JBR 2012-2 by office

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WETTEREN 1

P 702083

Volume 95 Page 61-122 March-April

Bimonthly

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2012

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

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

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

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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: Belgique Autres pays Envoi et port inclus.

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JBR-BTR ♦ 95/2 ♦ 2012 Journal Belge de ♦ Belgisch Tijdschrift voor ♦ RADIOLOGIE

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

The accessory spleen: prevalence and imaging findings in 1735 consecutuve patients examined by multidetector CT. T. Romer, W. Wiesner . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

US findings for chronic lateral epicondylitis. M. Obradov, P.G. Anderson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

A rare presentation of colonic duplication cyst: report of a case and review of the literature. K. Stefanidis, I. Lappas, Ch. Kolofousi, I. Kalogeropoulos . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Laryngopyocele. O. Lebecque, B. Coulier, V. Cloots . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Atypical presentation of a Langerhan’s cell histiocytosis of the forearm in a child. A. Rumy, A. Massez, C. Fricx, N. D’Haene, E.F. Avni, M. Cassart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Primary hyperparathyroidism presenting with bilateral slipped capital femur epiphysiolysis: a pictorial essay. T. De Beule, L. Ardies, Ph. Simons, P. Gillardin, P. Vanhoenacker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Heterotopic pancreas revealed by post-traumatic pancreatitis. F.C. Deprez, C. Pauls, B. Coulier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

A rare case of intradural spinal hydatid cyst in a paediatric patient. M. Ahmad, Ekramullah, I. Ahmas, S. Asmat Ali . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Unusual initial development of an esthesioneuroblastoma above the cribriform plate. G. Mazzamuto, P. Bosschaert . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Spontaneous transhepatic rupture of the gallbladder with massive hemoperitoneum. B. Coulier, Ph. Maldague, F. Pierard . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Post-contrast FLAIR imaging in a patient with posterior reversible encephalopathy syndrome (PRES). I. Celebi, M. Vural, B. Kahyaoglu, T. Guneysu . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

LETTER TO THE EDITOR Letter to the Editor: MDCT features of spontaneous pneumomediatinum by Macklin effect. G.C. Colin, F.C. Deprez, P. Bosschaert . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

IMAGES IN CLINICAL RADIOLOGY Pigmented villonodular synovitis of the ankle presenting as a persisting ankle effusion. C. Verlinden, F.M. Vanhoenacker, P. Boone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101 Heterotopic pancreatitis causing confusion in small bowel tumor. J. Joskin, L. Tselikas, N. Bleus, P. Meunier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 Sonographic findings of Meckel’s diveerticulitis. J. Samain, S. Maeyaert, E. Geusens, E. Mussen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 Supralabral air on plain radiography of the shoulder: first sign of an air-containing paralabral cyst. M. Demeter, Y. Vankan, A. Demeyere, D. Perdieus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104 Isolated splenic vein thrombosis. G. Karagiannis, A. Anagnostara, V. Samaras, S. Mylona . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105 Kohler’s disease of the patella. S.S. Suresh, M.S. Orth, M. Ch. Orth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106 Intracystic papilloma of the breast. M. Smets, C. Van Ongeval, A. Van Steen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 Bilateral intramuscular pseudotumor in a body-builder. L. Ardies, T. De Beule, T. Degroote, F.M. Vanhoenacker, P.K. Vanhoenacker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108 Amiodarone-induced pulmonary toxicity mimicking malignancy at initial presentation. M. Eyselbergs, I. Pilate, H. Rombouts, F.M. Vanhoenacker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109

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Proceedings of the Foot and Ankle meeting, Leiden, 25.03.2011 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110 News from the Universities: Prijs Pr Dr Em A.L. Baert 2011-2012 – Algemeen Reglement

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118

Forthcoming Courses and Meetings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 Grants of the RBRS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120 5th Senologic symposium, Oostduinkerke, june 2-3, 2012 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Classified services . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

91, 94

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

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

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Editor: J. Pringot

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

Managing Editor: P. Seynaeve

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

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

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

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

B. Op de Beeck, E. Danse

Bone and joints

P. Van Dyck, J.F. Nisolle

Breast imaging

C. Van der Merckt, A. Van Steen

Cardiac imaging

R. Salgado, O. Ghekière

Cardiovascular and interventional radiology

G. Maleux, M. Laureys

Chest radiology

B. Ghaye, W. De Wever

Head and neck radiology

J. Widelec, R. Hermans

Neuroradiology

P. Demaerel, N. Sadeghi

Pediatric radiology

B. Desprechins, L. Rausin

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

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

–

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

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

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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, references and acknowledgements should not be included. – In memoriams and News are essentially dealt with in the Editorial Office. Contributions 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, key-words, 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 references; turn off line spacing; turn off hyphen-

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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.: Pathogenic properties of invading microorganisms. 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 described 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 ⫻ 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.

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

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

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

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

Dynamische tomografie:

Onmiddellijk na een bolus injectie.

Vertraagde tomografie:

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

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

Imagerie dynamique

Immédiatement après l’injection en bolus

Imagerie retardée

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

Hersenen en ruggenmerg

Tot 60 minuten na toediening.

Système nerveux central

Jusqu’à 60 minutes après administration

MRA

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

ARM

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

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

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

www.bracco.com

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AD HEALTHCARE 4/2012_Opmaak 1 10/04/12 10:16 Pagina 1

The first time she touched his heart, she wasn’t wearing gloves. www.siemens.com/ultrasound

When Dr. Emily Chan walked into the operating room, she already knew what to expect—she had, after all, been following the progress of her patient’s mitral valve disease for years. Utilizing volumetric imaging and volume color Doppler quantification through eSie PISA™ volume analysis, Dr. Chan was able to confidently proceed with surgery for her patient’s asymptomatic mitral valve regurgitation. Measurements of the effective regurgitant orifice area,

regurgitant volumes, and regurgitant fractions made without 2D geometric assumptions provided the extra insight and assurance she needed to schedule the surgery. Siemens develops ultrasound solutions that provide vital information about the heart: detailed spatial resolution of intricate structures, real-time visualization of blood flow, and full-volume images made without stitching or gating. We pioneer ultrasound so that you can treat patients with confidence. Siemens. The Ultrasound Pioneers.

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Mastership 1 in detection,

delineation and characterization • about 50 % is eliminated via the renal pathway • about 50 % is eliminated via the biliary pathway.

Optimized Workflow of Liver MRI

• complete patient work up within 20–30 minutes in total • resulting in cost savings and higher patient throughput

NAME OF THE MEDICINAL PRODUCT Primovist 0.25 mmol/ml, solution for injection, pre-filled syringe QUALITATIVE AND QUANTITATIVE COMPOSITION Each ml contains 0.25 mmol gadoxetate disodium (Gd EOB DTPA disodium), equivalent to 181.43 mg gadoxetate disodium. 1 prefilled syringe with 5.0 ml contains 907 mg gadoxetate disodium, 1 prefilled syringe with 7.5 ml contains 1361 mg gadoxetate disodium, 1 prefilled syringe with 10.0 ml contains 1814 mg gadoxetate disodium. Contains 11.7 mg sodium/ ml. PHARMACEUTICAL FORM Solution for injection, prefilled syringe: Clear, colourless to pale yellow liquid free from visible particles. CLINICAL PARTICULARS Therapeutic indications Primovist is indicated for the detection of focal liver lesions and provides information on the character of lesions in T1-weighted magnetic resonance imaging (MRI). This medicinal product is for diagnostic use by intravenous administration only. Posology and method of administration Method of administration Primovist is a ready-to-use aqueous solution to be administered undiluted as an intravenous bolus injection at a flow rate of about 2 ml/sec. After the injection of the contrast medium the intravenous cannula/ line should be flushed using sterile 9 mg/ml (0.9 %) saline solution. Posology The recommended dose of Primovist is for Adults: 0.1 ml per kg body weight Primovist. Repeated use: No clinical information is available about repeated use of Primovist. Additional information on special populations Impaired renal function. Use of Primovist should be avoided in patients with severe renal impairment (GFR < 30 ml/min/1.73m2) and in patients in the perioperative liver transplantation period unless the diagnostic information is essential and not available with non-contrast enhanced MRI (see section 4.4). If use of Primovist cannot be avoided, the dose should not exceed 0.025 mmol/kg body weight. More than one dose should not be used during a scan. Because of the lack of information on repeated administration, Primovist injections should not be repeated unless the interval between injections is at least 7 days. Patients with hepatic impairment: No dosage adjustment is necessary. Paediatric population: The safety and efficacy of Primovist has not been established in patients under 18 years old. Therefore, use of Primovist in this patient group cannot be recommended. Elderly population (aged 65 years and above). No dosage adjustment is considered necessary. Caution should be exercised in elderly patients. Contraindications Hypersensitivity to the active substance or to any of the excipients. Undesirable effects Summary of the safety profile: The overall safety profile of Primovist is based on data from more than 1,900 patients in clinical trials, and from post-marketing surveillance. The most frequently observed adverse drug reactions (≥ 0.5 %) in patients receiving Primovist are nausea, headache, feeling hot, blood pressure increased, back pain and dizziness. The most serious adverse drug reaction in patients receiving Primovist is anaphylactoid shock. Delayed allergoid reactions (hours later up to several days) have been rarely observed. Most of the undesirable effects were transient and of mild to moderate intensity. Tabulated list of adverse reactions The adverse drug reactions observed with Primovist are represented in the table below. They are classified according to System Organ Class (MedDRA version 12.1). The most appropriate MedDRA term is used to describe a certain reaction and its synonyms and related conditions. Adverse drug reactions from clinical trials are classified according to their frequencies. Frequency groupings are defined according to the following convention: common: ≥ 1/100 to < 1/10; uncommon: ≥ 1/1,000 to < 1/100; rare: ≥ 1/10,000 to < 1/1,000. The adverse drug reactions identified only during post-marketing surveillance, and for which a frequency could not be estimated, are listed under ‘not known’. Within each frequency grouping, undesirable effects are presented in order of decreasing seriousness. Adverse drug reactions reported in clinical trials or during post-marketing surveillance in patients treated with Primovist System Organ Class (MedDra): Immune system disorders Not known Hypersensitivity /anaphylactoid reaction (e.g. shock*, hypotension, pharyngolaryngeal edema, urticaria, face edema, rhinitis, conjunctivitis, abdominal pain, hypoesthesia, sneezing, cough, pallor); System Organ Class (MedDra) Nervous system disorders; Common Headache Uncommon Vertigo, Dizziness, Dysgeusia, Paresthesia, Parosmia Rare Tremor, Akathisia Not known Restlessness System Organ Class (MedDra) Cardiac disorders Rare Bundle branch block, Palpitation Not known Tachycardia System Organ Class (MedDra) Vascular disorders Uncommon Blood pressure increased, Flushing System Organ Class (MedDra) Respiratory, thoracic and mediastinal disorders Uncommon Respiratory disorders, (Dyspnea*, Respiratory distress) System Organ Class (MedDra) Gastrointestinal disorders Common Nausea Uncommon Vomiting, Dry mouth Rare Oral discomfort Salivary hypersecretion System Organ Class (MedDra) Skin and subcutaneous tissue disorders Uncommon Rash Pruritus** Rare Maculopapular rash, Hyperhidrosis System Organ Class (MedDra) Musculoskeletal and connective tissue disorders Uncommon Back pain System Organ Class (MedDra) General disorders and administration site conditions Uncommon Chest pain, Injection site reactions, (various kinds)***, Feeling hot, Chills, Fatigue, Feeling abnormal Rare Discomfort Malaise * Life-threatening and/or fatal cases have been reported. These reports originated from post-marketing experience. **Pruritus (generalized pruritus, eye pruritus) ***Injection site reactions (various kinds) comprise the following terms: Injection site extravasation, injection site burning, injection site coldness, injection site irritation, injection site pain Description of selected adverse reactions Laboratory changes such as elevated serum iron, elevated bilirubin, increases in liver transaminases, decrease of hemoglobin, elevation of amylase, leucocyturia, hyperglycemia, elevated urine albumin, hyponatremia, elevated inorganic phosphate, decrease of serum protein, leucocytosis, hypokalemia, elevated LDH were reported in clinical trials. ECGs were regularly monitored during clinical studies and transient QT prolongation was observed in some patients without any associated adverse clinical events. Cases of nephrogenic systemic fibrosis (NSF) have been reported with other gadolinium-containing contrast agents. MARKETING AUTHORISATION HOLDER Bayer SA-NV J.E. Mommaertslaan 14, 1831 Diegem (Machelen) MARKETING AUTHORISATION NUMBER(S): Prefilled syringe 10ml BE281443 DATE OF REVISION OF THE TEXT 2011-09-28 DELIVERY: medical prescription L.BE.12.2011.0718 1 Hammerstingl et al. Diagnostic effi cacy of gadoxetic acid (Primovist)-enhanced MRI and spiral CT for a therapeutic strategy: comparison with intraoperative and histopathologic findings in focal liver lesions ; Eur Radiol 2008; 18:457–467

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We offer a full range of DR solutions, but only one level of image quality.

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Project1_Opmaak 1 8/03/12 09:14 Pagina 1

romer-wiesner_Opmaak 1 19/04/12 08:57 Pagina 61

JBR–BTR, 2012, 95: 61-65.

THE ACCESSORY SPLEEN: PREVALENCE AND IMAGING FINDINGS IN 1,735 CONSECUTIVE PATIENTS EXAMINED BY MULTIDETECTOR COMPUTED TOMOGRAPHY T. Romer, W. Wiesner1,2 Objective: To analyze the prevalence and CT findings of accessory spleens in the normal population. Material and methods: CT-examinations of 1735 consecutive patients, all examined by triple phase 16-row multidetector computed tomography (MDCT) of the abdomen, were retrospectively analyzed with special emphasis on the presence, location and imaging aspects of accessory spleens. Results: 199 patients showed an accessory spleen (11%). Size of accessory spleens ranged from 3 to 20 mm (mean 10 mm). In 60% the accessory spleen was located at the level of the splenic hilum and in 33% at the level of the lower pole. In 46% the accessory spleen was located medially and in 43% ventrally. 19 patients presented with two (1.1%) and seven patients with three accessory spleens (0.4%), respectively. One patient showed splenosis and one patient showed an enlarged accessory spleen (5 cm) secondary to a splenic apoplexy (i.e. hemorrhagic infarction) of the accessory spleen, caused by torsion. Conclusion: Accessory spleens may be identified by MDCT in about 11% of patients. Familiarity with normal imaging findings and knowledge on differential diagnoses, possible pathologies and potential pitfalls helps to differentiate from other findings in the upper abdomen. Key-words: Spleen, abnormalities.

Accessory spleens represent congenital variants of small isles of normally encapsulated splenic tissue with its own arterial and venous vascularisation and their prevalence seems to range between 10 and 20% (1-5). Accessory spleens do undergo the same pathophysiological mechanisms as the main spleen and, therefore, they may show all the potential lesions that may be observed in the main spleen, ranging from shrinking to swelling, from calcification to cyst or tumor formation and from haemorrhage to infarction. Most accessory spleens are located near the pancreatic tail and the splenic hilum and accurate identification of an accessory spleen may be important to avoid misinterpretation and differentiation from pathologic findings in the upper abdomen (6-8). The only study on accessory spleens – detected by CT – reported even a prevalence of 16% around ten years ago (9). However, this study was performed at the beginning of the era of multidetector computed tomography - using dual phase CT with a collimation of 8 mm for both, the unenhanced and the enhanced portal venous phase scans. Therefore, the present study was initiated with the intention to analyze if an increased spatial resolution by using triple phase MDCT with a slice

thickness of 3.75-5 mm would be able to detect more accessory spleens in the normal human population than reported in the literature until present. The present study addresses the CT-prevalence of accessory spleens in the normal population followed by a discussion of normal imaging findings, differential diagnoses and potential pitfalls that all may be helpful for their correct identification and differentiation from other findings in the upper abdomen. Material and methods 1735 consecutive patients, all examined over a time period of two years using 16-row MDCT (LightSpeed, GE, Milwaukee, USA) by triple phase CT (including unenhanced, arterial (35 sec.) and portalvenous phase (70 sec.) CT) were included into the study. Patients who have undergone splenectomy and patients with a potential reason for a splenic enlargement (liver cirrhosis, severe infection, sepsis, haematologic disorders etc.) were excluded from the study. All patients received positive oral contrast medium before CT (1 litre of Telebrix Gastro, orally taken over 1 hour, Guerbet, France). Triple phase MDCT was performed using 16-row MDCT. 100 ml of intravenous

From: 1. Department of Radiology, University Hospital Basel, Basel, Switzerland, 2. Institute for Diagnostic Radiology, Clinic Stephanshorn, St. Gallen, Switzerland. Address for correspondence: PD Dr. med. W. Wiesner, Clinic Stephanshorn, Brauerstrasse 95, 9016 St. Gallen, Switzerland.. E-mail: walter.wiesner@stephanshorn.ch

contrast material (Visipaque 320, GE Medical, Milwaukee, USA) was injected with a flow rate of 23 ml/sec. Arterial phase CT data acquisition started 35-40 seconds and portal-venous phase CT started 70-75 seconds after the intravenous administration of 100 ml of contrast material. CT parameters were as follows: Rotation time 0.8, helical thickness: 1.25 mm, pitch: 1.375:1, speed 27.5 mm, interval: 0.6 mm, KV 120, mAs (auto-mA): 400. Reconstructed slice thickness (and interval) was 5 mm for the unenhanced and the portal-venous phase images and 3.75 mm for the arterial phase images. Image analysis was performed on an integrated RIS/PACS work station (Centricity, GE Milwaukee, USA). All CT examinations were retrospectively analyzed by a radiologist, specialized in abdominal imaging on a double monitor work station of an integrated RIS/PACS System (Centricity, GE, Milwaukee) using both, slice after slice and cineviewing – technique in the axial plane, whereas multiplanar reconstructions were used only in selected and unclear cases. The reader was unaware of the reasons for the CT examination and of the clinical histories of the patients. Special emphasis was given on the presence, size, number and location, and if present, on visible pathologies of accessory spleens. The presence of an accessory spleen was confirmed only if it could be clearly depicted as a well circumscribed mass with similar attenuation and contrast enhancement as

romer-wiesner_Opmaak 1 19/04/12 08:57 Pagina 62

JBR–BTR, 2012, 95 (2)

Table I. — Location of accessory spleen. Location Upper pole dorsal ventral lateral medial Splenic hilum dorsal ventral lateral medial Lower pole dorsal ventral lateral medial

% 0.0% 3.5% 2.5% 0.0% 6.0% 2.5% 22.6% 1.5% 33.7% 60.3% 3.0% 17.1% 1.0% 12.6% 33.7%

Fig. 1. — Two accessory spleens (arrows) with a typical location near the splenic hilum.

the main spleen on all three phases. Two patients (one with splenosis following traumatic rupture of the spleen and one with apoplexy of his accessory spleen (i.e. haemorrhagic infarction due to torsion) were not excluded from the study according to the importance of the imaging findings, but they were excluded from the statistical analyses regarding number of accessory spleens and size, respectively. Results 199 patients (11.5%) showed at least one accessory spleen, which could clearly be depicted on all appropriate CT images, but usually was seen best on the thin collimated arterial phase CT. 19 patients had two accessory spleens (1.1%) and seven patients three accessory spleens (0.4%). 45,5% of the patients were male and 54,5% of the patients were female. Female patients showed accessory spleens in 11.7% and male patients in 11.2% of cases. The size of accessory spleens ranged from 3 mm to 20 mm (mean 10.3 mm) in female patients and from 3-24 mm (mean 9.8 mm) in male patients. In 60.3% of patients the accessory spleen was located near the splenic hilum and the pancreatic tail, and in 33.7% at the level of the splenic lower pole – usually ventrally (43.1%) and medially (46.4%) to the spleen, respectively, whereas only 6% of accessory spleens were found at the level of the upper pole (Table I, Fig. 1).

Fig. 2. — Multiple nodules spread within the peritoneal cavity in the left upper abdominal quadrant (arrows) in a patient with splenosis – mimicking nodular peritoneal carcinomatosis.

80% of the accessory spleens were round, whereas 20% showed a more oval shape. Attenuation and contrast enhancement paralleled the values of the normal spleen in all cases, in which the accessory spleen was larger than 5 mm, whereas accessory spleens measuring less than 5 mm usually seemed to show less enhancement than the spleen probably due to partial volume effects. One patient showed splenosis with multiple spleens throughout the entire abdomen, measuring between 1 mm and 20 mm and mainly located along the greater omentum (Fig. 2). Another patient showed a single, but enlarged accessory spleen, measuring 5 cm with inhomogeneous attenuation and

absence of contrast enhancement (despite the capsule) due to torsion and subsequent venous haemorrhagic infarction, (i.e. apoplexy of the accessory spleen) (Fig. 3). Discussion Accessory spleens may be found in up to 23.8% of golden hamsters (1), whereas their prevalence in the human seems to range between 10% to 20% as published by several studies based on anatomical and pathological examinations (2-5). However, the only publication that reported a prevalence of 20% was based on a quite small anatomical study including only 250 patients (6), whereas all other studies, and especially the largest and surely

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THE ACCESSORY SPLEEN — ROMER et al

Correct identification of an accessory spleen is also important in order to avoid misinterpretation of an accessory spleen for lymphadenopathy, a metastasis or an adrenal or renal tumor – and this is especially challenging when accessory spleens are found in an atypical locations – as for example in the pancreatic tail – where they may mimick a pancreatic neoplasm (1419). Such cases were not present in our study, but with modern CT- and MR-imaging this differentiation is usually possible nowadays.

Lesions and complications

B Fig. 3. — A. Large round lesion superior to the spleen with low attenuation. Except for some peripheral rim enhancement (arrow) the lesion does not enhance after contrast administration. B: Whirl sign (arrows), which shows torsion of the vessels supplying this mass and deriving from the splenic vasculature, confirms haemorrhagic infarction (i.e. apoplexy) of an accessory spleen.

most representative anatomical study, including 3000 patients (2), showed accessory spleens only in 311 cases – i.e. in around 10% of patients (2-5). Embryology and anatomy Accessory spleens are little islands of encapsulated splenic tissue with its own arterial and venous vascularisation and therefore they represent a kind of simple heterotopy. Accessory spleens develop during the fifth fetal week of life in the dorsal mesogastrium and move to the left upper abdomen due to the rotation of the stomach, finally fixed at this position by the gastrosplenic ligament ventrally and the splenorenal ligament dorsally (10, 11). Therefore, accessory spleens are usually located near the splenic hilum and close to the spleen, but sometimes they may be found also in the pancreatic tail, in the wall of

the stomach, the large bowel, the omentum, the mesentery and rarely even in the scrotum (6, 12, 13). Diagnosis and pitfalls An exact knowledge on the presence of an accessory spleen may be of great value – not only in cases in which splenectomy is necessary due to splenic rupture and where an accessory spleen should be preserved but also in cases of certain hematologic disorders, where all splenic tissue should be removed. Therefore, accessory spleens should be differentiated from other developmental anomalies such as splenic clefts and lobulations and one should be aware that sometimes venous collaterals in portal venous hypertension and rarely even aneurysms of the splenic artery may mimic accessory spleens at first sight, especially if only portal venous phase is acquired.

It is well known, that accessory spleens undergo the same pathophysiologic changes as the normal spleen: they may shrink in case of infarction, as for example in sickle cell disease and they may show a swelling, as for example in case of portal venous hypertension or in certain haematologic disorders causing splenomegaly (2, 7). This is especially evident after splenectomy - when the accessory spleen takes over the physiologic function of the main spleen, leading to an incredible enlargement of the accessory spleen, which may grow under these circumstances to a size of up to 7 cm although still keeping its original round shape (5, 20). Accessory spleens may show also the same focal lesions as the main spleeen – ranging from cyst or even tumour and abscess formation to rupture, haemorrhage and infarction (21-23). Although these findings are extremely rare according to the small size of accessory spleens, splenic apoplexy (i.e. haemorrhagic infarction of the accessory spleen) has occurred once in our series. Such apoplexy of an accessory spleen typically leads to unspecific subacute pain in the upper left abdominal quadrant and imaging findings consist of a mass with diffusely reduced and inhomogeneous attenuation and reduced or even absent contrast enhancement, which may be preserved only along the capsule (21-23). Although these imaging findings are not specific, identification of a "whirl sign" along the vessels leading to the lesion is almost pathognomonic for this rare condition (Fig. 3). Differential diagnoses A rare differential diagnosis of multiple spleens is splenosis, an acquired finding that was found

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once in our study population. Splenosis results from seeding and implantation (auto transplantation) of splenic tissue following splenic rupture, where the small and mostly multiple nodules, whose blood supply – unlike in an accessory spleen – derives from neovascularisation, may be found throughout the abdominal cavity - mostly adjacent to the greater omentum, the parietal peritoneum, the small bowel serosa or the diaphragm (24). Although these imaging findings may sometimes lead to a misdiagnosis according to the fact that they may mimic nodular peritoneal carcinomatosis knowledge about this entity, together with the patient’s history, usually allows one to make the correct diagnosis by CT (24). Another very rare differential diagnosis, that has to be differentiated from multiple accessory spleens is Polysplenia – in which up to 16 spleens may be found in the left upper abdomen – measuring from one to several centimeters each (25,26). Polysplenia is a congenital syndrome (synonyme: Isomerie, Ivemark-Syndrome, bilateral left sideness) in which various anatomical and especially cardiovascular anomalies are found in combination with a quite variable situs and which belongs to the same family of malformations as asplenia (i.e. bilateral right sideness) in which no splenic tissue at all will be found due to total agenesis of the spleen (27, 28).

JBR–BTR, 2012, 95 (2)

We did not use a slice thickness of 1 mm and we did not use a systematic postprocessing, which might be regarded as a certain limitation of our study, but although slice thickness was thinner (3.75-5 mm) in our study than in the study of Mortele (8 mm), and although all our patients were examined not only by dual phase but even by triple phase CT, we did not find more but less accessory spleens. One explanation for this discrepancy could be that this difference derives just from varying prevalences of accessory spleens in varying study populations or even from ethnic differences and although one might argue that we probably just missed some small accessory spleens in our study despite the fact that we used a higher resolution, it is obvious that our results are almost identical with the results of the most representative study ever, published by Halpert et al. who found 311 patients with accessory spleens among a total of 3,000 autopsies (2). Furthermore, there were no enlarged accessory spleens in our study according to our exclusion criteria which excluded patients with potential reasons for splenomegaly and, therefore, one might speculate about the varying number of very small accessory spleens that remained undetectable in the studies based on necropsies and also in our present study based on thin – slice MDCT – findings. Hypothesis

Prevalence and findings Accessory spleens seem to be quite common in the human population. They usually do not exceed a size of 25-30 mm and they typically are found mainly at the level of the middle third and the lower pole of the spleen located mostly medially or ventrally (3, 7, 8, 9). Accessory spleens may therefore be identified with a high accuracy by CT when a small round or oval mass is detected at the mentioned regions which shows an attenuation and an enhancement pattern similar to that of the spleen. Nevertheless, Mortele et al. investigated 1`000 patients by MDCT and they found accessory spleens in 16%, which stays in contrast to our results at first sight and especially to prior publications (9). Mortele et al. have therefore postulated that a thinner collimation at MDCT might probably lead to detection of even more accessory spleens – and this might even be right!

As explained in the beginning, accessory spleens undergo the same pathophysiological mechanisms as the main spleen and, therefore, they may show an enlargement in any situation that leads to splenomegaly. Certain authors have published an increased "incidence of accessory spleens" of up to 30% in patients with such haematologic disorders (5) and, although the term "incidence" is not appropriate in this setting (since accessory spleens are present or absent and since they never develop de novo!), these studies support the hypothesis, that even in the time of modern MDCT-scanning, probably more than 50% of all accessory spleens remain just undetectable during life due to their very small size as long as they are not forced to grow. Conclusion Even by using MDCT with a slice thickness of 3.75-5 mm accessory

spleens may be identified only in around 11% of patients during routine scans. Although it is obvious that such results will never be able to represent the real prevalence of all accessory splenic tissue in the human being, a detailed knowledge on the embryology and pathophysiology of this entity, together with its differential diagnoses and potential pitfalls will surely be helpful for a correct interpretation of this interesting, but statistically underestimated congenital condition. References 1. Yoon Y.S., Shin J.W., Park C.B., et al.: Morphological structure of accessory spleen in Chinese hamsters. J Vet Sci, 2000, 1: 73-75. 2. Halpert B., Gyorkey F.: Lesions observed in accessory spleens of 311 patients. Am J Clin Pathol, 1959, 32: 165-168. 3. Appel M.F., Bart J.B.: The surgical and hematologic significance of accessory spleens. Surg Gynecol Obstet, 1976, 143:, 191-192. 4. Curtis G.M., Movitz D.: The Surgical Significance of the Accessory Spleen. Ann Surg, 1946, 123: 276-298. 5. Olsen W.R., Beaudoin D.E.: Increased incidence of accessory spleens in hematologic disease. Arch Surg, 1969, 98: 762-763. 6. Wadham B.M., Adams P.B., Johnson M.A.: Incidence and location of accessory spleens. N Engl J Med, 1981, 304: 1111. 7. Hackl H.: Ueber Vorkommen und Entstehung von Nebenmilzen. Bruns Beitr Klin Chir, 1959,, 198: 128-138. 8. Barawi M., Bekal P., Gress F.: Accessory spleen: a potential cause of misdiagnosis at EUS. Gastrointest Endosc, 2000, 52: 769-772. 9. Mortelé K.J., Mortelé B., Silverman S.G.: CT features of the accessory spleen. AJR, 2004, 183: 1653-1657. 10. Varga I., Galfiova P., Adamkov M., et al.: Congenital anomalies of the spleen from an embryological point of view. Med Sci Monit, 2009, 15: 269276. 11. Walther M.M., Trulock T.S., Finnerty D.P., Woodard J.: Splenic gonadal fusion. Urology, 1988, 32: 521-524. 12. Altaf A.M.S., Sawatzky M., Ellsmere J., et al.: Laparoscopic accessory splenectomy: the value of perioperative localization studies. Surg Endosc, 2009, 23: 26752679. 13. Ungör B., Malas M.A., Sulak O., Albay S.: Development of spleen during the fetal period. Surg Radiol Anat, 2007, 29: 543-550. 14. Spencer L.A., Spizarny D.L., Williams T.R.: Imaging features of intrapancreatic accessory spleen. Br J Radiol, 2010, 83: 668-673.

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15. Meiler R., Dietl K., Novák K., Patzel C.: Intrapancreatic accessory spleen. Int Surg, 2010, 95: 183-187. 16. Schwartz T.L., Sterkel B.B., MeyerRochow G.Y., et al.: Accessory spleen masquerading as a pancreatic neoplasm. Am J Surg, 2009, 197: 61. 17. Schreiner A.M., Mansoor A., Faigel D.O., Morgan T.K.: Intrapancreatic accessory spleen: Mimic of pancreatic endocrine tumor diagnosed by endoscopic ultrasoundguided fine-needle aspiration biopsy. Diagn Cytopathol, 2008, 36: 262-265. 18. Meyer T., Maier M., Höller S., Fein M.: Intrapankreatische Nebenmilz als Differentialdiagnose des Pankreasschwanzkarzinomes. Zentralbl Chir, 2007, 132: 73-76. 19. Läuffer J.M., Baer H.U., Maurer C.A., Wagner M., Zimmermann A., Büchler M.W.: Intrapancreatic accessory spleen. A rare cause of a pancre-

THE ACCESSORY SPLEEN — ROMER et al

atic mass. Int J Pancreatol, 1999, 25: 65-68. Zwas S.T., Samra D., Samra Y., Sibber G.R.: Scintigraphic assessment of ectopic splenic tissue localization and function following splenectomy for trauma. Eur J Nucl Med, 1986, 12: 125-129. Impellizzeri P., Montalto A.S., Borruto F.A., et al.: Accessory spleen torsion: rare cause of acute abdomen in children and review of literature. J Pediatr Surg, 2009, 44: 15-18. Kim T.H., Kim J.K., Park M.J., Lee J.H.: Education and imaging. Hepatobiliary and pancreatic: torsion of an accessory spleen. J Gastroenterol Hepatol, 2009, 24: 1308. Pérez Fontán F.J., Soler R., Santos M., Facio I.: Accessory spleen torsion: US, CT and MR findings. Eur Radiol, 2001, 11: 509-512.

24. Tsitouridis I., Michaelides M., Sotiriadis C., Arvaniti M.: CT and MRI of intraperitoneal splenosis. Diagn Interv Radiol, 2010, 16: 145-149. 25. Maier M., Wiesner W., Mengiardi B.: Annular pancreas and agenesis of the dorsal pancreas in a patient with polysplenia syndrome. AJR, 2007, 188: 150-153. 26. Seo H., Jeon T.Y., Sim M.S., Kim S.: Polysplenia syndrome with preduodenal portal vein detected in adults. World J Gastroenterol, 2008, 14: 6418-6420. 27. Gayer G., Zissin R., Apter S., Atar E., Portnoy O., Itzchak Y.: CT findings in congenital anomalies of the spleen. Br J Radiol, 2001, 74: 767-772. 28. Mahlaoui N., Minard-Colin V., Picard C., et al.: Isolated Congenital Asplenia: A French Nationwide Retrospective Survey of, 20 Cases. J Pediatr, 2011, 158: 142-148.

20.

21.

22.

23.

5TH SENOLOGIC SYMPOSIUM Oostduinkerke, June 2 and 3, 2012. Venue: Holiday Centre “Ter Helme”, Kinderlaan 49-51, 8670 Oostduinkerke

Programme for radiologists Saturday June 2, 2012 8h00: Registration and welcome 8h35: Part I: Breast cancer: a national and international problem – chairwoman: C. Van Ongeval (UZ Leuven) 14h15: Part 2 (in collaboration with the Belgian Society of Senology): Breast changes and breast pathology during pregnancy and breast feeding – chairwoman: M. Van Goethem (UZ Antwerpen) 16h45-18h30: Practical part: digital reading (in groups) Sunday June 3, 2012 (in collaboration with the senology section of the Royal Belgian Radiological Society) Chairwoman: M. Mortier (UZ Gent) 9h00: Registration 9h30: Processing and evaluation from the radiologists’ point of view. C. Van Ongeval (UZ Leuven) 10h15: Breast density and cancer risk. A. Van Steen (UZ Leuven) 11h00-13h30: Digital mammography: is there a difference between CR and DR technique in diagnosis? Physicaltechnical: H. Bosmans (UZ Leuven) – Radiological: C. Van Ongeval (UZ Leuven) Cases presented by residents Follow-up of digital screening mammographies. A. Van Steen (UZ Leuven), M. Mortier (UZ Gent) Practical part: digital reading (in groups)

Programme for technologists (in Dutch only) Saturday June 2, 2012 8h00: Registration and welcome 8h30-11h30: see programme radiologists 11h30: Positioning – theory: A. Similon (UZ Leuven) 14h-16h: Start practical demonstrations: 4 groups 1. Positioning: A. Similon, D. Calvert (UZ Leuven) 2. Review of the mammographies (brought by the participants): K. Buelens (UZ Leuven) 3. Artefacts in mammography: A. Van Steen (UZ Leuven) 4. Execution and interpretation of the physical-technical analysis: H. Bosmans (UZ Leuven) For registration and information, please contact Ms. Monika Philips (monika.philips@uzleuven.be), secretariat of radiology, University Hospitals Leuven, Herestraat 49, 3000 Leuven (tel: 016/34.77.66)

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JBR–BTR, 2012, 95: 66-70.

ULTRA SONOGRAPHIC FINDINGS FOR CHRONIC LATERAL EPICONDYLITIS M. Obradov1, P.G. Anderson2 Purpose: To assess which individual gray-scale and color Doppler US findings and their combination are strongly associated with lateral epicondylitis. Also to determine whether chronic lateral epicondylitis is possible without any positive US findings. Methods: 49 patients (6 bilateral) underwent gray-scale ultrasonic imaging between 2005 to 2007. All had a history of lateral epicondylitis and had concordant pain during US probe compression in the common extensor region. Mean patient age was 47 (sd 7.7) years; M/F ratio 21/28; L/R ratio 17/32. Five symptom free volunteers (all bilateral) with a mean age of 36 (sd 8.7) years; M/F = 4/6; L/R = 5/5. Results: Neovascularity determined by color Doppler and four gray-scale US findings – a convex external contour, an erosive lateral epicondular cortex, internal calcifications, or a tear – have a specificity and PPV of 100% with conclusive likelihood ratios. However, only the sensitivity for neovascularity is above 50%. A combination of gray-scale and color Doppler shows a sensitivity between 92% to100%, a 90% specificity with a 98% PPV and a high likelihood ratio (9 to10). Conclusion: The combination of gray-scale and color Doppler changes is diagnostically superior to identify chronic lateral epicondylitis. Signs which confirm the diagnosis are a convex boundary, an erosive cortex, internal calcifications, a tear, and neovascularity. Patients with positive clinical signs and concordant pain but no US findings require further MRI evaluation. Key-words: Elbow, injuries – Extremities, US.

Lateral epicondylitis or tennis elbow is characterized by pain across the lateral epicondyle of the humerus that is aggravated by resisted dorsiflexion of the wrist or wrist supination against resistance (1). It is a self-limiting condition, often seen in athletes who engage in throwing sports and in tennis players. Treatment includes the conservative methods of rest, physical therapy, anti-inflammatory drugs, steroid injections, needling with or without steroid or autologous blood injection, and in the most refractory cases, surgery. Although the diagnosis is clinically based, ultra sonography (US) plays an important diagnostic role in chronic cases to asses the form, severity and location of the changes in epicondylitis and to exclude other possible causes of the lateral elbow pain. A US examination which includes both gray-scale and color Doppler US has been shown to have a 97% sensitivity and a 61% specificity (2), whereas for gray-scale changes alone these have been reported to be 72-88% and 36-100%, respectively; those for color Doppler alone are 95% and 88%, respectively (3, 4). Du Toit et al. recently concluded that lack of both neovascularity and gray-scale changes on US examination substantially increases

the probability that the condition is not present and should prompt the clinician to consider other causes for lateral elbow pain (2). A recent study by Noh et al., also reported that the induction of tenderness with a US probe at the site of tendon pathology increases the accuracy of US examination and rules out other causes of the chronic lateral elbow pain (5). This is important because differential diagnose of lateral elbow pain is broad and includes occult fracture, osteochondritis disseccans of the capitelum, osteoarthrosis, posterolateral rotatory instability, LUCL injury, lateral synovial plica, synovitis of the radiohumeral joint, and radial tunnel syndrome (6, 7). Purpose To evaluate the prevalence of US findings, including neovascularity determined by color Doppler, in a large group of patients with chronic lateral epicondylitis. The presence of induced pain by compression with a US probe in the region of the lateral epicondyle common extensor tendons was used as the gold standard for lateral epicondylitis. In addition, the possibility of a patient presenting with chronic lateral epicondylitis who had no gray-scale or color Doppler findings was determined.

From: 1. Department of Radiology, Sint Maartenskliniek Nijmegen, The Netherlands, 2. Experimental Psychologist, Researcher, Nijmegen, The Netherlands. Address for correspondence: Dr M. Obradov, M.D., Department of Radiology, Sint Maartenskliniek Nijmegen, the Netherlands, Hengstdal 3, Postbus 9011, 6500GM Nijmegen. E-mail:m.obradov@maartenskliniek.nl.

Material and methods Patients From June 2005 to March 2007 two experienced orthopedic surgeons, specialized in the upper limb, referred a total of 43 (6 bilateral) consecutive patients with chronic epicondilytis lateralis for US imaging, in total 17 left elbows and 32 right elbows. Cases were included in this historical cohort study if there had been at least a 6-month clinical history of epicondilytis lateralis with pain during a resisted dorsiflexion of the wrist or wrist supination against resistance, as well as concordant pain at the moment of imaging during compression with a US probe in the region of the lateral epicondyle/common extensor tendons. All had already received 6 months of conservative therapy consisting of rest, physical therapy, steroid injection or a brace, or a combination of these therapies. Patients who had had previous surgery related to lateral epicondylitis and patients who suffered from a systematic joint disease were excluded. In total 23 men and 20 women with a mean age of 47 (sd 7.7) years were included; for six patients both elbows were included. In addition, bilateral US was performed in 5 asymptomatic volunteers (two men, three women) with a mean age of 36 (sd 8.7) years. These volunteers were recruited from healthy hospital employees and had no history of elbow pain, no pain during resisted dorsiflexion of the wrist or wrist supination against

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ULTRA SONOGRAPHIC FINDINGS FOR CHRONIC LATERAL EPICONDYLITIS — OBRADOV et al

resistance and no concordant pain during compression with a US probe in the region of the lateral epicondyle/common extensor tendons. The internal review board approved this study. Imaging and interpretation All patients were examined by one of two experienced radiologists, each with at least 6 years of musculoskeletal US experience. A 5-12 MHz linear-array transducer (ATL 5000, Philips, The Netherlands) was used for all cases. The patient was in a sitting position, elbow in 90° flexion, wrist pronated with the underarm resting on the examination table. A standardized imaging protocol was used to image the area of the origin of the common extensor tendon up to the level of the radius head in longitudinal and transverse planes (Fig. 1). The patient’s clinical history and the clinical evaluation by the orthopedic surgeon and lateral epicondyle concordant pain during compression with a US probe were the reference standards. The symptoms included lateral elbow and forearm pain exacerbated by activities involving resistant wrist extension for at least 6 months during which the patient received conservative therapy; the tenderness of the lateral epicondyle at the common extensor origin did not abate. As a final check before the US examination, the radiologist identified the region of the common extensor tendon and compressed it with the US probe to see whether concordant pain was induced. Evaluation of the US images for each patient was performed retrospectively by each radiologist using a standardized scoring form; discrepancies were resolved by consensus. The following US findings were assessed: external border of the extensor tendon was defined as convex, neutral, or concave. The presence or absence of the following echological signs in either the extensor carpi radialis longus or the brevis was scored: focal hypoechoic area, tear, cortical bone irregularities, calcification which was classified as internal or external, and neovascularity. The evaluation of the US images for the volunteers was performed real time. It was therefore, possible to perform the tilting maneuver to eliminate anisotropy in longitudinal and transversal directions, twice for each direction with reposition of the probe in two angulations with

B Fig. 1. — Disappearance of hypoechogenic regions in the common extension tendons following the tilt maneuver. A is the longitudinal slice; 1: tilting proximally; 2: tilting distally. B is the transverse slice. 1: tilting medially; 2: tilting laterally.

approximately 90 degrees between them (Fig. 1). Statistical analyses To evaluate which individual grayscale changes are most strongly associated with the diagnosis of tennis elbow, the sensitivity, specificity, positive predictive value (PPV),and negative predictive value (NPV) were determined as well as the likelihood ratios obtained using these estimates. The same analyzes were conducted for the color Doppler finding and the combined US findings: gray scale and neovascularity. The images obtained from the ten healthy elbows were the controls. The 95% confidence intervals were calculated using the online program: www.causascientia.org/math_ stat/ProportionCI; the PPV and NPV as well as the likelihood ratios were calculated using the online program: www.medcalc3000.com/Bayesian Analysis. Because the patient images (static, digital images) had not been assessed in real time, these could not be corrected for anisotropy. Hence it can be expected that the number of patients assessed with a hypoechoic region will include a number of false positives. Therefore, for the combined US finding grayscale change and neovascularity two calculations were made: the first includes the hypoechoic region findings, the second excludes this possible gray-scale change. The first can be expected to be an estimation that is too high; the second can be expected to be the lower boundary.

Results As shown in Table I, each grayscale change was present in at least 7 affected elbows; the most prevalent change (hypoechoic regions) was found in 42 elbows. Only one elbow in the control group showed a positive US finding (external calcification). All 49 elbows had neovascularity and gray-scale changes when hypoechoic regions were included. However, when the hypoechoic regions were not included in the gray-scale changes because of the possibility of false positives due to anisotropy, there were 45 cases with positive combined findings. As shown in Table II, all measures show a high level of specificity. However only the combination of the grayscale changes with a positive color Doppler result for neovascularity has a high level of sensitivity. It was possible to indicate the extent of the possible overestimation on sensitivity and negative predictive value if the findings for focal hypoechoic regions are performed without correcting for anisotropy. The sensitivity for gray-scale changes drops about 15%; the change for the negative predictive value is more extreme: more than 30%. Discussion This study found that the combined US findings for gray-scale changes and neovascularity determined by color Doppler in patients with a clinical diagnosis of chronic lateral epicondylitis had a sensitivity of at least 92%, a specificity of 90%,

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JBR–BTR, 2012, 95 (2)

Table I. — The US findings for the patients with chronic lateral epicondylitis (n = 49) and the controls (n = 10) Ultra sonographic finding

Patients

Tear Erosive condylar cortex Convex external boundary Internal calcifications External calcifications Calcifications Hypoechoic regions Gray scale changes including hypoechoic regions Gray scale changes excluding hypoechoic regions Neovascularity Neovacularity and/or gray scale changes (including hypoechoic regions) Neovacularity and/or gray scale changes (excluding hypoechoic regions)

Volunteers

Present

Absent

Present

Absent

7 9 16 16 22 35 42 48 40 28 49

42 40 33 33 27 14 7 1 9 21 0

0 0 0 0 1 1 0 1 1 0 1

10 10 10 10 9 9 10 9 9 10 9

Table II. — Diagnostic evaluation, given as percentages, of the ultrasonographic findings present during examination with and without color Doppler. US findings

Sensitivity

Specificity

PPV

NPV

Positive LR

Negative LR

Tear

14 (8 to 27)

100 (72 to 100)

100 (63 to 100)

19 (11 to 32)

Infinity

0.86

Erosive condylar cortex

18 (10 to 11)

100 (72 to 100)

100 (69 to 100)

20 (11 to 33)

Infinity

0.82

Convex external boundary

33 (17 to 39)

100 (72 to 100)

100 (80 to 100)

23 (13 to 38)

Infinity

0.67

Internal calcifications

33 (21 to 47)

100 (72 to 100)

100 (80 to 100)

23 (13 to 34)

Infinity

0.67

External calcifications calcifications

45 (32 to 59) 71 (58 to 82)

90 (59 to 98) 90 (59 to 98)

96 (79 to 99) 97 (86 to 99)

25 (14 to 41) 39 (22 to 59)

4.49 7.14

0.61 0. 32

Focal hypoechoic regions

86 (73 to 93)

100 (72 to 100)

100 (100 to 100) 59 (36 to 78)

Infinity

0.14

Gray scale changes including hypoechoic regions

98 (89 to 100) 90 (59 to 98)

98 (89 to 100)

43 (59 to 98)

9.80

0.02

Gray scale changes excluding hypoechoic regions

82 (69 to 90)

90 (59 to 98)

98 (87 to 99)

50 (29 to 71)

8.16

0.20

Neovascularity

57 (43 to 70)

100 (72 to 100)

100 (96 to 100)

32 (19 to 50)

infinity

0.43

Neovascularity and/or gray scale changes including hypoechoic regions

100 (93 to 100) 90 (59 to 98)

98 (90 to 100)

100 (69 to 100)

10.00

0.00

98 (89 to 99)

69 (42 to 87)

9.180

0.091

Neovascularity and/or 92 (81 to 97) gray scale changes excluding hypoechoic regions

90 (59 to 98)

The 95% confidence interval is given in parentheses. LR, likelihood ratio; NPV, negative predictive value; PPV, positive predictive value.

a PPV of 98 % and a positive LR of at least 9 with a low negative likelihood ratio(0.09). The following individual US findings – a convex external contour, an erosive cortex of the lateral epicondyle, internal calcifications, a tear or neovascularity – had a specificity of 100%, PPV 100%, and a conclusive positive likelihood ratio. Unfortunately, the sensitivity for these four parameters is low; the

respective values for the affected elbows was 33%, 18%, 33%, and 14%. Thus individually these findings are not sufficient as a stand-alone diagnostic examination. Total sensitivity and specificity for the gray scale ultrasound varies in the literature between 72-88% and 36100% (3), respectively; in combination with power Doppler a sensitivity of 97% and specificity of 61% has

been found (2). In this study we found a gray scale sensitivity of 8298% and specificity of 90 %, PPV+ of 98-99%, with a positive LR 8-10% and in combination with color Doppler indicating a high accuracy. The lower values were calculated when hypoechoic reagions were not included in the gray-scale findings because of possible anisotropy, the higher values when they were

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included. In this study, more patients were included than in the Du Toit study (2), all the patients had been referred by experienced orthopedic surgeons specialized in the upper limb, and all patients had concordant pain induced by compression. Our study showed the absence of neovascularity in 21/49 symptomatic tendons, a proportion which is higher than in most other studies but comparable with the results found by Zanetti et al (8). Neovascularity had the highest sensitivity (57%) in the group of individual findings, with 100% specificity with a confidence interval of approximately Âą 10%. Presentation with neovascularity is a relatively specific US sign for a painful tendon (8). The literature reports a color Doppler sensitivity of 81-95% with a specificity of 9888% (3, 4) for tennis elbow while for painful patellar tendinopathy these values are 92% and 100%, respectively (2, 3, 4, 9) and for the Achilles tendon the respective values are 52% and 96% (5). Our study has a lower sensitivity and higher specificity for neovascularization than most other studies, but it is based on 49 patients while the other studies were based on fewer patients (ranging from 22-28) (3, 7, 10). In this study, calcification also has a relatively high sensitivity (71%) but only a 90% specificity. Superficial linear calcification at the origin of the ECRL has low specificity as it was demonstrated in 1 of the 10 volunteers. Our volunteer group had a mean age of 36 years compared to the mean age of 47 in the symptomatic group. It is reasonable to expect that in an older group more asymptomatic calcification may be presented at the origin of the ECRL. Furthermore, it has been reported that only 39% of all enthesophytes are symptomatic (11). In our study, the presence of a focal hypoechoic region had an 86% sensitivity with a 100% specificity. A sensitivity between 53% and 67% with a specificity between 81 to 89% has recently been published (3, 12). We do not think that previous treatment of the patients with corticosteriods has influenced our results since most animal studies indicate that intratendinous injection of corticosteroid results in collagen necrosis followed by a decrease in tensile strength of the tendons, no study shows correlation between those and eventual US findings. We suspect that the sensitivity we report is high because of the possibility of anisotropy in the patient

group compared to the volunteer group. As we retrospectively reviewed static, digital images, it is possible that the artifact anisotropy might be present for some symptomatic elbows. The extensor carpi radialis brevis tendons have an oblique course from depth to surface and are prone to anisotropy, which accounts for the well-known pitfall in US assessment for tendons. Therefore, we believe that the high sensitivity of hypoechoic region in our study is based on the fact that the US imaging for all symptomatic elbows had not been scored in real time. Based on the present study, it is unlikely that patients with chronic lateral epicondylitis would present without gray-scale or color Doppler findings. However, presentation with sonographic findings is not consistent and some can even be found in healthy volunteers. Although, Struijs et al found that gray scale sonographic findings had been identified and clinical diagnosis confirmed in only 75% of the imaged symptomatic patients (12), Du Toit et al. recently concluded that the lack of both neovascularity and gray scale changes on ultrasound examination substantially increases the probability that the condition is not present and should prompt the clinician to consider other causes for lateral elbow pain[9). Some other authors have found neovascularity at almost every symptomatic tendon Zeisg et al. 21/22 (10), Alfredson et al. 25/25 (13), Pederson et al. 9/20 (4). Although it is well known that in the acute phase of the disease, US changes can sometimes precede clinical symptoms of lateral epicondylitis, conversely, symptoms can sometimes proceed US changes (6, 12). Particularly for patients who are candidates for invasive therapy or operative treatment (chronic form), a low false positive rate is extremely important. The proposed combination neovascularity and gray-scale change is diagnostically superior to identify the chronic tennis elbow. For a clinician US is an important screening test. If the US is positive the patient should be planned for the therapeutic treatment of the lateral epicondylitis. If the US is negative the patient should be scheduled for the MRI arthrography of the wrist. Confirmation of the disease, and in the case of absence of US findings, the exclusion of other causes, is recommended before subjecting the patient to any sort of invasive therapy. The duration, sort, location,

extension and severity of abnormality determines the sort and extent of therapy, including a possible resection which should be based on the above mentioned ultrasound findings including the concordant pain during compression with a US probe as a gold standard. This study has limitations because the interpretation of the US findings in the patients was performed retrospectively. Each hypoechoic region seen on the static, digital images of a symptomatic elbow was interpreted as being positive while each hypoechoic region seen in the volunteers had been corrected for anisotropy. Consequently a part of those hypoechoic regions found in the symptomatic elbows can be explained as result of anisotropy. However, by calculating gray scale changes with and without hypoechoic regions we have been able to determine the range within which the gray scale changes should be corrected for anisotropy (a sensitivity between 83-98, both with a specificity of 90; a PPV of 98 with an NPV between 47-83). Our control sample was younger and on the small side, so that the PPV values are probably inflated. A further limitation is that sonoelastography was not included in the diagnostic work-up of the patients or the volunteers because at that time the machine did not have that function, making it not possible for us to further compare our results with those in the literature (14). In conclusion, a convex boundary of the extensor tendons, an erosive cortex of the lateral epicondyle, internal calcifications, a tear or neovascularity have a high diagnostic accuracy. If a patient shows one of these findings, one can confirm the diagnosis. However, the combination of gray scale and color Doppler changes is diagnostically superior to identify chronic lateral epicondylitis. Although absence of US findings in patients with positive clinical signs and concordant pain induced by US probe compression on the origin of the extensor tendons could indicate the absence of chronic lateral epicondylitis in acute cases (duration less than six months), it is wise to exclude other possible causes for the pain in the same region. Acknowledgment The authors thank Dr. Monique Reijnierse, Department of radiology, LUMC, Leiden, the Netherlands, for her participation in performing and evaluating the US examination.

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References 1. Cyriax J.H.: The pathology and treatment of tennis elbow. J Bone Joint Surg Am, 1936, 18 (4): 921-940. 2. Toit C., Stieler M., Saunders R., Bisset L., Vicenzino B.: Diagnostic accuracy of power Doppler ultrasound in patients with chronic tennis elbow. Br J Sport Med, 2008, 42: 572576. 3. Torp-Pedersen T., Torp-Pedersen S., Bliddal H.: Diagnostic Value of Ultrasonography in Epicondylitis. Ann Intern Med, 2002, 136 (10): 781. 4. Noh K.H., Moon Y.L., Jacir A.M., Kim K.H., Gorthi V.: Sonographic probe induced tenderness for lateral epicondylitis: an accurate technique to conform the location of the lesion. Knee Surg Sport Traumatol Arthrosc, 2010, DOI 10.1007/s00167-009-10371040. 5. Levin D., Nazarian L.N., Miller T.T., O’Kane P.L., Feld R.I., Parker L.,

10.

McShane J.M.: Lateral Epicondylitis of the Elbow: US findings. Radiology, 2005, 237: 230-234. Walz D.M., Newman J.S., Konin G.P., Ross G.: Epicondylitis: Pathogenesis, Imaging, and Treatment. RadioGraphics, 2010, 30: 167-184. Zanetti M., Metzdorf A., Kundert H.P., Zollinger H., Vienne P., Seifert B., Hodler J.: Achilles Tendons: Clinical Relevance of Neovascularization Diagnosed with Power Doppler US. Radiology, 2003, 227: 556-560. Breidahl W.H., Newman J.S., Taljanovic M.S., Adler R.S.: Power Doppler sonography in the assessment of musculoskeletal fluid collections. AJR, 1996, 1666: 1443-1446. Weinberg E.P., Adams M.J., Hollenberg G.M.: Technical Innovation: Color Doppler sonograpy of patellar tendinosis. AJR, 1988, 171: 743-744. Cornwall MW, McPoil TG: Plantar fasciitis: Etiology and Treatment. J Orthop Sports Phys Ther, 1999, 29, 12: 756-760.

11. Struijs P.A.A., Spruyt M., Assendelft W.J.J., Dijk van C.N.: The Predictive Value of Diagnostic Sonography for the Effectiveness of Conservative Treatment of Tennis Elbow. AJR, 2005, 185: 1113-1118. 12. Alfredson H., Ohberg L., Forsgren S.: Is vasculo-neural ingrowth the cause of pain in chronic Achilles tendinosis? An investigation using ultrasonography and colour Doppler, immunohistochemistry, and diagnostic injections. Knee Surg Sport Traumatol Arthrosc, 2003, 11: 334-338. 13. Zeisig E., Öhberg L., Alfredson H.: Extensor origin vascularity related to pain in patients with tennis elbow. Knee Surg Sport Traumatol Arthrosc, 2006, 14: 659-663. 14. Zordo de T., Lill S.R., Fink C., Feuchtner G.M., Jasckle W., BellmannWeiler R., Klauser A.S.: Real-time Sonoelastography of Lateral Epi condylitis: Comparison of Findings Between Patients and Healthy Volunteers. AJR, 2009, 193: 180-185.

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A RARE PRESENTATION OF COLONIC DUPLICATION CYST: REPORT OF A CASE AND REVIEW OF LITERATURE K. Stefanidis, I. Lappas, Ch. Kolofousi, I. Kalogeropoulos1 Duplication cyst is an uncommon congenital abnormality of the alimentary tract. It can occur anywhere in the alimentary tract with the ileum and the jejunum representing the most common sites of duplication. Most often the patients are asymptomatic and colonic duplication cysts remain undiagnosed for years. In this case report we present an unusual case of colonic duplication cyst with a transverse colon location. We present the radiological findings of this rare congenital malformation in order to be included in the differential diagnosis of cystic masses of the gastrointestinal tract. Key-word: Colon, abnormalities.

Duplication cyst is an extremely rare congenital malformation of the alimentary tract. It occurs most often in the ileum, accounting for over 60% of cases followed by the jejunum and the duodenum (1). The colon is the least common site of enteric duplication. In fact, in a review of 495 alimentary tract duplications only 7% of the duplications involved the colon (2). To our knowledge less than 100 cases have been described in the published literature (3). Case report We present an unusual case of colonic duplication cyst in a 45-yearold Caucasian man who presented to our hospital with lumbar pain. The patient had a medical history of constipation. On admission, the patient was afebrile. Physical examination revealed a large mass in the left upper quadrant with mild diffuse tenderness and no peritoneal signs. Blood laboratory tests were within normal limits. An initial plain X-ray was performed with no abnormal findings. Ultrasonography was insignificant due to gas filled bowels. After the first inconclusive radiological exams, a contrast Barium Enema study was decided to be performed. Barium Enema showed a large air-filled tubular structure in the left upper quadrant containing an air-fluid level (Fig. 1). The same cystic structure was partially filled with contrast due to communication with the transverse colon at the splenic flexure. The shape of the cystic structure changed with peristalsis and the position of the patient

Fig. 1. — Abdominal X-ray following the contrast barium enema study in upright position. It shows a large structure (white arrows) with contrast due to communication with the transverse colon with air-fluid level (black arrows).

(Fig. 2). At the same examination the gastric antrum was recognized as a smaller air-filled structure adjacent to the same tubular structure. Furthermore, Computed Tomography (CT) of the abdomen with

From: 1. Radiological Department, Evangelismos Hospital, Athens, Greece. Address for correspondence: Dr K. Stefanidis, M.D., Radiological Department, Evangelismos Hospital, Ipsilantou 45-47, 10676, Athens, Greece. E-mail: kostef77@gmail.com

oral contrast material was performed. It demonstrated a large airfilled 14 × 7 cm structure containing oral contrast in the left upper quadrant (Fig. 3). CT confirmed the findings of contrast Barium Enema study and a possible diagnosis of colonic duplication of the transverse common was concluded. A surgical intervention was decided in order to prevent complications of the colonic duplication cyst. At operation, the cyst was excised with a segment of

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Fig. 3. — Computed Tomography of the abdomen demonstrating the cystic structure (arrows) containing an air-fluid level.

Fig. 2. — Abdominal X-ray following the contrast Barium Enema study in supine position demonstrates the change of the shape of the cystic air-filled structure (arrowheads).

transverse colon and a colocolostomy was performed (Fig. 4). The duplication cyst was attached to the transverse colon with the presence of a small communication with the colonic lumen. Post-operative recovery was uneventful.

Fig. 4. — Surgical specimen including part of the transverse colon with the duplication.

Discussion Enteric duplications cysts are uncommon congenital malformations (4). They are usually discovered in infancy and childhood, but they may be discovered at any period of life. They occur anywhere along the length of the alimentary tract on the mesenteric side. The location at the transverse colon is extremely rare (2). Their walls may contain all of the normal bowel layers, including the mucosa, submucosa and muscularis. They may appear as cystic or tubular malformations. While duplication cysts typically do not communicate with the adjacent bowel lumen, tubular lesions, which usually arise near the colon, may communicate. Most colonic duplication cysts are asymptomatic and remain undiagnosed for years (5). If symptomatic, they manifest obstruction, bleeding,

infection or constipation (3, 6-9). In one race case of combined duplication of the colon and vermiform appendix, it was presented with hydronephrotic atrophy of the kidney (10). Also patients can present a variety of non-specific signs and symptoms like abdominal pain. Resection of the duplication cyst and the adjacent bowel is recommended because of the possibility of malignant changes and the risk of gastrointestinal ulceration and haemorrhage due to ectopic gastric mucosa (11). To avoid any future complications, cyst resection is indicated even in the asymptomatic patient (12-14). The diagnosis of a duplication cyst is difficult to be made clinically. Radiological studies play an important role in the detection and diagnosis of the duplication cysts. Plain film

radiography may be normal or may show a soft tissue mass with/without displacement of adjacent bowel or evidence of intestinal obstruction. Ultrasound is particularly well suited for the identification and characterization of duplication cysts, although in our case it was inconclusive (1516). Contrast examinations of the gastrointestinal tract can be useful in order to demonstrate displaced loops of bowel surrounding the presumed cyst and depict the communication with the gastrointestinal tract (17). In our case the use of contrast in the Barium Enema study revealed the origin of the cystic structure and depicted the communication with the transverse colon. In difficult cases which require a multiplanar approach to delineate the relationship between the cystic and peripheral structures, CT and MRI

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may be helpful. However, the contribution of sonography, CT and MRI has to be developed, in order to help radiologists to suggest such a disorder in their daily practise. In summary, colonic duplication share an extremely variable clinical presentation. The differential diagnosis of a cystic abdominal mass should always include enteric duplication, especially when associated with intestinal symptoms.

References 1. Pulingandla P.S., Nguyen L.T., StVil D., et al.: Gastrointestinal duplications. J Pediatr Surg, 2003, 38: 740744. 2. Stringer M.D., Spitz L., Abel R., et al.: Management of alimentary tract duplication in children. Br J Surg, 1995, 82: 74-78. 3. Fotiadis C., Genetzakis M., Papandreou I., Misiakos M.P., Agapitos E., Zografos G.C.: Colonic duplication in adults: report of two cases presenting with rectal bleeding.

8. 9. 10.

World J Gastroenterol, 2005, 11: 50725074. Macpherson R.I.: Gastrointestinal duplications: clinical, pathologic, etiologic, and radiologic considerations. Radiographics, 1993, 13: 1063-1080. Favara B.E., Franciosi R.A., Akers D.R.: Enteric duplications: thirty-seven cases – a vascular theory of pathogenesis. Am J Dis Child, 1971, 122: 501-506. Kekez T., Augustin G., Hrstic I., et al.: Colonic duplication in an adult who presented with chronic constipation attributed to hypothyroidism. World J Gastroenterol, 2008, 14: 644-646. Otter M.I., Marks C.G., Cook M.G.: An unusual presentation of intestinal duplication with a literature review. Dig Dis Sci, 1996, 41: 627-629. Van Elst F., Hubens A.: Duplication of the colon in the adult. Acta Chir Belg, 1978, 77: 335-342. Bremer J.L.: Diverticula and duplications of the intestinal tract. Arch Pathol, 1944, 38: 132-140. Kabay S., Yucel M., Yaylak F., et al.: Combined duplication of the colon and vermiform appendix in an adult patient. World J Gastroenterol, 2008, 14: 641-643.

11. Horie H., Iwasaki I., Takahashi H.: Carcinoid in a gastrointestinal duplication. J Pediatr Surg, 1986, 21: 902904. 12. Kim Y.W., Kim J., Lee K.Y., Kim N.K., Cho C.H.: Asymptomatic tubular duplication of the transverse colon in an adult. Yonsei Med J, 2005, 46: 189191. 13. Holcomb G.W., Gheissari A., O’Neill J.A. Jr.: Surgical management of alimentary tract duplications. Ann Surg, 1989, 209: 167-174. 14. Cavar S., Bogovic M., Luetic T., Antabak A., Batinica S.: Intestinal duplications – experience in 6 cases. Eur Surg Res, 2006, 38: 329-332. 15. Kangarloo H., Sample W.F., Hasen G., Robinson J.S., Sarti D.: Ultrasonic evaluation of abdominal gastrointestinal tract duplication in children. Radiology, 1979, 131: 191-194. 16. Hayden C.K. Jr. Ultrasonography of the gastrointestinal tract in infants and children. Abdom Imag, 1996, 21: 9-20. 17. Rathi V., Singh S., Bhargava S.K., Kaur N., Seth N.: Diagnosis of tubular colonic duplication by barium followthrough study. Australas Radiol, 2005, 49: 157-159.

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LARYNGOPYOCELE O. Lebecque, B. Coulier, V. Cloots1 An apparently healthy 31-year-old man presented with dysphonia. Laryngoscopy revealed a mass at the right side of epiglottis. He underwent a CT examination after intravenous injection of a iodinated contrast agent and this showed the presence of a paralaryngeal mass with rim enhancement. The diagnosis of laryngopyocele was made. Treatment consisted of endoscopic laser surgery, confirming the diagnosis and resolving the symptomatology. Key-word: Larynx, CT.

First described by Larrey in 1827, then by Virchow in 1867, simple laryngocele is an air-filled dilation of the saccule of the laryngeal ventricle, situated between the false and true vocal cords. While the saccule normally measures 5 to 15 mms, laryngocele will reach few centimeters. It is called laryngomucocele when fluid-filled. If infected and filled with pus, it is a laryngopyocele. Here is a case investigated by computed tomography after laryngoscopy showed submucosal swelling. Case report A 31-year-old man consulted his physician, complaining only about dysphonia. He reports singing from time to time and no other increasing intraglottic pressure factor. A laryngoscopy was performed first, revealing a smooth-surfaced mass at the right side of epiglottis, pushing to the left both epiglottis and glottic structures. Our patient went through a subsequent computed tomography with IV contrast which revealed a thin walled fluid-filled low density mass, with rim enhancement (Fig. 1). It was situated in the infra epiglottic para glottic place, pushing the thyrohoid membrane although not protruding through. The diagnosis of laryngopyocele was made. Original 3-D reconstructions and virtual endoscopy were performed (Fig. 2). He went through endoscopic laser surgery and complains no more. The fluid contained in the laryngocele was pus, confirming pyolaryngocele diagnosis. Since surgery was performed, patient's wife reports his husband is no more snoring.

Fig. 1. — CT Scan contrast enhanced, coronal view shows low density mass, with rim enhancement (arrow).

Fig. 2. — 3-D CT scan reconstructions. Left picture, 3-D overview: white square showing the laryngopyocele (upper middle shade is hyoid bone and lower middle shade is crico-thyroid cartilage). Right picture, virtual endoscopy: black square shows submucosal swelling, right sided.

Discussion According to the site of extension of the saccule, laryngocele can be

From: 1. Department of Radiology, Saint Luc Hospital, Bouge, Belgium. Address for correspondence: Dr O. Lebecque, M.D., Department of Radiology, Saint Luc Hospital, Rue Saint Luc 8, B-5004 Bouge, Belgium. E-mail: Olivier.lebecque@gmail.com

classified as internal, external or mixed type. Internal laryngocele is confined within the larynx, extending above the thyroid cartilage without piercing the thyrohyoid membrane. It extends postero superiorly into the aryepiglottic fold and false vocal folds. External laryngocele extends outside the thyrohyoid membrane to the neck, through what is believed to be a weak point caused by the opening for laryngeal nerves

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Fig. 3. — Left sided diagram shows normal larynx anatomy. Right sided diagram shows both internal (INT) and external (EXT) laryngocele. [Inspired from: Case of the month: What a blow. Br J Radiol, 1998, 71, 799-800].

Fig. 4. — CT scan contrast enhanced. Left picture, axial view showing a mixed laryngocele: an air-filled dilation of the saccule of the left Morgani's ventricle with virtual wall, protruding through the thyrohyoid membrane. Right picture, coronal view showing a laryngomucocele (arrow): a low density mass, with no rim enhancement.

and vessels (uncommonly, a case where the site of penetration was postero superior to the neurovascular bundle has been reported, 1) (Fig. 3). Mixed laryngocele is a combination of both internal and external forms. Laryngocele is more common in men after the 5th decade and in Caucasian population. It is more commonly acquired than congenital. Chronic increased intralaryngeal pressure may predispose to a laryngocele (for example: singers, glassblowers, chronic cough, wind instrument players, ...) (3, 4). 80-85% are unilateral with equal frequency between right and left sides (1, 2, 3). Of them, 20 to 40% are internal, 4050% are combined, and 20-30% are strictly external (2, 3, 5). Symptoms may include cough, hoarseness, dyspnea, inspiratory stridor, dysphagia, sore throat (2, 3).

The external and combined laryngocele can present as a swelling in the neck at the level of the hyoid bone, anterior to the sternocleidomastoid muscle. It may increase during a Valsalva's manoeuvre and shrink on palpation. In contrast to a saccular cyst for example, simple laryngocele maintains its communication with the laryngeal lumen. As a matter of fact, the lining of laryngocele contains mucous glands. If mucus does not collect, laryngocele will be an air filled dilation (Fig. 4, left picture). While a laryngeal mucocele is a fluid-filled laryngocele resulting from proliferation of mucous glands when duct is obstructed. Filled with low density mucus, we also talk about "laryngomucocele" (Fig. 4, right picture). If infection occurred (an estimated 8% of laryngoceles become infected (6, 8)), it may fill

with pus. They are then referred as pyolaryngocele and can be a vital emergency. Ventricular appendix is one of the entities to be considered in the differential diagnosis (11). When airfilled, this normal structure may mimic a small laryngocele but it does not lead to submucosal deformation. Depending on his location, an abscess (peripherally enhancing mass with central low density) can simulate a pyolaryngocele but would usually be surrounded with more inflammatory changes. Regarding cysts, the primary concern will be to define their location. Submucosal cysts are superficial structures protruding into airways and derived from submucosal glands. Their location is variable. Thyroglossal duct cysts are located on the midline, adjacent to midportion of hyoid bone and typically extralaryngeal. Second branchial cleft cysts are posterior to submandibular gland, at the angle of mandible and have no connection with the larynx. Finally, lying anterior to epiglottis and typically displacing it posteriorly, vallecular cysts (more common in children) are another possibility. Laryngoscopy is performed to search for evidence of an occult tumour and a guided biopsy is certainly justified at the entrance of the saccule (2). In a previous study, 17% of the cases of a laryngocele had an associated malignancy (3). That is the reason why patients should undergo laryngoscopy and biopsy (10). Surgery is treatment of choice. Internal laryngocele can be excised endoscopically with the use of a laser. External or combined laryngoceles are usually approached externally, through the neck (but for the 10 last years, some authors have

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published cases of endoscopic laser excision of combined laryngoceles (2)). Conclusion A standard radiography may have shown a soft tissue density projecting against air column in supraglottic region. Otherwise, it would have shown an air pocket in upper neck soft tissues with or without an associated fluid level. Ultrasound should be used in the initial evaluation of neck masses, to differentiate between fluid filled lesions and solid lesions (3, 7). Computed tomography scan of the neck – especially coronal reconstructed images – is needed to define the anatomy and nature of the defect. It will characterize and demonstrate very precisely anatomical extent of the lesion (7, 8). Only the laryngopyocele demonstrated peripheral rim enhancement on contrast CT and a thickening of the wall (6, 7). CT-Scan is also necessary to look for evidence of an occult tumour: incidence of laryngoceles in laryngeal carcinoma patients is

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higher than in the normal population (4). MRI with superior soft tissue resolution, may be alternative, also showing the laryngocele and any associated tumour (10). Not considering MRI's costs and poor availability, the excellent spatial resolution of a multi slice CTScan combined with coronal reconstructions, make contrast enhanced computed tomography an excellent imaging tool (11). References 1. Ingrams D., Hein D., Marks N.: Laryngocele: an anatomical variant. J Laryngol Otol, 1999, 113: 675-677. 2. Verret D.J., DeFatta R.J., Sinard R.: Imaging case study of the month: Combined Laryngocele. Ann Otol Rhinol Laryngol, 2004, 113: 594-596. 3. van Vierzen P.B., Joosten F.B., Manni J.J.: Sonographic, MR and CT findings in a large laryngocele: a case report. Eur J Radiol, 1994, 18: 45-47. 4. Akbas Y., Unal M., Pata Y.S.: Asymptomatic bilateral mixed-type laryngocele and laryngeal carcinoma. Eur Arch Otorhinolaryngol, 2004, 261: 307-309.

5. Swartz J.D., D'Angelo A.J., Harnsberger H.R., Zwillenberg S., Marlowe F.I.: The laryngeal mucocele: Imaging analysis of a rare lesion. Clin Imag, 1990, 14: 110-115. 6. Nazaroglu H., Ozates M., Uyar A., Deger E., Simsek M.: Laryngopyocele: signs on computed tomography. Eur J Radiol, 2000, 33: 6365. 7. Morgan N.J., Emberton P.: CT scanning and laryngocoeles. J Laryngol Otol, 1994, 108: 266-268. 8. Essaadi M., Raji A., Detsouli M., Kadiri F., Laraqui N.Z., Touhami M., Moukrim B., Chekkoury-Idrissi A., Benchakroun Y.: A propos d'une pathologie rare du larynx: la pyolaryngocèle. Rev Laryngol Otol Rhinol, 1995, 116 (5): 351-353. 9. Alvi A., Weissman J., Myssiorek D., Narula S., Myers E.N.: Computed tomographic and magnetic resonance imaging characteritics of laryngocele and its variants. Am J Otolaryngol, 1998, 19: 251-256. 10. Kumar G., Bradley P.J., Wastie M.L.: Case of the month: What a blow. Br J Radiol, 1998, 71: 799-800. 11. Harnsberger R., et al.: Diagnostic Imaging Head and Neck. Elsevier Saunders, III-3.6-9.

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ATYPICAL PRESENTATION OF A LANGERHAN’S CELL HISTIOCYTOSIS OF THE FOREARM IN A CHILD A. Rumy1, A. Massez2, C. Fricx3, N. D’Haene4, E.F. Avni1, M. Cassart2 We report a case of a 2-year-old child presenting with right forearm pain. Based on imaging analysis, the initial diagnosis was osteomyelitis but the final diagnosis demonstrated by histology was Eosinophilic Granuloma (EG) of the forearm. We detail the rare radiological presentation of such a lesion, the various clinical presentations and the work-up advised in this context. Key-words: Infants, skeletal system – Histiocytosis.

Eosinophilic granuloma is a solitary, non-neoplastic proliferation of Langerhan’s cell (LC). It was first described by Paul Langerhans in 1868. It occurs most commonly in children aged from 5 to 10 years and is uncommon in African population. The male to female ratio is two to one. The term histiocytosis X concerns the multiple organ involvement in disseminated Hand Schuler Christian disease. Neither the clinical nor the radiographic presentations of EG are specific, and the differential diagnosis is often difficult (1, 2). Case report A 2-year-old girl with no significant medical history presented with pain, swelling and restricted movements of the right forearm for two weeks. Physical examination revealed no history of fever, weight loss, or rash. Pain and deformity were not present at any other bony site or joint and there were no other soft tissue swellings. Laboratory values showed a total white cell count of 14500/mm3 among which there was 61% Polynuclear Neutrophils and 30% Lymphocytes; an elevated Erythrocyte Sedimentation Rate of 45 mm/h with a slightly elevated C - reactive protein at 5.6 mg/dl. The plain radiography of the affected forearm showed a globular aspect of the proximal part of the diaphysis of the radius bone associated with cortical irregularity, soft tissue swelling and periosteal reaction (Fig. 1). An MR- Imaging of the forearm was performed and demonstrated a hyper-intense bone lesion and hyperintensity of the surrounding

Fig. 1. — Plain X-rays of the forearm showing irregular periosteal margin of the right radius (arrows) AP (A) and lateral view (B).

tissues on T2-weighted sequences (Fig. 2). The bone lesion was hypo intense on T1 weighted sequences. Sequences with administration of gadolinium showed an intense cortical bone, periosteal and soft tissues enhancement (Fig. 3). A small fluid collection was protruding from the proximal radius which presented a broadened medullar cavity and cortical bone destruction (Fig. 4). A biopsy of the bone lesion was performed and the histological examination revealed Langerhan’s cell histiocytosis characterized by Langerhan’s cell proliferation accompanied by giant cell and inflammatory infiltrate. Langerhan’s cells were

From: 1. Radiology Department, 2. Pediatric Radiology Department, 3. Pediatric Department, 4. Anatopathology Department, Erasme University Hospital, Brussels, Belgium. Address for correspondence: Dr M. Cassart, M.D., Dept of Pediatric Radiology, Erasme University Hospital, Route de Lennik 808, B-1070 Brussels, Belgium. E-mail: mcassart@ulb.ac.be

positive for S-100 protein and CD1 (Fig. 5) (3, 4). Isotopic investigations enhanced the known lesion in the forearm but also a focal skull area. A head CT scan was performed and confirmed the presence of a solitary lytic lesion on the skull bone (Fig. 6). The child did not receive any treatment. A subsequent every 6month follow up by biological data and abdominal ultrasonography was programmed to exclude any further visceral involvement. Discussion Histiocytosis can present with various clinical manifestations (5-8). Eosinophilic Granuloma (EG)80%: EG is a self limited lesion in bone or lung. EG may be found in the skull, mandible, spine and long bones. EG can convert to more aggressive systemic forms described below.

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A Fig. 2. — Transverse section in T2-wt showing hyper-intense signal in the right upper radius surrounded by hyperintense soft tissue infiltration (arrow).

Fig. 3. — Transverse section of the forearm in T1-wt sequences showing hypo-intense radius (A) and after gadolinium injection (B) it showed broadening of the medullar cavity and destruction of the cortical bone. The surrounding soft tissue is also enhanced by gadolinium.

Fig. 4. — Sagittal section of the forearm in T1-wt sequences showing broadening of the medullary cavity and destruction of the cortical bone of the proximal radius (A); after Gadolinium injection a collection raising from the radius towards the surrounding tissue is well depicted (B) (arrow).

Hand-Schuller-Christian disease (HSC) -15-20% is a chronic disseminated form of Langerhan’s histiocytosis occurring in older patients. There is a well known triad of HSC which is diabetes insipidus, exopthalmos and skull lesions. Letterer-Siwe disease - 10% is a fulminant systemic disease that occurs in children under 3 years and is rapidly fatal. The radiologic appearance of EG is non-specific and differs by location. Cranial lesions may appear on plain X-ray with sharp, punched out borders. In the diaphysis or metaphysis of long bones, the lesions develop in the center of the medullary cavity. The lesion may then cause endosteal scalloping and periosteal reaction (9). Bone scintigraphy scanning is not useful in defining the EG by itself but is useful in detecting any other lesions after the diagnosis has been established (9). CT scan and MR-imaging are useful to delineate the extent of the intramedullary and cortical extension (7-9). The LCH imaging characteristics range between geographic non aggressive and highly aggressive appearance. Our case was the aggressive type of LCH with permeative and periosteal reaction. A fluid lesional component growing from the radius into the surrounding soft tissue was present resembling to an abscess formation. The radiologic differential diagnosis includes any aggressive bony lesion like Ewing's sarcoma,

Fig. 5. — Langerhan’s cell histiocytosis characterized by a proliferation of Langerhan’s cell CD1 a positive (CD1 a immunochemistry, original magnification (x200)).

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Conclusion The pathology of Langerhan’s cell histiocytosis is not clearly understood (10). The disease having an unpredictable outcome and a heterogenous clinical presentation makes the diagnostic work-up one of the most essential step in order to do a correct follow-up of patients. References

Fig. 6. — CT scan of the skull showing lytic lesion on the frontal bone.

osteosarcoma, metastases, leukemia and osteomyelitis. In bone tumours the soft tissue involvement is less common except for osteosarcoma. Leukemia is usually polyostotic. Osteomyelitis is most often metaphyseal in children (diaphyseal locations may be secondary to direct trauma). It is also very aggressive and permeative, and can be associated with reactive sclerosis and periosteal reaction. These features are very similar to LCH (10). The commonest sites of EG are skull, legs, ribs, pelvis, spine, jaw, humerus, and tibia (9, 10). Radial involvement is less frequent. Due to this uncommon location and its highly permeative nature leading to infiltration of the surrounding soft tissue, the diagnosis of osteomyelitis with an abscess formation was proposed. Only when the biopsy findings fail to show any germs in bacteriology, histiocytosis can be suspected. In our case, the MRI features were very much similar to osteomyelitis. The elevation of the periostium with presence of liquid around the damaged bone could be misleading. When the spine is involved, preservation of disc space

above and below the vertebral body helps to differentiate lesion from osteomyelitis (9). Treatment options and outcome Treatment of EG depends on the extent of the disease (9, 10). Treatment is planned after thorough evaluation of the patient to determine the extent of involvement. In localized disease, a biopsy alone is often enough to incite healing. In some cases the disease will regress without any treatment at all. Other treatment modalities of EG include curettage, excision, steroid injection, radiation (9). Chemotherapy (vinblastine) is recommended for systemic disease (8, 9). It is recommended to deliver the less possible aggressive treatment to keep the lesion under control and allowing it to heal without treatment. In our case, the affection was polyostotic without systemic involvement; therefore, it was decided to follow the child without treatment. The follow-up includes biological data and abdominal imaging to exclude visceral involvement. Until now, no new lesions have been detected.

1. Azouz E.M., Saigal G., Rodriguez M.M., Podda A.: Langerhans’ cell histiocytosis : pathology, imaging and treatment of skeletal involvement. Pediatr Radiol, 2005, 35 : 103-115. 2. Bollini G., Joure J.L., Gentet J.C., Jacquemier M., et al.: Bone lesions in histiocytosis X. J Pediatr Orthop, 1991, 11 : 469-477. 3. Valladeau J., Ravel O., DezutterDambuyant C., et al.: Langerin, a Novel C-Type Lectin Specific to Langerhans Cells is an Endocytic Receptor that Induces the Formation of Birbeck Granules. Immunity, 2000, 12 : 71-81. 4. Birbeck M.S., Breathnach A.S., Everall J.D.: "An Electron Microscope Study of Basal Melanocytes and High-Level Clear Cells (Langerhans cells) in Vitiligo." J Invest Dermat, 1961, 37 : 51-63. 5. Baumgartner I., von Hochstetter A., Baumert B., Luetolf U., Follath F.: Langerhans Cell Histiocytosis in Adults. Med Ped Oncol, 1997, 28 : 914. 6. Malpas J.S., Norton A.J.: Langerhans Cell Histiocytosis in the Adult. Med Ped Oncol, 1996, 27: 540-546. 7. Howarth D.M., Gilchrist G.S., Mullan B.P., Wiseman G.A., Edmonson J.H., Schomberg P.J.: Langerhans cell histiocytosis: diagnosis, natural history, management, and outcome. Cancer, 1999, 85, 10 : 22782290. 8. Schonfeld N., Frank W., Wenig S., Uhrmeister P., Allica E., Pressler H., Grassot A., Loddenkemper R.: Clinical and Radiologic Features, Lung Function and Therapeutic Results in Pulmonary Histiocytosis X. Respiration, 1993, 60: 38-44. 9. Writing Group of the Histiocyte Society. Histiocytosis Syndromes in Children. Lancet, 1987, 1 : 208-209. 10. Filipovich A., Mc Clain K., Grom A.: Histocytic Disorders: Recent insights into pathophysiology and Practical Guidelines. Biol Blood Marrow Transplant, 2010, 16: S82-S89. 11. Official website for the American Histiological society: www.histio.org.

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PRIMARY HYPERPARATHYROIDISM PRESENTING WITH BILATERAL SLIPPED CAPITAL FEMUR EPIPHYSIOLYSIS. A PICTORIAL ESSAY T. De Beule1, L. Ardies1, Ph. Simons1, P. Gillardin2, P. Vanhoenacker1 It has become rare to find the typical radiological manifestations of primary hyperparathyroidism like generalized osteoporosis, brown tumors and advanced bone resorption because of the generalized usage of biochemical screening techniques. We present a 17-year-old patient with a parathyroid adenoma resulting in these typical skeletal manifestation throughout the skeleton combined with secondary bilateral slipped capital femur epiphysiolysis. Key-word: Parathyroid, hyperparathyroidism.

Primary hyperparathyroidism is a rare condition caused by parathyroid adenoma, carcinoma or parathyroid gland hyperplasia. This condition is characterised by the elevated serum concentration of parathyroid hormone resulting in bone demineralisation throughout the whole skeleton and secondary hypercalcaemia. A generalized osteoporosis occurs if the disease is not treated in an early stage. These advanced signs of bone resorption are only seldom seen these days because of the widespread availability of diagnostic tests. We present a case of a young child with a delayed diagnosis of the disease, showing almost all the bony changes. A bilateral slipped capital femur epiphysiolysis (SCFE) was diagnosed as a complication of the bone resorption. Only five cases of SCFE in combination with primary hyperparathyroidism are reported in the literature to our knowledge. Case report We present a case of a 17-year-old patient with a long history of gait problems and a postural tension problem combined with symptoms of hyperflexia. Standard conventional radiographs were taken during a long diagnostic quest. These showed irregular translucent areas in the metaphysic bone adjacent to the growth plate (Fig. 1), an erosive delineation of the sacroiliac joints and the symphisis pubis (Fig. 2, 3), trabecular bone resorption throughout the skeleton (Fig. 4) and subligamentous bone resorption at tendon insertions (Fig. 5). A non-sclerotic lesion in the proximal tibia was found without any periosteal reaction (Fig. 6), this lesion fitted the description of a brown tumour. CT scan revealed multiple other brown

tumours (Fig. 7). Due to the secondary effects of this global bone resorption a rather rare secondary bilateral SCFE had developed (Fig. 8). These combined skeletal manifestations of global bone resorption and brown tumours lead to the assumption of hyperparathyroidism. The culprit lesion consisted of a parathyroid adenoma, which was surgically removed. Discussion Primary hyperparathyroidism is a common endocrine disease with a prevalence of 1 in 500 women a year and 1 in 2000 men. The incidence increases with age affecting about 1% of the population. A sporadic form (80%-85%) and a familial form exist. The sporadic form is in general caused by a solitary parathyroid adenoma creating an overproduction of parathyroid hormone (PTH) (1). Hyperparathyroidism is defined by the risen concentration of PTH, which affects the calcium metabolism. A risen PTH results in a higher bone mineralization turnover caused by an increased activation of osteoclastic cells. This demineralization creates an excess of calcium in the serum. PTH increases the calcium reabsorption at the level of the kidney and promotes the excretion of phosphates. PTH creates an intestinal absorption of calcium due to an overproduction of 1,25-dihydroxycalciferol. Overall, a risen concentration of PTH results in a higher serum calcium level which promotes the formation of kidney stones, osteoporosis with secondary fractures and neuromuscular weakness. These are all symptoms of a long-lasting disease. Due to the non-specificity of the symptoms, diagnostic delay was a common problem. In the

From: 1. Department of Radiology and Imaging, 2. Department of Pediatry, OLV Ziekenhuis, Aalst, Belgium. Address for correspondence: Dr T. De Beule, M.D., Dept of Radiology, Olv Ziekenhuis, Moorselbaan 164, 9300 Aalst, Belgium. E-mail: Tom.debeule@gmail.com

Fig. 1. â&#x20AC;&#x201D; Bilateral widening of the growth plate with an irregular sclerotic delineation.

early 1970s, biochemical screening became available creating the possibility for an early detection of the disorder without overt clinical manifestations. A marked decrease of symptomatic hyperparathyroid diseases is noted these days (2, 3). Because of the demineralization effects of PTH on the bone, radiographical changes at multiple locations throughout the skeleton can be noticed in late stage disease. One of the first possible presentations at imaging is the subphyseal, subchondral, subligamentous and trabecular bone resorption (4). Irregular translucent areas appear in the metaphysic bone adjacent to the growth plate as a result of subphyseal bone resorption caused by the higher level of serum PTH. This results in a widening of the growth plate with irregular sclerotic mar-

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Fig. 2. — Erosive delineation of the sacro-iliacal joints

Fig. 3. — Erosive delineation of the symphisis pubis

Fig. 4. — Trabecular bone resorption resulting in diffuse trabecular bone pattern. This resorption can occur throughout the skeleton.

Fig. 5. — Osseous resorption occurs at the sites of tendon and ligament attachment to bone and is mostly seen at the distal ends of the clavicula, trochanters, ischial tuberosties and humeral tuberosities.

gins. Subchondral bone resorption is most frequently seen in the sacroiliac, sternoclavicular and acromioclavicular joints, symphisis pubis, and the discovertebral junctions. This bone resorption is characterised by an erosive delineation located next to the articular surfaces. A third sign is the trabecular bone resorption throughout the skeleton. In the cranium, this resorption results in an osteopenic and speckled appearance represented by the multiple tiny hyperlucent areas throughout the skull vault. This sign is also known as the salt and pepper appearance or pepper pot skull (5). Subligamentous bone resorption can also be depicted at the sites of

tendon and ligament attachment to bone (6). This phenomenon can be seen at the distal ends of the clavicula, trochanters, ischial tuberosties and humeral tuberosities. Another finding due to this excess of osteoclast activity are is a brown tumor. In locations with particularly rapid octeoclastic activity, hemorrhage, reparative granulation and fibrous tissue can replace the normal bone. These localized accumulations of fibrous tissue and giant cells may produce osseous expansion. Brown tumors appear as single or multiple well-defined lesions of the axial or appendicular skeleton, without sclerosis on conventional radio graphy (7). The lesions may be in an

eccentric or cortical location. Computed tomography discloses a tissue mass that enhances after contrast injection but does not invade the soft tissues; in addition, there is no periosteal reaction. Brown tumours have a higher prevalence in association with secondary hyperparathyroidism and are more rarely associated with primary hyperparathyroidism (8). The effect of parathyroidectomy on brown tumors depends on their composition (9). Ossification can be expected if the cortex is blown out by a tissue mass that is reddishbrown as a result of interstitial bleeding. Fluid-filled masses, in contrast, tend to persist as cysts filled with hemorrhagic fluid. The main differential diagnosis is a giant-cell tumour, which is a highly vascular lesion located in the metaphysis or epiphysis of a limb bone or in the pelvis, sacrum, or spine.

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Fig. 7. — Brown tumor in the acetabular roof presented as a sharp demarcated lytic lesion with strong thinning of the surrounding cortex around the lytic lesion. Fig. 6. — Non-sclerotic, lytic lesion anteriorly localized in the proximal right tibia without a periosteal reaction.

Slipped capital femur epiphysis is another secondary finding due to the bone resorption around the growth plate of the femur capital. SCFE caused by hyperparathyroidism or other endocrine imbalances is well known and correlated (10). Trethowen's sign can be used to detect slippage of the femur capital, which is positve when Klein’s line no longer transects the lateral capital epiphysis. SCFE in case of primary hyperparathyroidism is a rare condition and to our knowledge only described in five case reports (11). Conclusion Excessive production of parathyroid hormone, termed hyperparathyroidism, is classified as primary, secondary, or tertiary in form. Primary hyperparathyroidism, due to autonomous hypersecretion of PTH, usually occurs in the setting of a parathyroid adenoma (80%), which is rather rare in children. Bone demineralisation throughout the skeleton can only be detected with conventional radiographs after a prolonged risen concentration of PTH. The excessive osteoclastic activity results in subperiosteal, endosteal, subchondral, trabecular, subphyseal and subligamentous and subtendinous bone resorption. These changes can be helpful in detecting asymptomatic lesions although biochemical tests are more sensitive. Brown tumours can occur because of a local higher osteoclastic activity and has to be differentiated from giant cell tumour, which are highly vascular compared to brown tumours.

Fig. 8. — Bilateral slipped capital femur epiphysis

Because primary hyperparathyroidism is regularly diagnosed earlier in the course of the disease, nowadays it is only rarely seen that the bony resorption occurs so manifest throughout the skeleton. It is important to keep the possibility of a SCFE in mind when young patients present with gait problems combined with hyperparathyroidism. Acknowledgements Special thanks to Dr. L. Lateur Dept. Radiology UZ Gasthuisberg who provided the case material. References 1. Elaraj D., Clark O.: Current status and treatment of primary hyperparathyroidism. The Permanent Journal, 2008, 12: 32-37. 2. Bilezikian J.P., Silverberg S.J.: Asymptomatic Primary Hyperparathyroidism. N Engl J Med, 2004, 350: 1746-1751. 3. McDonald D.K., Parman L., Speights V.O.: Primary Hyperparathyroidism Due to Parathyroid Adenoma. Radiographics, 2005, 25: 829-834. 4. Resnick D.: Resnick, Bone and joint imaging second edition Ch 52: p 552561.

5. Roche C.J., et al.: Selections from the Buffet of Food Signs in Radiology. Radiographics, 2002, 22: 13691384. 6. Teplick J.G., Eftekhari F., Haskin M.E.: Erosion of the sternal ends of the clavicles. A new sign of primary and secondary hyperparathyroidism. Radiology, 1974, 113: 323. 7. Merz M.N., Massich D.D., Marsh W., Schuller D.E.: Hyperparathyroidism Presenting as Brown Tumor of the Maxilla. Am J Otolaryngol, 2002, 23: 173-176. 8. Jouan A., Zabraniecki L., Vincent V., Poix E., Fournie B.: An unusual presentation of primary hyperparathyroidism: Severe hypercalcemia and multiple brown tumors. Joint Bone Spine, 2008, 75: 209-211. 9. Franco M., Bendini J.C., Albano L., et al.: Radiographic follow-up of a phalangeal brown tumor. Joint Bone Spine, 2002, 69: 506-510. 10. Qada L., et al.: Slipped Capital Femoral Epiphysis Associated with Primary Hyperparathyroidism and Severe Hypercalcemia. Clin Pediatr, 2003, 42: 43. 11. Loder R.T., Hensinger R.N.: Slipped capital femoral epiphysis associated with renal failure osteodystrophy. J Pediatr Orthop, 1997, 17: 205-211.

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HETEROTOPIC PANCREAS REVEALED BY POST-TRAUMATIC PANCREATITIS F.C. Deprez1, C. Pauls1, B. Coulier2 We report the case of an 82-year-old female presenting with acute epigastric abdominal pain after traumatic blow on the epigastrum. High-resolution multimodal imaging comprising Ultrasound, CT and MR, correlation with laboratory blood analyses and a 6 months CT follow-up allowed us to make a definite diagnosis of traumatic heterotopic pancreatitis. This case emphasizes the relevance of a well-targeted high-definition ultrasound study in the following of the first imaging modality. Key-words: Pancreatitis – Abdomen, injuries.

Heterotopic pancreas (HP) is characterized by pancreatic tissue found in ectopic locations at various sites of the body, most frequently in the gastrointestinal tract. This anatomic variation is quite frequently observed in postmortem examinations but is very rare and difficult to demonstrate by non-invasive imaging modalities. In this case, we would like to emphasize the relevance of a well-targeted high-definition ultrasound study to characterize non specific tissular abnormalities observed on the first imaging modality. HP is most often asymptomatic but can present the same pathology than normotopic pancreas or lead to mechanical complication due to aberrant localization. Pancreas inflammation can be idiopathic but is most often cause by biliary or gallstones and alcohol. Less common causes are auto-immune pancreatitis, drug-induced pancreatitis, vasculitis, viral infections, hypertriglyceridemia or hypercalcemia, porphyrias and direct trauma of the gland (including post ERCP). The diagnostic criteria for pancreatitis combine characteristic abdominal pain with serum elevation of amylase and/or lipase, and characteristic findings of acute pancreatitis on CT scan.

Case report An 82-year-old woman presented to the emergency room with a 12 hours history of increasing continuous epigastric abdominal pain. Symptoms began shortly after the patient received a blow on the epigastrum by falling on a small table.

Fig. 1. — Unenhanced abdominal CT. Axial (A,B), coronal (C) and sagital (D) views reveal an inflammatory round mass (white arrowhead) adjacent to the duodenojejunal flexure (asterisks), associated with focal bowel wall thickening, peripheral mesenteric fat infiltration and descending fluid collection along the proximal jejunum (black arrows). Pancreatic tissular lobules and fatty interstitium are well perceptible (white arrowhead), similar to normal pancreas (white arrows).

From: 1. Department of Radiology, Clinique St Pierre, Ottignies, Belgium, 2. Department of Radiology, Clinique St Luc, Bouge (Namur), Belgium. Address for correspondence: Dr F.C. Deprez, Department of Radiology, Clinique St Pierre, Avenue Reine Fabiola, B-1340 Ottignies, Belgium. E-mail: fabrice.deprez@uclouvain.be

Nausea, vomiting or melena were absent and the patient was apyretic. At physical examination central abdominal soreness was found, but peristaltism was still present and defense, rebound or organomegaly

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were absent. Pertinent laboratory values included normal liver function tests and normal white blood cell count but elevated serum amylase (158 IU/l), lipase (370 IU/l), LDH (619 IU/l) and CRP (14.3 mg/dl) were found. Unenhanced abdominal CT was performed on admission (Fig. 1) and revealed an inflammatory round mass snuggled up to the duodenojejunal flexure at the angle of Treitz. Peripheral mesenteric fat stranding, localized focal bowel wall thickening and ill-defined fluid collection along the proximal jejunum were associated. The round inflammatory mass had a lobulated appearance with fatty infiltration strongly resembling to elderly pancreatic tissue. High resolution ultrasound study was secondarily performed with a linear probe (3-9 MHz) and clearly delineated a 2,5 cm round echogenic homogenous mass, surrounded by an arciform non-peristalting and thickened duodenojejunal loop (Fig. 2). A central Y-shaped ductal system connected by a single duct to the thickened bowel wall was clearly delineated within the mass confirming the presumed diagnosis of heterotopic pancreatitis. Classic conservative treatment was proposed with imaging and biological follow-up. Spontaneous recovery was obtained. Pancreatic serum tests reached a maximum level 3 days after admis-

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Fig. 2. — High-resolution ultrasound study reveals a 2.5 cm in diameter round mass (arrows) adjacent to a non-peristaltic thickened duodenojejunal flexure. A branched ductal system (asterisk) connected to the inferior wall of the duodenojejunal loop (white arrowheads) is well observed, confirming the diagnosis of ectopic pancreas.

sion (amylase 170 IU/l, lipase 564 IU/l) and regained normal levels 18 days later (amylase 95 IU/l, lipase 61 IU/l). MR imaging was performed 10 days after admission. Axial T1weighted series showed an area

with a signal similar to that of the normotopic pancreas (Fig. 3). Unfortunately, this exam was of poor quality because of the difficulties of the patient to stay in apnea during the acquisitions. Moreover peripheral mesenteric fat infiltration and fluid

Fig. 3. — Axial MR series confirm the similar T1-weigthed (A) and T2-weighted (B) signal of normotopic pancreas (arrows) and ectopic pancreas (white arrowhead). Adjacent effusion is found (white asterisk).

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B Fig. 4. â&#x20AC;&#x201D; Contrast enhanced CT obtained 6 months after admission demonstrates spontaneous recovery, with disappearance of fluid collections. On MPR coronal oblique (A) and sagittal (B) view, ectopic pancreatic lobulation and enhancement (white arrows) is well visible and appears similar to normotopic pancreas (white arrow). HP is adjacent to the duodenojejunal flexure (black asterisks).

collections disturbed the precise visualization of the ectopic pancreas. The normotopic pancreas had a normal appearance. Abdominal CT with intravenous contrast agent injection was performed 6 months later. Fat infiltration and fluid collections had completely disappeared and the presumed heterotopic pancreas actually showed an homogenous enhancement pattern similar to that of normotopic pancreatic tissue (Fig. 4).

Pancreatic lobules and fatty interstitium were better characterized. There was no expansive process. The definite diagnosis of acute post-traumatic heterotopic pancreatitis was finally made on the basis of multimodality high-quality imaging, biological and clinical follow-up. Discussion Anatomical congenital pancreatic abnormalities are classified as: pan-

creas divisum, annular pancreas, agenesis of the dorsal pancreatic bud and ectopic pancreatic tissue. Heterotopic pancreas (HP) is defined as aberrant but well-developed pancreatic tissue lacking anatomic and vascular continuity with the main body of the pancreas. HP incidence ranges from 1% to 14% in literature (1). The most frequent localizations are the stomach, duodenum, jejunum and ileum (including Meckelâ&#x20AC;&#x2122;s or other diverticula). Less common sites include the liver, spleen, esophagus, biliary tract, fallopian tubes, mesentery and omentum, mediastinum or even umbilicus (1, 2). At least, heterotopic pancreatic tissue is frequently observed in gastric duplication cysts (3). HP can have a submucosal localization (75%), or can be present within the muscularis propria or the serosal surface of the GI tract (4). Variable amounts of pancreatic acinar and islet tissue are seen. The heterogeneity of these microscopic features is codified by the Heinrich classification. Class I lesions contain pancreatic acini, islets, and ducts; class II lesions contain acini and ducts but no islets; and class III lesions are composed of ducts alone. The proposed pathogeneses are transplantation of pancreatic cells to adjacent structures during embryonic development or metaplasia of multipotent endodermal cells. HP can be seen at any age, but because of its slow growing it is most often observed in adults (5). Moreover, in most cases HP remains asymptomatic and is an incidental finding. Symptomatic HP is usually found in the stomach or duodenum, with complaints of epigastralgia mimicking peptic disease (1). Potential complications of HP are mass effect causing bowel intussusception or obstruction, acute pancreatitis, and less frequently bleeding, cystic degeneration or malignancy of the exocrine or endocrine ectopic tissue. The need for treatment depends on symptoms and definite diagnosis, excluding particularly a malignant process (6). In our case, conservative treatment was privileged, like for classical mild entopic pancreatitis, after confirmation of clinical, biological and imaging recovery and owing to the patient old age. However, some investigators recommend surgical treatment (7-9), especially if diagnosis remains unclear. Incidental finding of HP does not require any operation (8).

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Heterotopic pancreatitis can lead to hemorrhage, necrosis, bowel perforation and acute or chronic inflammation, although being usually only as a microscopic finding. Late complications like pseudocyst formation have been reported (10). During acute HP inflammation, the elevation of serum amylase and lipase levels remain rather limited due to the small volume of pancreatic tissue in the heterotopic pancreas. In some systemic cause of pancreatitis, like drug-induced or autoimmune pancreatitis, simultaneous inflammation of the normotopic and ectopic pancreas can be observed (11). In our patient, typical CT appearance of elderly pancreatic tissue with lobulation and fatty infiltration was observed within the normotopic and the heterotopic pancreas, facilitating their characterization. The US demonstration of a central ductal system within the HP tissue was also of most importance to establish the correct diagnosis. Therefore we would like to put the emphasis on the relevance of a well-targeted high-definition ultrasound study in the following of the first imaging modality. In optimal conditions with cooperative patient, MRI exam could

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demonstrate the presence of a central ductal system, with T2-weigthed and cholangio-MR sequences (6). This result could equally be obtained with endoscopic ultrasound (EUS) if HP is localized in the stomach or the duodenum, especially if abdominal US exam is difficult (obesityâ&#x20AC;Ś) (6). At least, some authors reported the role of barium X-ray series to demonstrate nonspecific fold thickening with the characteristic appearance of a centrally umbilicated nodule in the gastric mucosa within the gastric heterotopic pancreatic rest (6).

References 1. Lai E.C., Tompkins R.K.: Heterotopic pancreas. Review of a 26 year experience. Am J Surg, 1985, 151: 697-700. 2. Siegel M.J.: Adrenal glands, pancreas, and other retroperitoneal structures. In: Siegel M.J. (ed) Pediatric body CT. Lippincott Williams and Wilkins, Philadelphia, 1999, pp 253-286. 3. Sinha A., Saluja S.S., Gamanagatti S.: Gastric duplication cyst with macroscopic serosal heterotopic pancreas. JOP, 2010, 11: 470-473. 4. Nijs E., Callahan M.J., Taylor G.A.: Disorders of pediatric pancreas:

9. 10.

11.

imaging features. Pediatr Radiol, 2005, 35: 358-373. Ogata H., Oshio T., Ishibashi H., Takano S., Yagi M.: Heterotopic pancreas in children: review of literature and report of 12 cases. Pedatr Surg Int, 2008, 24: 271-275. Shanbhogue A.K., Fasih N., Surabhi V.R., Doherty G.P., Shanbhogue D.K., Sethi S.K.: A clinical and radiologic review of uncommon types and causes of pancreatitis. Radiographics, 2009, 29: 1003-1026. Yuan Z., Chen J., Zheng Q., Huang X.Y., Yang Z., Tang J.: Heterotopic pancreas in the gastrointestinal tract. World Gastroenterol, 2009, 15: 3701-3703. Zinkiewicz K., Juskiewicz W., Zgodzinski W., Szumito J., Cwik G., Furtak J. et al.: Ectopic pancreas: endoscopic, ultrasound and radiological features. Folia Morphol, 2003, 62: 205-209. Fleischer D.E.: Endoscopic resection of gastrointestinal tumors. Endoscopy, 1993, 25: 479-481. Rubesin S.E., Furth E.E., Birnbaum B.A., Rowling S.E., Herlinger H.: Ectopic pancreas complicated by pancreatitis and pseudocyst formation mimicking jejunal diverticulitis. Br J Radiol, 1997, 70: 311-313. Benbow E.W.: Simultaneous acute inflammation in entopic and ectopic pancreas. J Clin Pathol, 1988, 41: 430434.

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A RARE CASE OF INTRADURAL SPINAL HYDATID CYST IN A PAEDIATRIC PATIENT M. Ahmad1, Ekramullah1, I. Ahmad1, S. Asmat Ali2 Intradural extramedullary type of spinal hydatid disease is a rare variety of hydatid disease, and is even rarer in paediatric age group. Spinal hydatid disease should be considered in the differential diagnosis of spinal cord compression syndrome in endemic countries and should be evaluated with imaging and serological investigations. Our case was a 9- year-old boy who presented with lower back pain lasting for 8 months and progressive bilateral lower extremities weakness lasting for 2 month. Neurological examination was suggestive of lower motor neuron type of paraperesis. Magnetic resonance images of the lumbar spine showed an intradural cystic lesion displacing and compressing the lower cord and cauda equina. The cystic mass was explored with L1-L4 laminectomy and after durotomy; it was separated from cord and dura mater by hydrodissection. It contained a clear fluid. The pathological diagnosis was hydatid disease. Key-word: Echinococcosis.

Hydatid (which means ‘watery cyst’ in Greek) disease is an uncommon but clinically and radiologically challenging parasitic disease in endemic areas. Bone involvement is a rare complication of this disease and spinal involvement in a child being even rarer. Despite the introduction of modern surgical and pharmacological therapy the disease still remains difficult to cure and highly prone to recurrence. The infestation persistently erodes the spinal column, eventually leading to its destruction and neurological deterioration.

Case report A 9-year-old boy presented to the neurosurgical out-patients’ department with complaints of back pain lasting for last 8 months as well as progressive weakness involving the lower limbs. He was also complaining of overflow urinary incontinence for a few days. On examination, there was wasting of muscles of both lower limbs (more severe on right side) with decreased power and absent tendon reflexes in bilateral knees and ankles. The chest radiograph was found to be normal. Abdominal ultrasound showed the presence of multiple, double walled cystic lesions of variable size within the right lobe of liver suggestive of hydatid cysts. MRI of the dorso-lumbar spine revealed the presence of a single, smooth walled, intradural cystic lesion extending from the level of D11-D12 intervertebral (IV)

Fig. 1. — Sagittal T1 (A) and T2 (B) weighted MR sequence of the dorso-lumbar spine showing presence of a single smooth walled intradural cystic lesion extending from the level of the D11-D12 disc to L3-L4 intervertebral disc level widening of the spinal canal and posterior scalloping of the vertebral bodies. Lower spinal cord and cauda equina are compressed and displaced towards the right side.

disc to L3-L4 IV disc causing widening of the involved spinal canal segment, lower spinal cord compression and displacement to the right (Fig. 1, 2). Immunologic studies were positive for Echinococcus granulosus. The erythrocyte sedimentation rate was 80 mm/h and the complete blood count showed an eosinophilia of 8%. On the basis of these radiographic, sonographic and immunological findings a diagnosis of hydatidosis was made, and treatment with albendazole was begun. In order to relieve the spinal cord compression, laminectomy was per-

From: 1. Department of Radiodiagnosis, 2. Department of Surgery, Jawaharlal Nehru Medical College, A.M.U. Aligarh, India. Address for correspondence: Dr M. Ahmad, M.D., H. No. 4/1309, New Sir Syed Nagar, Aligarh, U.P., India- 202002. E-mail: drmehtab@gmail.com

formed between the levels of L1 and L4. The dura mater was distended between these levels; the spinal cord was compressed and displaced to the right by the cyst. The dimensions of the cyst were 7 x 2 x 2 cm (Fig. 3). The histopathologic findings confirmed the diagnosis. The patient showed steady improvement after surgery and was discharged with a healthy note. Discussion Hydatid disease is a zoonotic disease caused by the larval stage of the tapeworm Echinococcus sp., and is known to be endemic in Middle Eastern, Mediterranean, and Australian regions (1). The first description of spinal hydatid disease was made by Churrier in 1807 and the first surgical intervention was

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Fig. 2. — Axial T1 (A) and T2 (B) weighted MR sequence of the dorso-lumbar spine at L2 level showing the presence of a single smooth walled intradural cystic lesion causing widening of the spinal canal and compressing and displacing the lower spinal cord and cauda equina towards right side.

Fig. 3. — Post- operative specimen of the excised cyst showing a glistening white membrane and containing clear fluid.

reported by Reydellet in 1819.The liver is most commonly involved, followed by the lungs. Bone involvement is rare and in most of these cases concerns the spine. Spinal hydatid cyst represents less than 1% of all hydatid cyst cases (2). The distribution of the disease in the spinal area is as follows: 10% in cervical area, 50% in thoracic area, 20% in lumbar area, and 20% in sacral area. Cervical spine involvement is least common (3). Spinal hydatid cysts are categorized morphologically into 5 groups (classification of Braithwaite and Lees (4)): 1- intramedullary HC, 2- intradural- extramedullary HC, 3extradural- intraspinal HC, 4- vertebral HC, and 5- paravertebral HC. In 90% of the cases the disease is confined to the bone and the epidural space. The first three groups are extremely rare and they are usually reported as sporadic cases. In spinal hydatid cysts, presentation differs according to the site of involvement of the spine and may vary from paraparesis (62%) or paraplegia (26%), backpain or radicular pain (55%), numbness or sensory loss (36%) and

sphincter disturbance (30%) (5). On MRI, hydatid cysts are seen as spherical lesions with well defined margins and fine walls (4). The fluid content of HC is isointense with CSF on T1 and T2 WI, but the cyst wall is seen as low signal intensity rim on both T1 WI and T2 WI. After IV contrast injection, the rim generally does not enhance, and calcification of the wall of the cyst is rare. Enhanced ring-shaped wall can be seen if the cyst is infected. In our case, no contrast enhancement or calcification was present. In the differential diagnosis of HC, archnoid cyst and epidermoid cyst of spine should always be considered, especially in children. As a conclusion, spinal hydatidosis is a rare entity. Among these, isolated intradural- extramedullary thoracolumbar hydatid cyst cases are extremely rare. In the pre-operative period, MRI is a useful imaging modality in diagnosis of spinal HD and can play a crucial role in the management. References 1.

2. 3. 4. 5.

King C. Cestodes. In: Mandel G.L., Bennet J.E., Dolin R. (eds). Principles and practice of Infectious diseases, 4th edn. Churchill & Livingstone, 2000, pp 2957-2965. Pamir M.N., Akalan N., Ozgen T., Erbengi A.: Spinal hydatid cysts. Surg Neurol, 1984, 21: 54-57. Is¸lekel S., Zileli M., Ers¸ahin Y.: Intradural spinal hydatid cysts. Eur Spine J, 1998, 7: 162-164. Braithwaite, P.A., Lees, R.F.: Vertebral hydatid disease: radiological assessment. Radiology, 1981, 140: 763-766. Abbassioun K., Amirjamshidi A.: Diagnosis and management of hydatid cyst of the central nervous system: part 2: Hydatid cysts of skull, orbit and spine. Neurosurgery, 2001, 11: 1-9.

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UNUSUAL INITIAL DEVELOPMENT OF AN ESTHESIONEUROBLASTOMA ABOVE THE CRIBRIFORM PLATE G. Mazzamuto, P. Bosschaert1 Esthesioneuroblastoma is a rare tumor localized in the superior part of the nasal cavity. Extension in the anterior cerebral fossa is sometimes observed. As we discovered in our patient, the location of the tumor above the cribriform plate was very unusual and meningioma was suspected. Features and prognosis are discussed below. Key-word: Nose, neoplasms.

Case report A 59-year-old man was admitted in the emergency room after convulsions and loss of consciousness. Computed tomography revealed a hypodense basi-frontal lesion with a barely perceptible erosion of the cribriform plate (Fig. 1). No calcifications were noted. Complementary preoperative investigation by MRI showed a hyperintense T2-weighted solid mass above the cribriform plate, surrounded by edema. Administration of gadolinium indicated a moderate to intense enhancement and a small bud tissue developed through the cribriform plate (Fig. 2). The diagnosis of meningioma was then made. The patient underwent a surgical resection by supra-orbital approach. There were no post-operative complications. Histological examination demonstrated typical features of esthesioneuroblastoma. Treatment was supplemented by radiotherapy. Unfortunately, a local recurrence was detected 1 year later (Fig. 3). A new surgical resection was therefore undertaken. No evidence of local recurrence or metastases has been identified after 2 years of observation. Discussion Esthesioneuroblastoma (ENB) or olfactory neuroblastoma was initially described by L. Berger in 1924 (1). This lesion represents 3% of all nasal tumors and occurs between ages 3 and 79, with a peak at age 10 and age 40 and occurring predominantly in males (1-2). The typical localization is under the cribriform plate. In fact, the lesion arises from sensory cells in the olfactory mucosa which is

Fig. 1. — Sagittal (A) and coronal (B) CT slices showing a slight erosion of the cribriform plate and the integrity of the superior nasal cavity (white arrow).

located in the most superior part of the nasal cavity. These cells originate in the neural crest and differentiate into olfactory elements. Many articles in the literature present ENB as a “site specific” tumor developing first in the superior nasal cavity, involving the nasal septum, turbinates, ethmoid. Maxillary sinuses, orbital cavities, and anterior cerebral fossa are occasionally affected. In our patient, the location of the ENB was very unusual, causing initial diagnostic confusion. By CT or MRI, the choice of sagittal and coronal planes is important to estimate the development of ENB into the superior nasal cavity and/or the anterior cerebral fossa. CT may show calcifications in the lesion. These are not constant nor are they specific. Bone erosions are also described, including the cribriform

From: 1. Department of Radiology, Clinique St-Pierre, Ottignies, Belgium. Address for correspondence: Dr P. Bosschaert, M.D., Department of Radiology, Clinique St-Pierre, Ottignies, Av. Reine Fabiola 9, B-1340 Ottignies, Belgium. E-mail: Pierre.bosschaert@skynet.be

plate. These erosions are not always easily visible. Enhancement is usually moderate after CA perfusion. Cystic component is sometimes reported. This may help to differentiate ENB and meningioma when the infringement is located above the cribriform plate. “Dural tail” is difficult to distinguish of meningeal infiltration. Finally, it is well known that meningiomas can cause hyperostosis by osteoblastic reaction. Bone erosion is rare with meningiomas, except in very aggressive cases. Differential diagnosis must include other regional tumors like epidermoid carcinoma, adenocarcinoma, lymphoma, metastasis of melanoma or hemangiopericitoma. The final diagnosis is histological in most cases. Hyams has proposed to differentiate low and high-grade ENB. He has shown in a retrospective series of 49 patients that the 5-year survival is influenced by the grade: 80% for the low grade and 40% for the high (3). However, this distinction is often difficult to appreciate, as reported in the literature (4-5). In 1992, Dulguerov

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B C A Fig. 2. — Axial FLAIR (A) and T1-weighted MR acquisition after gadolinium administration, with sagittal (B) and coronal (C) reconstructions, showing the ENB (asterisk) above the cribriform plate and surrounding edema. Enhancement is moderate to intense. A small extension along the nasal septum is present (white arrow).

Fig. 3. — MR examination realized 1 year later, with sagittal (A) and coronal (B) T1weighted slices, demonstrating a local recurrence of ENB.

and Calcaterra (6) proposed a TNM classification based on CT and MR imaging findings (Table I). This classification differs from that usually used for carcinomas of the nasal cavity and paranasal sinuses by the International Union Against Cancer (7). This is due to the great importance given to the extension of the tumor above the cribriform plate which involves difficulties in processing. In most studies, the long term survival varies between 50% and 80% (8). The prognosis is usually determined by the initial stage. Surgical total resection is sometimes impossible. Local recurrences are frequent and mostly intra-cranial, by meningeal or parenchymal extension. The largest study which was

Table I. — TNM classification of Dulguerov and Calcaterra. Classification Definition T1

Tumor involving the nasal cavity and/or paranasal sinuses (excluding the sphenoid), sparing the most superior ethmoidal cells

Tumor involving the nasal cavity and/or paranasal sinuses (including the sphenoid), with extension to – or erosion of – the cribiform plate

Tumor extending into the orbit or protruding into the anterior cranial fossa, with / without dural invasion

Tumor involving the brain

No cervical lymph node metastasis

Any form of cervical lymph node metastasis

No metastasis

Distant metastasis

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published by Duguerov and Allal shows a local rate of 29% (9). Distant recurrences are lung, liver, bone, but also meningeal or cerebro-spinal in 10%-25% of cases according to authors. The primary treatment for ENB is surgery followed by radiotherapy. A collaborative team of experienced medical and surgical specialists including neurosurgeons and otorhinolaryngologists is crucial to define the best treatment for each patient. To date, there is no evidence as to the effectiveness of chemotherapy (10,11). In conclusion, an extra-axial tumor centered on the cribriform plate should include the diagnosis of ENB although this lesion is less frequent than meningioma, and knowing that most of ENB have an intranasal development. The diagnosis is often difficult and is histological in many cases.

References 1. Broich G., Pagliari A., Ottaviani F.: Esthesioneuroblastoma: a general review of the cases published since the discovery of the tumor in 1924. Anticancer Res, 1997, 17: 2683-2706. 2. Dulguerov P., Allal A.S., Calcaterra T.C.: Esthesioneuriblastoma: a meta-analysis and review. Lancet Oncol, 2001, 2: 683-690. 3. Hyams V.J.: Olfactory neuroblastoma – Tumors of the upper respiratory tract and ear. Armed Forces Institute of Pathology, 1988, 240-248. 4. Gaye P.M., Mesbah L., Kanouni L. et al.: Esthesioblastome olfactif: experience de l’institut d’oncologie de Rabat et revue de la literature. J Afr Cancer, 2010, 2: 36-40. 5. Kadish S., Goodman G., Wang S.S.: Olfactory neuroblastoma: a clinical analysis of 17 cases. Cancer, 1976, 37: 1471-576. 6. Dulguerov P., Calcaterra T.C.: Esthesioblastoma: the UCLA experi-

7. 8.

10.

11.

ence 1970-1990. Laryngoscope, 1992, 102: 843-849. TNM - 7th edition, 2009 – UICC/AJCC Wiley and Sons Publishers Jethanamest D., Morris L.G., Sikora A.G., Kutler D.I.: Esthesioneuroblastoma: a population-based analysis of survival and prognostic factors. Arch Otolaryngol Head Neck Surg, 2007, 133: 276-80. Dulguerov P., Allal A.S.: Nasal and paranasal sinus carcinoma: how can we continue to make progress? Curr Opin Otolaryngol Head Neck Surg Review, 2006, 14: 67-72. Bassoulet J., Bourhis J., Cosnard G. et al.: Esthésioneuroblastome olfactif: étude clinique, radiologique, anatomopathologique et thérapeutique: à propos de trois observations. J Eur Radiother, 1988, 9: 159-166. Benfari G., Fusconi M., Ciofalo A. et al.: Radiotherapy alone for local tumor control in esthesioneuroblastoma. Acta Otorhinolaryngol Ital, 2008, 28: 292-297.

CLASSIFIED SERVICES FRANCE, NORD Groupe radiologique, département du Nord, cherche plusieurs associés. Multisites : 3 cabinets, scanner et IRM Radiologie conventionnelle, mammographie numérique, Scanner privé GE (128 coupes), IRM GE (450 W) Pas d’astreinte 4 jours de travail par semaine pour temps plein Mi-temps possible PAS DE DROIT D’ENTREE, PARTS GRATUITES Tél. 00.33.6.77.51.36.43 Mail : sipdf@wanadoo.fr » Nous restons à votre disposition pour tout renseignement complémentaire au 00.33.3.20.29.08.00

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SPONTANEOUS TRANSHEPATIC RUPTURE OF THE GALLBLADDER WITH MASSIVE HEMOPERITONEUM B. Coulier1, Ph. Maldague2, F. Pierard3 Perforation of the gallbladder has an incidence of 1.6 to 2.8% in gallbladder disease. Among these cases transhepatic rupture is a very rare event. We report a case associated with secondary massive hemoperitoneum, free gallstone spillage, partial portal vein thrombosis and secondary pulmonary embolism. Key-words: Gallbladder, perforation.

Transhepatic rupture of the gallbladder is rare, with fewer than 20 cases reported in the literature (1). We report an unusual case in which the patient initially presented with right basic thoracic pain evocating pulmonary embolism. The definite emergency diagnosis was obtained during pulmonary angioCT. Case report A 68-year-old patient presented in the emergency department with complaints of retrosternal and epigastric pain. Pain had suddenly led the patient to hypotensive syncope at home. There was a history of increasingly more frequent episodes of epigastric pain evolving for several days and for which the family practitioner had prescribed proton pump inhibitor for a week. At physical examination tenderness was found in the right upper quadrant and in the epigastric area but pulmonary examination appeared normal. Laboratory tests revealed a CRP level 118 mg/l (nl < 5 mg/l), D-Dimeres were > 4.0 mg/L (nl < 0.5), Got at 140 U/l (nl < 40), GPT at 118 U/l (nl < 41). Because of the association of an episode of hypotensive syncope at home and a retrosternal pain with elevated D-Dimeres, the patient was first considered as having pulmonary embolism. Pulmonary angio-CT was performed (not illustrated) and fresh clots were found in about 30% of the segmental branches of the right lower pulmonary artery. On the lower views of CT (not illustrated) ascite was found in both upper quadrants. Subphrenic strati-

B Fig. 1. — A, B: unenhanced abdominal CT views show stratified perihepatic fresh blood clots (black stars). Free ascitic fluid is found in the left perisplenic space (white star). The distended gallbladder (black arrow) appears spontaneously dense due to the presence of fresh blood. Groups of radiolucent gallstones are spontaneously visible in the hemorrhagic bile (small white arrows).

fied fresh blood clots were also visible in the hepatic area. For these reasons the patient was readmitted in the radiologic department for complementary abdominal CT.

From: Departments of 1. Diagnostic Radiology, 2. Gastro-enterology and 3. Visceral Surgery, Clinique St Luc, Bouge 5004 (Namur), Belgium. Address for correspondence: Dr B. Coulier, M.D., Department of Diagnostic Radiology, Clinique St Luc, Rue St Luc 8, 5004 Bouge (Namur) Belgium. E-mail: bcoulier@skynet.be

On the “almost” unenhanced views (Fig. 1) – pulmonary angio-CT having been performed only 30 minutes before – stratified fresh blood clots were confirmed in the perihepatic space. A very dense and distended hemorrhagic gallbladder was also found. Numerous radiolucent hypodense gallstones were seen floating in the dense hematic bile. On contrast enhanced MPR views (Fig. 2) a large defect was diagnosed in the hepatic side of the thickened wall of the hemorrhagic gallbladder.

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Fig. 2. — Axial CT views (A,B) and coronal MPR view (C) obtained after contrast enhancement. A large defect appears in the hepatic side of the thickened wall of the hemorrhagic gallbladder (black arrow). This defect appears in close relation with an hypodense area of dilacerated hepatic parenchyma (black star) in communication with the perihepatic clots (white star). A group of radiolucent hypodense gallstones obstruct the infudibulum (small black stars). Another is found in the fundus of the gallbladder (grey arrows). Free stone spillage has produced in the dilacerated hepatic parenchyma and in the perihepatic space (small white arrows). There is a thrombosis of the left intrahepatic portal vein (long white arrow).

Fig. 3. — Coronal oblique MPR view illustrating the partial thrombosis of the hilar portal vein (black arrow) and the complete thrombosis of the left intrahepatic portal vein (white arrow).

This defect appeared contiguous to a hypodense area of dilacerated hepatic parenchyma in close relation with the perihepatic fresh clots. Radiolucent hypodense gallstones were also found obstructing the infudibulum. Others were visible in the fundus of the gallbladder and

free gallstone spillage had also produced in the dilacerated hepatic parenchyma and in the perihepatic space. Additionally a thrombosis of the left intrahepatic portal vein was found (Fig. 2B and 3). The radiological diagnosis of spontaneous transhepatic hemor-

rhagic rupture of the gallbladder caused by gallstone obstruction was proposed. Emergency laparotomy was performed. A large hemoperitoneum was present and more than 1, 7 liter of blood was aspired. The right perihepatic space was packed with clots and during aspiration a large tear was found in the hepatic parenchyma at the level of the segment 6. This tear was in close relation with a perforation of thickened inflammatory gallbladder wall. Multiple spilled gallstones were found in the right upper quadrant. The partial thrombosis of the portal vein was considered to be the result of the septic dilaceration through the liver. Similarly the partial pulmonary embolism was considered as a collateral damage due to the migration of clots from sushepatic veins. Discussion In the presence of fresh perihepatic hematoma on emergency abdominal CT various hypotheses can be proposed included hepatic tumor (carcinoma or adenoma), a gallbladder cause or rupture of an arterial branch in the hepatic area (hepatic, cystic or pancreatic artery) (2). Perforation of the gallbladder occurs in 1.6-2.8 % of cases of gallbladder disease (3) and is one of the most life-threatening complications of acute cholecystitis with a reported prevalence of 2-11% (4-5). Risk factors include old age, male gender, previous cholecystitic attacks, association of severe systemic diseases in the same patient, arteriosclerosis, immunosuppression or prolongated corticoterapy (4, 6). The proposed mechanism of gallbladder perforation is stone impaction in the infudibulum or cystic duct, which leads to retention of secretion from mucus glands and distention leading to vascular compromise, followed by necrosis and perforation. During this process bleeding can occur that results in hemorrhagic cholecystitis with hemoperitoneum, a rather rare event (5-6). A gallstone impaction resulting in gallbladder distention and followed by massive transhepatic hemorrhagic rupture with hemoperitoneum and gallstone spillage was the proposed physiopathologic sequence for the reported case. Secondary partial pulmonary embolism was considered being caused by the migration of clots from suprahepatic veins to the inferior vena cava.

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In cases of bleeding of a perforated gallbladder, the source of bleeding is usually the gallbladder wall or the cystic artery, due to local extension of the inflammatory process, leading to focal necrosis, rupture and bleeding (1). Very rarely however – as seen in the reported case – the major cause of hemorrhage is the liver parenchyma through which the gallbladder has eroded (1, 4-5). Rare cases of perforation of the gallbladder due to blunt injuries to the abdomen with sometimes delayed presentation have also been reported (8-9). Finally the different causes of hemorrhagic cholecystitis are numerous and frequently associated : gallstones (50% of cases), anticoagulotherapy (5-6, 10) or coagulopathy, gallbladder cancer, hepatic or cystic aneurysm, trauma, portal hypertension, corticotherapy. A gallbladder tumor or an aneurysm of the cystic artery may also rupture into the gallbladder (2, 5). Gallbladder hemorrhage may first be evacuated through the cystic canal causing painful acute obstructive jaundice and/or with subsequent

hematemesis. On the other side when this canal is not permeable because obstructed by a gallstone or by blood clots, hemorrhage may distend the gallbladder and finally provoke rupture with free hemoperitoneum (5-6). The gallbladder fundus is the most common site of perforation due to poor vascular supply. Sometimes as in the reported case the rupture may produce directly through the hepatic parenchyma (24). References 1. Kolder D., Geiger T., Tharakan A.K., Kessel J.W., Awad Z.T.: Massive hemoperitoneum from transhepatic perforation of the gallbladder. Mt Sinai J Med, 2006, 73: 1135-1136. 2. Noel J.B., Sauvage PJ., Sommer V., Kuperas C., Naouri A.: Quid ? Gallbladder hemorrhage with intraperitoneal rupture. J Radiol, 1999, 80: 741-743. 3. Kim Y.C., Park M.-S., Chung Y.E., et al.: Gallstone spillage caused by spontaneously perforated hemorrhagic cholecystitis. World J Gastroenterol, 2007, 13: 5525-5526. 4. Nural M.S., Bakan S., Bayrak I.K., Baydin A., Danaci M.: A rare compli-

10.

cation of acute cholecystitis: trans hepatic perforation associated with massive intraperitoneal hemorrhage. Emerg Radiol, 2007, 14: 439-441. Tavernaraki K., Sykara A., Tavernaraki E., Chondros D., Lolis E.D.: Massive intraperitoneal bleeding due to hemorrhagic cholecystitis and gallbladder rupture: CT findings. Abdom Imaging, 2011, 36: 565-568. Morris D.S., Porterfield J.R., Sawyer M.D.: Hemorrhagic cholecysititis in an elderly patient taking aspirin and cilostazol. Case Rep Gastroenterol, 2008, 2: 203-207. Refsum S.E., Wilson R.H., Blake G.: Hemoperitoneum following gallbladder necrosis. Ulster Med J, 19923, 61: 207-208. Brainbridge J., Shaaban H., Kenefick N., Armstrong CP.: Delayed presentation of an isolated gallbladder rupture following blunt abdominal trauma: a case report. J Med Case Reports, 2007, 16: 52. Erb R.E., Mirvis S.E., Shanmuganathan K.: Gallbladder injury secondary to blunt trauma: CT findings. J Comput Assist Tomogr, 1994, 18: 778-784. Chen Y.Y., Yi C.H., Chen C.L., Huang S.C., Hsu Y.H.: Hemorrhagic cholecystitis after anticoagulation therapy. Am J Med, 2010, 340: 338339.

CLASSIFIED SERVICES FRANCE, POITIERS (1h30 de Paris par TGV – 1h30 du bord de mer) Ville Universitaire Groupe de 16 radiologues Cabinets 2 cliniques (400 lits) Plateau technique complet dont 2 TDM, 2 IRM, angiographie et radiographie interventionnelles Activité importante Cherche radiologue pour remplacement et succession. Contact: Docteur Luc DEVINEAU – Tél.: 06.34.01.25.01 – Email: luc.devineau@wanadoo.fr

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POST-CONTRAST FLAIR IMAGING IN A PATIENT WITH POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME (PRES) I. Çelebi1, M. Vural2, B. Kahyaog˘lu3, T. Güneysu4 We herein present a case of delayed enhancement of CSF on fluidattenuated inversion recovery (FLAIR) imaging in a patient with posterior reversible encephalopathy syndrome (PRES). In our case despite the settled clinical setting of PRES initial MR scan was negative and on repeated FLAIR imaging increased CSF signal intensity was more conspicuous than subtle cortical involvement. Key-word: Brain, diseases.

Case report A 65-year-old woman was admitted to the emergency service with sudden speech disturbance, difficulties in finding words, and numbness in right arm. Other findings of her neurologic examination were normal. Blood pressure on admission was 196/98 mmHg. There was no evidence of renal dysfunction by laboratory tests. MR imaging of brain and contrast enhanced (0.1 mmol/kg gadodiamid) supraaortic MR- angiography were performed. MR findings of brain were unremarkable, apart from periventricular white matter signal intensity consistent with chronic microangiopathic ischemic changes (Fig. 1A). Diffusion weighted images and apparent diffusion coefficient maps demonstrated no restricted diffusion. On MR-angiography supraaortic arterial system was unremarkable. Transient ischemic attack was suspected on the basis of clinical presentation and essentially negative MRI of the brain and anticoagulant therapy was started. Eight hours after the initial scan, MR examination of the brain was repeated because of persistent clinical statement. Unenhanced FLAIR images demonstrated elevated signal intensity throughout the subarachnoid spaces over both hemispheres and symmetric subtle cortical hyperintensity in the parietal and occipital lobes and inferior temporaloccipital junction, which had not been present on the initial scan (Fig. 1B). Subarachnoid hemorrhage was suggested as a possible explanation for the CSF signal elevation,

but subsequent CT examination was negative. The persistent clinical features and FLAIR imaging findings suggested PRES in the setting of hypertensive attack and anticoagulant theraphy was replaced with intravenous Nimodipin theraphy. Rapid clinical improvements were seen by the day two and follow-up FLAIR imaging revealed normal signal intensity of CSF and parenchyma (Fig. 1C). Discussion PRES is a neurotoxic state and typically characterized by headache, altered mental functioning, seizure and visual loss. The typical imaging finding is symmetric cortical and subcortical edema with a predominantly posterior distribution. The most common causes of PRES are preeclampsia/eclampsia, infection/ sepsis, autoimmune disease, cancer chemotherapy, transplantation and hypertension. Although there has been significant research regarding the pathophysiology of PRES it continues to be debated. Two opposing hypotheses exist. The earlier theory suggests that overreaction of brain autoregulation results in reversible vasoconstruction, and subsequent reversible ischemia. The newer and more favorable second theory suggests that severe hypertension exceeds the limits of autoregulation resulting in injury to the capillary bed and subsequent hyperperfusion and hyperpermeability of bloodbrain barrier. Hamilton et al. (1) presented a case of PRES with delayed enhancement of CSF and speculated that this finding provides additional

From: 1. Radiology Clinic, Sisli Etfal Training and Research Hospital, Istanbul, 2. Radiology Clinic, 3. Neurology Clinic, VKV American Hospital, Istanbul, 4. Radiology Clinic, Medmar Radiodiagnostic Center, Istanbul, Turkey. Address for correspondence: Dr I. Çelebi, M.D., Radiology Clinic, S¸is¸li Etfal Training and Research Hospital, 34377 S¸is¸li, Istanbul, Turkey. E-mail: irfancelebi@gmail.com

evidence in support of newer theory of hypertension/hyperperfusion. In many institution FLAIR pulse sequence has become a part of routine MR examination protocol due to CSF nulling and heavy T2 weighting. It is well known that varied pathologies increasing the CSF protein level or cellularity may result in increased signal intensity in CSF on FLAIR MR imaging and this signal change is more conspicuous than on standart T1 and T2 weighted spin echo sequences. CSF signal intensity changes have been observed with major disruptions of the blood-brain barrier in studies involving neurologic disorders such as ischemic stroke, epilepsy, tumors, acute inflammatory/infectious causes and vascular malformations (2, 3). In the literature, it is reported that the weakly paramagnetic effect of supplemental oxygen results in reduction of CSF T1-weighted relaxation time and subsequent high signal intensity on FLAIR images (4). However, our patient did not receive supplemental oxygen therapy. Artifact-related causes of hyperintensity on FLAIR images include; CSF pulsation, vascular pulsation, magnetic susceptibility and motion artifact (5). It can not be CSF pulsation artifact, since such artifacts tend to occur in the basal, prepontine, and cerebellopontine angle cisterns and in sections containing foramina of the ventricular system. These artifacts are less common and less intense over the convexities of the cerebral hemispheres, where CSF flow is diminished (6). Susceptibility artifacts and resultant FLAIR subarachnoid hyperintensity most commonly occur in the presence of metal, but more subtle local incomplete nulling of CSF can be caused by air in the paranasal sinuses and the temporal bones. The hyperintensities of our patient is at parietal and occipital lobes away from temporal bones and paranasal sinuses . It can not be vascular or motion artifact since they are not

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C Fig. 1. â&#x20AC;&#x201D; A. Initial axial FLAIR image is unremarkable apart from microangiopathic white matter intensities. B. Repeat FLAIR imaging reveals extensive CSF enhancement and mild cortical involvement with a predominantly posterior distribution. Cortical-based subtle lesions are difficult to appreciate owing to the adjacent hyperintense CSF. C. Follow-up FLAIR imaging obtained two days after the initial scan demonstrates complete resolution of lesions.

periodic with no synchrony between the phase-encoding steps. In our case, the imaging which repeated 8 hours after the first evaluation was carried out using the same device and same technical parameters. The hyperintensity in posterior cerebrospinal fluid areas which was not seen in the initial evaluation and

appeared after 8 hours takes us away from the opinion of artefactinduced hyperintensity. In the third follow-up examination, the same parameters were used again and CSF hyperintensity was disappeared. The main pathway of elimination of different gadolinium chelates is

glomerular filtration (7). The mean elimination half-life is 1.3 hours to 1.6 hours in healthy subjects (8). In patients with severe renal failure the mean elimination half-life has been shown to increased up to 30 hours (9). In the setting of renal insufficiency gadolinium accumulation in the CSF has been reported (10). Morris et.al has reported elevation of CSF intensity after prior administration of gadolinium on FLAIR imaging in subjects with normal renal function and without abnormalities known to disrupt the blood-brain barrier (11). Although the blood-brain barrier has been studied extensively, it remains unclear precisely where the gadolinium entered the CSF. The intact endothelium of brain capillaries has tight junctions and the blood-brain barrier is highly restrictive to passage of solutes, such as gadolinium. Blood-CSF barrier with fenestrated endothelium at the choroid plexus level and the circumventricular organs without the thight junctions in the capillary endothelium may allow the diffusion of gadolinium under certain conditions (12, 13). Ciliary body of eye has fenestrated capillary endothelium like choroid plexus and intraoccular T1 shortening effect after contrast administration was reported (14, 15). In our case despite the settled clinical setting of PRES initial MR scan was negative and on repeated FLAIR imaging increased CSF signal intensity was more conspicuous than subtle cortical involvement.

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POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME — C¸ELEBI et al

References 1. Hamilton B.E., Nesbit G.M.: Delayed CSF enhancementin posterior reversible encephalopathy syndrome. AJNR, 2008, 29: 456-457. 2. Levy L.M.: Exceeding the limits of the normal blood-brain barrier: Quo vadis gadolinium? AJNR, 2007, 28: 1835-1836. 3. Taoka T., Yuh W.T.C., White M.L., Quets J.P., Maley J.E., Ueda T.: Sulcal hyperintensity on fluid-attenuated inversion recovery MR images in patients without apparent cerebrospinal fluid abnormality. AJR, 2001, 16: 519-524. 4. Anzai Y., Ishikawa M., Shaw DW., Artru A., Yarnykh V., Maravilla K.R.: Paramagnetic effect of supplemental oxygen on CSF hyperintensity on fluid-attenuated inversion recovery MR images. AJNR, 2004, 25: 274-279. 5. Stuckey S.L., Goh T.D., Heffernan T., Rowan D.: Hyperintensity in the Subarachnoid Space on FLAIR MRI. AJR, 2007, 189: 913-921.

6. Rydberg J.N., Hammond C.A., Grimm R.C., et al.: Initial clinical experience in MR imaging of the brain with a fast fluid-attenuated inversion-recovery pulse sequence. Radiology, 1994, 193: 173-180. 7. Staks T., Schuhmann-Giampieri G., Frenzel T., Weinmann H.J., Lange L., Platzek J.: Pharmacokinetics, dose proportionality, and tolerability of gadobutrol after single intravenous injection in healthy volunteers. Invest Radiol, 1994, 709-715. 8. Joffe P., Thomsen H.S., Meusel M.: Pharmacokinetics of gadodiamide injection in patients with severe renal insufficiency and patients undergoing hemodialyis or continuous ambulatory peritoneal dialysis. Acad Radiol, 1998, 5: 491-502. 9. Shellock F.G., Kanal E.: Safety of magnetic resonance imaging contrast agents. J Magn Reson Imaging, 1999, 10: 477-484. 10. Rai A.T., Hogg J.P.: Persistence of gadolinium in CSF: a diagnostic pitfall in patients with end-stage renal

11.

12. 13. 14.

15.

disease. AJNR, 2001, 22: 13571361. Morris J.M., Miller G.M.: Increased signal in the subaracnoid space on fluid-attenuated inversion recovery imaging associated with the clearance dynamics of gadolinium chelate: a potential diagnostic pitfall. AJNR, 2007, 28: 1964-1967. Davson H.: Dynamic aspects of cerebrospinal fluid. Dev Med Child Neurol(Suppl), 1972, 27: 1-6. Carpenter M.B.: Coe Text of Neuroanatomy, (3rd ed) Baltimore: Williams & Wilkins, 1985: 1-19. Kanamalla U.S., Boyko O.B.: Gadolinium diffusion into orbital vitreus and aqueous humor, perivascular space, and ventricles in patients with chronic renal disease. AJR, 2002, 179: 1350-1352. Akın K., Agıldere A.M., Sezer S.: Hyperintense signal in the subarachnoid space and ocular globes in brain MRI of a patient with acute renal failure. Eur J Radiol, 2005, extra volume 55 issue 2:41-45.

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LETTER TO THE EDITOR MDCT FEATURES OF SPONTANEOUS PNEUMOMEDIASTINUM BY MACKLIN EFFECT G.C. Colin1, F.C. Deprez1, P. Bosschaert1

Dear editor, we read with great interest the two recent case reports about pneumomediastinum: “Complicated pulmonary interstitial emphysema” reported by C. Altay (JBR-BTR, 2011, 94: 84) and “Spontaneous soccer-induced pneumomediastinum in a 39-year-old man” reported by K. De Smet (JBR-BTR, 2011, 346-347). We would like to widen this subject, reporting a case of massive spontaneous pneumomediastinum by Macklin effect in a 25-year-old man. High quality MDCT series, associated to scientific literature review, allow us to highlight the the CT appearance of the Macklin effect leads us to affirm the spontaneous orgin of the pneumomediastinum and thus permitting to be reassuring. Our patient, a previously healthy 25-year-old man, entered the hospital complaining of acute retrosternal

pain which worsened with deep breathing and shortness of breath. Cardio-pulmonary examination, blood test and electrocardiogram were reassuring. Chest radiography revealed pneumomediastinum with gas collection dissecting the tissues of the neck (Fig. 1). A computed tomography (CT-scan) was performed and massive pneumomediastinum was confirmed, along with subcutaneous emphysema and a small left pneumothorax (Fig. 2-3). There was no pleural effusion. We also detected some free air collection along the segmental and lobar bronchi and pulmonary arteries representing interstitial pulmonary emphysema. These CT features indicated the spontaneous origin of pneumomediastinum which in turn helped us to be reassuring in our approach. Nevertheless, an esophagoscopy

and endoscopy of the upper airways were performed and were normal. The patient was treated with 48-hour medical observation. During that time, clinical manifestations were resolved and radiographic signs of conditions disappeared. Spontaneous pneumomediastinum (SP) is defined as the nontraumatic presence of free air in the mediastinum of a patient with no known underlying disease. It is a probably underestimated condition that has been observed to occur in young adults. According to scientific literature (1-4), the clinical presentation of SP in the majority of the cases associated with acute retrosternal chest pain (60 to 70%), coughing (25 to 40%), shortness of breath (25 to 67%) and subcutaneous emphysema (40 to 80%) at the physical examination. Dysphagia and neck pain are also

Fig. 1. — A. Initial anteroposterior radiograph shows continuous diaphragm sign (black arrowheads) due to air trapped posterior to the pericardium and linear band of mediastinal air outlining the descending aorta (horizontal black arrows). Subtle subcutaneous emphysema is observed over the right clavicle (asterisk). Pneumomediastinum reveals the pleural surface (white arrows) From: 1. Department of Radiology, Clinique St-Pierre, Ottignies, Belgium. delineating the mediastinal compartAddress for correspondence: Dr G. Colin, M.D., Clinique St-Pierre, Av. Reine Fabiola 9, ment. B. Detail of initial radiographs. B-1340 Ottignies, Belgium. E-mail: geoffreycolin1@hotmail.com

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Fig. 2. — Axial CT views of the (A) basicervical subcutaneous emphysemous, (B) sub-carina mediastinum and (C) inferior mediastinum with pneumoprecardium. (D) minIP sagittal reformat view demonstrates the pneumomedistinum extension. Medistinal structures are surrounded by air and become visible on radiographs.

possible. SP should be considered in the differential diagnosis of acute chest pain. In fact, the “spontaneous” mediastinum is rarely truly spontaneous, but caused by an acute raised intraalveolar pressure: a high-pressure gradient between distal alveoli and pulmonary interstitium leads to alveolar rupture. This cause the free gas to dissect along the peribronchovascular fascial sheaths (interstitial emphysema), into the hilum and then into the mediastinum. Once the gas is in the mediastinum, it can then track to cervical soft tissues (or even to retroperitoneum) producing subcutaneous emphysema. This physiopathology process was initially described by Macklin and Macklin. In the SP of a young adult, a precipi-

tating factor (related to Valsalva manoeuvre) is often present: exacerbation of asthma, cough (infection of upper airways), vomiting, sneezing, inhalation of drugs (speed, cocaine, amphetamine-derived drugs). In the case discussed above, the patient inhaled an illicit drug (amphetamine-derived) 36 hours before the symptoms reportedly began. In suspicion of pneumomediastinum, a CT-scan is the main relevant additional test to perform (5). A minority of cases of pneumomediastinum can be overlooked with chest radiography; alternately, CTscan reveals pneumomediastinum in 100% of the patients tested (1). After the diagnosis of pneumomediastinum, the most critical issue is in

determining if pneumomediastinum is spontaneous or secondary to esophageal or airway perforation. Actually, a lot of investigations are often performed (esophagography or contrast-enhanced swallow chestCT, esophagogastroduodenocopy and bronchoscopy), especially in presence of history of vomiting or cough. However, these patients are often over-evaluated and thus, the additional tests are almost invariably negative in their results (1, 4). In this context, perform a chest CT can allow the radiologist to diagnose the spontaneous origin of pneumomediastinum. At first, analysis of the pulmonary parenchyma should be normal. This rules out any underlying chronic pulmonary disease related to pneumomediastinum such as:

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Fig. 3. — Detail of axial CT views shows the “air around the artery” sign (black arrows) with air in the perivascular and peribronchial sheaths, surrounding main branches of pulmonary arteries. Theses characteristics are pathognomonic findings of pneumomediastinum by Macklin effect when they are found aloof from the hilum.

emphysema, cyst lesions, interstitial disease (2, 4). Secondly, examination of the pleural space is important in such a situation. A pneumothorax is associated in 6% to 30% of cases (4) and represents a potential serious complication of SP. Pleural effusion should be absent in cases of SP because it is more compatible with secondary pneumomediastinum (1). Finally, we want to point out CT features as indicative of the Macklin effect: free gas collection in the distal parenchyma and interstitial pulmonary emphysema (6, 7) with linear free air collection (aeric density without wall) around the bronchus or the vasculature dissecting the bronchovascular sheaths and spreading into the hilum (Fig. 3-4). To our knowledge, this effect has not yet been described in the case of secondary pneumomediastinum with airway or esophageal rupture and it is specific of a “spontaneous” origin of the pneumomediastinum if the pulmonary parenchyma appears normal. Note that on axial pictures free gas around the vessel can give the ring around the artery sign, but this sign is non-specific of the Macklin effect if found near the hilum. SP is a benign condition and presence of gas into the interstitium or

into the mediastinum does not affect gas exchanges nor blood gas analysis (8). A pneumothorax is sometimes associated and is often small. The outcome is usually positive, with resolution of symptoms within a few days. It can be treated expectantly with an admission to the hospital for 2 to 5 days for medical supervision, with reassuring treatment, bed rest, oxygen therapy and analgesics. Re-occurrence is exceptional and out-patient follow-up is usually not necessary. In conclusion, spontaneous pneumomediastinum is an often missed entity that should be considered in the differential diagnosis of acute chest pain, especially in young adults. We want to point out in particular that the performance of a chest CT in the management of spontaneous pneumomediastinum is important to remind us that the CT appearance of the Macklin effect leads to affirmation of the spontaneous origin of the pneumomediastinum, thus avoiding additional tests for the patient.

References 1.

Caceres M., Ali S.Z., Braud R., Weiman D., Garrett H.E. Jr.: Spontaneous Pneumomediastinum:

A Comparative Study and Review of the Literature. Ann Thorac Surg, 2008, 86: 962-966. Macia I., Moya J., Ramos R., Morera R., Escobar I., Saumench J., Perna V., Rivas F.: Spontaneous pneumomediastinum: 41 cases. Eur J Cardiothorac Surg, 2007, 31: 11101114. Andrew E., Newcomb C., Clarke P.: Spontaneous pneumomediastinum: a benign curiosity or a significant problem ? Chest, 2005, 128: 3298-302. Iyer V.N., Joshi A.Y., Ryu J.H.: Spontaneous pneumomediastinum: analysis of 62 consecutive adult patients. Mayo Clin Proc, 2009, 84: 417-421. Koullias G.J., Korkolis D.P., Wang X.J., Hammond G.L.: Current assessment and management of spontaneous pneumomediastinum: experience in 24 adult patients. Eur J Cardiothorac Surg, 2004, 25: 852-855. Wintermark M., Wicky S., Schnyder P., Capasso P.: Blunt traumatic pneumomediastinum: using CT to reveal the Macklin effect. Am J Roentgenol, 1999, 172: 129-130. Kemper A.C., Steinberg K.P., Stern E.J.: Pulmonary interstitial emphysema: CT findings. AJR, 1999, 172: 1642. Wintermark M., Schnyder P.: The Macklin effect: a frequent etiology for pneumomediastinum in severe blunt chest trauma. Chest, 2001, 120: 543547.

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JBR–BTR, 2012, 95: 101.

IMAGES IN CLINICAL RADIOLOGY Pigmented villonodular synovitis of the ankle presenting as a persisting ankle effusion C. Verlinden1, F.M. Vanhoenacker2,3,4, P. Boone1

A 38-year-old woman was referred to our department with persisting pain and swelling of the right ankle, 10 months following an inversion trauma. Initial standard radiographs were unremarkable. Conservative treatment with physiotherapy and local infiltration was unsuccessful. Three month later, repeated plain radiographs revealed a slightly radiodense mass at the anterior aspect of the talocrural joint (Fig. A, white arrow). An MRI was performed for further characterization. These images show an intra-articular nodular mass within the anterior ankle joint recess. The lesion was of intermediate to low signal intensity on axial T1-weighted (WI) images (Fig. B, star). On sagittal fatsuppressed T2-WI, the lesion contained multiple intralesional areas of low signal intensity interspersed with areas of high signal (Fig. C, star). A peripheral low signal intensity rim was seen, in keeping with hemosiderin deposition within the synovium (Fig. C, black arrow). Blooming artefact was seen on gradient echo imaging (not shown). Based on the imaging findings, the diagnosis of Pigmented VilloNodular Synovitis (PVNS) was made, which was confirmed on surgery (Fig. D, surgical view showing a lesion with black pigment within the synovium) and subsequent histological examination. The postoperative course was uneventful. Comment

PVNS is a relatively rare proliferative disorder of the synovium, characterized by the formation of nodular synovial masses with a unique histological structure mainly consisting of hemosiderin deposits. The predominantly affected joint is the knee, followed by the ankle and in rare cases the wrist, hip, shoulder and elbow. The etiology of the disease remains a matter of debate. Some authors indicate trauma and haemarthrosis as primary trigger of the synovial proliferation. The most typical clinical presentation is painful swelling around a joint. Standard radiographs may be normal in an early stage, or may reveal uncalcified radiodense masses. Later, rapid proliferation of the synovium may cause erosions and marginal sclerosis in the adjacent bone. CT is rarely used for diagnosis, but it may evaluate more subtle erosions and can be used for imaging guided core biopsy. For early detection, MRI is the preferred imaging technique and is currently referred as the gold standard. Both T1-and T2-WI images reveal hypointense intra-articular masses, indicative of hemosiderin deposition. Fatsuppressed T2-WI images may show areas of interspersed fluid entrapped within the thickened and hemosiderin-laden synovium. Gradient echo imaging may be useful to demonstrate “blooming” artefact of the hemosiderin deposits. After administration of gadolinium contrast, marked enhancement is the rule. These characteristic findings on MRI images allow a differentiation between other proliferative diseases about the joints, such as rheumatoid arthritis, synovial sarcoma, osteochondromatosis and lipoma arborescens. Surgery remains the gold standard in treatment of PVNS. A synovectomy with total excision should be performed in all cases. Overall, PVNS has a high risk of recurrence. Reference 1.

Hao D.P., Zhang J.Z., Xu W.J., Wang Z.C., Wang X.N.: Pigmented Villonodular Synovitis of the Ankle, Radiologic characteristics. J Am Podiatr Med Assoc, 2011, 101: 252-258.

D Department of 1. Orthopaedic Surgery, 2. Radiology, AZ Sint-Maarten Duffel-Mechelen, Mechelen, 3. Department of Radiology, Antwerp University Hospital, Edegem, 4. Faculty of Medicine and Health Sciences, University of Ghent, Ghent, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Heterotopic pancreatitis causing confusion in small bowel tumor J. Joskin1, N. Bleus1, T. Couvreur1, L. Tselikas2, M. Milicevic1 A 39-year-old man was admitted to our hospital for acute epigastric pain with nausea and vomiting. Physical examination was suggestive for acute abdomen without peritoneal irritation findings. Blood tests results were as follow: alanine aminotransferase (ALT): 87 U/L, aspartate aminotransferase (AST): 55 U/L, amylase: 135 U/L, lipase: 69 U/L, total bilirubin: 11,6 mg/l, creatinine: 9 mg/l, C-reactive protein (CRP): 108,4 mg/L, and white blood cells (WBC): 14640/mm3. A contrast-enhanced computed tomography (CT) scan of the abdomen was performed, including a reformatted image in the axial plane (Fig. A) and a reformatted image in the coronal plane (Fig. B) and revealed an ovoid soft-tissue mass depending on jejunal wall with homogeneous enhancement (arrows). A short segment of a bowel loop was asymmetrically thickened, with surrounding mesenteric edema and mesenteric lymph nodes. Abdominal ultrasound (US) confirmed the above-mentioned description and showed an ovoid soft-tissue mass at the expense of the jejunal wall. The Doppler-US showed vascularization of the ovoid mass. The diagnosis of the jejunal tumor (probably gastrointestinal stromal jejunal tumor or lymphoma) was suggested. A laparoscopy was performed and revealed a mass which was removed and a short bowel segment was resected. Frozen sections (Fig. C) demonstrated ectopic pancreas infiltrating the mesentery and the jejunal wall to the submucosa with signs of pancreatitis.

Comment Heterotopic pancreas is a congenital anomaly defined as pancreatic tissue in aberrant location lacking anatomic, ductal and vascular continuity with the eutopic gland. The origin of heterotopic pancreas is controversial. However the most accepted theory speaks of a separation during the endodermal embryogenic invagination of the primitive duodenal wall. The heterotopic tissue remains incorporated into the upper gastrointestinal tract within the bowel wall. The common sites of heterotopic pancreas are the duodenum, gastric antrum, jejunum and ileum. Jejunal location has been reported with an incidence of 16 to 35% and manifests as a submucosal or rarely as a subserosal mass. In uncommon cases, heterotopic pancreas has been found in the oesophagus, mediastinal teratoma, gallbladder, omentum, spleen, fallopian tubes, lymph nodes, jejunal diverticulum and Meckelâ&#x20AC;&#x2122;s diverticulum. Although most cases of heterotopic pancreas are asymptomatic, non specific gastrointestinal symptoms have been described in 3040%. The clinical signs are epigastric pain (77%), tarry stools (24%), vomiting (18%) or diarrhea (18%). Complications include mechanical obstructions, cyst degeneration, gastrointestinal bleeding, pancreatic cancer or acute pancreatitis. Those complications are the same as those for the eutopic pancreas.

C Reference 1.

Farrar W.B., Scott M., O'Dwyer P.J.: Heterotopic pancreas. Ir J Med Sci, 1990, 159: 19-20.

1. Department of Radiology, CHU Sart-Tilman, Liege, Belgium, 2. Department of Radiology, Georges Pompidou Hospital, Paris, France.

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JBR–BTR, 2012, 95: 103.

IMAGES IN CLINICAL RADIOLOGY Sonographic findings of Meckel’s diverticulitis J. Samain, S. Maeyaert, E. Geusens, E. Mussen1 An 18-year-old young man with no medical history presented at the emergency department with nausea, vomiting and pain in the right iliac fossa and the periumbilical region. Blood analysis was normal except for an elevated C-reactive protein (CRP) of 64 mg/L. High frequency gray-scale sonogram was performed and showed a normal presentation of the appendix. A tubular hypo-echogenic structure (length of 3 cm, width of 1 cm) with a cystlike center and an irregular thickened wall was discovered in the right periumbilical region (Fig. A). Color Doppler sonogram reveals a hypervascular wall (Fig. B) and infiltration of the surrounding mesenteric fat arrow in Fig. A and B). Diagnosis of Meckel diverticulitis was suggested, although a complicated duplication cyst could not be excluded. CT scan that followed showed a rim-enhancing tubular structure in the right peri-umbilical region with surrounding inflammatory changes (Fig. C). Surgery and pathology that followed confirmed a Meckel diverticulitis.

Comment Meckel's diverticulum is the most common congenital anomaly of the gastrointestinal tract, with an incidence of 1-3% of the population, although only 4% of those affected become symptomatic. When the vitelline (omphalomesenteric) duct fails to obliterate during fetal development, several anomalies appear, Meckel's diverticulum being the most frequent. B It occurs on the antimesenteric border of the ileum, 40-100 cm proximal to the ileocecal valve. Clinical symptoms arise from complications of the diverticulum, which are most common in male and in the pediatric population. Hemorrhage from peptic ulceration, small intestinal obstruction, and diverticulitis are the most frequent complications. Diverticulitis can mimic appendicitis clinically and on sonography the inflamed Meckel's diverticulum can be wrongly interpreted as an abnormal cecal appendix. Meckel’s diverticulitis appears as a round or tubular, cystlike structure with a thick, irregular hyperechoic internal wall and a hypoechoic external wall (Fig. A). The outer hypoechogenic layer corresponds to the muscularis propria of the intestinal wall, and the inner hyperechogenic layer corresponds to the mucosa and submucosal layers. This mural pattern of echogenicity is called the gut signature. The inflamed diverticulum may resemble appendicitis because it may be non-compressible when pressure is applied to the abdominal wall with the ultrasound transducer; in contrast, the inflamed diverticulum may be compressible and resemble a duplication cyst. In the latter circumstance, a duplication cyst usually has a smooth internal wall, compared with the irregular internal wall and the more tubular structure of an inflamed Meckel’s diverticulum. The presence of air inside the Meckel's diverticulum and its mobility during the peristaltic activity of the adjacent bowel loops can give the Meckel's diverticulum an appearance that is similar to the rest of the intestine. Color C Doppler sonography can be important in revealing hypervascularization, signs of inflammation of the Meckel's diverticulum and showing the presence of anomalous vessels, an appearance not found in the rest of the intestine. Echogenic foci in the lumen may represent enteroliths, fecoliths, or inflammatory debris. Sonography will not supersede 99mTc pertechnetate scintigraphy because scintigraphy is a highly accurate tool to use in establishing the diagnosis of an inflamed Meckel's diverticulum. Sonography may, however, be useful in patients who have rectal bleeding and whose scintigraphic findings are negative. For patients with diverticulitis and clinical signs and symptoms suggestive of appendicitis, a sonographic diagnosis may be made if the Meckel's diverticulum presents as a cystlike structure with a wall exhibiting the gut signature. Routine color Doppler sonography reveals anomalous vessels and signs of inflammation on the wall of the Meckel's diverticulum. Reference 1.

Baldisserotto M., Maffazzoni D., Dora M.: Sonographic findings of Meckel's diverticulitis in children. AJR, 2003, 180: 425-428.

1. Department of Radiology, University Hospital Leuven, Leuven, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Supralabral air on plain radiography of the shoulder: first sign of an air-containing paralabral cyst M. Demeter, Y. Vankan, A. Demeyere, D. Perdieus1

A forty-one-year-old male patient was referred to our department of Radiology for left shoulder pain and reduced mobility. There was no history of trauma, infection nor therapeutic intervention. A plain radiograph (Fig. A) of the left shoulder showed the presence of two small roundshaped lucent bubbles in the soft tissue above the glenoid. An additional ultrasound examination revealed the presence of a cyst in the suprascapular notch (Fig. B), slight atrophy and increased echogenicity of the infraspinatus muscle. Further investigation with T1 and T2 weighted pulsesequences on MRI revealed a loculated fluid-filled collection in the suprascapular notch, causing an impression on the suprascapular nerve and vessels. This fluid collection contained diminished signal intensity spots caused by the air collections. The infraspinatus muscle, innerved by the suprascapular nerve, showed on T2 weighted MR image a diffuse slightly increased intensity and thickening. Axial T2-weighted MR image (Fig. C) demonstrated communication between the paralabral fluid collection and the glenohumeral joint trough a tear in the superior and posterior glenoid labrum. Based on the imaging findings, the diagnosis of a large locular paralabral cyst, caused by a glenoid labral tear, was made. As a consequence, in this case, the suprascapular nerve was compressed and the infraspinatus muscle showed denervation signs. After arthroscopic decompression of the paralabral cyst, the patient complaints improved. Comment

Paralabral cysts in the shoulder (located in the suprascapular or spinoglenoid notch) are well known to cause suprascapular nerve impingement and are a risk for atrophy and denervation of the infraspinatus muscle. It is conceivable that cysts usually arise from a defect in the delineation of the shoulder joint, such as glenoid labral tears. Common complaints are shoulder pain and reduced functionality. Treatment of symptomatic paralabral cysts varies from observation, ultrasound-guided percutaneous aspiration, open excision, to arthroscopic decompression with or without labral repair. Ultrasound as a first diagnostic investigation tool can reveal the presence of a paralabral cyst. The additional value of MRI is that it mostly depicts the underlaying cause, such as a labral tear. MR arthrography or CT-artrography in our experience is the most sensitive investigation tool to demonstrate ruptures or fissures in the glenoid labrum. Most of the time, the initially plain radiography is negative for paralabral cysts. Though, the presence of air in the shoulder can be caused by trauma, degeneration, infections or iatrogenic by punctures, one should always consider supralabral air as a first sign of paralabral air-filled cyst, as shown in the present article. Reference 1.

Tung G.A., Entzian D., Stern J.B., Green A.: MR imaging and MR arthrography of paraglenoid labral cysts. AJR, 2000, 174: 1707-1715.

1. Department of Radiology, Imelda Hospital, Bonheiden, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Isolated splenic vein thrombosis G. Karagiannis1, A. Anagnostara1, V. Samaras2, S. Mylona1

A 70-year old woman presented to our hospital with a one month history of diffuse abdominal pain, vomiting, nausea and some diarrheic episodes alterning with constipation. She reported a personal history of autoimmune hemolytic anemia under cortisone for one year. Clinical examination was negative. Her laboratory tests except for the expected anemia (hematocrit 26%) revealed elevated inflammation signs (WBC: 15300, ESR: 122 and CRP: 231) and LDH (590 U/l) and a positive direct Coombs test for IgG antibodies. US of the abdomen showed a large hypoechoic lesion occupying the upper pole and middle part of the spleen (Fig. A). Splenic dimensions were measured as normal (craniocaudal diameter of about 11 cm). Abdominal CT confirmed the presence of a hypodense lesion in the splenic parenchyma reaching up to the splenic capsule. This finding was probably attributed to extensive splenic infarction (Fig. B). A large filling defect into splenic vein was clearly demonstrated (Fig. B and C, elbow arrows) while portal vein and superior mesenteric vein were shown patent (Fig. B and C, simple arrows). The final diagnosis was isolated splenic vein thrombosis and the patient underwent a splenectomy. The patient finally had a negative examination for thrombophilia (levels of antithrombin, protein C and S were normal) and was referred to hematologists for further evaluation. Comment

Isolated splenic vein thrombosis is an underrecognized clinical entity. Imaging procedures like abdominal US or CT play a crucial role to its early diagnosis, especially in patients, like our case, with atypical symptoms. Especially, contrast enhanced CT in both arterial and portal phase, is a suitable method for demonstrating splenic infarcts and potential causes (e.g. pancreatitis, pancreatic tumors) of splenic vein thrombosis as well as for examining splenic vessels patency. Splenic vein is mainly thrombosed together with superior mesenteric vein or portal vein as a result of neoplasms, cirrhosis or other causes of portal hypertenC sion. Isolated splenic vein thrombosis is a quite rare clinical condition (about 7% of splachnic vein thromboses). It appears clinically in most of the cases with upper gastrointestinal bleeding and clinical findings of left portal hypertension, mainly isolated gastric varices. This clinical condition does not affect normal liver function and symptoms of acute abdomen are extremely rare. Main causes of thrombosis are inflammation or neoplasms of the pancreas or less often left renal pathology. Splenic hypoperfusion has been proved reversible in some cases of acute thrombosis (e.g. due to inflammatory exacerbation of Crohnâ&#x20AC;&#x2122;s disease). Especially small focal infarcts can be treated satisfactorily with on time administration of antiplatelet therapy. On the contrary, extended infarcts occupying almost the whole spleen and wall to wall thrombus into the splenic vein, like in our case are particularly difficult to be treated pharmacologically. Furthermore, abdominal vein thromboses may be a complication of hematological disorders. Various hematological disorders have been correlated with thromboembolic predisposition. Polycythemia or other myeloproliferative disorders and some types of anemia, like sickle cell disease or hemolytic anemias, are considered thromboembolic risk factors. Autoimmune hemolytic anemia (AIHA) is a mainly idiopathic condition where the body attacks its own red blood cells leading to their destruction (hemolysis) usually performed in the spleen. Thus, splenectomy along with corticosteroid and immunodepressing therapies is the treatment in most of the cases. The most known mechanism of splenic vein thrombosis to these patients is a consequence of splenectomy. AIHA has been lately associated with venous thromboembolism (deep venous thrombosis, pulmonary embolism) especially to splenectomized patients. Another type of hemolytic anemia that increases the risk for thrombosis, especially to vein branches which are not usually affected like in our case, is paroxysmal nocturnal hemoglobinuria. The diagnosis of isolated splenic vein thrombosis is basically radiological in atypical cases and may indicate a hematologic disorder, especially when no other underlying cause is depicted. References 1. Ataga K.: Hypercoagubility and thrombotic complications in hemolytic anemias. Haematologica, 2009, 94: 1481-1484. 2. Thatipelli M.R., McBane R.D., Hodge D.O., et al.: Survival and recurrence in patients with splachnic vein thromboses. Clin Gastroenterol Hepatol, 2010, 8: 200-205.

1. Department of Radiology, 2. Department of Pathology, Korgialenio-Benakio, Hellenic Red Cross General Hospital, Athens, Greece.

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IMAGES IN CLINICAL RADIOLOGY Kohler’s disease of the patella S.S. Suresh, M.S. Orth, M. Ch. Orth1 An eight-year-old boy was referred to the trauma clinic with fracture of the patella. The boy had trivial trauma to the left knee when he fell down from a writing desk while in school. The boy walked in to our clinic. There was no effusion in the knee and the knee was not tender. He had full and pain-free range of movements of the knees. Radiographs of the left knee were available with the patient from the referring institution. This showed a hypoplastic patella with fragmentation and sclerosis (Fig. A). Antero posterior, lateral and skyline views of both knees were done, which showed similar radiologic features in both knees (Fig. B). His blood parameters, including sickling tests were done and found normal. No further radiological investigations were planned. Comment There are many incidences of out-patient clinic visits for anterior knee pain, and in some the patella is thought to be the origin. Osteochondrosis is an abnormal process in the secondary ossification centre, thought to be due to repeated trauma, at the time of growth spurt. One of the reported A causes of anterior knee pain in children between 5 and 9 years of age is osteochondrosis of the patella, otherwise known as Kohler’s disease. This affects the primary ossification centre of the patella. Osteochondrosis of the entire patella is thought to be rare. Patella is affected by two types of osteochondrosis, one affecting the entire ossification centres of the patella, and those affecting the secondary ossification centre. The commonest osteochondrosis in children is the Sinding-Larsen-Johansson disease which affects the child between 9 and 11 years, and is due to the affection of the secondary ossification centre in the lower pole. In the first 4 to 5 years of age, the patella is an expanding mass of cartilage, the shape of which is comparable to the final shape of the adult B patella. Between 4-6 years centrally located multifocal ossification centres appear which rapidly coalesce. The expanding ossification centre may become irregular giving the appearance of fragmentation in radiographs. As early as 1929 Moffat described Kohler’s disease as a disturbance of normal development of bone, occurring during the stage of ossification, and commented on the original paper by Kohler where he described abnormality of the patella in his case report on “isolated disease of the scaphoid”. There is fragmentation and sclerosis of the patella in the plain films. It is a condition of sinister significance and doesn’t require further investigations as the clinical course is that of a self limiting disease. Irregular ossification, fragmentation and sclerosis of the patella could be a normal developmental variation, or this could be an idiopathic self-limited disturbance of enchondral ossification in which rapid growth spurt is present. Some authors consider this as an overuse syndrome. In some children the expanding ossification centre is often irregular, which is a normal variant and diagnosis of osteochondrosis should be made with caution. It is a self limiting pathology with a very benign course and when seen incidentally in the radiographs, the patella is expected to be normal in around 2 years. If at all symptomatic, limitation of physical activity is all that required. Reference 1.

Pinar H., Gul O., Boya H., Ozcan C., Ozcan O.: Osteochondrosis of the primary centre of the patella (Kohler’s disease of the patella) report of three cases. Knee Surg Sports Traumatol Arthrosc, 2002, 10: 141-143.

1. Department of Orthopaedics, Ibri Regional Referral Hospital, Ibri, Sultanate of Oman.

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IMAGES IN CLINICAL RADIOLOGY Intracystic papilloma of the breast M. Smets, C. Van Ongeval, A. Van Steen1

A 53-year-old woman presented for work-up of a painless nodular breast mass. She had no significant personal or family history. Mammography and ultrasound were performed, as well as additional MRI. Mammography showed multiple large cysts in the left breast in (Fig. A). Ultrasound depicted these cystic lesions and showed additional intracystic solid wall proliferations (Fig. B). An MRI examination confirmed the large cysts with solid wall components with contrast enhancement of the solid lesions (Fig. C). Since this image was suspect for malignancy, additional fine needle aspiration cytology (FNAC) was performed. Based on the radiological (mainly ultrasound and MRI) and cytological findings, diagnosis of intracystic papilloma was made. Comment

An intracystic papilloma (ICP) is a benign papillary lesion supported by a fibrovascular stalk, growing inside an apparent cystically dilated duct. It may occur at any age but is most commonly seen between 30 and 55 years. It is very difficult to distinguish radiographically between ICP and intracystic papillary carcinoma (ICPC). ICP more often forms a single nodule protruding intracystically, while ICPC usually is larger (> 3 cm) and forms multiple aggregate nodules or even almost solid tumors with a small cystic part. Despite these guidelines, intracystic papillary lesions may be impossible to differentiate. The kinetic features for contrast enhancement on MRI are not helpful either since both the benign and malignant papillary lesions exhibit fast, strong, early enhancement and washout or a plateau enhancement pattern. Therefore, FNAC should be performed on all cystic breast masses with internal solid wall proliferations. To start, FNAC can help differentiate between intracystic debris and true solid components. And second, cytologic examination can help evaluate for malignant cells suggestive of ICPC. It should be noted however, that it is best not to completely evacuate the intracystic fluid as this can make it more difficult for the surgeon to locate the lesion peroperatively. In case of small lesions a marker, mostly a hooked wire, can be placed intracystically with the intent to locate the lesion more easily during the surgery. However, even FNAC as well as core biopsy with pathology of a intracystic papillary lesion can be misleading because cellular atypia is slight in the majority of ICPCâ&#x20AC;&#x2122;s. For this reason and because several studies have shown that a substantial number of lesions are upgraded in diagnosis at excision, all intracystic papillary lesions diagnosed by either imaging or cytology, should be excised surgically. Reference 1. Devan J.D., David E.M., Giovanna M.C., et al.: Complex cystic breast masses: diagnostic approach and imaging-pathologic correlation. RadioGraphics, 2007, 27: S53-S64.

1. Department of Radiology, University Hospitals Leuven, Leuven, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Bilateral intramuscular pseudotumor in a bodybuilder L. Ardies1, 2, T. De Beule1, T. Degroote1, F.M. Vanhoenacker2, P.K. Vanhoenacker1 A 29-year-old bodybuilder presented with a bilateral palpable and painful soft tissue mass in the deltoid region. CT scan showed a bilateral intramuscular mass within the deltoid muscle with intralesional fat (not shown). For further differentiation and exclusion of a fat-containing sarcomatous lesion, MRI of both shoulders was performed. Axial T1-weighted images (WI) of the right shoulder showed a heterogeneous mass lesion containing multiple fatty components (Fig. A, arrows). Axial T1-WI of the left shoulder depicted a mass with a T1-hyperintense fatty component and marked fat-fluid level (Fig. B, arrow). The lesion also demonstrated a fat-fluid level on a sagittal fat suppressed T2-WI (Fig. C, arrow). The presence of a bilateral fat containing soft tissue mass, combined with a history of local steroid injections were highly suggestive of pseudotumoral fat necrosis with surrounding inflammation rather than a fat-containing sarcoma. Because the lesions were painful, surgical removal was done. Pathological examination of the resection specimens showed fragments of necrotic muscle tissue with cystic degeneration, foamy macrophages and granulomatous foreign body inflammation. These findings confirmed the imaging diagnosis. Because both lesions showed no signs of malignancy and the patient was relieved of his complaints, no further follow-up exams were planned.

Comment

Anabolic steroids are synthetic derivatives of the male hormone testosterone, having an anabolic and androgenic effect. They are often used by bodybuilders to enhance muscle growth and maybe administered orally or by intramuscular injections. Parenteral intake of anabolic steroids results in an increased risk of systemic side effects such as hepatotoxicity, hypercholesterolemia, hypertension and also sex-specific side effects. Intramuscular injection of anabolic steroids may result in acute or chronic local complications. Acute complications include infection, abscess formation, arthritis, tendon tears or nerve damage, and are often caused by the injection technique itself. On rare occasions, injection of steroids can lead to chronic local disease with formation of soft tissue lesions mimicking sarcomas or liposarcomas. The most common sites of involvement are the deltoid and gluteus muscles. The biceps or quadriceps muscles are not commonly involved, because they are C less frequently used as injection sites. Histologically, there are several possible causative mechanisms explaining the origin of these soft tissue lesions: infectious non-sterile injections caused by needle sharing, physical trauma induced by recurrent intramuscular injections, reaction against the steroid or agent mixed with the steroid. In our case, the inflammatory response was characterized by macrophages, foam-cells and the presence of foreign material. These findings were indicative of a foreign body inflammation against the steroid, and more in particular the oilbased components mixed with the steroid. Besides the inflammatory reaction, the lesion also contained multiple areas of muscle necrosis with cystic transformation and fibrosis. Both on MRI and CT, the lesion featured multiple fatcontaining areas. A fat-fluid level can sometimes be seen and is a consequence of repeated trauma and fat-necrosis. Recurrent injections can also lead to intralesional bleeding and hemosiderin deposition, causing faster loss of signal intensity on T2-WI weighted images and gradient echo images. In conclusion, the presence of a bilateral fat containing lesion in the deltoid muscle in a young bodybuilder is highly suggestive for a local complication related to intramuscular injections rather than a tumoral mass lesion. Reference 1.

Al-Ismail K., Torreggiani W.C., Munk P.L., Nicolaou S.: Gluteal mass in a bodybuilder: radiological depiction of a complication of anabolic steroid use. EurRadiol, 2002, 12: 1366-1369. 1. Department of Radiology and Imaging, OLV Ziekenhuis, Aalst, Belgium, 2. Antwerp University Hospital and Universities of Antwerp and Ghent, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Amiodarone induced pulmonary toxicity mimicking malignancy at initial presentation M. Eyselbergs1,2, I. Pilate1, H. Rombouts3, F.M. Vanhoenacker1,2,4 An 81-year-old man with an extensive cardiac history was admitted to the cardiology department because of increasing shortness of breath. His medical history included melanoma and prostate adenocarcinoma 7 and 4 years ago respectively. His medication consisted of antihypertensive, anticoagulant and anti-arrhytmic drugs. Non-enhanced computed tomography (CT) of the chest revealed bilateral zones of consolidation (arrowheads) and multiple nodules of varying size (arrows) with predominant localization in the lower lobes (Fig. A). The lowest axial slices through the liver showed an increased attenuation of the liver parenchyma suggestive of amiodarone-induced liver disease (Fig. C(1), ROI: 78 HU). In view of his oncological history the multiple nodular lesions were primarily suspicious for metastasis. Combined pulmonary and liver imaging findings also raised the possibility of amiodarone induced pulmonary toxicity (AIPT). The patient – however – refused further diagnostic testing. Therefore await-and-see policy was implemented and amiodarone was withdrawn. Followup CT of the chest 4 months later showed marked regression of the lesions (Fig. B) and a decreased attenuation of the liver parenchyma confirming the diagnosis of AIPT (Fig. C(2), ROI: 56 HU).

Comment

Amiodarone is one of the most frequently prescribed anti-arrhythmic agents in Europe. It effectively reduces and prevents (supra)ventricular tachyarrhythmias. However, amiodarone also has multiple potentially life-threatening adverse reactions. The most important one is AIPT often starting within months after initiating therapy. Known risk factors are a high cumulative dose, a daily dose exceeding 400 mg/day, pre-existing lung disease and age. Symptoms are nonspecific and include a nonproductive cough and dyspnea. Pulmonary function testing unveils a restrictive or mixed obstructive-restrictive pattern and often a diminished lung diffusion capacity of more than 20%. Several forms of pulmonary disease can occur among patients treated with amiodarone. Nonspecific interstitial pneumonia (NSIP), cryptogenic organising pneumonia (COP formerly known as Bronchiolitis Obliterans Organising C Pneumonia (BOOP)) and acute respiratory distress syndrome are radiologically the most frequently encountered presentations. The combination of bilateral consolidations and multiple nodular lesions such as in our case, are typical features of COP. In the appropriate clinical context, malignancy is essential in the differential diagnosis of these nodules. Extrapulmonary involvement such as an increased attenuation of the liver or spleen on non-enhanced CT is an additional argument for possible amiodarone induced toxicity. The exact mechanism of the pulmonary toxicity is still highly debated but several mechanisms have been proposed. Cell injury can result from a cytotoxic reaction of the drug but an indirect immunological reaction has also been suggested. Other causes of respiratory failure such as pulmonary embolism, congestive heart disease or infection need to be ruled out in order to initiate the correct therapy. When amiodarone is considered the cause of the pulmonary toxicity, withdrawal of the drug is essential often in combination with low-dose corticosteroids. Resolution of the lesions on imaging can range from 2 to 24 months. Reference 1.

Papiris S.A., Triantafillidou C., Kolilekas L., Markoulaki D., Manali E.D.: Amiodarone Review of Pulmonary Effects and Toxicity. Drug Saf, 2010, 33: 539-558.

1. Department of Radiology, AZ Sint-Maarten Duffel-Mechelen, Duffel, 2. Department of Radiology, Antwerp University Hospital, Edegem, 3. Department of Cardiology, AZ SintMaarten Duffel-Mechelen, Duffel, 4. University of Ghent, Faculty of Medicine and Health sciences, Ghent, Belgium.

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CONTINUING EDUCATION PROCEEDINGS OF THE JOINT MEETING RBRS BONE SECTION AND NEDERLANDSE VERENIGING VOOR SKELETARADIOLOGIE, Leiden, The Netherlands, 25.03.2011 Ankle Distortion Related Lesions. Emphasis on Failed Radiographic Diagnosis J.L. Gielen, P. Van Dyck, J. Veryser1 Introduction Acute ankle distortion trauma is very frequent, it accounts for about 10% of emergency room admissions. In the acute setting, the Ottawa foot and ankle clinical decision rules are widely used to decide whether or not radiographic evaluation is needed. Although radiographs easily detect displaced fractures, occult fractures may occur. Also, sprains and peroneal tendon dislocation may go undetected using plain radiography. It is the purpose of this overview to briefly discuss ankle distortion related lesions with emphasis on failed radiographic diagnosis. Discussion Acute ankle distortion with inversion or eversion trauma is very frequent, it accounts for about 10% of emergency room admissions (1). In about 85% of ankle distortions, lateral collateral ligament lesion is present. A fracture is detected in about 15% (1) of cases. In the acute setting, the Ottawa foot and ankle clinical decision rules are widely used to decide whether or not radiographic evaluation is needed. By using these rules, about 35% of radiographic examinations can be avoided with a low rate of false negatives (1). Radiographic evaluation includes mortise and lateral views of the ankle and three-quarter views of the foot. An anteroposterior view of the lower leg is added in case of pain on palpation at the level of the proximal half of the fibula. These radiographs easily detect displaced fractures at the medial, lateral or tertiary malleolus, the fibula metaphysis and diaphysis, the fifth metatarsal, at the talus neck or dome and the posterior talus processus or os trigonum. Also grade III sprains of the syndesmosis may be detected on plain radiography. Appreciation of radiographs with the Lauge Hansen classification of ankle trauma has a major advantage compared to the Weber classification as it includes the trauma mechanism and position of the foot at the time of the injury (Fig. 1). Therefore, it gives a clue to accompanying ligament lesions and grades the lesion at the distal tibiofibular and ankle joint as being stable or unstable (2-7). In case of supination-adduction trauma (Weber A type), the presence of an

Fig. 1. — Weber and Lauge Hansen ankle trauma classification. In the Weber the higher the level the more chance for syndesmotic rupture and instability. The system by Lauge-Hansen (1950) is based on the position of the foot at the time of injury and the direction of the force on the talus with respect to the leg resulting in basic fracturetypes. It gives more insight in the trauma mechanism and associated injuries. In the Lauge Hansen classification the lesions are sequentially numbered. Supination-Adduction. • Stage 1. Transverse fracture of lateral malleolus, at or below the level of anterior talo-fibular ligament or a tear of LCL structures with the anterior talofibular ligament disrupted most often and frequently the calcaneofibular ligament also torn. • Stage 2. Oblique fracture of medial malleolus. Supination-External (Eversion) Rotation • Stage 1: Rupture of anterior inferior tibiofibular ligament. • Stage 2: Oblique fracture or spiral fracture of the lateral malleolus. • Stage 3: Rupture of post tibiofibular ligament or fracture of posterior malleolus of tibia. • Stage 4: Transverse (sometimes oblique) fracture of medial tibial malleolus. 40% - 70% of all ankle fractures Pronation-Abduction • Stage 1: Rupture of the deltoid ligament or transverse fracture of the medial malleolus. • Stage 2: Rupture of the anterior and posterior inferior tibiotalofibular ligaments or bony avulsion. • Stage 3: Oblique fracture of the fibula at the level of the syndesmosis. Less than 5% of ankle fractures. Pronation-Eversion • Stage 1: Rupture of the deltoid ligament or transverse fracture of the medial malleolus. • Stage 2: Rupture of the anterior nferior tibiotalofibular ligaments or bony avulsion. • Stage 3: Spiral/Oblique fracture of the fibula above the level of the syndesmosis. • Stage 4: Rupture of the posterior inferior tibiofibular ligament or fracture of the posterior malleolus.

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Fig. 2. — Fibulocalcanear ligament evaluation. Dynamic ultrasound examination of the fibulocalcanear ligament. A. Neutral position. The fibulocalcanear ligament (thin arrows) is slack with the peroneal tendons (thick arrows) superficial to the ligament. B. Foot in dorsiflexion and eversion position. In this position the fibulocalcanear ligament (thin arrows) is stretched with superficial displacement of the peroneal tendons. This superficial displacement is absent in torn (sprain grade III) or slackened (sprain grade II) ligaments. In case of retinaculum peroneorum superius tear or avulsive fracture the peroneus tendons may dislocate anterior relative to the lateral malleolus.

Fig. 3. — Talar neck fracture. Male, 53 y old. Magnetic resonance T2-WI sequences with fat suppression in axial (A) and coronal (B) planes. Complex talar fracture, sagittal and coronal hyperintense fractures (arrows). oblique (push off) fracture of the medial malleolus includes a major lateral lesion. As a consequence, in the absence of a transverse (avulsive) fracture of the malleolus lateralis, a sprain grade III of the anterior talofibular ligament and grade II or III of the fibulocalcanear ligament is present. In case of supinationexorotation trauma (Weber B type), a spiral fracture (push off type) of the fibula at the level of the syndesmosis implies a sprain grade III of the anterior inferior

tibiofibular ligament. If no accompanying avulsive (transverse) fracture of the medial malleolus is detected, a grade III (complete) tear of the deltoid ligament components is implied. In case of pronation-exorotation trauma (Weber C type), a fracture of the fibula metaphysis or diaphysis includes a tear of the anterior inferior tibiofibular ligament. If no accompanying transverse (avulsive) fracture of the medial malleolus is detected also a tear grade III of ligamentum deltoïdeum com-

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ponents are implied. In conclusion, this Lauge Hansen system is able to discriminate stable and unstable lesions at the level of the distal tibiofibular and talocrural joint and makes acute ligament evaluation by ultrasound or MRI obsolete in de acute setting. Despite the low rate of false negative radiographs in the acute setting, occult fractures may occur and recent reports calculate that 39% of ankle and midfoot fractures in ankle distortions are being missed on radiographs (8). Failed radiographic diagnosis does not only include non displaced fractures, but also minor sprains of medial and lateral ankle ligaments,syndesmosis and also, sprains or avulsive fractures of the dorsal calcaneocuboidal ligament, the ligamentum bifurcatum and the retinaculum peroneorum superior with possible peroneal tendon dislocation and concomitant tendinopathy. An undefined number of patients develop a sinus tarsus syndrome after ankle distortion. The frequency, clinical relevance and diagnostic and therapeutic management implications of failed diagnosis is dissimilar. These radiographically occult fractures can be visualized with MRI or CT. One week after acute ankle distortion, most patients (71%) declare symptom relief (8). In a prospective study in 38 patients without obvious fractures or syndesmosis lesions seen on radiographs, MRI detected ligament lesions in 63% of cases, 92% of them include LCL lesion (54.5% with single ATFL; 41% with ATFL and FCL lesion and 4.5% with lesions of all components of the LCL), 8% with MCL lesion and 8% with syndesmosis lesion (9). In this study, bone bruise was present in 8% (calcaneus, medial malleolus and calcaneus), osteochondral fracture of the medial talus in 8% and malleolus tertius fracture in 4% of cases. All these presented with effusion at the talocrural joint (9). A lesion is called highly significant if no return to sports activities was achieved after 12 months. This was the case in talar fractures and in case of complete calcaneofibular ligament tear (9). This can be explained by the stabilizing function of this ligament not only at the level of the talocrural joint but also at the level of the subtalar joint. Indeed, an association of sinus tarsus syndrome and subtalar intstability is well known (9). The fibulocalcanear ligament is best evaluated with dynamic ultrasound (Fig. 2). In another study (8), one week after the initial trauma, 0.4% of patients presented with residual clinical edema at the ankle, difficulty to bear weight and local tenderness above the anterior tibiofibular ligament while the ankle was held in plantar flexion and internal rotation. In these patients, non displaced talar neck fracture was detected with MRI (Fig. 3). Besides typical peroneal tendondislocation (Fig. 4), a so called ‘ intrasheath’ dislocation of the peroneal tendons may occur and be the cause of retromalleolar pain and clicking sensation (Fig. 5) (10). In this entity, the peroneal tendons switch place permanently or during ankle dorsiflexion and foot eversion maneuver. A longitudinal tear of the peroneus brevis may be

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Fig. 4. — Peroneal tendon dislocation. Male, 29y old. Multislice CT examination of the right ankle with coronal and axiale reconstructions in bone algorithm. Avulsive fracture of the retinaculum peroneorum superius with dissociated fracture fragment (long thin arrow) lateral-posterior to the distal fibula (triangle) with interposition and anterior dislocation of peroneal tendons (thick arrow). associated. This can easily be demonstrated with dynamic ultrasound. Anterior inferior tibiofibular ligament, calcaneocuboidal ligament, ligamentum bifurcatum and retinaculum peroneorum lesions may easily be evaluated with ultrasound. Additional evaluation is restricted to patients with residual pain during reevaluation one week after trauma. MRI or CT is used to detect occult fractures in case of residual talocrural joint effusion with anterior talar tenderness during endorotation and plantar flexion. Ultrasound is used in case of local tenderness posterior and inferior to the lateral malleolus to evaluate the fibulocal-

canear ligament and the superior peroneal retinaculum. Conclusion By using the Ottawa rules in the acute setting after ankle distortion, about 35% of radiographic examinations are avoided with a low rate of false negatives. Additional imaging evaluation is restricted to patients with residual pain during reevaluation one week after trauma and should focus on the detection of lesions that may go undetected using plain radiography. MRI or CT is used to detect occult fractures. Ultrasound is used in case of local tenderness posterior and

1. Stiell I.G., et al.: A study to develop clinical decision rules for the use of radiography in acute ankle injuries. Ann Emerg Med, 1992, 21: 384-390. 2. Lauge-Hansen N.: Fractures of the ankle. Arch Surg, 1948, 56: 259-317. 3. Lauge-Hansen N.: Fractures of the ankle II. Combined experimental-surgical and experimental-roentgenologic investigations. Arch Surg, 1950, 60: 957-987. 4. Lauge-Hansen N.: Fractures of the ankle. III. Genetic roentgenologic diagnosis of fractures of the ankle. AJR, 1954, 71: 456-471. 5. Lauge-Hansen N.: Fractures of the ankle IV. Clinical use of genetic roentgen diagnosis and genetic reduction. Arch Surg, 1952, 64: 488-500. 6. Lauge-Hansen N.: Fractures of the ankle. V. Pronation-dorsiflexion fracture. Arch Surg, 1953, 67: 813-820. 7. Weber B.G.: Die verletzungen des oberen sprunggelenkes 2nd ed. Bern, Switzerland: Huber, 1972. 8. Rodop O., Mahiro ulları M., Akyüz M., Sönmez G., Turgut H., Ku kucu M.: Missed talar neck fractures in ankle distortions. Acta Orthop Traumatol Turc., 2010, 44: 392-396. doi: 10.3944/AOTT.2010.2328. 9. Langner I., Frank M., Kuehn J.P., Hinz P., Ekkernkamp A., Hosten N., Langner S.: Acute inversion injury of the ankle without radiological abnormalities: assessment with high-field MR imaging and correlation of findings with clinical outcome. Skeletal Radiol, 2011, 40: 423-430 10. Raikin S.M., Elias I., Nazarian L.N.: Intrasheath subluxation of the per-

Fig. 5. — Intrasheath dislocation of peroneal tendons. Male, 28y old. Old inversion trauma with residual pain and clicking sensation during walking at left retromalleolal level. Ultrasound examinations in axial imaging plane at left retromalleolar level, right for comparison. At the left ankle the peroneus longus (oval) tendon is in contact with the malleolus lateralis with posterior displacement of the peroneus brevis (dotted line) tendon and muscle. At the normal right side the peroneus brevis (dotted line) is interposed between the malleolus lateralis and the peroneus longus (oval) tendon. Superficial to the tendons a normal thin retinaculum peroneorum superius is recognized with normal attachment to the fibula (arrow).

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PROCEEDINGS OF THE JOINT MEETING RBRS BONE SECTION oneal tendons. J Bone Joint Surg Am, 2008, 90: 992-999. 1. University Hospital Antwerp, Antwerp University. A challenging cause of mono-arthritis of the ankle S.A.J. ter Horst1, F.M. Vanhoenacker2,3, H.M. Kroon1 Case report A 24-year-old male presented with pain and swelling of the right ankle. He

C Fig. 1. â&#x20AC;&#x201D;

was diagnosed with mono-arthritis of unknown origin and treated with nonsteroidal anti-inflammatory drugs (NSAIDs) and intra-articular steroid injections. Four years later, due to insufficient effect of the treatment, he returned with persistent complaints. The initial conventional radiographs showed no abnormalities (not shown). An oblique radiograph (Fig. 1A) two years later showed a subtle juxtacortical lesion (arrow) on the superior side of talar neck. On MRI performed four years after the onset of symptoms, a significant joint effusion (asterisk) in the ankle joint was detected with extensive bone marrow

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edema (arrowheads) of the talus on fatsuppressed (FS) T2-weighted images (WI) (Fig. 1B). A juxtacortical, nodular lesion (arrow) of 10 mm was detected at the anteromedial aspect of the talar neck. The lesion was of intermediate signal intensity on T1-WI (Fig. 1C) and inhomogeneous with both high and low signal areas on FS T2-WI. The adjacent soft tissues showed reactive changes with high signal intensity on FS T2-WI (Fig. 1B). A follow-up conventional radiograph (Fig. 1D) showed a juxtacortical osteolytic lesion (arrow) in the medial talus surrounded by subtle sclerosis. The diagnosis of an intraarticular osteoĂŻd osteoma (O.O.) was

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made. The lesion was successfully treated with radiofrequency ablation and the patient was symptom-free two week after treatment.

of joint pain in the young adult, especially when conventional treatment fails.

Comment

O.O. is a benign bone-forming tumor accounting for 12% of all benign skeletal neoplasms. The tumor has a male to female ratio of 2-3:1 and is most commonly found in adolescents or young adults (10-25 years). The classical O.O. is located in the cortex of the diaphysis of long bones. Patients typically present with pain starting at rest and worsening during the night responding very well to NSAIDs. The diagnosis on imaging is usually straightforward on plain films or even better on CT-scan. A small osteolytic lesion (the nidus) with variable central ossification surrounded by sclerosis and subperiosteal new bone formation is seen within the cortex. The scintigraphic hallmark of an O.O. is the ‘double density sign’, characterized by intense accumulation of the radionuclide centrally in the nidus and less activity peripherally in the reactive sclerotic bone. The treatment of choice for O.O. consists of radiofrequency ablation. However, in approximately 13% the O.O. is located in the subperiosteal juxtaor intra-articular location with different clinical and diagnostic presentation resulting in a diagnostic challenge. The hip joint is most commonly affected, followed by the ankle, elbow, wrist and knee. Intra-articular O.O. presents with symptoms similar to any mono-articular inflammatory arthritis with joint tenderness, soft-tissue swelling, joint effusion and synovitis. The pain is often indistinguishable from other arthropathies and the night pain is usually absent or less typical. Moreover, intra-articular O.O. is less responsive to NSAIDs. On plain radiographs the sclerosis around the nidus is less striking or even absent due to the anatomical location of trabecular bone in the epi/metaphysis. Therefore, the nidus is often overlooked on the initial plain radiograph. As periosteum is not present within the joint capsule, periosteal new bone formation is absent or may occur distant from the lesion. On scintigraphy a nonspecific diffuse activity is seen instead of the ‘double density’ sign, due to associated synovitis and hyperaemia. On MRI, a small nidus is lost in the surrounding reactive changes. The variable signal intensity of the nidus on MRI depends on size, vascularity, maturity and the degree of surrounding sclerosis. Furthermore, the joint effusion and bone marrow edema are prominent and misinterpreted as signs of arthritis and not as a reactive phenomena of an intracapsular nidus. CT remains the preferred modality for identifying the nidus. The different clinical and radiological characteristics frequently result in a diagnostic delay of 2,5 to 3,5 years. Due to this delay, secondary osteoarthritis may complicate an intra-articular O.O. In conclusion, intra-articular O.O. must be included in the differential diagnosis

Reference Allen S.D., Saifuddin A.: Imaging of Intra-articular Osteoid Osteoma. Clin Radiol, 2003, 58: 845-852

no local recurrence but instead a stress fracture dorsal in the calcaneus was seen (Fig. 2A-C). Additional history revealed a recent strong increase of physical activity. He had recently resumed an intense training schedule to be able to participate in a field hockey competition. Case 3

1. Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands. 2. Department of Radiology, AZ Sint-Maarten, Duffel-Mechelen, Duffel, Belgium 3. Department of Radiology, University Hospital Antwerp, UZA, University of Antwerp, Edegem, Belgium.

Calcaneal stress fracture revisited N. Voormolen 1, A. Navas Canete2, M. Reijnierse2 Introduction Classically stress injuries of the calcaneus have been related to repetitive trauma, like long distance marching in military recruits, first described in 1939. However, with current trends of an increasingly health conscious society, which often undertakes new and unsupervised exercise regimes, calcaneal stress injuries may be underdiagnosed. Especially older people performing recreational sport activity and also patients with an (extended) medical history including diabetes and immunosuppressant therapy are at risk. Stress injuries of the calcaneus often show a nonspecific clinical presentation and therefore the radiologist may play a key role in the early detection of abnormalities and early diagnosis of stress injury. Illustrative case series Case 1 51-year-old male. The medical history revealed a liver transplantation due to a primary biliary cirrhosis necessitating admittance in the intensive care unit with good recovery despite a critical illness polyneuropathy. Four months before the clinical presentation the patient performed extensive exercise by making a new wooden floor in his living room on his own. Since that time he has been complaining of increasing pain and swelling of his foot. Clinically a Charcot foot was suspected. Radiographs (Fig. 1A) and Magnetic Resonance (MR) images (Fig. 1B-C) showed a classic stress fracture dorsally in the calcaneus. Patient confirmed local compression tenderness over the calcaneus. Case 2 18 year old male treated with radiofrequency ablation (RFA) for an osteoblastoma in the calcaneus five years before. He presented with new local complaints and a local recurrence was suspected clinically. MRI was performed showing

60-year-old female known with diabetes mellitus complicated by a foot ulcer with prolonged cast immobilisation. Patient complained of increasing of pain over the calcaneus during mobilisation. Radiographs showed subtle changes consistent with a stress fracture (Fig. 3A). However MRI showed clearly two stress fracture lines in the calcaneus with an associated stress reaction in the distal tibia (Fig. 3B-C). Clinical symptoms and risk factors The symptoms of stress injuries are nonspecific and often consist of an insidious onset of increasing of pain and tenderness over the calcaneus. Initially pain does not interfere with normal physical activity; however pain increases during the physical activity. If the physical activity continues the healing process fails and a stress fracture occurs. Risk factors include repetitive trauma like prolonged marching and long distance running. However other conditions like nutritional disorders, especially in young (female) athletes, osteoporosis, hormonal disorders, neuropathy, arterial vascular disease, tarsal coalition and immunomodulating drugs are related with the development of stress fractures (1-4). Epidemiology In military recruits in a large study from Finland the incidence of calcaneal stress fractures was of 2.6/10.000 person years (5). Calcaneal stress fractures may be the most common tarsal stress injury in children (6). There are no studies considering the incidence of stress injuries in populations at a higher risk of insufficiency fractures. Classification and imaging characteristics Stress reactions are classically divided into fatigue and insufficiency fractures. Fatigue fractures occur when excessive repetitive stress is applied to normal bone. Insufficiency fractures occur when normal stress is applied to abnormal or weakened bone (Case 1). In practice stress reactions usually are a combination of both (Case 2 and 3). Stress reactions can also be divided into several types based on the degree of severity represented by MRI characteristics. This scheme was originally developed for tibial stress fractures but seems to be applicable to other sites of stress injuries as well (7) (Table I). However other staging systems have been proposed (8). None of these has been correlated to prognosis. A

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C Table I. — Table with grading of stress injuries by MR characteristics according to Fredericson (7). Grade of MR Imaging characteristics stress injury Grade 0 Grade 1 Grade 2 Grade 3 Grade 4

No abnormality Periosteal edema. No associated marrow abnormalities Periosteal edema and mild edema like lesions of trabecular bone, only visible on T2-weighted images Periosteal edema and extensive edema like lesions of trabecular bone, visible on both T1 and T2-weighted images All of the above and intracortical signal abnormality

B Fig. 1. — Case 1. Lateral radiograph (A), T1 (B) and T2 (C) TSE weighted sagittal MR image of the calcaneus. A clear fracture line, surrounded by edema is visible (arrow). spectrum of abnormalities can be detected with MRI, ranging from subtle periosteal increased signal intensity on T2 weighted images (stress reaction or ‘pre-fracture’) to a real fracture line (Fig. 1). The increased signal intensity on T2 fat saturated images with associated decreased signal intensity on T1 weighted images is classically called ‘bone marrow edema’. This bone marrow edema has been correlated with the presence of clinical symptoms in some studies. However increased signal intensity at certain sites may also occur in asymptomatic athletes (9) and the term ‘edema like lesions’ is probably a better descriptor. The presence of a fracture line or cortical signal abnormalities seems to correlate better with the duration of the symptoms (10). In the calcaneus high grade injury with a clear fracture line represents only about 10% of stress injuries, in almost 90% only edema like lesions are found (11). To our knowledge no stud-

ies correlating these changes to clinical outcome in the calcaneus are performed. Most fatigue fractures of the calcaneus are found in the upper and dorsal part of the calcaneus, however fractures can occur in other locations(5). It has been hypothesized that most of the stress fractures are oriented in the same plane as the traction or compression trabeculae of the calcaneus (12). Imaging protocol The sensitivity of radiographs for stress fractures is low, initial radiographs have a sensitivity of 15-30% to detect stress fractures in general, increasing to 30-70% at follow up. Stress reactions only become apparent after signs of healing are present like sclerosis, bone formation and periosteal reaction, often difficult to visualize in the calcaneus, therefore these numbers are probably even lower in the calcaneus. Radiographs are

however useful to exclude other causes of pain. Ultrasound may give an indication that fracture is present by hyperaemia and thickening of the periosteum, is however non specific (13). Nuclear imaging has a high sensitivity but low specificity for this type of injury. MRI is the gold standard for imaging stress injuries (14). Stress injuries can be detected in an early stage. A dedicated protocol involving high resolution imaging with an appropriate field of view should be used, including the whole ankle, to identify possible concomitant stress injury. It is recommended to place a marker (vitamin pearl) over the painful area in order to correlate the evaluation of the radiological abnormalities with the clinical symptoms. T1-weighted sequences TSE images for anatomical purposes and fluid sensitive sequences (T2 TSE fat suppresed or STIR sequences) to detect “edema like” lesions. A good interobserver agreement has been shown for T2 weighted and STIR imaging (15). The more widely use of an MR extremity scanner can make MRI easily accessible. Aetiology/Pathophysiology In normal cancellous or trabecular bone a certain amount of trabecular microfrac-

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JBR–BTR, 2012, 95 (2) lesions. Histopathologically these signal changes can reflect transient bone marrow edema due to interstitial edema with increased osteoblastic activity and fibrosis and woven bone formation as seen in bone marrow edema syndrome or a process of increased osteoclastic activity with fibrosis as seen in avascular necrosis or the hemorrhage and trabecular destruction seen in bone bruise (18). Treatment and complications Calcaneal stress fractures in military recruits were associated with other stress injuries in 65% (11). Most of them were fractures of the navicular. In fatigue injuries the prognosis of these fractures is good with military recruits resuming and completion of duty within 2 years of diagnosis (5). Even with limited measures calcaneal insufficiency fractures in athletes belong to the lesions at low risk of non union (19). There is no evidence regarding prognosis and best treatment options for insufficiency fractures.

Conclusion Calcaneal stress reactions may have a non specific, prolonged clinical presentation. The diagnosis can be easily made by MR, and allows classification of the stress reaction into low grade injuries represented by “edema like” lesions, or higher grade injury in which progression to a fracture line has occurred. Early diagnosis allows timely clinical measures to prevent progression to complete fracture. The implementation of readily available MR extremity scanners might be of additional value. References

Fig. 2 . — Case 2. Sagittal T1 weighted TSE (A) and coronal T1 weighted TSE (C) and axial STIR images (B) of the calcaneus show intraosseous edema and a fracture line in the inferior part of the calcaneus. Anteriorly the sequellae of previous radiofrequent ablation of an osteoblastoma are visible. tures is present during physical activity. These fractures heal with the formation of microcallus and woven bone. If accumulation of these fractures occurs exceeding the healing capacity of the bone, a stress injury may occur. The accumulation of microfractures or stress injuries can finally result in a complete fracture (16). Normal fracture healing is complex, involving three phases, an inflammatory phase, a proliferative phase and a remodelling phase. The inflammatory phase involves bleeding, and the invasion of macrophages and attraction of mesenchymal stem cells. After 24 hours the proliferative phase starts with the differentiation of stem cells into an osteogenic

and a chondrogenic lineage. The proliferative phase normally lasts three weeks. After three weeks the remodelling phase involves the replacement of woven bone by an organised lamellar bone. In this phase healing osteoclasts are dominant in achieving a normal bone structure with sufficient stability (17). At which stage of the healing process the normal healing of cancellouos bone is interrupted, leading to a stress fracture is not known, but most probable the proliferative phase is compromised with insufficient response in the remodelling phase. The hallmark of stress injuries is an increased signal on T2 and a decreased signal on T1 reflecting “edema like”

1. Peris P.: Stress fractures in rheumatological practice: clinical significance and localizations. Rheumatol Int, 2002 , 22: 77-79. 2. Maenpaa H., Lehto M.U., Belt E.A.: Stress fractures of the ankle and forefoot in patients with inflammatory arthritides. Foot Ankle Int, 2002, 23: 833-837. 3. Moe D.C., Choi J.J., Davis K.W.: Posterior subtalar facet coalition with calcaneal stress fracture. AJR, 2006, 186: 259-264. 4. Ito K., Hori K., Terashima Y., Sekine M., Kura H.: Insufficiency fracture of the body of the calcaneus in elderly patients with osteoporosis: a report of two cases. Clin Orthop Relat Res, 2004, (422): 190-194. 5. Sormaala M.J., Niva M.H., Kiuru M.J., Mattila V.M., Pihlajamaki H.K.: Stress injuries of the calcaneus detected with magnetic resonance imaging in military recruits. J Bone Joint Surg Am, 2006, 88: 2237-2242. 6. Oestreich A.E., Bhojwani N.: Stress fractures of ankle and wrist in childhood: nature and frequency. Pediatr Radiol, 2010, 40: 1387-1389. 7. Fredericson M., Jennings F., Beaulieu C., Matheson G.O.: Stress

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C A 12.

13.

14.

15.

16.

B Fig. 3. â&#x20AC;&#x201D; Case 3. Lateral radiograph shows a subtle sclerotic change (A), more conspicious when comparing with previous radiographs a month earlier which showed no abnormalities (not shown). Sagittal T1 weighted TSE (B) and STIR images (C) show two fracture lines in the calcaneus and a concomitant stress reaction without an overt fracture line in the tibia. (arrows). fractures in athletes. Top Magn Reson Imaging, 2006, 17: 309-325. 8. Kiuru M.J., Pihlajamaki H.K., Perkio J.P., Ahovuo J.A.: Dynamic contrast-enhanced MR imaging in symptomatic bone stress of the pelvis and the lower extremity. Acta Radiol, 2001, 42: 277-285. 9. Kornaat P.R., de Jonge M.C., Maas M.: Bone marrow edema-like signal in

the athlete. Eur J Radiol, 2008, 67: 4953. 10. Yao L., Johnson C., Gentili A., Lee J.K., Seeger L.L.: Stress injuries of bone: analysis of MR imaging staging criteria. Acad Radiol, 1998, 5: 3440. 11. Niva M.H., Sormaala M.J., Kiuru M.J., Haataja R., Ahovuo J.A., Pihlajamaki H.K.: Bone stress injuries

17.

18.

19.

of the ankle and foot: an 86-month magnetic resonance imaging-based study of physically active young adults. Am J Sports Med, 2007, 35: 643-649. Sabry F.F., Ebraheim N.A., Mehalik J.N., Rezcallah A.T.: Internal architecture of the calcaneus: implications for calcaneus fractures. Foot Ankle Int, 2000, 21: 114-118. Arni D., Lambert V., Delmi M., Bianchi S.: Insufficiency fracture of the Calcaneum: Sonographic findings. J Clin Ultrasound, 2009, 37: 424427. Kiuru M.J., Pihlajamaki H.K., Hietanen H.J., Ahovuo J.A.: MR imaging, bone scintigraphy, and radiography in bone stress injuries of the pelvis and the lower extremity. Acta Radiol, 2002, 43: 207-212. Ahovuo J.A., Kiuru M.J., Kinnunen J.J., Haapamaki V., Pihlajamaki H.K.: MR imaging of fatigue stress injuries to bones: intraand interobserver agreement. Magn Reson Imaging, 2002, 20: 401-406. Fazzalari N.L.: Trabecular microfracture. Calcif Tissue Int, 1993, 53 Suppl 1: S143-S146. Mabilleau G., Edmonds M.E.: Role of neuropathy on fracture healing in Charcot neuro-osteoarthropathy. J Musculoskelet Neuronal Interact, 2010, 10: 84-91. Thiryayi W.A., Thiryayi S.A., Freemont A.J.: Histopathological perspective on bone marrow oedema, reactive bone change and haemorrhage. Eur J Radiol, 2008, 67: 62-67. Kaeding C.C., Yu J.R., Wright R., Amendola A., Spindler K.P.: Management and return to play of stress fractures. Clin J Sport Med, 2005, 15: 442-447.

1. Medical Center Haaglanden, 2. Leiden University Medical Center, The Netherlands.

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NEWS FROM THE UNIVERSITIES WETENSCHAPPELIJKE PRIJS EM. PROFESSOR DOCTOR A. L. BAERT PERIODE 2011-2012 Algemeen reglement Artikel 1 Een tweejaarlijkse prijs voor een bedrag van € 2500 wordt opgericht door de stichting “Wetenschappelijke Prijs Em. Prof. Dr. A. L. Baert te Leuven, met als doel het fundamenteel en klinisch wetenschappelijk onderzoek in de radiologie aan te moedigen. Artikel 2 Deze prijs kan worden toegekend aan een radioloog, opgeleid aan één van de vier Nederlandstalige universiteiten in België, op basis van een met goed gevolg verdedigde doctoraatsthesis, door een jury die zal benoemd worden door het stichtingscomité. Artikel 3 Slechts werken die minder dan 2 jaar oud zijn op de datum van hun indiening kunnen in aanmerking worden genomen. Het werk moet opgesteld zijn in het Nederlands of in het Engels, met in beide gevallen, een uitgebreide samenvatting van minstens 15 bladzijden in het Nederlands (interlinie 1, ca. 47 regels per blz.). Artikel 4 De prijs kan slechts toegekend worden aan een nog niet bekroond werk. De auteur van het bekroonde werk krijgt de titel “Laureaat Wetenschappelijke Prijs Em. Prof. Dr. A. L. Baert”. Artikel 5 De jury van de prijs is samengesteld uit 7 personen, aangeduid door het stichtingscomité volgens de regels van het intern reglement. Em. Prof. Dr. A. L. Baert is voorzitter van de jury. Het staat de jury vrij de prijs al dan niet toe te kennen. Artikel 6 De gevallen waarin door het reglement van de prijs niet is voorzien of betwistingen die zouden kunnen ontstaan betreffende de interpretatie ervan, de beoordeling van de ontvankelijkheid van de werken en/of van de kandidaten e.a. worden onherroepelijk door de jury beslecht. Er wordt geen briefwisseling gevoerd over de uitspraak van de jury. Artikel 7 De kandidaten moeten hun werk samen met hun curriculum vitae indienen in 6 gedrukte exemplaren bij Em. Prof. Dr. A. L. Baert en 1 exemplaar bij de secretaris, uiterlijk op 30 september 2012. Het stichtingscomité bepaalt de exacte datum van de toekenning van elke tweejaarlijkse prijs, voorzien in de maand december. De eerste toekenning van de prijs is uitgereikt in december 1998. Em. Prof. Dr. A. L. Baert Voorzitter Trolieberg 58 3010 Kessel-Lo

Prof. Dr. Ph. Demaerel Secretaris Dienst radiologie, UZ Leuven Herestraat 49 3000 Leuven

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FORTHCOMING COURSES AND MEETINGS NATIONAL MEETINGS 21.05.12 RBRS – Neuroradiology Section Information: nsadeghi@ ulb.ac.be 25-26.05.12 COURS CEPUR DU PONT D’OYE Imagerie de l’œil, de l’orbite et des voies visuelles Habay-la-Neuve, Château du Pont d’Oye Information: anne.bauwens@bordet.be 01.06.12 RBRS – Section Head and Neck Radiology Joint Meeting with the Nederlandse Vereniging voor Radiologie, sectie HoofdHalsradiologie Hasselt, Radisson Blu Hotel Organization: Dr B. Termote Information: Pr Dr R. Hermans, robert.hermans@uzleuven.be 02-03.06.12 FIFTH CONGRESS OF SENOLOGY Oostduinkerke Information: Monika.Philips@uzleuven.be 07-08.06.12 ATELIERS DE COLONOSCOPIE VIRTUELLE DEDIES A LA LECTURE EN FILET VIEW ET VUES DE DISSECTION Liège, Clinique St Joseph Information: anne-marie.mandic@chc.be

RBRS – Pediatric Radiology 12.06.12

09.06.12 INTERVENTIONELE MUSCULOSKELETALE ECHOGRAFIE. THEORIE EN PRAKTIJK Antwerpen, UZA Informatie : jan.gielen@uza.be 12.06.12 RBRS – Pediatric Radiology Leuven, UZ Information: Luc.Breysem@kuleuven.ac.be 28-30.06.12 GLOBAL CONGRESS ON PROSTATE CANCER Brussels, The Egg Information: www.prosca.org 06-08.09.12 UPDATE IN ABDOMINAL AND UROGENITAL IMAGING Bruges, Congress Centre Oud Sint-Jan Information: www.update-medical-imaging.be

19-22.09.12 22ND ANNUAL MEETING MUSOC – MUSCULOSKELETAL ULTRASOUND SOCIETY Leuven Information: www.musoc.com 05.11.12 RBRS – Neuroradiology Section Information: nsadeghi@ulb.ac.be 10-12.01.13 5TH LEUVEN COURSE ON EAR IMAGING Leuven, Huis van Chièvres Information: Monika.Philips@uzleuven.be 10.11.12 LUNG CANCER IMAGING IN 2012: UPDATES AND INNOVATIONS Tervueren, Palais des colonies / Koloniënpaleis Organization: Dr B Ghaye, Pr E Coche Information: martine.vanwambeke@uclouvain.be

17.09.12 RBRS – Neuroradiology Section Information: nsadeghi@ulb.ac.be

RBRS – Neuroradiology Section 21.05.12, 17.09.12, 05.11.12

Miscellaneous 02-03.06.12, 07-08.06.12, 28-30.06.12, 0608.09.12, 19-22.09.12, 10.11.12, 10-12.01.13

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

INTERNATIONAL MEETINGS 01-05.03.12 ECR 2012 Vienna, Austria Information: http://www.myesr.org 30.03.12 JOURNEE DE PRINTEMPS DE LA SIAD Theme : Tumeurs malignes du foie Paris, France Information: siad@sfradiologie.org 15-18.04.12 THE BREAST COURSE 2012 Lisbon, Portugal Information: info@thebreastpractices.com 03-06.05.12 27TH CONGRESS OF RADIOLOGY ICR 2012 Sao Paulo, Brasil Information: www.icr2012.org

12-15.06.12 ESGAR 2012 23RD ANNUAL MEETING AND POSTGRADUATE COURSE Edinburgh, UK Info : www.esgar.org

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

16.06.12 9EME JOURNEE DE RADIOLOGIE HEPATOBILIAIRE ET DIGESTIVE DU CH BICETRE PAUL BROUSSE France, Paris Organization: Pr MF Bellin, Dr F. Kunstlinger, Pr M.Lewin Information: veronique.rey@bct.aphp.fr

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

22.06.12 ESTI EUROPEAN SOCIETY OF THORACIC IMAGING London, UK Information: www.esti-society.org

00.10.12 JOURNÉES FRANÇAISES DE RADIOLOGIE Paris, France Information: sfr@sfradiologie.org 25-30.11.12 RSNA 2012 Chicago, USA Information: www.rsna.org

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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

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 KBVR 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 SRBR.

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 KBVR.

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.

b) Bourse de recherche : Le candidat déposera un projet de recherche approuvé par le titulaire de l’enseignement de radiologie de son université auprès du Bureau de la SRBR. 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. b) Bourse de recherche :

BELGISCHE

de kandidaat legt een studieproject voor aan het bureau van de KBVR 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. Researchbeurs: de kandidaat legt een researchproject voor aan het bureau van de KBVR 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. 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. 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 SRBR.

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

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 SRBR.

binnen de 5 maanden na het beëindigen van de buitenlandse stage brengt de studiebeurslaureaat mondeling verslag uit bij het bureau van de KBVR 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 :

b. Researchbeurs:

Dans l’année suivant l’attribution de la bourse, le candidat présentera un rapport auprès du Bureau de la SRBR.

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

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 SRBR.

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 SRBR 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 KBVR genomen te worden ten laatste binnen de 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 SRBR. b) Bourse de recherche :

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. 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.

BOURSE DE LA SRBR POUR LA RECHERCHE À L’ÉTRANGER

KBVR BEURS VOOR RESEARCH IN HET BUITENLAND

La SRBR instaure une bourse d’un montant de 25.000 € mise à disposition de la communauté radiologique belge dans le but de réaliser une recherche relevant du domaine de l’imagerie médicale dans un hôpital universitaire étranger.

Door de KBVR wordt een beurs ten bedrage van € 25.000 ter beschikking gesteld aan Belgische radiologen om gedurende 1 jaar in een buitenlandse universitaire dienst van radiologie research te verrichten binnen het domein van de radiologie.

Règlement

Reglement

1. Les candidat(e)(s) seront radiologues reconnus faisant preuve dune activité de recherche dans une Université Belge. Ils (elles) seront de nationalité belge et faire preuve qu’au moment de la candidature ils (elles) ont obtenu ou ont entrepris un programme de recherche en vue de l’obtention d’un doctorat en sciences médicales ou d’une thèse d’agréation (une attestation de la faculté de médecine sera requise). Les candidat(e)(s) fourniront un curriculum attestant de travaux publiés dans des revues internationales à comité de lecture, de présentations à des réunions internationales et de l’obtention éventuelles de prix ou de bourses. Les candidat(e)(s) doivent être membre titulaire de la SRBR.

1. Als kandida(a)t(e) komt in aanmerking iedere erkende specialist in de radiologie die op het ogenblik van de aanvraag actief betrokken is in de radiologische research aan een Belgische universiteit. De kandida(a)t(e) dient de Belgische nationaliteit te hebben en op het ogenblik van de aanvraag een doctoraat in de medische wetenschappen behaald te hebben of deel te nemen aan het programma voor het behalen van dit doctoraat (certificaat van de faculteit is vereist). De kandida(a)t(e) moet zijn/haar research activiteiten bovendien bewijzen d.m.v. vroegere publicaties in internationale tijdschriften, voordrachten op internationale symposia, het eventueel verworven hebben van andere beurzen of prijzen. De kandida(a)t(e) moet titulair lid zijn van de KBVR.

2. La bourse peut être attribuée 1 fois à chaque Université belge, les candidatures devant être introduites entre le 01-01-2012 et le 31-12-2012.

2. De beurs kan 1 maal toegekend worden aan elk van de 7 universitaire opleidingscentra voor radiologie en dit in de periode tussen 1/1/2012 en 31/12/2012.

3. Les candidat(e)(s) déposeront à l’appui de leur candidature un document (minimum 4 pages à simple interligne) décrivant les buts et modalités de leur recherche d’un an et décrivant les conditions de recherche de l’institution d’accueil qui devra être reconnue comme étant de haut standard. Le document détaillera le shéma de la recherche entreprise qui comportera au moins 70% d’activité de recherche pure, à l’exclusion de prestations cliniques. Le documents sera accompagné d’une attestation du responsable du service d’accueil établissant la validité de la recherche et l’acceptation du (de la) candidat(e). De plus le chef de service du service universitaire d’origine attestera des activités de recherche du (de la) candidat(e) et du soutien de l’institution d’origine.

3. De kandida(a)t(e) legt een document (minimaal 4 getypte pagina’s) voor aan het bureau van de KBVR waarin het concept en de doelstellingen van het 1 jaar durende research project worden uitgelegd en waarin ook de research faciliteiten van het buitenlands centrum worden beschreven. Dit buitenlands centrum moet algemeen erkend zijn als kwalitatief hoogstaand. In het document wordt ook een gedetailleerde omschrijving gegeven van het geplande werkschema dat alleszins minstens 70% labowerk dient te omvatten. Het document dient vergezeld van een brief van het diensthoofd van het buitenlands centrum waarin duidelijk gesteld wordt dat zowel kandida(a)t(e) als research project aanvaard zijn. Verder dient er ook een brief te zijn van het diensthoofd radiologie van de Belgische universiteit waar de kandida(a)t(e) op het ogenblik van de aanvraag research verricht en waarin vermeld wordt dat de aanvraag gesteund wordt.

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4. La décision sur les projets introduits sera prise au plus tard 4 mois après le dépôt des documents.

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

5. Le(la) Candidat(e) devra envoyer un rapport intermédiaire auprès du Bureau de la Société à l’échéance des six mois écoulés après l’attribution de la Bourse. Ce rapport devra décrire le stade d’avancement et les résultats préliminaires de l’étude. Un rapport définitif sera envoyé au Bureau après complétion de l’étude. En outre, le (la) titulaire de la bourse rédigera deux articles pour publication, l’un à l’intention du Journal Belge de Radiologie (JBR-BTR) l’autre à l’intention d’European Radiology.

5. Zes maanden na de start van het project dient de kandita(a)at(e) een tussentijds rapport te versturen naar het bureau van de KBVR waarin de stand van het project en de voorlopige resultaten van de reeds gedane wetenschappelijke studies worden weergegeven. Bij het einde van het project dient een volledig en uitvoerig rapport gemaakt. Verder dienen er door de kandida(a)at(e) twee artikels geschreven te worden, één voor publicatie in het Belgische Tijdschrift van Radiologie en één voor publicatie in European Radiology

6. Payement

6. Betaling

€ 12.500,00 seront payés 1 mois avant le départ du (de la) titulaire de la bourse. € 6.250,00 seront payés au 6e mois, après le dépôt du rapport intermédiaire € 6.250,00 seront payés après la complétion du projet et dépôt du rapport définitif et lorsque les deux articles seront écris et envoyés. Le montant de la bourse sera versé au service d'origine ou son Université qui la payera au ( à la) titulaire.

€ 12.500,00 zal uitbetaald worden 1 maand voor het vertrek van de titularis. € 6.250,00 wordt uitbetaald na 6 maanden, nadat de kandida(a)t(e) het tussentijds verslag heeft verstuurd naar het bureau. € 6.250,00 na het beëindigen van het project, op het ogenblik dat het eindrapport is voorgebracht en dat de 2 manuscripten afgewerkt en verstuurd zijn. De studiebeurs wordt uitbetaald aan de dienst radiologie of aan de universiteit die het geld bezorgt aan de kandida(a)t(e).

BOURSE COUVRANT DES FRAIS DE THESE

BEURS TERUGBETALING ONKOSTEN THESIS

La SRBR crée une bourse de 1860 € à l’intention des docteurs en médecine, spécialistes en radiologie, membres de la Société, qui ont présenté à partir de 1998 une thèse de doctorat ou d’agrégation. Cette bourse est destinée à couvrir les frais d’impression de cette thèse.

Door de KBVR wordt een beurs ten bedrage van € 1.850 ter beschikking gesteld aan radiologen, titulaire leden van de vereniging die vanaf het jaar 1998 een doctoraats- of aggregaatsthesis (echter geen biomedische thesis) hebben verdedigd. Het doel van deze beurs is de onkosten gemaakt voor het drukken van deze thesis te vergoeden.

Règlement :

Reglement

1. Le candidat doit être docteur en médecine, avoir acquis la spécialisation en radiologie ou être en formation dans une université belge, y inclus les stages non universitaires. Le candidat doit être membre titulaire de la SRBR.

1. Als kandidaat komt in aanmerking iedere 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 KBVR.

2. Le candidat doit déposer l’épreuve imprimée de sa thèse accompagnée de la facture d’impression.

2. De kandidaat legt de gedrukt thesis voor tezamen met een onkostennota die de uitgaven voor het drukken van de thesis bewijst.

3. La demande est introduite au Bureau de la SRBR qui doit approuver la demande.

3. De aanvraag dient voorgelegd te worden aan het bureau van de KBVR en door dit orgaan te worden goedgekeurd.

4. Le montant est attribué en fonction des justificatifs avec une demande maximale de € 1.850.

4. Het uitgekeerd bedrag staat in functie van bewezen onkosten en bedraagt maximaal € 1.850.

5. Le Bureau de la SRBR statuera sur l’attribution de la bourse dans les quatre mois suivant l’introduction.

5. De beslissing over het toekennen van de beurs dient door het bureau van de KBVR genomen te worden ten laatste binnen de 4 maanden na het indienen.

6. Le paiement de la bourse sera versé au chef de service de l’institution universitaire , qui le mettra à la disposition du boursier.

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

7. La facture des frais d’impression peut être libellée au nom du service auquel appartient le candidat ou au nom de la Société Royale Belge de Radiologie.

7. De factuur van de drukkosten kan gemaakt worden op naam van de dienst waartoe de kandidaat behoort of op naam van de KBVR.

00b-JBR-Adv.index-2011-6_JBR-Adv.index-2003/6 26/04/12 08:52 Pagina 1

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Pages III IV VII, VIII IX X XI, XII XIII CIV

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