ter beschikking gesteld aan elk van de 7 universitaire opleidingscentra voor radiologie. Deze zijn: KUL, RUG, VUB, UIA, UCL, ULB, ULg. Deze beurs zal dienen om ofwel de reiskosten te dekken van een studiereis uitgevoerd door één van haar leden ofwel om kosten voor research te dekken uitgevoerd door één van haar leden.

Règlement

Reglement

1. Sera prise en considération la candidature de tout docteur en médecine, accomplissant ou ayant accompli sa formation de spécialiste en radiodiagnostic dans une université belge ou un centre de stage non-universitaire y attaché. Le candidat doit être membre titulaire de la SBR.

1. Als kandidaat komt in aanmerking iedere arts of doctor in de genees-, heel- en verloskunde die een opleiding volgt of gevolgd heeft tot specialist in de radiologie aan één van de Belgische universiteiten met inbegrip van de hieraan verbonden niet-universitaire stagecentra. De kandidaat moet titulair lid zijn van de BVR.

2. a) Bourse de voyage :

2. a. Voor de reisbeurs:

Le candidat déposera un projet d’étude approuvé par le responsable du département de radiologie de son université. Si la formation s’effectue en tout ou en partie dans un centre de stage non-universitaire, la demande sera préalablement approuvée par le maître de stage ou encore par le responsable du département de radiologie de l’université ayant délivré au candidat son diplôme de docteur en médecine, chirurgie et accouchements.

de kandidaat legt een studieproject voor aan het bureau van de BVR dat door de titularis van de leerstoel radiologie van zijn universiteit is goedgekeurd. Ingeval de kandidaat een gedeeltelijke of volledige opleiding volgt in één van de niet-universitaire stagecentra dient zijn aanvraag goedgekeurd te worden door zijn stagemeester en de titularis radiologie van de universiteit waaraan het stagecentrum verbonden is of van de universiteit waar de kandidaat zijn einddiploma van doctor in genees-, heel- en verloskunde heeft gehaald.

b) Bourse de recherche :

b. Researchbeurs:

de kandidaat legt een researchproject voor aan het bureau van de BVR dat door de titularis van de leerstoel radiologie van zijn universiteit is goedgekeurd. Dit project dient welomschreven te zijn zowel naar inhoud als naar nodige werkingsmiddelen.

Le candidat déposera un projet de recherche approuvé par le titulaire de l’enseignement de radiologie de son université auprès du Bureau de la SBR. Ce projet structuré comprendra la description de la recherche ainsi que les moyens nécessaires.

3. a) Bourse de voyage :

Le choix se portera préférentiellement sur des projets d’études effectués lors d’un séjour d’environ deux mois dans un centre de radiologie étranger, dans le but d’acquérir ou de perfectionner une expérience particulière de l’une ou l’autre méthode d’investigation radiologique ou dans le but d’améliorer les connaissances du candidat dans l’un ou l’autre domaine de la radiologie.

3. a. Reisbeurs: als studieprojecten komen bij voorkeur in aanmerking: een verblijf van ongeveer 2 maanden in een buitenlands centrum voor radiologie met het oog op het verwerven of verdiepen van een bijzondere ervaring in één of andere radiologische onderzoeksmethode of met het oog op het verbeteren van de kennissen van de kandidaat in één of ander domein van de radiologie.

b) Bourse de recherche :

b. Researchbeurs:

Peut être pris en considération le projet s’inscrivant dans le domaine de la radiologie susceptible de représenter une contribution importante aux sciences radiologiques et qui est susceptible d’être publié dans une revue internationale à comité de lecture sélectif.

als project komt in aanmerking een welomschreven studie in één of ander domein van de radiologie waarvan mag verwacht worden dat ze een belangrijke bijdrage levert tot de radiologische wetenschap en dat ze zal leiden tot een publicatie in een reviewed tijdschrift.

4. Les demandes de bourse de voyage et de bourse de recherche seront soumises au Bureau de la SBR.

4. Zowel voor de reisbeurs als voor de researchbeurs dient het project voorgelegd te worden aan het bureau van de BVR.

5. a) Bourse de voyage :

5. a. Reisbeurs:

Endéans les cinq mois suivant la fin de stage à l’étranger, le lauréat de la bourse d’étude présentera un compte-rendu oral de son voyage d’étude au Bureau de la SBR.

Grants kopie.indd 54

binnen de 5 maanden na het beëindigen van de buitenlandse stage brengt de studiebeurslaureaat mondeling verslag uit bij het bureau van de BVR over zijn studiereis. De reisbeurslaureaat verbindt er zich toe een wetenschappelijke bijdrage met betrekking tot zijn project te publiceren in het JBR-BTR.

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b) Bourse de recherche : Dans l’année suivant l’attribution de la bourse, le candidat présentera un rapport auprès du Bureau de la SBR.

b. Researchbeurs:

binnen het jaar na het toekennen van de beurs brengt de kandidaat verslag uit bij het bureau van de BVR.

6. Les demandes doivent être introduites au 31 décembre de l’année en cours. Les candidatures seront adressées à l’un des Secrétaires Généraux de la SBR.

6. De periode tijdens dewelke de aanvragen kunnen ingediend worden en dienen toe te komen bij de Algemene Secretarissen loopt tot en met 31 december van het lopende jaar.

7. L’approbation du projet par le Bureau de la SBR sera notifié au candidat au plus tard quatre mois après la réception du projet.

7. Een beslissing over een ingediend project dient door het bureau van de BVR genomen te worden ten laatste binnende 4 maand na het indienen.

8. a) Bourse de voyage :

8. a. Reisbeurs:

La moitié du montant de la bourse sera versée avant la date du départ du boursier. Le solde sera libéré après présentation du compte-rendu de son séjour au Bureau de la SBR.

de helft van de studiebeurs zal uitbetaald worden voor het vertrek van de kandidaat. De overige helft wordt uitbetaald nadat de kandidaat verslag heeft uitgebracht bij het bureau.

b) Bourse de recherche :

b. Researchbeurs:

La moitié du montant de la bourse sera versée dès son attribution. Le reliquat sera versé après le rapport présenté auprès du Bureau.

de helft van de beurs zal uitbetaald worden bij het toekennen. De overige helft wordt uitbetaald nadat de kandidaat verslag heeft uitgebracht bij het bureau.

9. Le montant de la bourse sera versé au maître de stage, qui le mettra à la disposition du boursier.

9. De studiebeurs wordt uitbetaald aan het diensthoofd die het geld bezorgt aan de kandidaat.

BVR beurs voor Research in het buitenland / Bourse de la SBR pour la recherche à l’étranger and Beurs terugbetaling onkosten thesis / Bourse couvrant des frais de these See previous issues of JBR-BTR.

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– Opinion articles are special articles dealing with controversial topics of specific concern to radiologists. They may include tables and figures, and must provide a references list. – Letters to the Editor and their replies present objective and useful criticism over an article published in one of the lest four issues of the JBR-BTR. They will be published with the name and address of the author. References are necessary, tables and figures are accepted but acknowledgements are not appropriate. – Meeting news are reports of national or international congresses, symposia and meetings of radiology. Full references of the meeting, including date, place and summary of the main topics should be mentioned. Text should be kept to major facts. Figures, tables, refe rences and ac knowledgements should not be included. – In memoriams and News are essentially dealt with in the Editorial Office. Con tributions may however be submitted under the form of letters addressed to the Editorial Office which will check the adequacy of the information.

General Guidelines for Papers Manuscript Requirements Send 3 copies of the manuscript, including tables and figures (1 original set + 2 copies of the text and 2 original sets + 1 copy of the illustrations) and the corresponding diskette (see below Instructions for Electronic Manuscript Submission). In keeping with sound environmental and economic principles, the JBR-BTR encourages all authors to submit manuscripts printed on both sides of the page. The practice not only will save paper but also will reduce the price of postage required to mail the manuscript. Note that failure to provide an electronic version of manuscript will result in costs to be charged to the author. The original set should mention the personal references of the author. The copies should be nameless (including the figures). Each section of the manuscript begins on a new page in the following order: titre page running title page + key-words, abstract, text, acknowledgements, references, tables and captions for illustrations. Use English or one of the national languages. In the latter case, an English version of the titre, abstract, keywords, legends must necessarily be provided. Note that the author will be charged the costs of translation. Submitted manuscripts may not be covered by a previous copyright. The author will be held responsible for any litigation that might possebly ensue. Manuscripts will be submitted to a review Committee whose decision is final. Authors are usually notified within eight weeks as to the acceptability of their paper. Instructions for Electronic Manuscript Submission

Please send an electronic version of your manuscript either a floppy disk or a CD-rom in conjunction with the traditional paper version or separately as an e-mail with attachments to JBR-BTR@skynet.be. Please follow the general instructions on style/ arrangements and, in particular, the reference style as given in the present “Instructions to Authors”. Note, however, that while the paper version of the manuscript must be presented in the traditional double spaced format, the electronic version will be typeset and should not contain any extraneous instructions. For exemple: use hard carriage returns only at the end of paragraphs and display lines (e.g. titles, subheadings); do not use an extra hard return between paragraphs; do not use tabs or extra space at the start of a paragraph or for list entries; do not indent runover lines in refer ences; turn off line spacing; turn off

hyphenation and justification; do not specify pages breaks, page numbers, or headers; do not specify typeface. Care should be taken to correctly enter “one“ (1) and longer case “el“ (l), as well as “zero” (O) and capital “o“ (O). Illustrations and tables will be handled conventionally. However, figures and table legends should be included at the end of the electronic file. Nonstandard characters (Greek letters, mathematical symbols, etc.) should be coded consistently throughout the text. Please make a list of such characters and provide a listing of the codes used. Note that disks and CD-roms will not be returned to authors. Title – Keep it short and relevant. – Title must be followed by the surname(s) and first name(s) (for computer processing purposes, 2 initial letters only will be admitted) of all authors. – The position held by the authors, their academic degrees, the name of the institution to which they belong and/or from which the article originates and the name of the department Head (if required) must be indicated at the bottom of the first page. – The titIe in the national language of the text should be noted after the key-words. – A running title in English should be provided on a separate page. – Two copies of a blind titre page are included, giving only the titre (without the authors names) for use in the review process. Abstract and Key-words Written in English exclusively, the abstract should head the manuscript and summarize the aim, the methods, results and conclusions. It should not exceed 200 words for major papers and 100 words for the other studies. No abbreviation or references are used in the abstract. Three to six key-words from the terms used in the JBR-BTR Subject Index (and/or the most recent three-year cumulative index of Radiology) should be listed. Text The text should be clearly divided in the followingsections: introduction, material and methods, results, discussion and conclusion. Abbreviations should be defined in an ry note before being used as such. explanato The definitive text should be typed on one side only of a standard size (A4) typewriting paper, in doublespacing throughout and have at least 3 cm margins. The manuscript should not be longer than 16 typewritten pages, including references and summary for a major paper unless otherwise agreed by the Editor (one typewritten page is equivalent to approximately 250 words) and no longer than 6 typewritten pages for the other types of work. Specific guest editorials Specific guest editorials are invited papers written by selected distinguished specialists. They should summarize in concise the stase of the art in one specific field of medical imaging or related sciences in no more than 8 typewritten pages, including either 1 table or illustration (drawing or graph). The bibliography should not exceed 12-15 recent and/or fundamental references. References References should be numbered consecutively in the order in which they appear in the text. Their number should be kept down to 20 for major papers and 8 for case reports and other papers.

They should be given as follows: a) abridged titles of periodicals should conform to those in the Index Medicus. All authors are listed when six or fewer; when seven or more authors, the first three are listed, followed by “et al.”. Ex.: Bomsel F., Couchard M., Henry E.: Respiratory distress in the newborn. J Belge Radiol, 1980, 63: 89-107. b) in the case of books, references should indicate: the authors of the chapter, the title of the chapter, the title of the book, the editor(s), publisher, edition, city, year and specific pages. – Ex.: Isengrin P.: Radiologie stomacale. 3e édition, Arscia, Bruxelies, 1974, p. 22. – Ex.: Weinstein L., Swartz M.N.: Patho genic properties of invading micro organisms. In: Pathologic physiology: mechanisms of disease. Edited by Sodeman W.A. Jr, Sodeman W.A., Cds. Printed by Saunders, Philadelphia, 1974, pp. 457-472. Quote the name and address of the author to whom the reprints will be sent, at the end of the references. Corresponding author and Reprints The name and address of the corresponding author to should be mentioned affer the references. 25 reprints, are offered free by the JBR-BTR. Tables Tables should be presented on a separate page and numbered in Roman numerals in the order in which they are cited in the text. They should have an English title and legend. Abbreviations should be defined in a foot note. Only commonly admitted measurement standards should be used. Figures and Legends Illustrations should be restricted to the minimum required to show the essentiel features describ ed in the paper. They must be mentioned in the text. Two complete unmounted sets of original figures in labeled envelopes should be provided. All figure parts relating to one patient should have the same figure number. Use capital letters A, B, C, in the ieft longer corner to distinguish figures from one set. Figures should be marked on the back with an arabic numeral indicating the sequence in which they are to be referred to, with a lightly pencilled “top“ indicating their topside and the name of the first author. Never use ink on front or back of any figure. For uniformity purposes, points of interest should be showed on the figures with removable (Letraset) arrows or/and letters, or should be indicated on an accompanying photocopy of the figures, in order to enable our services to use their own characters. Images should be uniform in size and magnification. 1. Radiographs Cost and number: depending on the length of the manuscript (a total of 2 to 6 times 14 3 15 cm is availabie free of charge). Presentation: glossy prints, no larger than 18/24 cm. It is advisable for films to be centered on the zone of major interest and they should be grouped. Arrows should indicate the important points. 2. Photographs and drawings Four-colour illustrations will be printed at the expense of the authors. Drawing and graphs should be of professional quality. They should illustrate — not duplicate — data given in the text. Legends are typed separately and preceded by the number of the corresponding illustration. Note that illustrations will not be returned to authors.

(*) Pr J. PRINGOT, Avenue W. Churchill 11/30, B-1180 Bruxelles, Belgique (tél.: 02-374.25.55, fax: 02-374.96.28, e-mail: jbr-btr@skynet.be).

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GOLD SPONSOR

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The Belgian radiology journal wishes to thank Guerbet for their continuous support

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The Belgian radiology journal wishes to thank Philips for their continuous support

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The Belgian radiology journal wishes to thank GE for their continuous support

Editor: Professor J. PRINGOT, Koning Leopold III laan 20, B‑3001 HEVERLEE Membre de l’Union des Editeurs de la Presse Périodique Lid van de Unie van de Uitgevers van de Periodieke Pers Printed in Belgium by UNIVERSA PRESS, Honderdweg 24 ‑ B‑9230 Wetteren

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