JBR 2014-5 by office

WETTEREN 1

P 702083

Volume 97 Page 271-324

September-October

Bimonthly

–

2014

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

ORGANE DE LA SOCIETE BELGE DE RADIOLOGIE (SBR) ORGAAN VAN DE BELGISCHE VERENIGING VOOR RADIOLOGIE (BVR) 00a-Couv-2014 (5).indd 1

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Subscribers’ information The JBR-BTR is published 6 times a year. Subscription of members of the Belgian Society of Radiology are included in membership dues and are handled by the Society. Non-members’ subscriptions are available from the ARSMB-KVBMG. The rate is valid to date and can be amended without notice according to fluctuation of printing and material costs. Annual subscriptions or single issue orders should be made promptly. The publishers cannot guarantee supply of back issues. Change of address must be notified 60 days in advance. RATES: Annual Single issue Belgium 175 € 42 € Other Countries 200 € 49 € All amounts are net and include postal and handling charges. You are kindly invited to address all your correspondence to Mrs A. Hirsch and execute all payments to ARSMBKVBMG (see below).

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

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

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

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

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JBR-BTR  97/5  2014 Journal Belge de  Belgisch Tijdschrift voor  RADIOLOGIE

Founded in 1907 A bimonthly journal devoted to diagnostic and interventional imaging, related imaging sciences, and continuing education Contents Sonographic evaluation of the plantar fascia in asymptomatic subjects N. Gadalla, M. Kichouh, C. Boulet, F. Machiels, J. de Mey, M. De Maeseneer. . . . . . . . . . . . . . . . . . . . . . . . . . . . 271 Giant cavernous malformations in young adults: report of two cases, radiological findings and surgical consequences M.R. Parizel, T. Menovsky, V. Van Marck, M. Lammens, P.M. Parizel. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 274 Multidetector computed tomography diagnosis of gastric volvulus through the foramen of Morgagni S. Lecouvet, B. Coulier, F. Pierard, M. Gogoase, J.P. Coppens, M. Van Hoof. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279 Amyloidosis: an unusual cause of mesenteric, omental and lymph node calcifications F.M. Vanhoenacker, K. Vanwambeke, G. Jacomen. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283 Spontaneous rupture: a rare complication of hepatic hemangiomas P. De Beul, B. Claikens, G. Heirwegh, A. Janssen. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 287 Granular cell tumor in the breast mimicking breast carcinoma J. Huyskens, C. Geniets, E. Van Hedent. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289 Correlative imaging in gallbladder carcinoma I. Willekens, L.R. Goethals, C. Brussaard, D. Verdries, J. de Mey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291 Axial osseous lesions mimicking disseminated metastases. A report of osseous mastocytosis E. Desportes, J. Lincot, A. Hess, V. Descamps, B. Dallaudière. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 295 Solitary fibrous tumor of the kidney P. Tritschler, B. Coulier, I. Gielen. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 298 Mesenteric inflammatory myofibroblastic tumor : MRI and CT imaging correlated to anatomical pathology Th. Kirchgesner, E. Danse, Ch. Sempoux, L. Annet, Ch. Anca Dragean, P. Trefois, N. Abbes Orabi, A. Kartheuser . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301 Rapid malignant transformation of primary synovial chondromatosis into chondrosarcoma J. Jonckheere, M. Shahabpour, I. Willekens, N. Pouliart, M. Dezillie, F. Vanhoenacker, J. De Mey . . . . . . . . . . 303 A rare case of early onset type abdominal trocar site hernia (TSH) with atypical externalizing in two-step: multidetector row CT diagnosis B. Coulier, A. Ramboux, F. Pierard. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308

IMAGES IN CLINICAL RADIOLOGY Diffusion restriction of posterior uveal melanoma on MR imaging R. Semnic, D. Kozic, K. Petrovic, F.M. Vanhoenacker. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 312 Delayed onset muscle soreness L. Delcour, B. Dallaudière, P. Omoumi, T. Kirchgesner, B. Vande Berg, C. Cyteval, A. Larbi . . . . . . . . . . . . . . . . 313 Idiopathic intracranial hypertension G. Vandekerckhove, V. VandeVyver. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 314 Hemangioperiocytoma simulating meningioma in a 41-year-old man E. Rabaey, K. Desmet, M. De Maeseneer, T. Vanderhasselt, T. Stadnik . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315 Proximal avulsion fracture of the long head of the triceps brachii muscle M. Vansevenant, F.M. Vanhoenacker, T. Wauters. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 316 Secondary infertility caused by midline cyst of the prostate T. Dewaele, L. D’Hooghe, K. Everaert, P. Devisschere . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317 Lunate dislocation F. Filippitzi, B. Dallaudière, P. Omoumi, F.E. Lecouvet, M. Lefere, B. Vande Berg, A. Larbi . . . . . . . . . . . . . . . . . 318

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LETTER TO THE EDITOR Acute renal failure due to bilateral upper ureteral stoneÂ : a rare occurrence I. Mocanu, N. Verbeeck, F. Prospert. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319 Abstract of paper for full membership at the Royal Belgian Society of Radiology (Van den Bossche). . . . . . . . . . 321 Forthcoming Courses and Meetings. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322 Postgraduaat Radiologie van de Vlaamse Universiteiten. Programma 2014-2015 . . . . . . . . . . . . . . . . . . . . . . . . . . 323 Instructions to Authors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iii Subscribers information. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . cii Advertising index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322

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

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Editor-in-Chief: J. Pringot

Board of the Belgian Society of Radiology:

Consulting Co-Editor: Ph. Grenier (Paris)

President: G. Villeirs

Managing Editors: P. Seynaeve

Vice-President: D. Henroteaux

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

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

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

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

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

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

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

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

(possibly made up of different parts) per 3 pages of manuscript. All the material should be made available to the JBR- BTR editorial office (2 copies of the manuscript with 2 sets of illustrations) with the corresponding diskette though there will not be peer review. – Images in Clinical Radiology are short (max. 1 typed page) case reports designed to illustrate with max. 3 figures a specific enti ty. The report should not include abstract nor discussion but consist of a synthetic description of the clinical and radiological features as well as the final diagnosis and one major reference. Technical notes are short descriptions of a specific technique, procedure or equipment of interest to radi ologists. Technical notes may originate from radiologists having experience of the item presented or from commercial firms (these should contact the Editorial Office to obtain specific guidelines for publication). The manuscript length should be inferior to 1 typed page, original language should be English, the manuscript may be accompa nied by maximum 1 b/w figure, and include one major reference. – Book reviews should be limited to one typed page, mention full references of the book, including number of pages, of illus trations (when available), and price. The author should specify to whom the book is intended and give a personal apprecia tion. They will be published with the initial lettersof the signature. (continued on p. 324)

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NAAM VAN HET GENEESMIDDEL: MultiHance, 0.5 M oplossing voor injectie. DENOMINATION DU MEDICAMENT: MultiHance 0,5 M solution injectable. COMPOSITION KWALITATIEVE EN KWANTITATIEVE SAMENSTELLING: 1 ml oplossing voor injectie QUALITATIVE ET QUANTITATIVE: 1 mL de solution contient : acide gadobénique 334 mg bevat: 334 mg gadobeenzuur (0,5 M) als het dimeglumine-zout [gadobeendimeglumine (0,5 M) sous forme® de de diméglumine. [529 mginjectable de gadobénate de diméglumine = MULTIHANCE 0,5selmmol/ml : Solution en flacon ou en seringue pré-remplie. 529 mg = gadobeenzuur 334 mg + meglumine 195 mg]. 5 ml oplossing voor injectie 334 mg d’acide gadobénique + 195 de diméglumine]. 5 mL de solution contient diméglumine. [529 mg de mg gadobénate de diméglumine = 334: acide mg d’acide gadobéniqu bevat: 1.670 mg gadobeenzuur (2,5 mmol) als dimegluminezout. [gadobenaatdimeglumine gadobénique 1670 mg (2,5 mmol) sous forme de sel de diméglumine. [2645 mg de injectable en flacon ou en seringue pré-remplie. Solution aqueuse limpide, incolore, rem 2.645 mg = gadobeenzuur 1.670 mg + meglumine 975 mg]. 10 ml oplossing voor gadobénate de diméglumine = 1670 mg d’acide gadobénique + 975 mg de diméglumine]. 5,3 pHcontient : : 6,9-7,3. CLINIQUES : Indications : Ce m injectie bevat: 3.340 mg gadobeenzuur (5 mmol) als dimegluminezout [5.290 mg 10 mLmPa.s. de solution acide DONNEES gadobénique 3340 mg (5 mmol) sous forme de selthérapeutiques de dansde: •diméglumine IRM du foie pour détection des lésions hépatiques magnétique gadobenaatdimeglumine = 3.340 mg gadobeenzuur + 1.950 mg meglumine]. 15 ml diméglumine.(IRM) [5290et mgindiqué de gadobénate = 3340 mg la d’acide gadobénique oplossing voor injectie bevat: 5.010 mg gadobeenzuur (7,5 mmol) als dimegluminezout + 1950 mg de diméglumine]. 15 mL de solution contient : acide gadobénique 5010 mg épinière où il améliore la détection des lésions et apporte des informations diagnostiques supplémen [7.935 mg gadobenaatdimeglumine = 5.010 mg gadobeenzuur + 2.925 mg meglumine]. 20 ml oplossing voorlainjectie bevat:de la maladie (7,5 mmol)vasculaire sous forme desténo-occlusive sel de diméglumine.cliniquement [7935 mg de gadobénate de diméglumine = 5010 mg d’acidevasculaire gadobéniquedes + 2925 diagnostique pour détection significative lorsqu’une pathologie artères abdominales o 6.680 mg gadobeenzuur (10 mmol) als dimegluminezout [10.580 mg gadobenaatdimeglumine = 6.680 mg gadobeenzuur mg de diméglumine]. 20 mL de solution contient : acide gadobénique 6680 mg (10 mmol) sous forme de sel de diméglumine. (IRM) indiqué dans le cadre de : • L’IRM du foie la détection focales chez les patients chez l l’imagerie par résonance magnétique [10580 + 3.900 mg meglumine]. FARMACEUTISCHE VORM: Oplossing voor injectie. Heldere waterige oplossing, afgevuld in kleurloze mg de gadobénate de diméglumine = 6680 mgpour d’acide gadobéniquedes + lésions 3900 mghépatiques de diméglumine]. FORME améliore la détection des lésionsPHARMACEUTIQUE: et apporte des Solution informations diagnostiques comparativement uneincolore.Osmolalité IRM sans produit de contraste. Po glazen injectieflacons. Osmolaliteit bij 37 ºC: 1,97 osmol/kg. Viscositeit bij 37 ºC:car 5,3il mPa.s KLINISCHE GEGEVENS: injectable. Solution aqueusesupplémentaires limpide, incolore, remplie dans des flacons deàverre Therapeutische indicaties: Dit geneesmiddel is uitsluitend bestemd voor diagnostisch gebruik. 37°C : 1,970 Viscosité 37°C : 5,3 mPa.s. DONNEES nerveux CLINIQUES:central Indications thérapeutiques: Ce médicament 0,05MultiHance mmol/kgis een de paramagnetische poids corporel, soit à0,1 ml/kg deOsmol/kg. la solution 0,5àM. • IRM du système (flacon et seringue pré-remplie) : La dose re contrastvloeistof die wordt gebruikt voor de magnetische resonantie tomografie (MRI) geïndiceerd voor: • MRI van de lever voor de est à usage diagnostique uniquement. Produit de contraste paramagnétique utilisé dans l’imagerie par résonance magnétique (IRM) (flacon) : 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. Flacon : MultiHance doit être introd detectie van focale leverlaesies bij patiënten met bekende of verdachte primaire leverkanker (b.v. hepatocellulair carcinoom) of et indiqué dans : • IRM du foie pour la détection des lésions hépatiques lorsqu’un cancer hépatique secondaire ou primitif ne doit pas être d’autres examens IRM. Seringue(carcinome pré-remplie : MultiHance doit être utilisé immédiatement metastasen. • MRI van de hersenen en het ruggenmerg, waar het de detectie van laesiespour verbetert en aanvullende diagnostische hépatocellulaire) est suspecté ou connu. • IRM du cerveau et de laaprès moelle ouverture épinière où il et améliore la détection desdilué. lésions Tout reliquat éventu être MR-angiografie vissée dans (MRA) le piston dans le sens des aiguilles d’unediagnostiques montre, puis enfoncée de quelques millimètres éliminer toute• Angiographie friction entre le piston et le c informatie kan geven op de informatie uit de niet contrast-versterkte MRI. • Contrast-versterkte bij patiënten et apporte des informations supplémentaires comparativement à une IRM sanspour produit de contraste. met verdachte of bekende vasculaire ziekten van de abdominale of perifere arteriën. • MRI van de voor het opsporen van (ARM)jetable, où il améliore l’exactitude diagnostique détection de laaux maladie deborst l’extrémité de la seringue etpary résonance fixer soitmagnétique une aiguille stérile, soit une tubulurepour 5/6lacompatible vis vasculaire Luer ensténo-occlusive exerçant une poussée rotative. canule kwaadaardige laesies bij patiënten met een gekende of vermoede borstkanker op basis van de resultaten van een voorafgaande cliniquement significative lorsqu’une pathologie vasculaire des artères abdominales ou périphériques est suspectée connue. le risque d’extrav ou que la tubulure soit complètement remplie. L’injection doit être réalisée en respectant la procédure d’aspiration habituelle. Pouroudiminuer mammografie of echografie. Dosering en wijze van toediening: MRI van de lever: de aanbevolen dosis MultiHance bij • IRM du sein, pour la détection des lésions malignes chez les patients pour lesquels un cancer du sein est connu ou suspecté, voie intraveineuse, soit en bolus, soit en injection lente (10 ml/min). ARM dans la veine. Foie et système nerveux central : le produit doit être administré par volwassenen bedraagt 0,05 mmol/kg lichaamsgewicht, hetgeen overeenkomt met 0,1 ml/kg van de 0,5 M oplossing. MRI van de sur la base des résultats disponibles de mammographie ou d’échographie. Posologie et mode d’administration: IRM du foie : être suivie d’unouder embol chlorure deLasodium à 0,9 %. Acquisition images : •0,1 Foie (flacon et seringue pré-remplie) hersenen en het ruggenmerg: de aanbevolen dosis MultiHance bij volwassen en pediatrische patiënten dande 2 jaar is dose recommandée chez l’adulte estdes de 0,05 mmol/kgpost-contraste de poids corporel, soit ml/kg de la solution 0,5 M. IRM du système : Imagerie dynam typeded’imagerie nécessaire. central (flacon et seringue : Jusqu’à après de admi niscorporel, tration.soit • ARM (flacon) : Immé duMRA: 0,1 mmol/kg lichaamsgewicht, hetgeen overeenkomt met 0,2 ml/kg van de 0,5 M oplossing. aanbevolen dosis MultiHance• Système nerveuxnerveux central : La dose recommandée chez l’adultepré-remplie) et l’enfant de plus de 2 ans60 estminutes de 0,1 mmol/kg poids bij volwassenen is 0,1 mmol/kg lichaamsgewicht hetgeen overeenkomt met 0,2 ml/kg vandudebolus. 0,5 M oplossing. MRI van deautomatique borst: 0,2 de la solution 0,5 M. ARM :pulsée La dose recommandée chez l’adulte est de 0,1 mmol/kg de poids soit 20,2ml ml/kg Si la détection duml/kg contraste en séquence n’est pas utilisée, alors l’injection d’un boluscorporel, test de de deproduit au maximum de aanbevolen dosis MultiHance bij volwassenen is 0,1 mmol/kg lichaamsgewicht hetgeen overeenkomt met 0,2 ml/kg van de la solution 0,5 M. IRM du sein : La dose recommandée chez l’adulte est de 0,1 mmol/kg de poids corporel, soit 0,2 ml/kg de la MultiHance doit être évitée chez les patients présentant une insuffisance rénale sévère (DFG < 30 ml/min/1,73 m²) et en période périopératoire de transp 0,5 M oplossing. MultiHance moet onmiddellijk voor het gebruik in de injectiespuit worden opgezogen en mag niet worden verdund. solution 0,5 M. MultiHance doit être introduit dans la seringue immédiatement avant l’injection et ne doit pas être dilué. Tout reliquat du contraste Mises en jeté garde précautions particulières dedeMultiHance Eventuele ongebruikte restanten contrastvloeistof moeten worden vernietigd, en mogenrehaussement niet worden gebruikt voor ander (voir MRI rubrique éventuel doit être et nespéciales doit pas êtreetutilisé pour d’autres examens IRM.d’emploi). Pour diminuerSilel’administration risque d’extravasation MultiHance ne peut être évitée une ARM et men la dose netedoit mmol/kg de poids lorsqu’elle administrée une IRM foie. Ne administrer plus d’une ouvoorkomen onderzoek. Om de mogelijke risico’s van extravasatie van MultiHance in het spierweefsel te dient erop toe zien pas excéder dans les 0,05 tissus mous environnants, il estcorporel conseillé de s’assurer deest la bonne dispositionpour de l’aiguille ou dedu la canule danspas la veine. dat de i.v. naald of canule zorgvuldig in de vena wordt aangebracht. Lever en hersenen ruggenmerg: de sauf oplossing dient Foie etles système nerveux le produit doit être administré intraveineuse soit :enAucune bolus soitadaptation en injectionposologique lente estcentral d’au :moins 7 jours. Sujets âgéspar(àvoie partir de 65 ans) n’est nécess pasenêtre réitérées, si l’intervalle entre injections intraveneus te worden toegediend als bolus of als langzame injectie (10 ml/min.). MRA: de oplossing dient intraveneus als een bolus (10 mL/min). ARM : le produit doit être administré par voie intraveineuse en bolus, soit manuellement soit à l’aide d’un injecteur dans l’IRM du système nerveux central n’est pas recommandée chez l’enfant de moins de 2 ans. L’utilisation dans l’IRM du foie et l’ARM n’est pas recom injectie te worden toegediend, handmatig of gebruikmakend van een automatisch injecteersysteem. Na de injectie dient een spoeling automatique. L’injection doit être suivie d’un bolus de chlorure de sodium à 0,9%. Acquisition des images post-contraste : met fysiologische zoutoplossing plaats te vinden. Post-contrast tomogrammen acquisitie: hypersensibilité à l’un de ses constituants. - Les patients ayant des antécédents d'allergie ou d'effets indésirables liés à d'autres chélates de gadolinium. Mi Imagerie dynamique Immédiatement après l’injection en bolus graves surviennent dans cette période. Le patient devra rester dans un environnement les 15 minutes suivant l’injection, puisque la majorité des réactions Dynamische tomografie: Onmiddellijk na een bolus injectie. Foie en particulier l’exclusion de tout patient matériel ferromagnétique (pace-makers ou clips vasculaires par e appliquées lors de l’emploi de MultiHance, porteur de minutes Entre 40 et 120 après l’injection (IRM retardée), Imagerie retardée Lever Tussen de 40 en 120 minutendiagnostiques na de injectie, doit être réservée aux établissements dont le personnel est formé en d’imagerie nécessaire et dans lesquels le matériel de réanimation à lafonction prise du entype charge des urgences Vertraagde tomografie: afhankelijk van de individuelede tomografische behoefte. diméglumine durant son stockage. Système En conséquence, MultiHance doit pasaprès êtreadministration administré aux patients présentant des antécédents d’allergie à l’alcool b nerveux central Jusqu’àne 60 minutes de contraste afin de permettre l’élimination de MultiHance par l’organisme. • Insuffisance rénale : Avant l’administration de MultiHance, des examens de Hersenen en ruggenmerg Tot 60 minuten na de toediening. Immédiatement après l’administration, avec un délai d’acquisition calculé sur la base du bolus néphrogénique systémique (FNS) ont été rapportés après injection de certains produits de contraste contenant du gadolinium chez des patients ayant une Onmiddellijk na toediening, met scan vertraging die op basis van de testbolus of automatische test ou par la technique de détection automatique du bolus. Si la détection automatique du ARM hépatique l’incidence de l’insuffisance rénale aiguë élevéed’undans Etant donné qu’il est pos transplantation bolus detectie techniek wordt berekend. Indien een automatische contrastdetectie puls- sont particulièrement à risque, car contraste en séquence pulsée n’est pas utilisée, alorsest l’injection bolusce testgroupe. de 2 ml de MRA préauoumaximum post-opératoire d’une transplantation hépatique, sauf si le diagnostic ne peut être obte insuffisance sequentie niet wordt gebruikt voor bolus timing, dan dient een test bolusrénale injectie sévère et chez les patients durant la période produit devra être réalisée pour calculer le timing d’acquisition adéquat. Il n’est pas établi que l’instauration d’une hémodialyse puisse prévenir ou traiter la F MultiHance pourrait faciliter l’élimination de ce produit de l’organisme. ≤2 ml van de oplossing gebruikt te worden om de geschikte scan vertraging te berekenen. Acquisition dynamique en séquence pondérée T1 après administration d’un bolus et répétée Sein altérée chez les sujets de rechercher un dysfonctionnement rénal chez les sujets âgés de 65 ans et plus. Interaction T1-gewogen, dynamische acquisitie onmiddellijk na de bolus injectie en opnieuw na âgés, il est particulièrement important après 2, 4, 6 et 8 minutes. Borst spécifique d’interaction n’a été menée. Cependant, il n’a pas été rapporté d’interaction entre MultiHance et d’autres médicaments durant les essais clinique 2, 4, 6 en 8 minuten. Populations particulières: Insuffisants rénaux: L’administration MultiHance(≥doit être évitée présentant uneneurologiques : céph 1/100 - < chez 1/10)les: patients • Manifestations sujets adultes. Aucun effet indésirable de fréquence supérieure à 2 % n’a été rapporté.deFréquent Speciale populaties: Nierfunctiestoornis: Het gebruik van MultiHance dient te worden vermeden bij patiënten met een insuffisance rénale sévère (DFG < 30 mL/min/1,73 m²) et en période périopératoire de transplantation hépatique, sauf si les (≥ 1/1.000 -informations < 1/100)diagnostiques : • Manifestations infectieuses : rhinopharyngite. Manifestations paresthésies, sensations v nierfunctiestoornis (glomerulaire filtratiesnelheid (GFR) < 30 ml/min/1,73 m²) endebijchaleur. patiëntenPeu in Fréquent de perioperatieve sont indispensables et ne peuvent être obtenues au •moyen d’une IRM sansneurologiques rehaussement du :contraste. systoles ventriculaires, bradycardie sinusale. • Manifestations vasculaires : hypertension artérielle, hypotension artérielle. Manifestations respiratoires, th levertransplantatieperiode, tenzij de diagnostische informatie essentieel is en niet kan worden verkregen met niet-contrastversterkte Si l’administration de MultiHance ne peut être évitée, la dose ne doit pas excéder 0,1 mmol/kg de poids corporel •dans le cas d’une MRI. Indien gebruik van MultiHance niet kan worden vermeden, dient de dosis niet groter tehypersialorrhée, zijn dan 0,1 mmol/kg lichaamsgewicht du cerveau et de lacutanées moelle épinière ou d’une angiographie par résonance magnétique (ARM)œdème et 0,05 mmol/kg de poids corporel hypersudation. • M douleur abdominale. IRM • Manifestations et sous-cutanées : prurit, éruption cutanée, de la face, urticaire, wanneer gebruikt voor een MRI van de hersenen en ruggenmerg of MR angiografie en niet groter dan 0,05 mmol/kg dans le cas d’une IRM du foie. Ne pas administrer plus d’une dose au cours de l’examen IRM. En raison du manque d’information d’injection : asthénie, fièvre, frissons, douleur thoracique, douleurs, douleur au point d’injection, extravasation au point d’injection. • Anomalies des exame lichaamsgewicht wanneer gebruikt voor een MRI van de lever. Niet meer dan één dosis mag worden gebruikt bij een scan. Wegens sur les administrations répétées, les injections de MultiHance ne doivent pas être réitérées, sauf si l’intervalle entre les injections est Manifestations neurologiques : hyperesthésie, tremblements, hypertension intracrânienne, hémiplégie. • Troubles oculaires : conjonctivite. • Manifestations O het ontbreken van informatie over herhaalde toedieningen dient MultiHance niet herhaald te worden toegediend, tenzij het interval d’au moins 7 jours. Sujets âgés (à partir de 65 ans): Aucune adaptation posologique n’est nécessaire. Utiliser avec prudence chez médiastinales : dyspnée, laryngospasme, sifflements respiratoires, congestion pulmonaire. Troubles thoraciques etwordt tussen de injecties ten minste 7 dagen bedraagt. Ouderen (van 65 jaar en ouder): en dosisaanpassing niet noodzakelijk les sujets âgés. Enfants: Aucun ajustement posologique n’est nécessaire.pulmonaire, L’utilisation dansœdème l’IRM du système nerveux•central n’est gastro-intestinaux : • Manifestations et au point chez d’injection inflammation au point dans d’injection. Leset anomalies biologiques précédemment observée impérieuses. geacht. Voorzichtigheid is geboden bij oudere patiënten. Pediatrische populatie: Er is geen dosisaanpassing nodig. Gebruik voorgénérales pas recommandée l’enfant de: moins de 2 ans. L’utilisation l’IRM du foie l’ARM n’est pas recommandéecitées chez l’enfant MRI van de hersenen en de wervelkolom wordt niet aanbevolen bij kinderen jonger dan 2leucopénie, jaar. Gebruik voor MRI van de lever en de moins de 18 ans. Contre-indications: MultiHance est contre-indiqué chez :• les patients présentant une hypersensibilité à l’un hématurie, hyperlip augmentation des basophiles, hypoprotéinémie, hypocalcémie, hyperkaliémie, hyper- ou hypoglycémie, albuminurie, glycosurie, MRA wordt niet aanbevolen bij kinderen jonger dan 18 jaar. Contra-indicaties: MultiHance is gecontraïndiceerd bij: • patiënten de ses constituants.Cependant, • les patientsces ayantphénomènes des antécédentsont d’allergie ou d’effetlement indésirable liés à d’autres chélates de gadolinium. de la lactico-deshydrogénase et de la créatininémie. été essentiel observés chez des patients présentant une insuffisan met overgevoeligheid voor het werkzame bestanddeel of voor een van de hulpstoffen. • patiënten die eerder allergische reacties of Effets indésirables: Les effets indésirables suivants ont été observés au cours du développement clinique de MultiHance sur 2637 ont régressé spontanément sans séquelle. Aucune pu être établie le sexe ou la dose administrée. Pédiatrie : Au cours des et quitoediening andere bijwerkingen hebben ondervonden met andere gadoliniumchelaten. Bijwerkingen: Tijdens aan 2637 volwassenen sujets adultes. Aucun effet corrélation indésirable de n’a fréquence supérieure à 2avec % n’a l’âge, été rapporté. Manifestations infectieuses. Peu fréquent (0,9een%). La fréquence et la nature des événements indésirables à celles observées chez(≥1/1 l’adulte. (0,9 %)geen et l’hyperhidrose gedurende de klinische ontwikkeling van MultiHance zijn de volgende bijwerkingen gemeld. Er zijn bijwerkingen die met (≥1/1 000, <1/100) : rhinopharyngite. Manifestations neurologiques.étaient Fréquentsimilaires (≥1/100, <1/10) : céphalée. Peu fréquent 000, Depuis la comme frequentie van meer dan 2% voorkomen. Infecties en parasitaire aandoeningen. Soms (≥ 1/1.000, <1/100): nasofaringitis.cliniques <1/100) : paresthésies, sensations vertigineuses, syncope, parosmie. Rare (≥1/10 000, <1/1 000): hyperesthésie, tremblements, vomissements, manifestations plus ou moins sévères d’hypersensibilité comprenant : choc anaphylactique, réactions anaphylactoïdes, angioœdème, s Zenuwstelselaandoeningen. Vaak (≥ 1/100, <1/10): hoofdpijn. Soms (≥ 1/1.000, <1/100): paresthesie, duizeligheid, syncope, hypertension intra-crânienne, hémiplégie, convulsion. Troubles oculaires. Rare (≥1/10 000, <1/1 000): conjonctivite. Manifestations localement une douleur ou une sensation de brûlure, voire une tuméfaction ou un décollement cutané, ont également été rapportées. Des cas isolés de fib stoornis van het reukvermogen. Zelden (≥ 1/10.000, < 1/1.000): hyperesthesie, tremor, intracraniële hypertensie, halfzijdige ORL. Rare (≥1/10 000, <1/1 000): acouphènes. Troubles cardiaques. Peu fréquent (≥1/1 000, <1/100) : tachycardie, fibrillation base de gadolinium en garde spéciales et précautions particulières d’emploi). PROPRIETES PHARMACOLOGIQUES : Produ contraste à Evenwichtsorgaanverlamming, convulsie. Oogaandoeningen. Zelden (≥ 1/10.000, < 1/1.000): conjunctivitis. en (voir chapitre auriculaire, mises bloc auriculo-ventriculaire du 1er degré, extrasystoles ventriculaires, bradycardie sinusale. Rare (≥1/10 000, <1/1 000): doitPR. être collée dansvasculaires. le dossier patient afin000, de<1/100) permettre un suivi précis d injectables. L’étiquette détachable de arythmie, traçabilité placée sur les flacons/seringues ooraandoeningen. Zelden (≥ 1/10.000, < 1/1.000): oorsuizen. Hartaandoeningen. Soms (≥ 1/1.000, <1/100): tachycardie, ischémie myocardique, allongement de l’intervalle Manifestations Peudu fréquent (≥1/1 : atriumfibrilleren, eerste-graads atrioventriculair block, ventriculaire extrasystoles, sinus bradycardie. Zelden: 5(≥ ml 1/10.000, hypertension artérielle, hypotension artérielle. Manifestations thoraciques Peu fréquent:(≥1/1 000,en flacon (verre), 60 en flacon (verre), 25,44 € - 3400934741296 : 10 ml en respiratoires, flacon (verre), 42,55et€médiastinales. - 3400934741357 15 ml 3400934741128 < 1/1.000): aritmie, myocard ischemie, verlengd PR interval. Bloedvataandoeningen. Soms (≥ 1/1.000, <1/100): : rhinite.préremplie, Rare (≥1/10 000, <1/1 €000): dyspnée, laryngospasme, respiratoires, congestion pulmonaire, œdème 3400938879728 : 15hypertensie, ml de solution<1/100) en seringue 60,93 - 3400938879896: 20sifflements ml de solution en seringue préremplie, 77,11 € - Liste I - Rem hypotensie. Ademhalingsstelsel-, borstkas- en mediastinumaandoeningen. Soms (≥ 1/1.000, <1/100): rhinitis. Zelden pulmonaire. Troubles gastro-intestinaux. Fréquent (≥1/100, <1/10) : nausée. Peu fréquent (≥1/1 000, <1/100) : sécheresse de révision de la monographie : Octobre 2012. Pour une information complète, se référer au dictionnaire Vidal. Titulaire de l’AMM et exploitant : Brac (≥ 1/10.000, < 1/1.000): dyspnoe, laryngismus, hijgende ademhaling, pulmonale congestie, pulmonaal oedeem. buccale, dysgueusie, diarrhée, vomissement, dyspepsie, hypersialorrhée, douleurs abdominales. Rare (≥1/10 000, <1/1 000): Maagdarmstelselaandoeningen. Vaak (≥ 1/100, <1/10): misselijkheid. Soms (≥ 1/1.000, <1/100): droge mond, smaakverandering, constipation, incontinence faecale, pancréatite nécrosante. Manifestations cutanées et sous-cutanées. Peu fréquent (≥1/1 000, diarree, braken, dyspepsie, overmatig speekselvloed, abdominale pijn. Zelden (≥ 1/10.000, < 1/1.000): obstipatie, fecale <1/100) : prurit, éruption cutanée, œdème de la face, urticaire, hypersudation. Manifestations musculaires, ostéoarticulaires et du incontinentie, necrotiserende pancreatitis. Huid- en onderhuidaandoeningen. Soms (≥ 1/1.000, <1/100): pruritus, rash, tissu conjonctif. Peu fréquent (≥1/1 000, <1/100) : douleurs dorsales, myalgies. Troubles rénaux et manifestations urinaires. Rare gelaatsoedeem, urticaria, zweten. Bot-, skeletspierstelsel- en bindweefselaandoeningen. SomsCavagna, (≥ 1/1.000, rugpijn,chelates(≥1/10 000, <1/1 000):toincontinence urinaire,A mictions impérieuses. Manifestations générales et auContrast point d’injection. Fréquent 1- F.M. et <1/100): al. Gadolinium with Weak Binding Serum Proteins. New Class of High Efficiency, General Purpose Agents for Magnetic Resonance Imagin myalgie. Nier- en urinewegaandoeningen. Zelden (≥ 1/10.000, < 1/1.000): urine-incontinentie, pollakisurie. Algemene (≥1/100, <1/10) : réaction au pointContrast d’injection, sensationJCAT de chaleur. (≥1/1 000, <1/100) asthénie,Vidal. fièvre,4frissons, and Physicochemical Properties of a New Magnetic Resonance Imaging Medium. 1999; Peu 23 fréquent (Suppl. 1): S161-S168. 3-: Source J.M. Idée, et al. Clinical and aandoeningen en toedieningsplaatsstoornissen. Vaak (≥ 1/100, <1/10): reactie op de plaats van injectie, warmte gevoel. Soms douleur thoracique, douleurs, douleur au point d’injection, extravasation au point d’injection. Rare (≥1/10 000, <1/1 000):multicenter intraindivid 563-576- Erratum in: Fundam Clin Pharmacol. 2007 Jun; 21(3): 335. 5- K.R. Maravilla, et al. Contrast enhancement of central nervous system lesions: (≥ 1/1.000, <1/100): asthenie, koorts, rillingen, pijn op de borst, pijn, pijn op de plaats van injectie, extravasatie op de plaats van inflammation au point d’injection. Anomalies des examens paracliniques. Peu fréquent (≥1/1 000, <1/100) : examens de laboratoire crossover comparison of contrast enhancement after gadobenate dimeglumine versus established gadolinium comparators. Acad. Radiol. 2006; 13: 744-751. 7- J. Pintaske et a injectie. Zelden (≥ 1/10.000, < 1/1.000): ontsteking op de plaats van injectie. Onderzoeken. Soms (≥ 1/1.000, <1/100): afwijkende anormaux, ECG anormal, allongement de l’intervalle QT. Les anomalies biologiques citées ci-dessus, observées chez 0,4 % des and 3 Tesla. Invest Radiolomschreven 2006; 41: 213-221 et erratum. 8- Giesel al.Influence of serumincluent albumine on longitudinal andhyperleucocytose, tranverse relaxation (R1 and R2) of magnetic co laboratoriumwaarden, afwijkingen in het ECG, verlengd QT-interval. Afwijkende laboratoriumwaarden zoals hierboven patients au maximum aprèsetadministration de human MultiHance, : anémie hypochrome, leucopénie, bevatten hypochrome anemie, leukocytose, leukopenie, basofilie, hypoproteïnemie, hypocalciëmie, hyperkaliëmie, hyperglykemie of augmentation des basophiles, hypoprotéinémie, hypocalcémie, hyperkaliémie, hyper- ou hypoglycémie, albuminurie, glycosurie, hypoglykemie, albuminurie, glucosurie, hematurie, hyperlipidemie, hyperbilirubinemie, toename van commercial serumijzer, en toename van hématurie, destinés hyperlipidémie, duLes fer sérique et augmentation tauxréservées sériques àdes transaminases, Le service dispose de moyens informatiques à gérerhyperbilirubinémie, plus facilement laaugmentation relation client. informations enregistréesdessont l’usage du service concerné et ne peuven serum transaminasen, alkalische fosfatase, lactaatdehydrogenase en serumcreatinine werden bij minder dan van et deaux patiënten phosphatases alcalines, de la lactico-deshydrogénase et de laoucréatininémie. Cependant, ces laphénomènes onts’adressant été l’informatique, aux0,4% fichiers libertés, toutedes personne peut obtenir communication et, le cas échéant, rectification suppression des informations concernant, en au pharmacien re gesignaleerd na toediening van MultiHance. Echter, deze bevindingen hadden voor het grootste deelappréciation betrekking opdepatiënten bij wie chezpar descourrier patientsàprésentant connue ou une maladie métabolique sous-jacente. de votre cette visite, notammentessentiellement sur sa qualité observés scientifique, l’attentionune du insuffisance pharmacienhépatique responsable. voordien al sprake was van een verminderde leverfunctie of een bestaande metabole aandoening. Voor het grootste deel waren deze Dans la plupart des cas, il s’agissait d’événements non-graves, transitoires et qui ont régressé spontanément sans séquelle. Aucune bijwerkingen niet ernstig, van voorbijgaande aard en verdwenen zij spontaan zonder effecten na te laten. Er werd geen verband corrélation n’a pu être établie avec l’âge, le sexe ou la dose administrée. Pédiatrie Au cours des essais cliniques chez l’enfant, les gezien met leeftijd, geslacht of dosering. Kinderen Bij pediatrische patiënten opgenomen in klinische onderzoeken omvatten de événements indésirables les plus fréquemment rapportés incluent les vomissements (1,4%), la fièvre (0,9%) et l’hyperhidrose (0,9%). meest gerapporteerde bijwerkingen braken (1,4%), koorts (0,9%) en hyperhydrose (0,9%). De frequentie en de aard van de La fréquence et la nature des événements indésirables étaient similaires à celles observées chez l’adulte. Depuis la commercialisation bijwerkingen waren gelijk aan die bij volwassenen. In minder dan 0,1% van de patiënten zijn, sinds het product op de markt is, de MultiHance, des effets indésirables ont été rapportés, chez moins de 0,1 % des patients. Les plus fréquents sont : nausées, bijwerkingen gemeld. De meest voorkomende bijwerkingen waren: misselijkheid, braken, signalen en symptomen van vomissements, manifestations cliniques plus ou moins sévères d’hypersensibilité comprenant : choc anaphylactique, réactions overgevoeligheidsreacties inclusief: anafylactische shock, anafylactoïde reacties, angio-oedeem, larynxspasme en huiduitslag. anaphylactoïdes, angioœdème, spasme laryngé et éruption cutanée. Des réactions au point d’injection, consécutives à une Reacties op de plaats van injectie als gevolg van extravasatie van het contrastmiddel leidend tot lokale pijn of branderig gevoel, extravasation du produit de contraste, entraînant localement une douleur ou une sensation de brûlure, voire une tuméfaction, un zwelling, blaarvorming en, in zeldzame gevallen wanneer de lokale zwelling ernstig is, tot necrose zijn gemeld. Lokale tromboflebitis décollement cutané ou, dans de rares cas de tuméfaction locale sévère, une nécrose ont également été rapportées. Une werd ook in zeldzame gevallen gemeld. Geïsoleerde gevallen van Nefrogene Systemische Fibrose (NSF) zijn gemeld met MultiHance thrombophlébite locale a également été reportée dans de rares cas. Des cas isolés de fibrose néphrogénique systémique (FNS) ont bij patiënten die gelijktijdig andere gadoliniumhoudende contrastmedia toegediend kregen. HOUDER VAN DE VERGUNNING VOOR été rapportés avec MultiHance chez des patients ayant également reçu d’autres produits de contraste contenant du gadolinium. HET IN DE HANDEL BRENGEN: Bracco Imaging Deutschland GmbH, Max-Stromeyer-Straße 116, 78467 Konstanz, Duitsland. TITULAIRE DE L’AUTORISATION DE LA MISE SUR LE MARCHE: Bracco Imaging Deutschland GmbH, Max-Stromeyer-Straße 116, NUMMERS VAN DE VERGUNNING VOOR HET IN DE HANDEL BRENGEN: MultiHance 5 ml: BE199963, MultiHance 10 ml: 78467 Konstanz, Allemagne. NUMEROS D’AUTORISATION DE MISE SUR LE MARCHE: MultiHance 5 ml: BE199963, MultiHance BE199972, MultiHance 15 ml: BE199981 MultiHance 20 ml: BE199997. AFLEVERINGSWIJZE: Op medisch voorschrift. DATUM 10 ml: BE199972, MultiHance 15 ml: BE199981, MultiHance 20 ml: BE199997. MODE DE DÉLIVRANCE: Sur prescription médicale. VAN HERZIENING/GOEDKEURING VAN DE TEKST: Datum van herziening van de tekst: 10/2013. DATE DE MISE A JOUR/D’APPROBATION DU TEXTE: Date de mise à jour : 10/2013. Informatie over de rubrieken Bijzondere waarschuwingen en voorzorgen bij gebruik, Interacties, Vruchtbaarheid, zwangerschap en borstvoeding, Beïnvloeding van de rijvaardigheid en het vermogen om machines te bedienen, Overdosering, Farmacologische eigenschappen en Farmaceutische gegevens kan u vinden in de volledige versie van de Samenvatting van de Productkenmerken.

Des informations sur les rubriques Mises en garde spéciales et précautions d’emploi, Interactions, Fécondité, grossesse et allaitement, Effets sur l’aptitude à conduire des véhicules et à utiliser des machines, Surdosage, Propriétés pharmacologiques et Données pharmaceutiques se trouvent dans le Résumé des Caractéristiques du Produit complet.

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• MultiHance® is 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) • 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 SmPC Please consult locally approved information.

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MRI and MDCT of the Abdomen Workshop February 7 – 9, 2015, Muscat, Oman Workshop organiser Saqar Altai

22nd Hands-on Workshop on CT Colonography April 15 – 17, 2015, Bruges, Belgium Workshop organisers Philippe Lefere, Stefaan Gryspeerdt

Liver Imaging Workshop April 24 – 25, 2015, Novi Sad, Serbia Workshop organiser Sanja Stojanovic

4th Pancreas Workshop May 7 – 8, 2015, Athens, Greece Workshop organiser Charina Triantopoulou

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JBR–BTR, 2014, 97: 271-273.

Sonographic evaluation of the plantar fascia in asymptomatic subjects N. Gadalla1, M. Kichouh1, C. Boulet1, F. Machiels2, J. De Mey1, M. De Maeseneer1 Purpose: To evaluate the appearance of the plantar fascia in asymptomatic subjects. Materials and methods: Thirty-one asymptomatic subjects were examined by 2 musculoskeletal radiologists. The plantar fascia was evaluated for thickness, echogenicity, vascularity on power Doppler, rupture, fluid adjacent to the fascia, and calcifications. Results: The study included 14 men and 17 women (age, 17-79 years; mean, 45 years). The mean thickness of the plantar fascia in men was 3.7 mm (range 2.5-7 mm), and in women 3.5 mm (range, 1.7-5.1 mm). The thickness was greater than 4 mm in 4 men (bilateral in 2). The mean thickness of fascias thicker than 4 mm in men was 5.4 mm (range, 4.3-7 mm). The thickness was greater than 4 mm in 5 women ( bilateral in 4). The mean thickness of fascias thicker than 4 mm in women was 4.7 mm (range, 4.2-5.1 mm). There was no statistically significant difference between men and women and between both heels. Hypoechogenicity was observed in 3 men (bilateral in 2), and in 5 women (bilateral in 6). Hypervascularity, rupture, fluid adjacent to the fascia, and calcifications were not observed. Conclusion: A thickness greater than 4 mm and hypoechogenicity, are common in the plantar fascia of asymptomatic subjects. Findings that were not seen in asymptomatic subjects include a thickness greater than 7 mm, hypervascularity on power Doppler, rupture, fluid adjacent to the fascia, and calcifications. Key-word: Foot, US.

Plantar fasciitis is a low-grade inflammation of the plantar fascia and perifascial tissues. It is a common cause of heel pain and usually affects middle-aged women, as well as younger, predominantly male, runners (1). The condition is likely related to repeated strain, leading to microtears and inflammation. Imaging is commonly used to confirm the diagnosis, and exclude other causes of posterior heel pain (2). Although MR imaging may be used to diagnose plantar fasciitis, many authors suggest ultrasound is an accurate, simple, and noninvasive technique to diagnose the condition. Previous investigators have reported that the most important diagnostic findings in plantar fasciitis are thickening and hypoechogenicity, and occasionally fluid collections adjacent to the fascia. Wall et al. (3) suggest that a plantar fascia thickness greater than 4 mm is consistent with plantar fasciitis. This value has been used as a reference value in several studies (4-6). To our knowledge, there are no data about the ultrasound appearance of the plantar fascia in asymptomatic subjects. Hence, it is not known if certain commonly used ultrasound criteria of plantar fasciitis might be seen in such a population. If so, this may entail the risk of attributing the patients’ symptoms to

plantar fasciitis while other abnormalities may be overlooked and not further investigated. Therefore we decided to evaluate the plantar fascia in asymptomatic subjects with high resolution ultrasound. Materials and methods Institutional Review Board approval for our study was obtained and consent from the asymptomatic subjects. They were interviewed to confirm they had not been symptomatic at the sole of the foot. Other exclusion criteria were a history of foot surgery, foot and ankle trauma, arthritis, gout, neuropathic foot disease, and diabetes mellitus. Both heels of the 31 asymptomatic subjects were scanned by one of two experienced musculoskeletal radiologists using a 12 MHz linear-array transducer on a state of the art system (Toshiba Applio XG, Tokyo, Japan). The examinations were performed with the subjects in prone position and the feet hanging freely over the edge of the examination table. Acoustic coupling gel, but no standoff-pad, was applied to the plantar surface of the foot. The focal zone was adjusted to the depth of the fascia. The central band of the plantar fascia was examined from its origin up to the metatarsal head region. The thickness was measured at

From: 1. Department of Radiology, Universitair Ziekenhuis Brussel, Brussels, Belgium, 2. Clinique du Parc Léopold, Brussels, Belgium. Address for correspondence: Dr N. Gadalla, M.D., Department of Radiology, UZ B russel, Laarbeeklaan 101, 1090 Jette, Belgium. E-mail: ngadalla@hotmail.com

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a reference point where the plantar fascia crossed the anterior aspect of the inferior border of the calcaneus. The measurement points are indicated in the figures by calipers (Figs. 1-3). The plantar fascia was evaluated for echogenicity. It was only considered hypoechoic if its echogenicity was markedly decreased with respect to the subcutaneous heel fat. The plantar fascia was also assessed for presence of calcification defined as markedly hyperechoic foci, with or without acoustic shadowing, vascularity with Doppler, tear, and fluid adjacent to the fascia. The saved images were reviewed by 2 investigators. Statistical analysis was performed using a t-test (independent samples) (IBM SPSS Statistics 20, Armonk, NY). The significance threshold was set at p = 0.05. Results A total of 62 plantar fascias in 31 subjects (14 men, 17 women), aged from 17 to 79 years (mean age, 45 years) were evaluated (Fig. 1-3). The results are shown in Tables I and II. The mean thickness of the plantar fascia in men was 3.7 mm (range, 2.5-7 mm), and in women 3.5 mm (range, 1.7-5.1 mm). There was no statistically significant difference between the thickness of the fascia in men and women (p = 0.21). There was no significant difference between the right and the left foot (p = 0.64). The thickness of the plantar fascia was greater than 4 mm in 4 men

2/10/14 08:37

272

JBR–BTR, 2014, 97 (5)

A Fig. 1. — Asymptomatic 74-year-old woman. Right side. Thickness was 1.9 mm. The calcaneal insertion of the plantar fascia (arrows) is hyperechoic, and the middle portion is somewhat more hypoechoic compared to fat (this was not considered hypoechoic for analysis) (Cal, calcaneus).

B Fig. 2. — Asymptomatic 44-year-old woman. Right side (A) and left side (B). Thickness of 5 mm is seen bilaterally. Both fascias (arrows) also appear hypoechoic relative to the subcutaneous fat plane. No vascularity is seen on power Doppler (box) (Cal, calcaneus).

Fig. 3. — Right heel in asymptomatic 78-year-old man. Note markedly thickened (7 mm) and hypoechoic fascia (arrow) (Cal, calcaneus).

(28.5%, bilateral in 2 volunteers). The mean thickness of fascia thicker than 4 mm in men was 5.4 mm (range, 4.3-7 mm). The thickness was greater than 4 mm in 5 women (29%, bilateral in 4 volunteers). The mean thickness of fascia thicker than 4 mm in women was 4.7 mm (range, 4.25.1 mm). For our study, hypoechogenicity was considered present only if it was graded as 3 (very clearly hypoechoic). This was observed in 7 women

(42%, bilateral in 6) and 3 men (21.7%, bilateral in 2). The plantar fascia was both thicker than 4 mm and hypoechoic in 3 men (18%, bilateral in 2 men), and in 5 women (23%, bilateral in 4 women). All fascia that were thicker than 4 mm, were also hypoechoic. However some fascia in women were hypoechoic but not thicker than 4mm. Hypervascularity, rupture, fluid collections, and calcifications were not observed in any of the subjects.

Discussion The plantar fascia is a fibrous poneurosis, which inserts along the a plantar aspect of the calcaneus. It has a central, medial, and lateral component and supports the longitudinal arch of the foot. Often the term plantar fascia is used to refer to the large central component, which inserts at the medial calcaneal tuberosity, and is considered most important in the setting of plantar fasciitis.

Table I. — Measured thickness in men and women (in mm). Mean and range, mean and range of thicknesses greater than 4 mm. Mean Range

> 4 mm (mean)

> 4 mm (range)

Men

3.7

2.5-7

5.4

4.3-7

Women

3.5

1.7-5.1

4.7

4.2-5.1

Table II. — Number of volunteers with specific findings. > 4 mm hypoechoic both findings

hypervascularity fluid calcification tear

Men

Women

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SONOGRAPHIC EVALUATION OF THE PLANTAR FASCIA — GADALLA et al

The medial and lateral components overlie the intrinsic muscles. The normal fascia is reported to be 2 to 4 mm thick and has a slightly echogenic fibrillar pattern at ultrasound (7). With plantar fasciitis, usually the calcaneal insertion is involved, although occasionally the area of thickening can be localized at a distance from the calcaneal insertion. It is however, more typical for ruptures to be located distal to the calcaneal insertion. On ultrasound, commonly used criteria of plantar fasciitis are increased thickness (greater than 4 mm), and hypoechogenicity (9-11). Ultrasound has been shown to have good reproducibility for measurement of plantar fascia thickness and appreciation of hypoechogenicity (12, 13). The typical presentation of plantar fasciitis is pain during the first few steps after rest or pain on arising in the morning. Pain is usually worse with exertion. On clinical exam, tenderness at the calcaneal origin may be evident (1, 9). Although plantar fasciitis may resolve after a few weeks, in some patients symptoms may become chronic. The best management of chronic plantar fasciitis is not entirely agreed upon and a variety of conservative approaches as well as more invasive treatments has been suggested (13-19). Our study results, however, showed that a thickness greater than 4 mm could be observed in nearly 30% of asymptomatic subjects. We did not assess differences between men and women, due to the sample size. Hypoechogenicity of the plantar fascia, also a commonly used criterion of plantar fasciitis was seen in 21.7% of men, and 42% of women, in our study. The plantar fascia was both thicker than 4 mm and hypo echoic in 17.8% of men and 23.5% of women. Actually all fascias thicker than 4mm were also hypoechoic. Hence, the two most commonly used criteria of plantar fasciitis with ultrasound, are both seen together in asymptomatic subjects. Although no histological studies are available of the plantar fascia in asymptomatic subjects we speculate that the observed hypoechogenicity may reflect a degenerative phenomenon. When the plantar fascia was thickened and hypoechoic in asymptomatic subjects, this was often the case bilaterally. Hence, we recommend a comparison with the contralateral

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side when performing an ultrasound study of the plantar fascia. Hyperemia has been considered to be an important feature of acute plantar fasciitis in some studies. When evaluating hyperemia, care should be taken to exert as little pressure with the ultrasound probe as possible. Still because of heel thickness this may be difficult, and small vessels could potentially be compressed. None of our volunteers showed hyperemia. Fluid adjacent to the plantar fascia and tear are less commonly demonstrated in plantar fasciitis. In our study none of the asymptomatic subjects had fluid adjacent to the plantar fascia or tear. Our study has some limitations. First, the study population is relatively small. Second, there was no follow up of our study subjects and hence we cannot entirely exclude that subjects with increased fascia thickness or hypoechogenicity ultimately will not develop symptoms of plantar fasciitis. However we detected these abnormalities in about 25% of our study population. Third, with regard to the evaluation of echogenicity, we acknowledge this is a somewhat subjective feature that may be difficult to appreciate due to anisotropy and inhomogeneous penetration of thick plantar skin and subcutaneous tissues (20). In summary, thickness greater than 4 mm and hypoechogenicity, and both findings, can be seen in the plantar fascia of asymptomatic subjects. We suggest prudence when attributing the patients’ symptoms to plantar fasciitis only based on these ultrasound findings. This could entail the risk of missing another diagnosis. Often these findings are bilateral, and a comparison with the contralateral side may be helpful. Findings that were never observed in asymptomatic subjects, include a thickness greater than 7 mm, and we would suggest this as a new cutoff value. Hypervascularity, rupture, fluid collections adjacent to the fascia, and calcifications also were never observed in asymptomatic subjects. References 1. DeMaio M., Paine R., Mangine R.E., et al.: Plantar fasciitis. Orthopedics, 1993, 16: 1153. 2. Barret S.L., O’Malley R.: Plantar fasciitis and other causes of heel pain. Am Fam Phys, 1999, 59: 2200.

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3. Wall J.R., Harkness M.A., Crawford A.: Ultrasound of plantar fasciitis. Foot Ankle Int, 1993, 14: 465. 4. Kane D., Greaney T., Shananhan M., et al.: The role of ultrasonography in the diagnosis and management of idiopathic plantar fasciitis. Rheuma tology, 2001, 40: 1002. 5. Huang Y.C., Wang L.Y., Wang H.C., et al.: The relationship between the flexible flatfoot and plantar fasciitis: ultrasonographic evaluation. Chang Gun Med J, 2004, 27: 443. 6. Sabir N., Demirlenk S., Yagci B., et al. Clinical utility of sonography in diagnosing plantar fasciitis. J Ultrasound Med, 2005, 24: 1041. 7. Chew N.S., Lee J., Davies M., et al.: Ankle and foot injuries. In: Essential Radiology for Sports Medicine, Philip Robinson, Department of Radiology Leeds Teaching Hospitals, 2010, pp 82. 8. Uzel M., Cetinus E., Ekerbicer H.C., Karaoguz A.: The influence of athletic activity on the plantar fascia in healthy young adults. J Clin Ultrasound, 2006, 34: 17-21. 9. Cardinal E., Chhem R.K., Beauregard C.G., et al.: Plantar fasciitis: sonographic evaluation. Radiology, 1996, 201: 257. 10. Fessel D.P., van Holsbeeck M.: Ultrasound of the foot and ankle. Semin Musculoskel Radiol, 1998, 2: 271. 11. Walther M.: Power Doppler findings in plantar fasciitis. Ultrasound in Med Biol, 2004, 30: 435. 12. Cheng J.W., Tsai W.C., Yu T.Y., Huang K.Y.: Reproducibility of sonographic measurement of thickness and echogenicity of the plantar fascia. J Clin ultrasound, 2012, 40: 14-9. 13. Wolgin M., Cook C., Graham C., et al.: Conservative treatment of plantar heel pain: long term follow up. Foot Ankle Int, 1994, 15: 97. 14. Wapner K.L., Sharkey P.F.: The use of night splints for treatment of recalcitrant plantar fasciitis. Foot Ankle, 1991, 12: 135. 15. Sollitto R.J., Plotkin E.L., Klein P.G., et al.: Early clinical results of the use of radiofrequency lesioning in the treatment of the plantar fasciitis. J Foot Ankle Surg, 1997, 36: 215. 16. Gudeman S.D., Eisele S.A., Heidt R.S. Jr, et al.: Treatment of plantar fasciitis by iontophoresis of 0,4% dexamethasone. A randomized double-blind, placebo-controlled study. Am J Sports Med, 1997, 25: 312. 17. Lester D.K., Buchanan J.R.: Surgical treatment of plantar fasciitis. Clin Orthop, 1984, 186: 202. 18. Barrett S.L., Day S.V., Pignetti T.T., et al.: Endoscopic plantar fasciotomy: A multisurgeon prospective analysis of 625 cases. J Foot Ankle Surg, 1995, 34: 400. 19. Baxter D.E., Thigpen C.M.: Heel pain operative results. Foot Ankle, 1984, 5: 16. 20. Fornage B.D.: The hypoechoic normal tendon. A pitfall. J Ultrasound Med, 1987, 6: 19-22.

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JBR–BTR, 2014, 97: 274-278.

Giant cavernous malformations in young adults: report of two cases, radiological findings and surgical consequences M.R. Parizel1, T. Menovsky2, V. Van Marck1, M. Lammens1, P.M. Parizel3 Cerebral cavernous malformations, also known as cavernous angioma or cavernoma, are a type of vascular disorder. They consist of abnormally large vascular cavities or sinusoid channels of varying size. The majority of cavernous malformations in the brain are small and do not always present with symptoms. A minority of large cavernous malformations, known as giant cavernous malformations (GCM), can cause neurological symptoms (such as headaches, focal neurologic deficits and seizures), which are probably related to hemorrhage and mass effect. GCM grow steadily in size over time, due to repetitive episodes of bleeding. The purpose of this paper is to document two case reports of patients with GCM, illustrate the radiological appearance, discuss the neurosurgical consequences, and to provide a literature analysis. Key-words: Cerebral blood vessels, abnormalities – Cerebral blood vessels, MR.

Cerebral cavernous malformations represent a special subtype of low-flow vascular disorder. Histopathologically, these lesions consist of sinusoid-like capillary channels of varying sizes, containing slowly flowing blood. These lesions are located inside the brain, but do not invade the adjacent brain parenchyma, and are usually not surrounded by perilesional edema (1). The cavernous malformation is also known as cavernous angioma or cavernoma, The majority of cavernous malformations in the brain are small, with a mean size of 14.2 mm in diameter (2). Often these lesions are asymptomatic and are discovered on imaging studies as incidental findings. A minority of cavernous malformations may increase in size, due to repeated episodes of hemorrhage; these larger lesions cause neurological symptoms such as headaches, focal neurologic deficits and seizures (3). A clinically important subgroup is the so-called “giant” cavernous malformation (GCM). The size criterion for GCM is not sharply defined; some authors use a minimum diameter of 6 cm as threshold (4), while most other authors use a diameter of 4 cm as cut-off (3). GCM are rare tumorlike lesions, which are characterized by a typical layered appearance on MR imaging studies. In this paper we report on two patients with GCM, describe the radiological characteristic, discuss the neurosurgical consequences, and provide a literature analysis. Case reports Patient 1 This 16-year-old high-school student presented with recurrent head-

aches, intermittent nausea, and sensory disturbances involving the left hand and fingers. Over the past year, his school performance had steadily deteriorated, without specific explanation. Three months prior to admission, he had been involved in a roadtraffic accident when a car hit his motorcycle, but he did not sustain any neurological injury. Previous medical history was otherwise unremarkable, and the young man was generally in good health. Clinical neurological examination showed a mild paresis in the lower left leg, but was otherwise normal. The patient was referred for an MR examination of the brain. Before contrast administration, the following sequences were obtained: axial fluid attenuated inversion recovery (FLAIR), axial T2-weighted images, axial diffusion-weighed images, axial gradient echo T2*, axial susceptibility-weighted (SWI) images, axial T1-weighted images. After intra venous injection of a gadoliniumchelate, axial, coronal and sagittal T1-weighted sequences were obtained. The MR examination revealed a large mass, in the deep right frontal-parietal region (Fig. 1). The largest diameters of the mass were 43 mm antero-posteriorly, 31 mm left-right, and 38 mm head-feet. The lesion was sharply circumscribed, but contained markedly hetero geneous signal intensities, suggestive of recent as well as old blood degradation products. The mass was surrounded by perilesional edema in the white matter of the right centrum semiovale. The lesion caused mass effect on the right lateral ventricle and displaced and compressed the corpus callosum. Imaging findings were consistent with a giant cavernous malformation.

From: Department of 1. Pathology, 2. Neurosurgery, and 3. Radiology, Antwerp University Hospital and University of Antwerp, Belgium. Address for correspondence: Dr M.R. Parizel, Dept of Pathology, Antwerp University Hospital, University of Antwerp, Wilrijkstraat 10, 2650 Antwerp (Edegem), Belgium. E-mail: MaximR.Parizel@uza.be

parizel-.indd 274

The patient underwent a under neurosurgical intervention. A rightsided parafrontal craniotomy was performed. Via a paramedical approach, along the falx, the mass was resected using microsurgical techniques. The giant cavernous malformation could be removed completely, as well as an old and liquefied hematoma next to the large mass. Deposits of hemosiderin and reactive gliosis were observed. The layer of hemosiderin was carefully removed by microsurgical suction. The post-operative course was uneventful (with the exception of a pneumothorax caused by placement of a subclavian catheter). Neurologically the patient was intact. A postoperative CT scan one day after surgery of the brain showed a resection cavity with no further abnormalities (Fig. 2). Pathological examination confirmed the diagnosis of a giant cavernous malformation (Fig. 3). Follow-up visits confirmed that this young man is clinically doing well, without any neurological deficit, at 15 months post operatively. Follow-up MR examination showed a small resection cavity, partially lined with hemosiderin, but no other abnormalities. Patient 2 This 25-year-old woman was admitted with complaints of gradually worsening nausea and vomiting, headache and anorexia. She had experienced a weight loss of 9 kg during the 5 weeks prior to admission. At the age of 19, she had been treated for syringomyelia, with placement of a syringo-dural shunt and posterior cervical decompression surgery. Previous medical history reveals chronic fatigue syndrome and fibromyalgia. Clinical examination revealed a lethargic woman. There were no neurological deficits.

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Fig. 1. — Patient 1, pre-operative MRI of the brain with axial TSE T2-WI (A), axial TSE T1-WI (B), axial gradient echo T2* (C), s agittal TSE T1-WI (D), coronal TSE T1-WI (E) and coronal gradient echo T2* (F). A sharply marginated mass lesion is identified in the deep right frontal-parietal lobes. The mass presents with a heterogeneously layered appearance with blood degradation products of varying age. The hyperintense signal intensity components represent extracellular methemoglobin, while the hypointense portions indicate the presence of hemosiderin. Behind the giant cavernous malformation, there is a liquefied hematoma.

MR examination of the brain (Fig. 4) was performed including axial T2-weighted images, axial FLAIR, axial diffusion-weighed images, axial gradient echo T2*, axial sus ceptibility-weighted (SWI) images, axial T1-weighted images; after intravenous injection of a gadoliniumchelate, additional axial, coronal and sagittal T1-weighted sequences were obtained. The MR examination revealed a large left frontal mass lesion, with heterogeneous signal architecture, involving the head of the left caudate nucleus and the lentiform nucleus, and extending across the midline in the suprasellar region. In the axial plane, the largest diameter of the mass is 43 mm. The lesion was partially surrounded by a halo of vasogenic edema, and compressed and displaced the frontal horn of the right lateral ventricle; the midline structures were shifted to the right. Imaging findings were highly suggestive for a giant cavernous malformation, after recent episode of hemorrhage.

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A neurosurgical intervention was performed and consisted of a left frontal craniotomy, with a left-sided transcallosal approach. The mass was completely removed using microsurgical techniques. Adjacent to the giant cavernous malformation, an old and liquefied hematoma was found; this was evacuated together with a layer of hemosiderin and reactive gliosis. The post-operative course was free of complications. A CT examination one day post-operatively revealed a sharply defined resection cavity, with a limited amount of intracranial air, consistent with a recent status post surgery (Fig. 5). The patient was discharged in good clinical condition on day 4 after the surgical procedure. The patient is clinically doing well without any neurological deficit at 14 months post operatively. Discussion Cavernous malformations also known as cavernous angioma or

cavernoma, are a type of vascular disorder, consisting of abnormally large vascular cavities or sinusoid channels of varying size. These lesions have alternately been classified as neoplastic or hamartomatous. Cavernous malformations can occur in mostly any organ. In the brain, cavernous malformations account for 5-10% of all vascular malformations (5). They occur with an incidence of approximately 0,5-1% in the general population. Most lesions are small and do not always cause neurological symptoms; it is estimated that only 1 in 3 cavernous malformations causes clinical symptoms, mostly seizures, progressive neurologic deficits and hemorrhage. Although almost all of the cases have micro-bleedings, bleeding leading to clinical symptoms is a rare entity in cavernomas (0,256%) (6). Symptoms are reported to occur when the lesion diameter is greater than 1,75 cm (7). Cavernous malformations are found in the cerebral hemispheres (66%), brainstem

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Fig. 2. — Patient 1, post-operative follow-up. Axial non-contrast CT examinations, 24 hours after surgery (A) and 4 months later (B). In the immediate postoperative period (A), the surgical cavity is sharply defined and dry; four months after surgery (B), the resection cavity has further decreased in size.

Fig. 3. — Giant cavernous malformation (haematoxylin/eosin stained paraffin section, bar: 500 µm). The wall of the lesion is covered by fibrinous material (arrow). Inset, left (CD34 immunohistochemical staining, bar: 100 µm) shows that the vessel wall is lined by a single-layered endothelium.

(18%), basal ganglia or thalamus (8%), cerebellum (6%), and other locations (2.5% [combined supra- and infratentorial, callosal or insular] (8). The natural history of cavernous malformations is to increase in size due to repeated episodes of hemorrhage (9). This leads to their markedly heterogeneous internal architecture on MR imaging, with blood degradation products of varying age.

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The presence of vasogenic edema in the surrounding brain tissue, as seen in our patients, indicates a recent episode of bleeding. The hemorrhage of the cavernoma can increase the edema. The increase in size of the cavernoma can be explained by re-endothelisation of the hemorrhagic cavity, formation of new blood vessels and proliferation of granulation tissue. New bleedings

from this hemorrhagic cavity may further increase the size in time . This is analogue to the growth of a subdural hematoma (10). The rate of bleeding is higher when the size of the lesion is greater than 10 mm and when the patient is aged 35 years or younger (11). There is a small, but clinically important, subgroup of so-called giant cavernous malformations (GCM). Unlike giant aneurysms, defined as having a diameter of at least 25 mm, no real threshold dimension has been agreed upon for giant cavernous malformation. Some authors define GCM as having a diameter of greater than 6 cm (4), while others use 4 cm as a cut-off (3). Because of their slow development and size, GCM present with subtle symptoms, that can mimic depression or brain tumor. Their clinical presentation depends on size and location, and is affected by recent episodes of bleeding. GCM occur more often in children and adolescents (12). In children they are frequently associated with intractable epilepsy (13, 14). The MRI characteristics of GCM are variable, depending on the presence of hemorrhage breakdown products and calcifications. The typical MR appearance of a GCM is that of a heterogeneous “popcorn-like” mass lesion (15, 16). We compare

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Fig. 4. — Patient 2, pre-operative MRI of the brain with axial TSE T2-WI (A), axial TSE T1-WI (B), axial gradient echo T2* (C), axial susceptibility WI (D), axial first eigenvector fractional anisotropy map (E), sagittal TSE T1-WI (F). There is a large heterogeneous mass in the suprasellar region involving the left caudate and lentiform nuclei. The mass presents a layered appearance, with mixed signal intensity components indicating various stages of blood degradation products. On the T2* and SWI sequences, the lesion is predominantly hypointense due to susceptibility effects caused by hemosiderin. Adjacent to the giant cavernous angioma, there is a layer of liquefied blood. The lesion is surrounded by vasogenic edema in the deep frontal white matter.

the appearance of the GCM in our two patients to a freshly cracked “walnut” with a heterogeneously mixed signal core and a hypointense hemosiderin rim. This heterogeneous signal architecture, with high and low signal intensity components, is explained by the presence of old and fresh blood breakdown products. The mottled appearance is best appreciated on T2* gradient echo or susceptibility weighted images (SWI); in these sequences, old blood degradation products (hemosiderin) appear hypointense (black) whereas fresh blood is hyperintense (white). These lesions are more conspicuous on high-field MR systems, because of their greater sensitivity to susceptibility artifacts. Diffusionweighted images may show throm-

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bosed blood clots as areas of diffusion restriction. Innovative imaging techniques, such as diffusion tensor imaging and functional MR imaging, have been applied to the preoperative and intra-operative management of these lesions. Histopathologically, cavernous malformations are well-circumscribed, lobulated, red to purple, raspberry-like lesions. They consist of thin hyalinized vascular channels without interposed brain tissue. Their size varies from punctate to several centimeters. On microscopic examination, cavernous malformations are shown to be composed of dilated, thin-walled capillaries that have one layer of endothelial lining and a variable layer of fibrous adventitia. Elastic fibers are absent in the

walls of these vascular caverns. There is usually evidence of previous hemorrhage on pathological examination. Thrombosis may be present within some of the lumens. Although not present in these two cases, literature describes that cavernous malformations may be associated with venous malformations (17). There is growing evidence that cavernous malformations and venous developmental anomaly (DVA) co-exist, and may even be different manifestations of the same disease spectrum (18-20). When these patients present with hemorrhage, it is often the cavernous malformation that has bled and not the venous developmental anomaly. In fact, it is exceedingly rare for a venous anomaly alone to hemorrhage.

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Fig. 5. — Patient 2, post-operative contrast enhanced CT scan (A) and CT angiography (B) on day 1 after surgery. There is a sharply defined, non-enhancing post-operative resection cavity in the suprasellar and left caudato-lenticular region; note the presence of intracranial air, consistent with a recent post-operative status. CT-angiography with volume rendering shows that the blood vessels of the circulus of Willis are intact.

The subgroup of giant cavernous malformations constitutes a formidable challenge to the neurosurgeon. These lesions need to be removed by circumferential dissection of the malformation. In both our patients, evacuation of the liquefied hematoma created space to facilitate surgical removal. Incomplete removal increases the risk of a post-operative hemorrhage or recurrence of the cavernous malformation. In conclusion, we have documented two patients with giant cavernous malformations. Clinical presentation may be insidious. The diagnosis is made with MR imaging, and both of our patients presented with a typical “walnut” appearance on T2* and SWI sequences. The neurosurgical approach consists of circumferential dissection with complete removal of the lesion. References 1. de Andrade G.C., Prandini M.N., Braga F.M.: Giant cavernous angioma: report of two cases. Arq Neuropsiquiatr, 2002, 60: 481-486. 2. Son D.W., Lee S.W., Choi C.H.: Giant cavernous malformation: a case report and review of the literature. J Korean Neurosurg Soc, 2008, 43: 198-200. 3. Kan P., Tubay M., Osborn A., et al.: Radiographic features of tumefactive giant cavernous angiomas. Acta Neurochir (Wien), 2008, 150: 49-55. 4. Lawton M.T., Vates G.E., QuinonesHinojosa A., et al.: Giant infiltrative

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cavernous malformation: clinical presentation, intervention, and genetic analysis: case report. Neurosurg, 2004, 55: 979-980. 5. Rigamonti D., Hadley M.N., Drayer B.P., et al.: Cerebral cavernous malformations. Incidence and familial occurrence. N Engl J Med, 1988, 319: 343–347. 6. Avci E., Ozturk A., Baba F., et al.: Huge cavernoma with massive intracerebral hemorrhage in a child. Turkish Neurosurg, 2007, 17: 23-26. 7. El-Koussy M., Stepper F., Spreng A., et al.: Incidence, clinical presentation and imaging findings of cavernous malformations of the CNS. A twentyyear experience. Swiss Med Wkly, 2011, 141: w13172. 8. Gross B.A., Lin N., Du R., et al.: The natural history of intracranial cavernous malformations. Neurosurg Focus, 2011, 30: E24. 9. Steiger H.J., Markwalder T.M., Reulen H.J.: Clinicopathological relations of cerebral cavernous angiomas: observations in eleven cases. Neurosurg, 1987, 21: 879-884. 10. Nanko N., Tanikawa M., Mase M., et al.: Involvement of hypoxia-inducible factor-1alpha and vascular endothelial growth factor in the mechanism of development of chronic subdural hematoma. Neurol Med Chir (Tokyo), 2009, 49: 379-385. 11. Alba T., Tanaka R., Koike T., et al.: Natural history of intracranial cavernous malformations. J Neurosurg, 1995, 83: 56-59. 12. Ozgen B.: Radiological features of childhood giant cavernous malformations. Neuroradiology, 2011, 53: 283289.

13. Rocamora R., Mader I., Zentner J., et al.: Epilepsy surgery in patients with multiple cerebral cavernous malformations. Seizure, 2009, 18: 241-245. 14. Thakar S., Furtado S.V., Ghosal N., et al.: A peri-trigonal giant tumefactive cavernous malformation: case report and review of literature. Childs Nerv Syst, 2010, 26: 1819-1823. 15. Gelal F., Feran H., Rezanko T., et al.: Giant cavernous angioma of the temporal lobe: A case report and review of the literature. Acta Radiol, 2005, 46: 310-313. 16. Kuhn J., Knitelius H.O., Bewermeyer H.: Multiple cerebral cavernous malformations: typical pattern on MR imaging and appearence of a new lesion in the follow-up MRI. Rontgenpraxis, 2004, 55: 200-202. 17. Campeaua N.G., Lane J.I.: De novo development of a lesion with the appearance of a cavernous malformation adjacent to an existing developmental venous anomaly. AJNR, 2005, 26: 156-159. 18. Hong Y.J., Chung T.S., Suh S.H., et al.: The angioarchitectural factors of the cerebral developmental venous anomaly; can they be the causes of concurrent sporadic cavernous malformation? Neuroradiology, 2010, 52: 883-891. 19. Sharma A., Zipfel G.J., Hildebolt C., et al.: Hemodynamic effects of developmental venous anomalies with and without cavernous malformations. AJNR, 2013, 34 (9): 1746-51. 20. Zhang P., Liu L., Cao Y., et al.: Cerebellar cavernous malformations with and without associated developmental venous anomalies. BMC Neurol, 2013 (Epub ahead of print), 13: 134.

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Multidetector Computed Tomography Diagnosis of Gastric Volvulus through the Foramen of Morgagni S. Lecouvet1, B. Coulier1, F. Pierard2, M. Gogoase1, J.P. Coppens1, M. Van Hoof3 Morgagni hernia is considered to be the rarest form of all diaphragmatic hernias. It develops through a congenital defect in the retrosternal area. Usually asymptomatic, this entity can lead to life-threatening complications such as incarceration, strangulation or volvulus of the herniated viscus. We hereby report a rare case of organoaxial gastric volvulus producing through the foramen of Morgagni in a 78-year-old woman. The full diagnosis was made by upper gastro-intestinal series and multidetector computed tomography (MDCT). The basic anatomy, physiopathology, diagnostic methods, complications and surgical treatment of Morgagni hernia are briefly reviewed. Key-words: Hernia, diaphragmatic – Stomach, volvulus.

Morgagni hernia (MH), an uncommon anteromedial subcostosternal diaphragmatic hernia, represents 3% of all surgically repaired diaphragmatic hernia. More frequently observed among women, MHs occur in most cases on the right side (90%). Most MHs are discovered incidentally. Despite a non obvious symptomatology or an asymptomatic character, MHs need an appropriate care and a prompt treatment to avoid lifethreatening complications such as gastric volvulus. Case report A 78-year-old woman presented with complains of abdominal pain,

pyrosis and post-prandial dyspepsia associated with symptoms of gastrooesophageal reflux. Since 2005, the patient had had a medical history of esophagitis associated with a hiatal hernia and was treated by proton pump in hibitor. Based on the history and current symptoms, gastroscopy was performed and confirmed a grade C esophagitis. At the same time, a massive amount of fluid was found in the stomach and one litre was sucked up. The endoscope could not progressd beyond the pylori. The procedure was repeated with a longer endoscope but remained unsuccessful.

Upper gastro-intestinal series were performed to investigate chronic gastric emptying disorders, to estimate the size and reducibility of the alleged hiatal hernia, to localize the gastro-oesophageal junction and to exclude a duodenal obstruction (Fig. 1A). The morphology of the oesophagus and the position of the cardia appeared normal but the largest part of the stomach comprising the distal fundus and the antrum were found within the thorax suggesting a clockwise intrathoracic gastric volvulus through an anteromedial retrosternal orifice. Contrast-enhanced Multidetector Computed Tomography (MDCT) of the thoraco abdominal junction (Fig. 1B

Fig. 1. — Global anteroposterior plain film (A) obtained during upper gastrointestinal series illustrates the intrathoracic clockwise gastric volvulus (curved arrow) producing through an anterior defect of the diaFrom: Department of 1. Diagnostic Radiology, 2. Visceral Surgery, 3. Gastroenterology, phragm. The same situation is spontaneClinique St Luc, Bouge (Namur), Belgium. ously found on the CT topogram (B). Address for correspondence: Dr S. Lecouvet, MD, Department of Diagnostic Radiology, Clinique St Luc, Rue St Luc 8, B-5004 Bouge (Namur) Belgium. E-mail: stephleco@gmail.com

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of diameter) was firmly sutured (Fig. 3). The post-operative period was uneventful. Discussion

Fig. 2. — A series of selected MPR views obtained in the anterior coronal (A), posterior coronal (B), nearly medial sagittal (C), axial (D) and axial oblique planes (E) illustrates the complex anatomy of herniating process. The esophagus and the cardia are in place (black arrows on B & C). The greater tuberosity appears distended by fluid and but remains in the left upper quadrant. A large portion of the gastric body and gastric antrum clockwise protrude within the thorax (white curved arrow on A) through a retrosternal orifice (straight white arrow on C). The diaphragmatic landmark of the orificeis clearly delineated (small white arrows on D) and finally the stretched distal antrum is seen reintegrating the epigastric area (short black arrow on E).

and 2) confirmed a typical Morgagni hernia (MH) complicated by an organoaxial gastric volvulus. During laparotomy, the stomach was first carefully decompressed

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allowingthe complete reduction of the volvulus. There was no sign of necrosis or perforation and gastric resection can be avoided. The distended foramen of Morgagni (6 cm

In 1769, thanks to his studies of autopsy specimens, Morgagni, an Italian anatomist and pathologist, was the first to describe the Morgagni orifice as a triangular anterior diaphragmatic defect (the foramen of Morgagni) between the muscle fibres of the xiphisternum and the costal margin (1-2). The defect also is referred to as the space of Larrey who described it as a foramen through which pericardial tamponade could be treated (3-4). This space is the result of a failure of fusion between the musculo-fibrotendinous elements of the diaphragm that come from the xiphisternum and the costal margin and insert on the central tendon of the diaphragm (5-6). Usually the defect has a greater transverse diameter than the anteroposterior one (3, 6). The internal mammary artery and its vein and lymphatics are the only anatomic structures that cross over this space to become the epigastric artery (5- 6). The physiopathology of the Morgagnihernia (MH) is currently explained as an acquired herniation of abdominal contents through this congenital defect in the anteromedial diaphragm. Although this defect is congenital, MH is extremely rare in children. The congenital weakness of the diaphragm resulting in a small defect tends to enlarge with age as a result of raised intra-abdominal pressure, explaining a more common presentation in adulthood (1, 4, 7). The main factors that increase abdominal pressureare pregnancy, multiparity, obesity , chronic constipation and chronic cough (3-5, 8). MHs can also be acquired secondary to a traumatic injury (9). Accounting for 3% of all surgically repaired diaphragmatic hernias, it is the rarest diaphragmatic hernia (5, 10). It occurs far more common on the right side of the diaphragm (90%) despite protection of the liver (3, 5-6, 8). Only 8% of MHs occur on the left side. One hypothesis to explain it is that the extensive pericardial attachments on the left provide additional supports for that side of the diaphragm (3, 5, 11). So the left diaphragmatic defects are covered by the heart and pericardium, constituting an obstacle to the herniating process (1). However, a MH acquired secondary to a traumatic injury is

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Fig. 3. — Surgical views. During laparotomy a large anterior retroxyphoidian orifice is found (A). The deflated gastric body clockwise protrudes within the thorax through this orifice (white arrow). The volvulus is reduced and the 6 cm wide open foramen of Morgagni clearly appears (white star on B & C) and is firmly sutured (black arrow on D).

more frequently seen at the left side because of the protection of the right diaphragmatic cupola by the liver (9). Bilateral presentations are exceptional (2%) (1, 5, 7). 70% of the patients presenting with MH are women (3, 5-6, 8). The average age of presentation is 58 years in female and 50 years in males (4). Most patients with MH do not have any symptom and the hernias are usually discovered incidentally (4, 6-8). Symptoms occur mainly in patients who have a hollow viscus included in the herniation (6, 10-11). Symptoms are nonspecific, fre quently digestive or pulmonary such as abdominal discomfort, fullness, bloating, nausea, vomiting, cramps, cough, dyspnea, pain in the chest (45, 12). The diagnosis of MH may be suggested on plain chest or abdominal X-rays which may show a mass at the cardiophrenic angle with the density of the heart or a bowel gas pattern within the chest when the

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stomach or the intestines are herniated (1, 3, 5, 13). Barium investigations can help to the diagnosis but their contribution may be limited when the herniating sac doesn’t contain any hollow viscera, for example when it only contains the greater omentum (8, 14). In our situation, contrast studies were first performed to investigate and evaluate the alleged and symptomatic hiatal hernia and the gastric emptying disorders (SAGES guidelines) (15). Furthermore, barium investigations are frequently carried out before surgery for better delineation of the anatomy, especially to localize the gastro-oesophageal junction (15). However, in acute situations with suspected complications, contrastenhanced MDCT is the diagnostic method of choice, making the correct diagnosis in 100% of cases (5, 7). It is essential for a complete pre operative anatomic diagnosis, able to determine the site, the level and

the cause of many digestive obstructions including the MH. It can identify the specific herniated organs and the potential accompanying complications (1-2, 5). Furthermore, when the hernia is purely omental, this exam can make the distinction between herniated fat of the greater omentum and epicardial fat pad or lipoma thanks to the identification of the rich vascular network of the greater omentum (3-6). In fact, the presence of fine curvilinear or linear densities within the fat represents omental vessels and confirms without doubt a hernia of the greater omentum with intrathoracic topography (1, 14). After a MDCT showing an anterior mediastinal mass with partially fat density, MRI can be interesting to distinguish between a chest- and an abdominal process, especially when the differential diagnosis includes mediastinal tumours (3, 5). Apart from mediastinal tumours, the main differential diagnosis in-

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cludes atelectasis, pneumonia, mesothelioma, pulmonary sequestrum (3, 11). Endoscopy is not helpful to make the diagnosis but the inability to pass the endoscope beyond the duodenal bulb suggests some gastric anomaly (7). The most common contents of the hernia sac are omentum exclusively (31%) or colon and omentum (29%). More rarely, the stomach (15%) (generally secondary to the incarceration of the transverse colon), the small bowel (11%) and the liver (4%) can also herniate (3, 5-6). The main but infrequent complications of a Morgagni hernia are incarceration, strangulation, bowel obstruction and volvulus of the herniated organ (7). These lifethreatening complications need a prompt diagnosis. The incidence of an acute stran gulation complicating a MH is about 10-15% and among these strangu lations, gastric volvulus (GV) is particularly uncommon (5). The main aetiologies of GV include diaphragmatic anomalies (hernias, eventrations, etc), splenic anomalies (wandering spleen, aspleny), liver anomalies (aplasia of the left liver lobe) and gastric lesions (gastric ulcus or neoplasm, pyloric hypertrophy) (5, 16). Ligament laxity is an essential and constant factor to arise a GV (13, 16). Some others predisposing factors are mentioned such as gastric repletion, repeated vomiting and factors that increase the abdominal pressure. GV may be organoaxial (59%), me sentericoaxial (29%), combined (2%) or not classified (10%) (5, 16). The classical symptoms of GV are known as the Borchardt’s triad including severeepigastric or thoracic pain, abdominal distension with unproductive vomiting and difficultiesor impossibility to put a nasogastric tube (5, 16). Given the potentially severe and life-threatening complications of MHs, surgery is indicated in all cases, symptomatic or not (1, 3-4, 6, 11). Several surgical approaches have been used to repair MHs: laparo tomy, thoracotomy and minimal invasive surgery (laparoscopic and thorascopic). The optimal surgical treatment is still controversial (4). For acute surgical presentation, laparotomy is the most common surgical approach (4).

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Thoracotomy remains the best approachto allow the dissection of the hernial sac (3-4). Laparoscopy provides the benefit of an excellent view of the defect and abdominal contents, minimal tissue trauma, superior cosmetics, rapid recoveryof the patient and earlier returnat home (2, 4). Laparoscopic is actually considered as a safe and effective alter native to laparotomy or thoracotomy (1, 11-12). There is no consensus related to the management of the hernial sac (4, 8). Some surgeons don’t recommend the resection of the hernial sac to avoid some fatal complications secondarily to the dissection of intrathoracic adhesions, such as pneumopericardium, injury to the lung, pericardium and mediastinal structures (3, 8). Other surgeons recommend removing the sac when it is small, without intrathoracic adhesions and when there are few risks of injuring thoracic structures (3). The necessity to close or not the defect with prosthetic mesh is also a matter of debate. The use of prosthetic mesh is recommended if the defect is larger than 3 cm. The smallest defects can be repaired with a simple suture (4). Conclusion Morgagni hernia (MH), a rare and usually asymptomatic diaphragmatic hernia needs an appropriate and prompt diagnosis because a late diagnosisor misdiagnosis can be fatal. In fact, the entity can lead to life-threatening complications. For patients with suspected complications, contrast-enhanced MDCT is currently the diagnostic method of choice, providing two- or threedimensionalreformatted images of high quality and allowing correct diagnosisin 100% of cases. Modern surgical techniques as laparoscopy allow an effective, minimally invasive and safe repair of MHs but laparotomy remains the most common surgical approach for acute surgical presentation. References 1. Altinkaya N., Parlakgümüs A., Koc Z., Ulusan S.: Morgagni hernia: diagnosis with multidetector computed tomography and treatment. Hernia, 2010; 14: 277-281.

2. Arora S., Haji A., Ng P.: Adult Mor gagni hernia: the need for clinical awareness, early diagnosis and prompt surgical intervention. Ann Roy Coll Surg Engl, 2008; 90: 694-695. 3. Albarracin Marin-Blazquez A., Candel M.F., Parra P.A.: Morgagni hernia : Repair with a mesh using laparoscopic surgery. Hernia, 2004; 8: 70-72. 4. Griffiths E.A., Ellis A., Mohamed A., Tam E., Ball C.S.: Surgical treatment of a Morgagni hernia causing intermittent gastric outlet obstruction. BMJ Case Reports, 2010; 10: 1-6. 5. Coulier B., Broze B.: Gastric volvulus through a Morgagni hernia: multidetector computed tomography diagnosis. Emerg Radiol, 2008; 15: 197-201. 6. Coulier B.: Hernias of the greater omentum through the antero-superior abdominal wall: an extensive pictorial MDCT review with emphasis on typical anatomic landmarks. A pictorial essay. JBR-BTR, 2012; 95: 191-214. 7. Borodyansky Dodis L., Bennett M.W.: Gastroduodenal obstruction from Mor gagni hernia in an elderly patient. Med scape General Medicine, 2005; 7: 70. 8. Cybulsky I., Himal H.S.: Gastric volvulus within the foramen of Morgagni. Can Med Assoc J, 1985; 133, 209-210. 9. Machtelincks C., De Man R., De Coster M., Ghillebert G., Provoost V.: Acute torsion and necrosis of the greater omentum herniated into a foramen of Morgagni. Abd Imag, 2001; 26: 83-85. 10. Rai S.P.V., Kamath M., Shetty A., Shenay S., Kumar A.: Symptomatic Morgagni’s hernia in an elderly patient. J Emerg, Trauma and Shock, 2010; 3: 89-91. 11. Horton John D., Hofmann Luke J., Hetz Stephen P.: Presentation and management of Morgagni hernias in adults: a review of 298 cases. Surg Endoscopy, 2008; 22: 1413-1420. 12. Vassileva C.M., Shabosky J., Boley T., Hazelrigg S.: Morgagni hernia presenting as a right middle lobe compression. Ann Thorac Cardiovasc Surg, 2012; 18: 79-81. 13. Aghajanzadeh M., Khadem S., JahromiS.K., Gorabi H.E., Ebrahimi H., Maafi A.A.: Clinical presentation and operative repair of Morgagni hernia. Interactive Cardiovascular and Thoracic Surgery, 2012; 15: 608-611. 14. Gossios K.J., Tatsis C.K., Lykouri A., Constantopoulos S.H.: Omental herniation through the foramen of Morgagni. Diagnosis with chest computed tomography. Chest, 1991; 100: 1469-1470. 15. Kohn G.P., Price R.R., Demeester S.R. et al.: Society of American Gastrointestinal and Endoscopic Surgeons: Guidelines for the Management of Hiatal Hernia, 2013. 16. Bedioui H., Bensafta Z.: Gastric Vol vulus: diagnosis and management. Presse Med, 2008; 37: 67-76.

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Amyloidosis: an unusual cause of mesenteric, omental and lymph node calcifications F.M. Vanhoenacker1,2,3, K. Vanwambeke1, G. Jacomen4 We present a rare case of amyloidosis initially presenting with giant calcified inguinal adenopathy. Further imaging revealed diffuse calcifications within the mesentery and greater omentum. Amyloid deposition may mimic chronic granulomatous disorders and primary or secondary neoplastic conditions. Although definite diagnosis is made on histology, the radiologist should include amyloidosis in the differential diagnosis in the absence of a clinical history of neoplastic disorders or chronic infection, especially if extensive intralesional calcifications are seen. Ultrasound may be useful to target solid noncalcified areas in easily accessible extraabdominal locations. Key-word: Amyloidosis.

Case report An 81-year-old female presented with bilateral inguinal soft tissue swellings. The lesions were painless and of hard consistency on palpation. The clinical notes of the patient mentioned biopsy of a similar soft tissue lesion at the left groin 20 years earlier, revealing a nonspecific benign fibrous lesion at histology. Further clinical history was unremarkable. According to the patient, the masses were slowly increasing in volume during the last 6 months. Computed Tomography (CT) showed bilateral giant adenopathy with intralesional coarse calcifications (Fig. 1). In addition, multiple small nodular calcifications were seen in the omentum. Subsequent CT of the upper abdomen confirmed diffuse calcifications along the greater omentum, mesentery, the hepatic fissure, peritoneal surface of the spleen and splenic hilum (Fig. 2). Magnetic Resonance Imaging (MRI) of the groin showed heterogeneous signal of the enlarged inguinal lymph nodes on both pulse sequences. There was no enhancement of the intralesional calcifications, whereas the noncalcified areas showed vivid enhancement (Fig. 3). Lesion heterogeneity was also seen on ultrasound. The calcified areas showed retroacoustic shadowing, whereas the solid components were hypoechoic with increased power Doppler signal (Fig. 4). An ultrasound guided biopsy was performed at the level of the noncalcified solid portions of the left groin

From: 1. Department of Radiology, AZ Sint-Maarten, Duffel-Mechelen, 2. Department of Radiology, Antwerp University Hospital, University of Antwerp, Edegem, 3. Faculty of Medicine and Health Sciences, University of Ghent, 4. Department of Pathology, AZ Sint-Maarten, Duffel-Mechelen, Belgium. Address for correspondence: Prof. dr. F.M. Vanhoenacker, M.D., Dept. of Radiology, AZ Sint-Maarten, Duffel-Mechelen, Rooienberg 25, 2570 Duffel, Belgium.

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Fig. 1. — CT scan of the pelvis. Axial (A) and coronal reformatted image (B) shows bilateral massive inguinal adenopathy with intralesional coarse calcifications (black arrows). Note also small nodular calcifications within the omentum (white arrowheads).

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C A

A B Fig. 2. — CT scan of the upper abdomen. Coronal reformatted image (A) showing thickening of the omentum which contains a mantle of speckled calcifications (black arrows). Axial image (B) revealing multiple nodular calcifications within the mesentery, the splenic hilum and the posterior surface of the spleen. Axial image at a slightly lower level (C). Note subtle calcification at the hepatic fissure (white arrowheads).

lesion. Histology of the biopsy specimen showed amyloid deposits on Congo red stain, exhibiting applegreen birefringence on polarized light (Fig. 5). Discussion Amyloidosis consists of a heterogeneous group of disorders characterized by widespread extracellular deposition of amyloid, an insoluble fibrillar protein, in multiple organs and tissues (1-4). The current classi-

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B Fig. 3. — MR imaging of the groins. Axial T2-WI (A) and coronal fat-suppressed T1-WI after intravenous administration of gadolinium contrast (B). The enlarged lymph nodes and are of heterogeneous signal on T2-WI, with the calcified areas being hypointense (white arrows). The noncalcified components showed vivid enhancement (white arrows), whereas the calcified solid components are nonenhancing (black arrows) (B).

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Fig. 4. — Ultrasound of the groins showing enlarged inguinal lymph nodes with calcified areas demonstrating retroacoustic shadowing (white arrows). The noncalcified solid parts are hypoechoic with foci of increased Doppler flow (white arrowheads).

fication of amyloid disease is based on the specific type of protein fibril involved in the amyloid deposits, and uses an abbreviation of the protein, prefixed with the letter A. For example, amyloidosis caused by transthyretin (TTR) is termed “ATTR”. The nomenclature of amyloid protein fibril is complex and has been revised recently by the nomenclature Committee of the International Society of Amyloidosis (5, 6). The literature contains many clinical and histochemical classifications that were used when the chemical diversity of amyloid disease was poorly understood. One such historical classification distinguishes systemic and localised forms of amyloidosis. Systemic amyloidosis refers to involvement of more than one body organ or system, whereas localised amyloidosis affects only one body organ or tissue type. Another older classification divides primary or secondary forms. Primary amyloidosis arises from a disease with disordered immune cell function such as multiple myeloma and other immunocyte dyscrasias. Secondary amyloidosis occurs as a complication of some other chronic inflammatory or tissue destructive disease. The Committee of the International Society of Amyloidosis recommends to suppress these confusing alternative classifications. Amyloidosis has been described in various anatomic locations including the central nervous system, head and neck, chest, heart, lymph nodes, breast, gastrointestinal and genitourinary tract, spleen, subcutis, musculoskeletal system (1-4, 7-10).

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Fig. 5. — Photomicrograph of the histopathologic specimen (Congo red stain) showing apple-green birefringence on polarized light.

Involvement of the omentum, mesentery and peritoneum are extremely rare manifestations of this disease (1-4). The disease may be either nodular or diffuse (4). In the diffuse form, amyloid deposition in the greater omentum, mesentery and retroperitoneum usually results in hazy infiltration of the fat within these structures on CT (4). Extensive calcifications within these deposits are rare (2), but are highly suggestive of amyloidosis (2, 4). Enlargement of retroperitoneal lymph nodes is seen in the nodular form. Lymph node involvement occurs in up to 37% of patients and the hilar, mediastinal and para-aortic lymph nodes are most commonly involved, but other locations have been reported as well (8, 9). In our patient, the dominant finding at presentation was the presence of huge calcified inguinal lymphadenopathy. On imaging, the involved lymph nodes are usually enlarged and may contain intralesional calcifications. CT is the preferred technique for demonstration of calcifications, although ultrasound may be a useful technique for guiding biopsy, particularly in lymph nodes which are easily accessible. The biopsy should be targeted to noncalcified solid parts, because of the soft consistency of these components. Non calcified areas may demonstrate increased color Doppler signal, in keeping with vascularized components. Apart from evaluation of cardiac amyloidosis (7), MRI of amyloid deposition in soft tissues and lymph nodes has been rarely described (10).

MR appearance may be variable and is usually heterogeneous on all pulse sequences. Densely packed amyloid fibrils, dense collagen and calcifications appear hypointense on T2-weighted images. High signal intensity areas on T2-WI may be due to necrosis, whereas hemorrhagic, proteinaceous or eosinophilic components may be of high signal (10). Contrast enhanceon T1-WI ment can also be observed in lymph nodes (8). The differential diagnosis of calcified peritoneal, mesenteric and omental amyloidosis includes primary or metastatic neoplasms that may provoke desmoplastic reaction, such as peritoneal mesothelioma and ovarian carcinoma (2). Ascites is usually present in these cases, whereas ascites is only seen in 20% of cases of peritoneal amyloidosis, secondary to associated cardiac, hepatic or renal failure (4). In our case, there was no ascites. Another differential diagnosis consists of infectious disorders of the peritoneum and greater omentum, such as tuberculosis. The differential diagnosis of massive lymphadenopathy includes lymphoma, infection, metastatic disease, and granulomatous diseases. Rosai-Dorfman disease, Castleman’s disease, Bartonellosis, and rare inflammatory disorders such as Kimura’s disease and Kichuchi- Fujimoto disease should be considered in the differential diagnosis in case of enhancing lymph nodes (8). Chronic tuberculosis or granulomatous disease should be excluded when lymph nodes are calcified.

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Histologic confirmation is required for definite diagnosis of amyloid deposition. Although routine hematoxylin-eosin stains can be suggestive, the diagnosis should be confirmed by a Congo Red stain, where examination under polarized light reveals a characteristic applegreen colour, due to the birefringence of the amyloid deposition. Conclusion Although rare, amyloidosis should be considered in the differential diagnosis of diffuse omental, mesenteric and peritoneal calcifications and in the presence of massive calcified lymphadenopathy. References 1. Allen H.A., Vick W., Messner J.M., Parker G.A.: Diffuse mesenteric amyloidosis: CT, sonographic and

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JBR–BTR, 2014, 97 (5) pathologic findings. J Comput Assist Tomogr, 1985, 9: 196-198. 2. Coumbaras M., Chopier J., Massiani M.A., Antoine M., Boudghene F., Bazot M.: Diffuse mesenteric and omental infiltration by amyloidosis with omental calcification mimicking abdominal carcinomatosis. Clin Radiol, 2001, 56: 674-676. 3. Horger M., Vogel M., Brodoefel H., Schimmel H., Clausen C.: Omental and peritoneal involvement in systemic amyloidosis: CT with pathologic correlation. Am J Roentgenol AJR, 2006, 186: 1193-1195. 4. Coulier B., Monfort L., Doyen V., Gielen I.: MDCT findings in primary amyloidosis of the greater omentum and mesentery: a case report Abdom Imaging, 2010, 35: 88-91. 5. Sipe J.D., Benson M.D., Buxbaum J.N., et al.: Amyloid fi bril protein nomenclature: 2010 recommendations from the nomenclature committee of the International Society of Amyloidosis. Amyloid, 2010, 17: 101-104.

6. Sipe J.D., Benson M.D., Buxbaum J.N, et al.: Amyloid fibril protein nomenclature: 2012 recommenda tions from the Nomenclature Committee of the International Society of Amyloidosis. Amyloid, 2012, 19: 167170. 7. Bauner K.U., Wintersperger B.: MRI in cardiac sarcoidosis and amyloidosis. Radiologe, 2013, 53: 54-60. Horger 8. Vogel M.N., Wehrmann M., M.S.: Massive cervical and abdominal lymphadenopathy caused by localized amyloidosis. J Clin Oncol, 2007, 25: 343-344. 9. Terrier B, Hummel A, Servais A, Delarue R, Fournier P, Fakhouri F.: An unusual cause of lymph nodes enlargement. Am J Med, 2007, 120: e13. 10. Maheshwari A.V., Muro-Cacho C.A., Kransdorf M.J., Temple H.T.: Soft- tissue amyloidoma of the extremities: a case report and review of literature. Skeletal Radiol, 2009, 38: 287-292.

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SPONTANEOUS RUPTURE: A RARE COMPLICATION OF HEPATIC HEMANGIOMAS P. De Beul1, P. Roels1, G. Heirwegh1, A. Janssen2, B. Claikens1 Hepatic lesions are one of the possible visceral causes of spontaneous hemoperitoneum. Hepatic hemangiomas are congenital vascular malformations and are the most common benign tumours of the liver. Most cases are asymptomatic. Although they seldom rupture, it is important to diagnose them as their global mortality rate is high. An accurate diagnosis of a hemangioma as cause of a hemoperitoneum would result in correct clinical decision making and treatment. Key-word: Angioma.

Case report A 46-year-old woman was admitted to our hospital complaining of diarrhea, syncopal episodes and heavy abdominal cramps. Physical examination revealed remarkable pain and sensitivity over the whole abdomen. The patient’s medical history was unremarkable, except having taken birth control pill for several years. Blood analysis showed increased white blood cells, anaemia, thrombocytopenia, increased Gamma-GT and lactate dehydrogenase. Due to the acute situation, no US was performed, but a CT scan with intravenous contrast was promptly performed. CT-scan revealed a massive hemoperitoneum with multiple voluminous hypodense lesions in the right and left liver lobes with inlying fluid-fluid levels and with peripheral enhancement. The imaging aspect of the biggest lesion of 10 centimeters rose the suspicion of acute rupture of a giant cavernous hemangioma (Fig. 1). Because of the emergency and the instability of the patient, no angiography was performed. The patient was urgently admitted to the Department of Surgery for a laparoscopic approach with reconversion. Partial capsulectomy with transparenchymal suturing was done. Peroperative images were taken (Fig. 2). Discussion Hepatic hemangiomas are congenital vascular malformations and are considered as the most common benign tumours of the liver and can measure up to 20 centimetres. These

Fig. 1. — CT scan revealed a massive hemoperitoneum with a giant hemangioma as possible cause.

tumours can be found at any age, 7095% occur in women especially in their fourth and fifth decades of live (1). Macroscopically, they are wellcircumscribed, reddish-purple, hyper vascular lesions. Hepatic hemangiomas can be divided in two major groups: capillary hemangiomas and cavernous hemangiomas. Respectively they are generally peripheral, small, and sometimes multiple and the second group are more rare and larger. Lesions larger than 4 cm are called ‘giant hemangiomas’. Hepatic hemangiomas enlarge by ectasia rather than neoplastic growth. Malignant transformation is extremely rare. They are often diagnosed as incidental findings on

From: 1. Dept. of Radiology, 2. Dept of Surgery, AZ Damiaan, Ostend, Belgium. Address for correspondence: Dr P. De Beul, M.D., Dpt of Radiology, AZDamiaan, Gouwelozestraat 100, 8400 Ostend, Belgium. E-mail: pakeezah.debeul@student.kuleuven.be

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imaging studies of the abdomen or during exploratory surgeries. Most cases of hepatic hemangiomas are asymptomatic although a few patients may present with a wide variety of clinical symptoms like intermittent right upper quadrant pain. Increasing size or intratumoral thrombosis or hemorrhage can cause pain, possibly secondary to capsular distension, focal necrosis or compression of adjacent structures. Giant hemangiomas can also cause biliary colic, obstructive jaundice, and gastric outlet obstruction. Laboratory studies show an elevation of transaminases, bilirubin and alkaline phosphatase even in asymptomatic cases. Spontaneous rupture of hepatic hemangiomas is an uncommon complication representing 1-4% (2). In cases where spontaneous rupture occurs, clinical manifestations consist of sudden abdominal pain, and anemia secondary to a hemoperitoneum. As the size of the hemangioma increases, the chance of rupture also

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Fig. 2. — Peroperative image confirms the giant hemangioma as the cause of the hemoperitoneum.

increases, especially if the tumour is located on the surface of the liver and shows extrahepatic growth. If the patient receives steroid therapy for a coexisting disorder, the chance of rupture is even higher (3). The global mortality rate is high and about 60-75%. Spontaneous rupture of a (giant) hepatic hemangioma can give rise to a spontaneous hemoperitoneum. Hepatic hemangioma can be diagnosed in most patients using noninvasive studies inter alia ultrasonography, contrast-enhanced computed tomography and magnetic resonance imaging. Describing imaging features is beyond the purpose of this article. Because most cases of hepatic hemangiomas are asymptomatic they could be followed up by periodic radiological examination. Surgery should be restricted to specific situations. Liver biopsy is contra indicated because of an increased risk of hemorrhage and should be used only when imaging studies and alpha fetoprotein (as a tumor marker

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of liver cancer) testing are inconclusive. Absolute indications for surgery are spontaneous or traumatic rupture with hemoperitoneum, intratumoral bleeding, consumption coagulopathy (Kasabach-Merritt syndrome), when malignancy cannot be excluded and rapid growth. Lesions exceeding more than 10 to 11 centimeters in diameter may have greater likely hood for internal bleeding, further growth or rupture and here a preventive excision is proposed (4). Persistent abdominal pain, obstructing jaundice, portal hypertension, a size greater than 5 cm, superficial localization because of traumatism risk, and an uncertain diagnosis are relative surgical indications. The proposed surgical procedures are anatomic, nonanatomic resection, enucleation, use of transcatheter arterial embolization and liver transplantation. Surgical resection and enucleation with temporary inflow occlusion (Pringle maneuver) are considered the treatments of choice (5). Segmental resection is usually selected if a hemangioma is localized in a single segment, and enucleation is usually selected if it is localized in the center of the liver (6). Transcatheter arterial embolization has been suggested as a good treatment used either alone or as a preoperative procedure prior to surgical resection (7). In cases of arterial rupture, transcatheter embolization results in stanching or reducing the hemorrhage. In conclusion, hepatic hemangiomas are congenital vascular malformations and are considered the most benign tumours of the liver. Most cases are asymptomatic. But they are a rare cause of spontaneous

rupture. Because of the high global mortality associated with it, every radiologist may not overlook a spontaneous ruptured hemangioma as possible cause of a hemoperitoneum. So whenever a hemoperitoneum is presented with a liver lesion, radiologists should look for spontaneous rupture of hepatic hemangiomas. References 1. Abrams R.M., Bernbaum E.R., Santon J.S., Lipson J.: Angiographic features of cavernous hemangioma of the liver. Radiology, 1969, 92: 308-312. 2. Jain V., Ramachandran V., Garg R., Pal S., Gamanagatti S.R., Srivastava D.N.: Spontaneous rupture of a giant hepatic hemangioma – sequential management with transcatheter arterial embolization and resection. Saudi J Gastroenterol, 2010, 16: 116-119. 3. Aiura K., Ohshima R., Matsumoto K., Ishii S., Arisawa Y., Nakagawa M., et al.: Spontaneous rupture of liver hemangioma: risk factors for rupture. J Hep Bil Pancr Surg, 1996, 3: 308312. 4. Donati M., Stavrou G.A., Donati A., Oldhafer K.J.: The risk of spontaneous rupture of liver hemangiomas: a critical review of the literature. J Hepatobiliary Pancreat Sci, 2011, vol. 18, Issue 6 , pp 797-805. 5. Corigliano N., Mercantini P., Amodio P.M., Balducci G., Caterino S., Ramacciato G., et al.: Hemoperito neum from a Spontaneous Rupture of a Giant Hemangioma of the Liver: Report of a case. Surg Today, 2003, 33 : 459-463. 6. Seo H., Jo H.J., Sim M.P., Kim S.: Right trisegmentectomy with thoraco abdominal approach after transarterial embolization for giant hepatic hemangioma. World J Gastroenterol, 2009, 15: 3437-3439. 7. Deutsch G.S., Yeh K.A., Bates W.B. III, Tannehill W.B.: Embolization for management of hepatic hemangiomas. Am Surg, 2001, 67: 159-164.

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Granular cell tumor in the breast mimicking breast carcinoma J. Huyskens, C. Geniets Granular cell tumor is also known as a granular cell myoblastoma, Abrikossoff’s tumor, granular cell nerve sheath tumor or granular cell scwhannoma. It is a rare soft-tissue mass that can develop in any soft tissue. Most commonly it appears in the tongue (40%), the oral cavity or in the subcutaneous tissue. In rare occasions it is reported as a breast mass, mimicking a carcinoma. Not only clinically, but also on mammography, ultrasonography and macroscopically. Diagnosis can only be made on histology, emphasizing once again the importance of a thorough preoperative multi-disciplinary assessment. We describe a case in which a woman presents herself with a palpable nodule in the breast in which clinical investigation, mammography and especially sonography indicated the presence of a malignancy. Only after we conducted a core biopsy for pre-operative histological investigation, we could make the diagnosis of a granular cell tumor, preventing an unnecessary mastectomy. The patient refused however local excision and was followed up with mammography and sonography. Key-word: Breast neoplasms, diagnosis.

Case report A black woman of 30 years old presented to the gynecologist with a mass in the right breast. On clinical investigation a hard palpable mass was identified in the medial part of the right breast. There was no skin retraction or nipple discharge, nor were there palpable axillary lymph nodes. A mammography revealed an asymmetric stellate mass of 20 millimeter, located deep and me dial in the right breast. It is causes distortion and retraction of the pec toral muscle, as shown on the cra niocaudal images of the right breast (Fig. 1 and 2). The mass had irregular borders and was clearly identified, because of the relative low density of the breast tissue and the type 3 amount of tissue, i.e. between 25 and 50% of glandular tissue, relative to the amount of fatty tissue. Imme diately after, we performed a sono graphy, showing a hypodense mass of 15 millimeter medial in the right breast. The mass had irregular bor ders, showed marked posterior acoustic shadow and had increased vascularity with a ‘feeding vessel’ as shown on Doppler (Fig. 3 and 4). As part of the pre-operative investiga tion for typing and grading of a breast carcinoma we performed 4 ultrasound-guided core biopsies of this lesion. Histology showed prolif eration of loose cells with an eosino phylic cytoplasm with a small round core without nuclear atypia, indicat ing a benign granular cell tumor. Also immunuhistochemical findings showed staining typical for a benign

Fig. 1. — Craniocaudal and mediolateral oblique mammography of the right (RCC) breast showing a stellate mass deep and medial in the right breast with attraction of the prepectoral muscle.

granular cell tumor, thus preventing unnecessary and mutilating mastec tomy. The patient refused local excision. After a half year and a year follow up, the tumor showed no growth and the patient was lost from follow-up. Discussion Granular cell tumor was first escribed in 1924 by the Russian d pathologist Aleksei Ivanovich Abrikossoff who referred to it as a myeloblastoma because of the simi lar appearance of striped muscle

From: Department of Radiology, Algemeen Stedelijk Ziekenhuis Aalst, Aalst, Belgium. Address for correspondence: Dr J. Huyskens, M.D., Department of Radiology, Algemeen Stedelijk Ziekenhuis Aalst, Merestraat 80, 9300 Aalst, Belgium. E-mail: jef_huyskens@hotmail.com

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cells and the believe that they arise from myoblastic cells. This is a rare tumor, and recent studies suggest that they are from neural origin and arise from Schwann cells. However because on a cellular level they are much differences with schwannoma, it should still be regarded as a sepa rate entity. Some still believe that it is a degenerative process that can arise in all cells. It can appear in vir tual any soft tissue with a predilec tion in the head and neck area (4565%). It is most commonly found in the tongue (40%) and the oral cavity. It is relatively rare (5-8%) in the breast area. We found 47 case reports and several series, including lesions in other regions. Mostly it is benign tu mor and only a minority is malignant (2,5%). Only in a minority of the

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Fig. 2. — Enlargement mammography of the right (RCC) breast, showing a stellate mass deep in the breast with attraction of the prepectoral muscle.

Fig. 3. — Ultrasound of the right breast shows a hypodense mass with a marked retro-acoustic shadow and irregular borders. Diameters of 14,8 × 14,0 millimeter.

Fig. 4. — Ultrasound with colour Doppler mapping shows a large irregular mass with an adjacent ‘feeding’ vessel and marked hypervascularity in the margin.

c ases a benign one mimics a malignancy, as shown in the study of Boulat et al. in 1994 were 3 of 159 reported granular cell tumors in the breast mimicked breast carcinoma. Overall a ratio of 1 granular cell tumor to 1000 carcinomas of the breast is likely. It is more common found in premenopausal black woman. It is treated by local wide excision and however it has relative high recurrence rate after excision, it has a good prognosis. The diagnosis is exclusively made on pathology. Microscopic investigation of the benign form show polygonal cells with a granular eosinophylic cytoplasm and small round nuclei without atypia. The malignant form shows high

mitotic activity and pleiomorphic cellular tissue. Immuno-histochemical staining shows reactivity for S100 protein, CD 68 and neuron specific endolase. Recommended surgical treatment is wide local excision with tumor-free margins. Malignancy is rare and therefore radical mutilating surgery should be avoided especially in the breasts of a young woman like in our case. However is best removed, patients still can decide by themselves and can never be obligated, like in our case.

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References 1. Abrikossoff A.: Ueber myome, ausgehend von der quergestreifen willkurli-

chen muskulatur. Vorchows Arch Patholog Anat Physiol Klin Med, 1926, 260: 215-233. 2. Sussman E.B., Hajdu S.I., Gray G.F., et al.: Granular cell myoblastoma of the breast. Am J Surg, 1973, 126: 669670. 3. Umansky C., Bullock W.D., et al.: Granular cell myoblastoma of the breast. Ann Surg, 1968, 168: 810-817. 4. Mariscal A., Perea R.J., Castella E., et al.: Granular cell tumor of the breast in a male patient. AJR, 1995, 165: 6364. 5. Brown A.C., Audisio R.A., Regitnig P., et al.: Granular cell tumour of the breast. Surg Oncol, 2011, 20: 97-105. 6. Matrai Z., Langmar Z., Szabo E., et al.: Granular cell tumour of the breast. Case series and review of the literature. Eur J Gyn Oncol, 2010, 31: 636640. 7. Gogas J., Markopoulos C., Kouskos E., et al.: Granular cell tumor of the breast: a rare lesion resembling breast cancer. Eur J Gyn Oncol, 2002, 23: 333-334. 8. Lellé R.J., Park H., Brow C.A., et al.: Benign granular cell tumor mimicking carcinoma of the breast. Report of a case. Eur J Gyn Oncol, 1992, 13: 390393. 9. Boulat J., Mathoulin M.P., Vacheret H., et al.: Granular cell tumor of the breast. Anatomic Pathol, 1994, 14: 93100. 10. Ordoñez N.G., et al.: Granular cell tumor: a review and update. Advances in Anatomic Pathology, 1999, 6: 186-203. 11. Becelli R., Perugini M., Gasparini G., et al.: Abrikossoff’s tumor. J Cranio facial Surg, 2001, 12: 78-81. 12. Le B.H., Boyer Ph.J., Lewis J.E., et al.: Granular cell tumor. Immunohistochemical assessment of inhibin alfa, Protein gene product 9.5, S100 Protein, CD 68 and Ki 67 Proliferative index with clinical correlation. Arch Pathol Lab Med, 2004, 128: 771775. 13. Wang J., Zhu X.Z., Zhang R.Y., et al.: Malignant granular cell tumor: a clinicopathologic analysis of 10 cases with review of the literature. Zonghua Bing Li Xue Za Zhi, 2004, 33: 497-502. 14. Simsir A., Osborne B.M., Greenebaum E., et al.: Malignant granular cell tumor: a case report and review of the recent literature. Human Pathology, 1996, 27: 853-858. 15. Hahn H.J., Iglesias J., Flenker H., et al.: Granular cell tumor in differential diagnosis of tumors of the breast. The role of fine needle aspiration cytology. Pathology Research and Practice, 1992, 188: 1091-1094. 16. Akatsu T., Kobayashi H., Uematsu S., et al.: Granular cell tumor of the breast pre-operatively diagnosed by fine-needle aspiration cytology: report of a case. Surgery Today, 2004, 34: 760-763.

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Correlative Imaging in Gallbladder Carcinoma I. Willekens1,2, L.R. Goethals1,2, C. Brussaard2, D. Verdries2, J. de Mey2 Gallbladder carcinoma is a relatively rare malignant epithelial neoplasm, arising from gallbladder mucosa. It is the fifth most common gastrointestinal malignancy and the most common biliary tract cancer. Early diagnosis remains difficult, because clinical symptoms are sparse and non-specific, often resulting in advanced stage disease at the time of diagnosis. The most common feature of gallbladder carcinoma on different imaging modalities is focal wall thickening, associated with a large eccentric tumor mass. In this case we report the imaging characteristics of gallbladder carcinoma on ultrasound, MDCT and 18F-FDG PET/CT. Key-word: Gallbladder, neoplasms.

Gallbladder carcinoma (GBCA) is a relatively rare malignancy with bad prognosis. Is was first described in 1777 by deStoll (1), and is the most common malignant neoplasm of the biliary tract and the fifth most common gastrointestinal cancer. Patients with GBCA have usually advanced disease at the time of diagnosis. GBCA is associated with porcelain gallbladder and chronic inflammation, secondary to gallstones. Ultrasonography is often the first step to the diagnosis. CT and MRI are used for further characterization of the gallbladder lesions and metastatic survey. 18F-FDG PET/CT is useful in diagnosing ambiguous primary lesions, uncovering distant disease and detecting residual disease after cholecystectomy. In this report, we present these imaging findings in 4 patients with gallbladder carcinoma.

Case reports

E F An 82-year-old woman was admitted to our hospital with congestive Fig. 1. — Sagittal (A) and coronal (B) ultrasound image reveals heart failure. Abdominal history ina hypoechogenic mass adjacent to the wall of the gallbladder. cluded diverticulosis, diverticulitis, Axial (C) and coronal (D) multiplanar reformatted computed cholangitis, pancreatitis, and a partomography images after IV contrast injection displays a contial colectomy for an ileocaecal adetrast-enhancing mass adjacent to the wall of the gallbladder, noma. Seven years earlier, there was with possible local invasion of the liver parenchyma. Axial (E) an increased CA19.9 without signs of and coronal (F) FDG-PET/CT images show a solitary hypermeta18 malignancy on F-FDG PET/CT or bolic focus at the fundus of the gallbladder, corresponding to the US-endoscopy. The patient had no contrast-enhancing mass adjacent to the wall of the gallbladder. abdominal pain. Physical examination revealed a flexible abdomen with normal peristalsis. Blood sample demonstrated increased levels of gallbladder wall. This finding was men (Fig. 1C and D) demonstrated a alkaline phosphatase, gamma-further investigated by CT. A consuspicious, contrast-enhanced mass glutamyl transferase, lactate dehydro trast-enhanced (80 cc non-ionic ioadjacent to the wall of the gallbladgenase (LDH), and lipase. Abdominal dinated contrast medium, Ultravist®, der and possibly locally invading the ultrasound (Fig. 1A and B) revealed a liver. Non-contrast enhanced 18F-FDG Bayer HealthCare Pharmaceuticals) hypoechogenic mass adjacent to the multidetector CT scan of the abdoPET/CT (Fig. 1E and F) confirmed a mass lesion with hypermetabolic characteristics at the fundus of the gallbladder and suggested local inFrom: 1. In vivo Cellular and Molecular Imaging (ICMI), Vrije Universiteit Brussel (VUB), vasion of the liver parenchyma. SurBrussels, 2. Department of Radiology, UZ Brussel, Brussels, Belgium. gery was no option due to the imporAddress for correspondence: Dr I. Willekens (MD), Dpt. of Radiology, UZ Brussel, Vrije tant comorbidity of the patient. Universiteit Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium. E-mail: Inneke.willekens@gmail.com Palliative chemotherapy was pro-

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Fig. 2. — Ultrasound (A) image shows an enlarged gallbladder with thickened wall and gallstones. Axial (B) and coronal (C) multiplanar reformatted computed tomography images after IV contrast injection displays a hydrops of the gallbladder with thickening of the wall and enclosed gallstones. One of the gallstones is impacted in the neck of the gallbladder. The liver is surrounded by free fluid. An acute cholecystitis was diagnosed.

posed, if the patient would become symptomatic due to tumor progression. Follow-up was organized, and two years later the patient died due to cardiovascular disease. An 83-year-old woman was admitted to the emergency department of our institution with abdominal pain since 10 days, fever and hypotension. The pain was initially continuous and located in the right hypochondrium, subsequently migrating to the right fossa region. Medical history included gastric ulcers, gallstones, diverticulosis, chronic renal insufficiency, and appendectomy. Physical examination revealed a tense, diffusely sensitive abdomen. Blood sample demonstrated increased levels of C-reactive protein, alkaline phosphatase, gamma-glutamyl transferase, and lipase. Abdominal ultrasound (Fig. 2A) revealed an enlarged gallbladder with thickened wall and gallstones. The gall A contrast-enhanced (80 cc nonionic iodinated contrast medium, Ultravist®, Bayer HealthCare Pharmaceuticals) multidetector CT scan of the abdomen (Fig. 2 B and C) confirmed a hydrops of the gallbladder with thickening of the wall and enclosed gallstones. One of the gallstones is impacted in the neck of the gallbladder. The liver is surrounded by free fluid. An acute cholecystitis was diagnosed. A laparoscopic cholecystectomy was performed. Pathological analysis revealed an adenocarcinoma of the gallbladder. Due to the chronic renal insufficiency, chemotherapy could not be started. Two weeks after surgery the patient died due to septicemia. An 80-year-old woman was admitted to the nuclear medicine depart-

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Fig. 3. — Axial (A, C) and coronal (B, D) FDG-PET/CT images show a mass lesion with hypermetabolic characteristics at the gallbladder with invasion of the liver.

ment of our hospital for a follow up of a carcinoma of the anal canal. Abdominal history included a squamous cell carcinoma of the anal canal treated by abdominoperineal resection and radiotherapy and an appendectomy. The patient had no abdominal pain. Physical examination revealed a painless abdomen with normal peristalsis. Contrast enhanced 18F-FDG PET/CT (Fig. 3A, B, C and D) showed a mass lesion with hypermetabolic characteristics at the gallbladder with invasion of the liver. Diagnosis of a solitary metastasis was suggested and a partial hepatectomy with resection of the gallbladder was performed. Pathological

analysis revealed a primary gallbladder carcinoma. Adjuvant chemotherapy was initiated and during one year follow-up, a liver metastasis of the gallbladder carcinoma was diagnosed and treated by radiofrequency ablation. A 65-year-old woman was admitted to our hospital with progressive dyspnea. Medical history includes arterial hypertension, choledocolithiasis treated by sphincterotomy and stenting, and diabetes with a recent leg amputation (4 months ago). Blood sample showed increased inflammatory markers and liver enzyme values. A chest X-ray demonstrated bilateral pleural effu-

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Fig. 4. — Ultrasound (A) image shows a porcelain gallbladder. Axial (B) and coronal (C) multiplanar reformatted computed tomo graphy images after IV contrast injection displays a porcelain gallbladder, a hypodense liver lesion, abdominal and retroperitoneal adenopathies, peritoneal metastases, and ascites.

sion. A pleural puncture showed a chylothorax with metastatic cells. Additional blood samples showed an elevated CA 125 level. Abdominal ultrasound (Fig. 4A) showed a porcelain gallbladder. Further investigation by contrast-enhanced (80 cc non-ionic iodinated contrast medium, Ultravist®, Bayer HealthCare Pharmaceuticals) multidetector CT scan of the abdomen (Fig. 4B and C) confirmed a porcelain gallbladder, a solitary hypodense liver lesion, abdominal and retroperitoneal adenopathies, peritoneal metastases, and ascites. The patient died 15 days after hospitalization. Autopsy established macroscopically a gallbladder filled with gallstones. The wall was thickened and contained a mass with central necrosis. Microcopy confirmed the presence of a gallbladder carcinoma. Discussion Gallbladder carcinoma is a relatively infrequent neoplasm in most Western countries. The most common incidence rates have been reported in women from India, Chile, Pakistan and Ecuador. GBCA is up to 3 times higher among women than men (2). GBCA is found incidentally in 1-3% of cholecystectomy specimens and in 0.5%-7.4% of autopsies (3). Gallstones are identified as the major risk factor, being present in 60% to 90% of cases (4). Obesity is also associated with an increased risk of GBCA (5). A strong association has been described with mixed bacterial and Salmonella infec(6) and porcelain gallbladtions der (7). Anomalous pancreatobiliary ductal junction (APDJ) is a rare congenital anomaly considered to be an

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etiological factor in the development of GBCA, especially in young women without stones (8). The clinical presentation of GBCA remains unspecific and may include abdominal pain, weight loss, fever, and jaundice (9). Sonography is often the first imaging technique (10). CT and MRI are widely used for further characterization of potentially malignant gallbladder lesions and metastatic survey (11). At any of these imaging techniques, GBCA may appear as a mass completely occupying or replacing the gallbladder lumen (4065%), a focal or diffuse asymmetric gallbladder thickening (20-30%), or an intraluminal polypoid lesion (1525%) (12). The mass appears on US as a heterogeneous, predominantly hypo echoic tumor. Anechoic foci of trapped bile or necrotic tumor can be present, as well as echogenic shadowing from gallstones, porcelain gallbladder, or tumor calcifications (13). GBCA are usually hypodense on unenhanced CT, with up to 40% of lesions showing hypervascular foci of enhancement equal to or greater than that of liver after IV contrast administration (14). On MRI, GBCA usually shows hypo- to isointense signal characteristics on T1-weighted and moderately hyperintense signal characteristics on T2-weighted sequences. On CT and MRI, intense irregular enhancement may occur at the periphery during early arterial phase. During portal venous and delayed phases, contrast enhancement may be retained in fibrous stromal components (12). At 18F-FDG PET, an intense tracer accumulation in the region of the

gallbladder suggests malignancy, although this lacks specificity in distinguishing GBCA from other malignant lesions (15). MDCT has an accuracy of up to 84% in determining the local extent (T staging) of GBCA (16) and 85% in predicting resectability (17). MRI with cholangiographic and contrastenhanced arterial and portal phase 3D angiographic images may be up to 100% sensitive for bile duct and vascular invasion, but only only 67% sensitivity for hepatic invasion and 56% for lymph node metastases (18). In patients with suspected GBC, depending on the disease stage, open surgical resection is appropriate. Adjuvant combination chemotherapy and molecular targeted therapy are emerging as therapeutic options in those with advanced GBC (19). The poor prognosis associated with GBC is mainly related to advanced stage of disease at diagnosis, which is mainly due to the vague and non-specific clinical symptoms. Conclusion Gallbladder carcinoma is a relatively rare type of cancer, associated with a poor prognosis, related to the advanced tumor stage at diagnosis. Advances in radiological imaging have aided early detection and accurate staging of the tumor. References 1. DeStoll M.: Rationis mendendi, in nosocomio pactico vendobo-nensi. Part 1 lugduni batavarum, Haak et Socios et A. et J. Honkoop 1788. 2. Randi G., Franceschi S., La Vecchia C.: Gallbladder cancer worldwide: geographical distribution and risk factors. Int J Cancer, 2006, 118: 1591-1602.

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294 3. Lack E.E.: Tumors of the gallbladder and cystic duct. In: Lack E.E., editor. Pathology of the pancreas, gallbladder, extrahepatic biliary tract and ampullary region. Oxford: Oxford university Press, 2003, p. 465-510. 4. Goldin R.D., Roa J.C.: Gallbladder cancer: a morphological and molecular update. Histopathology, 2009, 55: 218-229. 5. Larsson S.C., Wolk A.: Obesity and a risk of gallbladder cancer: a metaanalysis. Br J Cancer, 2007, 96: 14571461. 6. Dutta U., Garg P.K., Kumar R., Tandon R.K.: Typhoid carriers among patients with gallstoned are at increased risk for carcinoma of the gallbladder. Am J Gaastroenterol, 2000, 95, 784-787. 7. Stephen A.E., Berger D.L.: Carcinoma in the porcelain gallbladder: a relationship revisited. Surgery, 2001, 129: 699-703. 8. Sasatomi E., Tokunaga O., Miyazaki K.: Precancerous conditions of gallbladder carcinoma: overview of histopathologic characteristics and mole

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JBR–BTR, 2014, 97 (5) cular genetic findings. J. Hepatobiliary Pancreat Surg, 2000, 7: 556-567. 9. Reid K.M., Ramos-De la Medina A., Donohue J.H.: Diagnosis and surgical management of gallbladder cancer: a review. J Gastrointest Surg, 2007, 11: 671-681. 10. Rodriguez-Fernandez A., GomezRio M., Medina-Benitez A., et al.: Application of modern imaging methods in diagnosis of gallbladder carcinoma. J Surg Oncol, 2006, 93: 650-664. 11. Furlan A., Ferrris J.V., Hosseinzadeh K., et al.: Gallbladder carcinoma update: multimodality imaging evaluation, staging, and treatment options. AJR, 2008, 191: 1440-1447. 12. Levy A.D., Murakata L.A., Rohrmann C.A.: Gallbladder carcinoma: radiologic-pathologic correlation. RadioGraphics, 2001, 21: 295-314. 13. Tsuchiya Y.: Early detection of the gallbladder: macroscopic features and sonographic findings. Radiology 1991, 179: 171-175. 14. Yun E.J., Cho S.G., Park S., et al.: Gallbladder cancer and chronic cholecystitis: differentiation with two-phase

spiral CT. Abdom Imaging, 2004, 29: 102-108. 15. Corvera C.U., Blumgart L.H., Akhurst T., et al.: 18F-fluorodeoxyglucose positron emission tomography influences management decision in patients with biliary cancer. J Am Coll Surg, 2008, 206: 57-65. 16. Kim S.J., Lee J.M., Lee J.Y., et al.: Accuracy of preoperative T-staging of gallbladder carcinoma using MDCT. AJR, 2008, 190: 74-80. 17. Kalra N., Suri S., Gupta R., et al.: MDCT in the staging of gallbladder carcinoma. AJR, 2006, 186: 758762. 18. Kim J.H., Kim T.K., Kim B.S., et al.: Preoperative evaluation of gallbladder carcinoma: efficacy of combined use of MR imaging, MR cholangiography, and contrast-enhanced dualphase three-dimensional MR angio graphy. J Magn Reson Imag, 2002, 16: 676-684. 19. Dutta U.: Gallbladder cancer: can newer insights improve the outcome? J Gastroenterol Hepatol, 2012, 27: 642-653.

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Axial osseous lesions mimicking disseminated metastases, a report of osseous mastocytosis E. Desportes1, J. Lincot1, A. Hess1,2, V. Descamps1, B. Dallaudière1,2 This article reports a case of osseous mastocytosis, a relatively rare pathology that shows nonspecific osteolytic and osteoblastic bone lesions on CT. As metastatic disease is the most frequent pathology that results in incidentally discovered diffuse osteoblastic lesions, biopsy should be performed in case of doubt. Key-word: Mastocytosis.

Case report A 58-year-old man consulted our hospital emergency room for acute abdominal pain. Apart from an overall tender abdomen, clinical examination revealed multiple diffuse cutaneous plaques of brown maculae and papulae predominantly affecting the legs, and telangiectasic lesions affecting shoulders (Fig. 1). Contrastenhanced CT showed diffuse mesenteric infiltration with lymphadenopathy; bone windows showed a moth-eaten appearance of most of axial skeletal bone matrix with global distribution with predominant areas of osteosclerosis associated with osteolytic areas involving vertebrae, sternum, sacrum and hip bones (Fig. 2) without cortical thickening but with predominant areas of osteosclerosis and also areas of osteolysis involving all parts of vertebral bodies and mainly sacrum. There were no signs of aggressiveness as posterior wall rupture of vertebrae, fracture or narrowed spinal canal. For this patient the hypothesis of a fortuitously discovered diffuse osteocoblastic secondary spine from unknown primary neoplasm with paraneoplastic skin eruption seemed fairly likely. A cutaneous biopsy concluded to an urticaria pigmentosa, the cutaneous form of mastocytosis, due to an abnormal mastocytic proliferation in sub-epidermal skin layers. Osseous disseminated condensing abnormalities and abdominal lymphadenopathy were compatible with associated mastocytic localizations thus falling within the scope of systemic mastocytosis. Discussion Metastases are dissemination of tumoral cells, mainly hematogenous-

B Fig. 1. — 58-year-old man, cutaneous mastocytosis. Photographs of typical urticaria pigmentosa with brown papules on foot and ankle (A) and telangiectatic form on shoulder (B).

ly, at distance of the primitive lesion. Skeletal metastases represent the most common malignant bone tumor. They occur mainly in adults and their prevalence increases with

From: 1. Service de Radiologie, Hôpital Bichat-Claude Bernard, Paris, France, 2. UFR de Médecine Xavier Bichat, Université Paris 7 Diderot, Paris, France. Address for correspondence: Dr E. Desportes, Service d’Imagerie Médicale, CHU Bichat – Claude Bernard, Assistance Publique – Hôpitaux de Paris, 46 Rue Henri Huchard, 75018 Paris, France. E-mail: desportes.emilie@yahoo.fr

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patient’s age. The spine and pelvis are the most common metastatic sites due to the presence of a high amount of red hematopoietic, strongly vascularized, bone marrow. Imaging exams, such as CT or MRI, performed in an elderly population may incidentally discover osseous aspecific lesions which evocate metastases even in the absence of a known primitive neoplasia (1-4).

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Fig. 2. — 58-year-old male, osseous mastocytosis. Findings: Abdominal CT, sagittal (A) and axial reconstructions centred on pelvis (B) and 3rd lumbar vertebra (C) showing a moth-eaten appearance of most of axial skeletal bone matrix with predominant osteo blastic areas (arrowheads) and areas of osteolysis (arrows) involving vertebral bodies and sacrum. Technique: 400 mA, 120 kV, 0.6 mm slice thickness.

Table I. — Summary table for systemic mastocytosis. Etiology Abnormal proliferation of mast cells in different tissues, as osseous one’s, due to a mutation of c-Kit gene lncidence Systemic mastocytosis: 1/20 000 to 1/40 000 Osseous mastocytosis 1/3 of mastocytosis: 1/60 000 to 1/120 000 Gender ratio Male:female 1:1 Age predilection 60 years Risk Factors Triggering factors - Unknown - Drugs (morphine, salicylic acid, injection of iodinated contrast...) - Trauma (surgery, wasp sting...) - Food (alcohol, bananas, crustacean...) Treatment

- Symptomatic treatment included bisphosphonates and antihistamine for the indolent type - Corticotherapy and interferon for the aggressive type

Prognosis

Variable - Normal life expectancy for the indolent type (chronic forms) - 2 to 4 years for the aggressive type

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Table II. — Differential diagnosis table for osseous mastocytosis. Modality

Osseous mastocytosis

Osteoporosis

Metastasis

Paget disease

Condensing or lytic or mixt osseous lesions

Diffuse demineralization of the spine

Condensing or lytic or mixt lesions

Vertebral compression fractures

lnvasion of adjacent soft tissue

Lytic or sclerotic Condensing or lytic or mixt lesions lesions Rise of vertebral Spleen body diameter enlarged and nodes associated

Vertebral compression fractures

Characterization of these lesions can be difficult and should be considered globally taking into account clinical, biological and radiological data. Differential diagnosis of diffuse axial osteopathies should always be considered in these cases. In unusual radiological presentations consensus should be sought and a biopsy, either osseous or of another pathologic site is often necessary to reach the diagnosis (3). We reported a case illustrating an axial osteopathies mimicing secondary neoplastic localizations. The moth-eaten appearance axial bone matrix, alternating areas of osteosclerosis and osteolysis were findings of osseous lesions of systemic mastocytosis. Cutaneous mastocytosis is most often isolated, urticaria pigmentosa being the predominant form, but can occasionally be associated with other organs involvement through a systemic mastocytosis (Table I). Abdominal lymphadenopathy has been reported in our case but systemic mastocytosis might give other symptoms: hematologic (anemia, myeloproliferative syndroms) and paroxysmal access (flush, palpitations, headaches, diarrhea) (5-6). When affecting bone, lesions are generally asymptomatic but they also can provide arthralgia, pain, bone tumefaction or fractures. It can proceed in two patterns: osteoblastic areas preferentially affecting the axial skeleton (skull, spine, pelvis) and

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Vertebral compression fractures

occasionally involving proximal long bones with a variably marked cortical thickening. Conversely a diffuse more common aspect of demineralization can be observed, possibly associated with vertebral collapse resembling postmenopausal osteoporosis. As a matter of fact these demineralizing forms could be more frequent than the osteoblastic ones. Mixed osteolytic-osteoblastic lesions also occur (7-8). Other differential diagnoses than metastases have been discussed for this kind of images. Paget disease shows osteolysis, trabecular coarsening, cortical thickening and osseous expansion (9). Lymphoma is often symptomatic, associated with enlarge spleen and lymphadenopathy (10). Negative protein electrophoresis rules out myeloma (11) (Table II). In conclusion, our reported experience tends to illustrate that incidentally discovered disseminated osteolytic or osteoblastic lesions in an advanced age population are not always metastases, even in case of fairly evocative images and of a known primary tumor. When imaging findings are inconclusive, biopsy is advocated. References 1. Guillevin R., Vallee J.N., Lafitte F., Menuel C., Duverneuil N.M., Chiras J.: Spine metastasis imaging: review of the literature. J Neuroradiol, 2007, 34: 311-321.

Lymphoma

Myeloma Diffuse demineralization only (5%) Lysed pedicles lnvasion of adjacent soft tissue Vertebral compression fractures

2. Cotten A., et al.: Imagerie musculosquelettique: pathologies générales. Masson, 2005. 3. Resnick D., et al.: Bone and Joint Disorder, Vol. 3. Philadelphia, Saunders, 1995. 4. Laredo J.-D., Morvan G., Wybier M.: Imagerie ostéo-articulaire. Paris, Flammarion médecine-sciences, 1998. 5. Quintás-Cardama A., Jain N., Verstovsek S.: Advances and controversies in the diagnosis, pathogenesis, and treatment of systemic mastocytosis. Cancer, 2011: 117: 5439-5449. 6. Pardanani A.: Systemic mastocytosis in adults: 2011 update on diagnosis, risk stratification, and management. Am J Hematol, 2011, 86: 362-371. 7. Manara M., Varenna M., Cantoni S., Parafioriti A., Gallazzi M.B., Sinigaglia L.: Osteoporosis with vertebral fractures in young males, due to bone marrow mastocytosis: a report of two cases. Clin Exp Rheumatology, 2010, 28: 97-100. 8. Metzgeroth G., Dinter D., Erben P., La Rosée P., Hehlmann R., Hastka J.: Systemic mastocytosis simulating osseous metastatic disease. Br J Haematol, 2007, 136: 1. 9. Theodorou D.J., Theodorou S.J., Kakitsubata Y.: Imaging of Paget Disease of Bone and Its Musculoskeletal Complications: Review. AJR Am J Roentgenol, 2011, 196: WS53-56. 10. Freedman A.: Follicular lymphoma: 2012 update on diagnosis and management. Am J Hematol, 2012, 87: 988-995. 11. Nystrom L.M., Buckwalter J.A., Syrbu S., Miller B.J.: Serum protein electrophoresis in the evaluation of lytic bone lesions. Iowa Orthop J, 2013, 33: 114-118.

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SOLITARY FIBROUS TUMOR OF THE KIDNEY P. Tritschler1, B. Coulier1, I. Gielen2 Solitary fibrous tumor (SFT) is an unusual spindle cell neoplasm rarely described in the kidney. Usually occurring in the pleura, it has also been described in various extrapleural sites. We report a rare case of SFT of the kidney fortuitously found in a 55-year-old patient. The imaging features are illustrated. The definite diagnosis was made through histological and immunohistochemical study after radical nephrectomy. Key-word: Kidney, neoplasms, diagnosis.

Solitary fibrous tumor (SFT) is a rare lesion representing 2% of all soft tissue tumors (1). Described for the first time in the pleura by Klemperer and Rabin in 1931 (2), SFTs can also rarely occur in intra- or extrathoracic site. Imaging features on SFT are mostly non specific and essentially show a highly vascularised tumor. The definite diagnosis can only be made through histological and immunohistochemical study. We report a new case of solitary fibrous tumor of the kidneys fortuitously found in a 55-year-old patient. Case report A 55-year-old patient was referred to our radiology department with a few weeks history of right upper quadrant pain. Nausea, vomiting, diarrhea or hematuria were absent. Abdominal physical examination and blood tests were normal. The patient had no previous medical or surgical history. Abdominal ultrasound demonstrated uncomplicated gallstones but extended examination revealed a central mass in the right kidney (Fig. 1A,C). There was no pyelectasy. This well circumscribed solid mass was developing in the renal sinus. Slight cortical atrophy was associated and power Doppler showed a high vascularisation (Fig. 1B). The arterial phase of contrast enhanced mdCT confirmed a 5 × 7 cm well circumscribed and richly vascularised mass developing in the right renal sinus (Fig. 1C, D, E). The tumor appeared separated from the renal cortex. Areas of parenchyma atrophy

of the renal cortex were visible adjacent to the tumor. No delay of renal excretion was seen. The hypothesis renal cell carcinoma or atypical urothelial carcinoma was retained. Radical uretero-nephrectomy was first planified. Nevertheless intraoperative opening of the resected kidney (Fig. 1F) restricted the diagnosis to a non-urothelial neoplasm and complementary resection of the uretera was avoided. Histological examination showed a hypercellular solid tumor made by spindles cells with rounded or oval nucleus, arranging in all directions with formation of vortices hemangiopericytoma like (Fig. 2B). The cytoplasm was moderately abundant with imprecise boundaries. No mitotic activity nor atypia were found. This tumor invades the hilar fatty tissue (Fig. 2A). Immunohistochemical examination revealed a positivity on numerous cells for the CD99, Bcl2, CD34, vimentine and a minority of cells for the actine. Desmine and EMA are negative. The Ki67 nuclear proliferation index is low 3%. A diagnosis of solitary fibrous tumor of the kidney is then evoked. Discussion Solitary fibroma tumors (SFTs) are mesenchymal tumors, now considered a variant of hemangiopericytomas (3). SFTs were described for the first time in the pleura but they can affect all the body at any location (4). Cases have been described in upper respiratory tract, lung, nasal cavity, paranasal sinuses, orbits, glands, mediastinum, salivary

From: 1. Department of Medical Imaging, Clinique St Luc, Bouge, Belgium, 2. Institute of Pathology and Genetics, Loverval, Belgium. Address for correspondence: Dr P. Tritschler, M.D., Department of Diagnostic Radiology, Clinique St Luc, Rue St Luc 8, 5004 Bouge (Namur) Belgium. E-mail: pierre.tritschler@student.uclouvain.be

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breast, meninges, liver and urogenital organs (3). Thus, there are intra and extra-thoracic locations but most of cases are intra-thoracic (5). Intra-thoracic and extra-thoracic SFTs are often considered benign neoplasms but the incidence of aggressive forms manifested by local invasion or distant metastases (6) is about 10-15% for intra-thoracic SFTs and more than 10% for extra-thoracic SFTs (7). Therefore all patients with SFT need to be on long-term follow-up (3). SFTs of kidney is very rare with only about 40 cases described in the (1). The origin of most literature cases kidney SFTs is difficult to determine and may originate from the capsule, interstitial tissues, or peripelvic connective tissues (3). The average age of presentation is 51 years (1), with a small female predilection (6) but usually the addition of intra and extra-thoracic forms revealed no preference, male and female being equally affected. Clinical examination can show a palpable mass, a flank pain and often hematuria. Blood test are non contributive. Sometimes hypoglycaemia is described for extra or intra thoracic forms but never for kidney SFTs (7). The diagnosis is often delayed because these tumor are usually asymptomatic when they have a small size. Histopathological nature of SFTs is distinguished by a hypercellular stroma of bland spindles cells with a patternless architecture. Typical immunohistochemicals characteristics are a high positivity for CD34 – regarded as an indispensable finding in the diagnosis (3) and to a lesser extent for Bcl2, vimentin and CD99 (1, 8). The differential diagnosis is large and includes highly vascularized tumors as renal cell carcinoma, sarcomatoid renal cell carcinoma, angiomyolipoma, fibroma, fibro sarcoma, and leiomyosarcoma (3). The therapeutic management is surgery with a high survival rate approaching 100% at 5 years (1).

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Fig. 1. – A. US study, coronal view, demonstrates a rather homogeneously hypoechoic tumor developed in the sinus of the right kidney. This relatively well circumscribed tumor measures 5 × 5 × 4,5 cm. B. Coronal power Doppler view demonstrates a rather homogeneously hypoechoic and hypervascular tumor developed in the sinus of the right kidney. C. Transverse gray-scale ultrasound (white star) and MDCT (black star) views demonstrate a homogeneously hypoechoic and hypodense tumor developed in the sinus of the right kidney. D. Corresponding coronal oblique contrast enhanced mdCT view shows a well circumscribed homogenous hypervascular tumor occupying the renal sinus. The excretory cavities appear only moderately compressed. E. Volume rendering view obtained during the early arterial phase of contrast enhanced mdCT shows a large tumor highly vascularized by larges vessels. F. Gross anatomy of the resected kidney (sagital section through the organ) shows a well circumscribed, non necrotic white color pink mass of firm consistency protruding within the hilar area.

Imaging is an important tool for the evaluation of extension and recurrence of renal SFT. Neverthe less CT, ultrasound and MR imaging features are not specific for the defi-

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nite characterization of SFT. Radiologists could only consider SFT in the differential diagnosis of a renal mass if the lesion is a large, situated in the renal sinus with lobulated margins

and highly vascularized by larges vessels (4). Finally the final diagnosis is always based on histopathology and immunohistochemical study.

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Fig. 2. – A. Photomicrograph (hematoxylin-eosin stain) shows at low power field view (×10) a rather well circumscribed hyper cellular tumor (white star) invades the sinusal fat (black star). B. Photomicrograph (hematoxylin-eosin stain) shows at higher power field view (×40) the hypercellular tumor appears composed of numerous bland uniform spindle cells with a patternless architecture.

References 1. Shanbhogue A.K., Prasad S.R., Takahashi N., et al.: Somatic and visceral solitary fibrous tumors in the abdomen and pelvis: cross-sectional imaging spectrum. Radiographics, 2011, 31: 393-408. 2. Hanau C.A., Miettinen M.: Solitary fibrous tumor: histological and immunohistochemical spectrum of benign and malignant variants presenting at different sites. Hum Pathol, 1995, 26: 440-449. 3. Naveen H.N., Nelivigi G.N., Venkatesh G.K., Suriraju V.: A case of

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solitary fibrous tumor of the kidney. Urol Ann, 2011, 3: 158-160. 4. Wignall O.J., Moskovic E.C., K., Thomas J.M.: Solitary Thway fibrous tumors of the soft tissues: review of the imaging and clinical features with histopathologic correlation. AJR Am J Roentgenol, 2010, 195: W55-62. 5. Gold J.S., Antonescu C.R., Hajdu C., et al.: Clinicopathologic correlates of solitary fibrous tumors. Cancer, 2002, 15, 94: 1057-1068. 6. Katabathina V.S., Vikram R., Nagar A.M., Tamboli P., Menias C.O., Prasad S.R.: Mesenchymal neoplasms

of the kidney in adults: imaging spectrum with radiologic-pathologic correlation. Radiographics, 2010, 30: 1525-1540. Hsieh T.Y., ChangChien Y.C., 7. Chen W.H., et al. De novo malignant solitary fibrous tumor of the kidney. Diagn Pathol, 2011, 5, 6: 96. 8. Bugel H., Gobet F., Baron M., Pfister C., Sibert L., Grise P.: Solitary fibrous tumour of the kidney and other sites in the urogenital tract: morphological and immunohistochemical characteristics. Prog Urol, 2003, 13: 1397.

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MESENTERIC INFLAMMATORY MYOFIBROBLASTIC TUMOR: MRI AND CT IMAGING CORRELATED TO ANATOMICAL PATHOLOGY Th. Kirchgesner1, E. Danse1, Ch. Sempoux2, L. Annet1, Ch. Anca Dragean1, P. Trefois1, N. Abbes Orabi3, A. Kartheuser3 Inflammatory myofibroblastic tumor (IMT) is a rare tumor, classified by WHO of intermediate biological potential with tendency for local recurrence and small risk for distant metastasis. Histologically IMT is a mixture of inflammatory cells and myofibroblastic spindle cells proliferation. To our knowledge there is no MRI description of mesenteric IMT in the literature. We would like to emphasize the correlation between medical imaging and anatomical pathology based on our experience of a mesenteric IMT in a 28-year-old patient. Key-word: Mesenteric, inflammatory, myofibroblastic, tumor, MRI.

Case report An abdominal CT performed in a 28-year-old woman suffering from asthenia, appetite loss and intermittent hypogastric abdominal pain with night sweats and fever for six weeks demonstrates an 8 cm diameter pelvic mass, possibly from mesenteric origin. The non calcified mass shows well-defined margins, homogeneous attenuation before contrast injection and peripheral enhancement after contrast injection at portal phase that slightly progresses at late phase, while the center stays hypoattenuated (Fig. 1). Three weeks later MRI is also performed with T2, T2 fat sat, TSE and T1 fat sat weighted images with and without Gadolinium injection (Fig. 2). Patient is then admitted for surgical laparotomic exploration, which demonstrates a large pelvic mass from mesenteric origin near the terminal ileum (Fig. 3). Twenty-five centimeters of the terminal ileon and the appendix are resected along with six lymph nodes and ileocecal anastomosis is performed. Anatomical pathology examination of the mass concludes with inflammatory myofibroblastic tumor based on proliferation of spindle cells and inflammatory infiltration of lymphocytes at histology (Fig. 4). Ileum, appendix and lymph nodes are normal. Evolution after surgery is good with an uneventful follow-up. Discussion Inflammatory myofibroblastic tumor (IMT) is a rare tumor, classified by WHO of intermediate biological potential with tendency for local recurrence and small risk for distant

Fig. 1. — Axial CT demonstrating a large mesenteric pelvic mass with well-defined margins and heterogeneous peripheral enhancement after iodine IV injection at portal phase.

Fig. 2. — MRI axial T1FS with gadolinium IV injection (4 minutes) demonstrating intense enhancement of the peripheral inflammatory component while the central fibrotic component is hypovascular.

metastasis. It is also known as inflammatory pseudotumor, inflammatory fibrosarcoma, xanthogranu-

From: Dpt of 1. Radiology, 2. Anatomical pathology, 3. Colorectal Surgery, Cliniques Universitaires Saint-Luc, Brussels, Belgium. Address for correspondence: Dr Th. Kirchgesner, M.D., Service de Radiologie, Cliniques Universitaires Saint-Luc, Avenue Hippocrate 10, B-1200 Bruxelles, Belgium. E-mail: Thomas.Kirchgesner@gmail.com

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loma or myofibroblastoma among others. Histologically IMT is a mixture of inflammatory cells and myofibroblastic spindle cells proliferation. ALK gene abnormalities, typically associated with anaplastic large cell lymphoma, are seen in approximately 50% of IMT cases (1). Pathogenesis in unknown and several hypotheses

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Fig. 3. — Macroscopic study - Eight centimeters diameter mesenteric mass with well-defined margins adhering to the terminal ileum: inflammatory myofibroblastic tumor confirmed at histology. Note the central fibrotic component and the encapsulated aspect.

have been made: low-grade fibrosarcoma with inflammatory cells, inflammation following minor trauma or surgery, immune/autoimmune mechanism or reaction secondary to infection. IMT is ubiquitary and has been described in almost every body sites. It most occurs during the first two decades of life, usually solitary but some multifocal cases have been described. Clinically abdominal IMT is nonspecific: fever, night sweating, malaise, weight loss, abdominal pain, palpable abdominal mass or diarrhea. Laboratory findings are also nonspecific, reflecting the chronic inflammation: elevation of CRP, anemia, thrombocytosis and hypergammaglobulinemia. In ultrasonography, mesenteric IMT appears as a well-defined or infiltrating solid mixed-echostructure mass within the mesentery. Vascularization may be seen with Doppler ultrasound. Typical CT findings are those of a slow growing unique mass with well-defined or infiltrating margins (2). Calcifications are uncommon. Involvement of adjacent bowel segments is exceptional. The mass is typically heterogeneous in attenuation and largest lesions may have central areas of hypoattenuation suggestive of necrosis. Enhancement after iodine IV injection is variable, from non-enhancing to peripheral or heterogeneous enhancement and may be related to fibrosis age: early enhancement if fibrosis is «young» with a larger inflammatory component and late enhancement if

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Fig. 4. — Histology - Proliferation of spindle cells (arrowheads) and inflammatory infiltration of lymphocytes (circle).

fibrosis is «old» with a larger fibrotic component (3). To our knowledge there is no MRI description of mesenteric IMT in the literature. With this case we would like to emphasize the correlation between MRI imaging of IMT and its histological aspect. In our present case, the lesion has a homogeneous signal intensity on T1 weighted sequence without contrast. On T2 weighted sequence, the lesion presents two components: an irregular central fibrotic component with low signal intensity and a peripheral inflammatory component with relatively high signal intensity. T1 weighted sequence four minutes after Gadolinium injection demonstrates intense enhancement of the peripheral inflammatory component while the central fibrotic component is hypovascular. MRI aspect on T1 weighted images after Gadolinium injection is very similar to the CT aspect at portal venous phase. Peripheral enhancement in both techniques is highly representative of the inflammatory component, but medical imaging is still nonspecific of IMT requiring histological confirmation. Given the similar results of both techniques and the young age of the concerned population (mostly first two decades), MRI should be preferred to CT because of its non- irradiating nature. Range of differential diagnosis for mesenteric IMT is wide including benign tumors and pseudo-tumors like mesenteric fibromatosis (desmoid tumor) or sclerosing mesenteriris

and malignant tumors like lymphoma, GIST or carcinoid tumor metastasis (4). Nonspecific CT and MRI imaging aspect does not ensure certainty of diagnosis so that surgical exploration and anatomical pathology examination are required to differentiate IMT from other tumors. Treatment of choice consists in excision with clear resection margins except for orbitary locations treated by high doses of systemic steroids which can be associated to low-dose radiation therapy. Local recurrences occur in about 10% to 25% cases of abdominal IMT especially within a year of surgery. Distant metastases are rare, about less than 5%. References 1. Coffin C.M., Patel A., Perkins S., Elenitoba-Johnson K.S., Perlman E., Griffin C.A.: ALK1 and p80 Expression and Chromosomal Rearrangements Involving 2p23 in Inflammatory Myofibroblastic Tumor. Mod Pathol, 2001, 14: 569-576. 2. Levy A.D., Rimola J., Mehrotra A.K., Sobin L.H.: Benign Fibrous Tumors and Tumorlike Lesions of the Mesentery: Radiologic-Pathologic Correlation. RadioGraphics, 2006, 26: 245264. 3. Aptel S., Gervaise A., Fairise A., Henrot P., Leroux A., Guillemin F., Laurent V., Régent D.: Abdominal inflammatory myofibroblastic tumour. Diagn Interv Imaging, 2012, 93: 410412. 4. Sheth S., Horton K.M., Garland M.R., Fishman E.K.: Mesenteric Neoplasms: CT Appearances of Primary and Secondary Tumors and Differential Diagnosis. RadioGraphics, 2003, 23: 457-473.

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RAPID MALIGNANT TRANSFORMATION OF PRIMARY SYNOVIAL CHON DROMATOSIS INTO CHONDROSARCOMA J. Jonckheere1, M. Shahabpour1, I. Willekens1, N. Pouliart2, M. Dezillie3, F. Vanhoenacker4, J. De Mey1 Chondrosarcoma of the synovium is rare. It may arise de novo from the synovium or pre-existing synovial chondro matosis may undergo malignant transformation into chondrosarcoma. Diagnosing a malignant transformation of the synovium remains a big challenge. It is based on the correlation of clinical findings, imaging and histology, as illustrated in this case report. Key-word: Bone neoplasms, MR.

Case report A 45-year-old woman presented with recurrent swelling, pain and stiffness of the left knee. Initial plain radiography depicted small round and oval radio-opaque frag ments within the joint as well as joint effusion. No osteophytes, sub chondral sclerosis or other signs of osteoarthrosis were seen (Fig. 1). MR imaging demonstrated in detail the synovial changes and suspected the presence of loose bodies. T2weighted images (WI) showed mul tiple, round synovial nodules with

low-to-intermediate signal inten sity in the popliteal fossa and in the posterior intercondylar fossa as well as joint effusion (Fig. 2A-B). Some of the nodules enhanced after intra venous (IV) Gadolinium con trast administration (Fig. 2C). Two months later an arthroscopic syno vectomy was performed. Histologically, the diagnosis of synovial chondromatosis was made. Within the following 2 months, the clinical symptoms of the patient aggravated and malignancy was suspected on subsequent follow-up MR examination. Despite the arthros

Fig. 1. — Initial lateral radiograph of the left knee. Radiopaque round calcifications in popliteal fossa (open arrow) and associated soft tissue swelling (black arrows).

From: 1. Department of Radiology, 2. Department of Orthopedic Surgery, Universitair Ziekenhuis Brussel, Brussels, 3. Department of Orthopedic Surgery, AZ Groeninge, Kortrijk, 4. Department of Radiology, AZ Sint Maarten, Mechelen, Belgium. Address for correspondence: Dr J. Jonckheere,MD, Department of Radiology, Universitair Ziekenhuis Brussel, Laarbeeklaan 101, B-1090 Brussels, Belgium. E-mail: Jan Jonckheere@uzbrussel.be

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copic synovectomy, there was a recurrence of multiple intra-articular nodules of low-to-intermediate signal intensity on T2-WI. The extracapsular retrotibial nodules as well as the supracondylar retrofemoral nodules recurred and clearly increased in size and were of a higher signal intensity (Fig. 3A). Multiple new nodulesof low-to-intermediate signal intensity on T2-WI appeared in the lateral and medial parapatellar pouches (Fig. 3B-C). Joint effusion and soft tissue extension were also detected (Fig. 3A). Consequently, an open total synovectomy and capsulectomy were performed. Again, histology confirmed the diagnosis of synovial chondromatosis. Follow-up plain radiographs three months after this surgery depicted joint destruction with obliteration of the joint line and subchondral bone cyst formation in the femoral condyle and the tibial plateau. Posterior subluxation of the tibia was present (Fig. 4A). MR examination showed diffuse soft tissue extension, especially posteriorly. Several areas of subchondral bone erosions and subchondral bone sclerosis were apparent (Fig. 4B). Progression of the disease to cruciate ligament caused the posterior subluxation of the tibia. Finally, the diagnosis of low-grade chondrosarcoma was made by the interdisciplinary bone tumor commission. This diagnosis was based on the postoperative recurrence, the rapid clinical and radiological progression and the marked hypercellularity and nuclear atypia on histological examination (Fig. 5). An above-knee amputation was performed. Discussion Primary synovial chondromatosis (PSC) is a non-neoplastic, proliferative and metaplastic disorder of the synovium. It is characterized by the formation of multiple cartilaginous nodules in the synovium of joints,

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B Fig. 2. — A. Initial sagittal fast spin echo (FSE) T2-weighted MR image. Suprapatellar joint effusion and multiple intra- and extra capsular round nodules of intermediate-to-low signal intensity (open arrow) in the posterior intercondylar area with retrofemoral and retrotibial extension resulting in a posterior displacement of the medial head of the gastrocnemius muscle. B. Initial axial T2weighted MR Image. Multiple nodules in the posterior intercondylar area (black arrowheads), and fluid effusion in the patellar pouch (black arrow). C. Initial sagittal fat-suppressed T1-WI after IV administration of Gadolinium contrast. Some of the hypointense nodules without enhancement (open arrow), whereas others enhanced heterogeneously (black arrow).

C tendons and bursae (1, 2). PSC can occur in virtually every joint. The knee is the most commonly affected site, followed by the hip. Monoarticular involvement is the rule (3). Synovial chondrosarcoma is an extremely rare condition. It may occuras a primary process or as a transformation of PSC into a lowgrade chondrosarcoma. It affects patientsbetween the fourth and seventhdecades of life and is slightly more common in men than women (4, 5). Strictly spoken, if there is no documented radiological or histo

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logical evidence of pre-existent PSC, the synovial chondrosarcoma should be regarded as primary (6). The distinction between PSC and malignant transformation is problematic, either clinically, histologically and radiologically. Therefore the diagnosis should be based on a combination of clinical, radiological and histological parameters to minimize the risk of misinterpretation of PSC as chondrosarcoma and vice versa (6, 7). The clinical manifestation of PSC includes pain, joint swelling and re

striction of joint movement. Physical examination reveals diffuse joint swelling, articular tenderness, articu lar crepitus, locking and pal pable nodules or a mass. However, in synovial chondrosarcoma similar symptoms and signs may be present. In case of known PSC with rapid deterioration of the clinical symp toms, transformation to synovial chondrosarcoma should be sus pected (2, 7, 8). The histological findings in PSC are variable, but in general, the degree of cellularity is fairly striking. The cartilage is hypercellular with plump hyperchromatic nuclei and binucleate forms that would be interpreted as malignant if the car tilage occurred within a bone. Despite the cellularity of chondro matosis, individual chondrocytes often have a very definite pattern characterized by arrangement into micronodular clones (4, 6, 7). On the contrary, histological features that are in favour of a synovial chondrosarcoma include: loss of the micronodularity of the chondrocytes,

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A Fig. 3. — A. Sagittal T2-WI. Recurrence of multiple intracapsular nodules of low-to-intermediate signal intensity two months after total arthroscopic synovectomy (black arrow). The extracapsular retrotibial nodule (open arrow) and the supracondylar retrofemoral nodules (white arrow) were larger and of predominantly high signal intensity. B. Axial T2-weighted MR Image two months after arthroscopic synovectomy. Multiple new nodules in the medial patellar pouch (black arrow), increase in size of multiple nodules in the posterior intercondylar area (black arrowheads), as well as a huge new nodule of intermediate signal intensity (size: 4 cm) in the lateral patellar pouch (white arrow). C. Axial MR image in T2 FSE sequence performed 2 months after a total arthroscopic synovectomy. Retrotibial nodule (white arrowheads) associated with a tibial bone erosion (black arrow). Posterior displacement of the gastrocnemius muscle and of the neurovascular popliteal bundle. Post-operative thickening of the patellar tendon (black arrowheads) and fibrous scar formation in the medial aspect of the Hoffa fat pad (open arrow).

decreased cellularity compared to PSC, myxoid tranformation of the matrix and chondrocyte necrosis. The most reliable histological sign consists of osseous permeation by cartilage with extension of cartilage matrix into intertrabecular spaces (4, 5, 7). A preliminary study suggests that reduced or absent expression of the immunohistochemical marker Bcl2 is associated with malignant transformation of chondromatosis (9). The imaging techniques in differentiating PSC and synovial chondrosarcoma are conventional radiography, computed tomography (CT) and magnetic resonance imaging (MRI). A rapidly enlarging extra-articular mass and true cortical destruction with bone marrow invasion and permeation are imaging features that should be considered as potential signs of malignancy (7, 8, 11).

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C Bone scintigraphy and ultrasound have not yet been extensively evaluated. Conventional radiography in PSC can demonstrate multiple intra-articular calcifications with a very similar shape and typically distributed evenly throughout the joint. A typical chondroid ring-and-arc pattern of mineralisation is common. Further maturation of the fragments is possible with enchondral ossification. A

target appearance is also possible, consisting of a central focus and a single peripheral rim of calcification. Joint effusion can be seen. The joint space is typically maintained, however, asymmetric joint space narrowing is possible in chronic disease (8). Extrinsic erosion of the bone, usually on both sides of the joint, has also been reported (10). In 5-30% of patients with PSC radiography can be normal (3). The radiographical diag-

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Fig. 4. — A. Lateral radiograph, 3 months after open synovectomy and capsulectomy: obliteration of the femorotibial joint line (black arrows). The popliteal loose bodies have disappeared. B. Sagittal T2-WI of the final MR examination depicted severe thinning of the articular cartilage with hypointensity of the subchondral bone with subchondral sclerosis and cyst formation (open arrows). Irregular delineation of the patellar tendon and fibrous scar formation in Hoffa’s fat pad (white arrow).

B Fig. 5. — Pathologic appearance of primary synovial chondromatosis and malignant transformation to synovial chondrosarcoma. A. Photomicrograph shows chondrocytes arranged in clusters with acellular stroma in the background (on the left); typical of synovial chondromatosis. Adjacent to this area (on the right) are larger areas in which the cartilage cells have lost their clustering effect, with a myxoid background. There is a marked increase in cellularity and nuclear pleomorphism. Malignant transformation to a chondrosarcoma has occurred. B. Photomicrograph at low magnification shows a nodule of synovial chondromatosis. C. Photomicrograph at higher magnification shows nuclear pleiomorphism and mitotic figures as seen in synovial chondrosarcoma.

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co-existing chondrosarcoma or malignant transformation to chondrosarcoma. A multidisciplinary discussion is required, as the definitive diagnosis can only be made on a combination of clinical, radiological and histological criteria. References

Fig. 6. — Peroperative photograph during open arthrotomy. Posterior view of the knee demonstrates a huge synovial cartilaginous mass.

nosis of malignant transformation can be difficult because of its possible radiographically similar appearances with PSC. An extensive calcified soft-tissue mass about and within the joint (with potential extension into the adjacent soft tissues) and extrinsic erosion of bone can occurboth in PSC as in chondrosarcoma. However, a rapidly enlarging extra-articular mass and true cortical destruction are radiographical features that should be considered as potential signs of malignancy. CT in PSC is superior to conventional radiography (CR) in distinguishing low attenuation synovial thickening with lobular outer contour from synovial fluid. Furthermore, CT is superior to CR in detection and characterisation of calcifications and subtle extrinsic erosion of bone. In combination with arthrography, CT may define the precise location of the chondral nodules (intra-articular, bursal, tenosynovial) (3, 8, 12). The potential signs of malignancy on CT are similar to those on CR. MRI in PSC can provide adjacent information by depicting subtle extrinsic bone erosion, not seen on radiography . Peripheral and septal contrast enhancement may be seen in the nodules (8). MRI may sub divide PSC in three subtypes according to the classification of Kramer et al. (13). The most frequent pattern consists of intra-articular lobules of homogeneous intermediate signal intensity similar to muscle on T1WI, high signal intensity on T2-WI

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images and intralesional areas of low signal intensity on all pulse sequences. The areas of signal void may correspond to regions of calcification on radiographs or CT scan and are more conspicuous on gradient-echo MR images owing to magnetic susceptibility effects. The second most common subtype is similar, except for the absence of focalintra-articular areas of low signal. No calcifications are seen on corresponding radiographs or CT. The third pattern has features similar to those of the other patterns but also includes high-signal-intensity foci, iso-intense relative to fat with a peripheral rim of low signal intensity. MRI is superior to CR and CT for the assessment of bone marrow invasionas a potential sign of malignancy (14). Conclusion The most important features that would suggest malignant transformation of PSC into low-grade chondrosarcoma are: a rapid increase in size of the lesion, a rapid clinical deterioration, cortical destruction on radiography and medullary invasion on MRI. In these cases biopsy may contribute to the correct diagnosis. From a surgical point of view, any patient with recurrent synovitis of the knee and difficult histological differential diagnosis between synovial chondromatosis and chondrosarcoma, should be suspected of having

1. Villacin A.B., Brigham L.N., Bullough P.G.: Primary and secondary synovial chondrometaplasia: histopathologic and clinicoradiologic differences. Hum Pathol, 1979, 10: 439451. 2. Murphy F.P., Dahlin D.C., Sullivan R.: Articular synovial chondromatosis. J Bone Joint Surg [Am], 1962, 44A: 77-86. 3. Crotty J.M., Monu J.U.V., Pope J.R.T.L.: Synovial osteochondromatosis. Radiol Clin North Am, 1996, 34: 327-342. 4. Hermann G., Klein M.J., Adbelwahab I.F., Kenan S.: Synovial chondrosarcoma arising in synovial chondromatosis of the right hip. Skeletal Radiol, 1997, 26: 366-369. 5. Wittkop B., Davies A.M., Mangham D.C.: Primary synovial chondromatosis and synovial chondrosarcoma. Eur Radiol, 2002; 12: 2112-2119. 6. Davis R.I., Hamilton A., Biggart J.D.: Primary synovial chondromatosis: a clinicopathologic review and assessment of malignant potential. Hum Pathol, 1998, 29: 683-688. 7. Bertoni F., Unni K., Beabout J.W., Sim F.H.: Chondrosarcoma of the synovium. Cancer, 1991, 67:155-162. 8. Murphey M.D., Vidal J.A., FanburgSmith J.C., Gajewski D.A.: Imaging of synovial chondromatosis with radiologic-pathologic correlation. Radiographics, 2007, 27: 1465-1488. 9. Sperling B.L., Angel S., Stoneham G., Chow V., McFadden A., Chibbar R.: Synovial chondromatosis and chondrosarcoma: a diagnostic dilemma. Sarcoma, 2003, 7:69-73. 10. Norman A., Steiner G.C.: Bone erosion in synovial chondromatosis. Radiology, 1986, 161: 749-752. 11. Goldman R.L., Lichtenstein L.: Synovial chondrosarcoma. Cancer, 1964, 17: 1233-1240. 12. Ginaldi S. Computed tomography feature of synovial osteochondromatosis. Skeletal Radiol, 1980, 5: 219222. 13. Kramer J., Recht M., Deely D.M., et al.: MR appearance of idiopathic synovial osteochondromatosis. J Comput Assist Tomogr, 1993, 17:772–776. 14. Wuisman P.I., Noorda R.J., Jutte P.C.: Chondrosarcoma secondary to synovial chondromatosis: report of two cases and a review of the literature. Arch Orthop Trauma Surg, 1997, 116: 307-311.

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A Rare Case of Early Onset Type of Abdominal Trocar Site Hernia (TSH) with Atypical Externalizing in Two-step: Multi detector Row CT diagnosis B. Coulier1, A. Ramboux2, F. Pierard2 We report a rare case of early onset type Trocar Site Hernia (TSH) producing in the right lower abdominal quadrant of a 64-year old obese woman. The patient was admitted in the emergency room for abdominal pain producing four days after laparoscopic adnexectomy. The hernia atypically externalized in two-steps creating two superposed concentric small bowel strangulating hernias producing through two distinctive superposed orifices. A precise and complete anatomic diagnosis was made by contrast enhanced 64-row multidetector computed tomography (MDCT). The imaging features are presented with a short review of the literature. The case emphasizes the high performances of MDCT for the early diagnosis of Trocar Site Hernias. Key-word: Abdomen, interventional procedure.

Laparoscopic surgery developed in the eighties and rapidly emerged as a major innovation in surgery offering a drastic reduction of the classical complications of classical open surgery. Benefits include decreased postoperative pain, quicker return to normal activity, and less postoperative complications. Nevertheless laparoscopic surgery can be associated with new specific type of complications including incisional hernia through the trocar site (1-2). This new type of incisional hernia occurring on the trocar incision site after minimally invasive surgery is called a Trocar Site Hernia ernia (TSH) but the term of Port Site H is also common. We report a rare case of early TSH diagnosed four days after laparoscopic adnexectomy in an obese female and atypically externalizing in two-step. The detailed anatomic diagnosis was made by contrast enhanced Multidetector Computed Tomography. The imaging features are presented with a short review of the literature. The case emphasizes the high performances of MDCT for the diagnosis of acute Trocar Site Hernias (3-4). Case report A 64-year old obese woman was admitted in the surgery department for elective minimally invasive laparoscopic removal of a slow growing postmenopausal left ovarian cyst. Three trocars were used during laparoscopy comprising a 5 mm optical

umbilical trocar, a 5 mm nonbladed trocar in the left lower quadrant and a 10 mm nonbladed main trocar in the right lower quadrant. Twin cysts of two centimeters were confirmed on the left ovary and subsequent bilateral classical adnexectomy was performed with endobag extraction of the specimens through the 10 mm right lower quadrant port site. The port sites were not specifically sutured. The patient was discharged after 24 hours. Four days after surgery the patient was readmitted in the emergency department for abdominal pain. This pain lasted for 48 hours and had started the day after leaving the hospital. This pain had continuously amplified the next day to become constant at the time of readmission. It was maximal in the right lower quadrant where a 6-8 cm painful mass was clearly palpable. The patient remained afebrile and the laboratory tests were normal with a white cell count at 6800 mm³ and a CRP level at 1, 79 mg/L (normal < 5 mg/L). Emergency contrast-enhanced Multidetector Computed Tomography (MDCT) (Fig. 1) revealed a small intestine occlusion due to bowel strangulation through a “Spiegelian like” interstitial hernia of the right lower quadrant. This hernia produced through a 19 mm orifice through the transverse and small oblique muscles (nearly at the level of the Spiegelian line) and expanded under the distended large oblique muscle. Careful multiplanar analysis revealed another simultaneous but more

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

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s uperficial small bowel strangulating hernia producing through a more anterior and superficial 19 mm other orifice. This second orifice was situated in the anterior root of the distended large oblique muscle and presented with an angle of 90 degrees from the deepest orifice. The small subcutaneous strangulated intestinal loop represented a small portion of the intraparietal strangulated incarcerated loops. This atypical hernia complex appeared thus unusually constituted by two superposed concentric strangulating hernias as schematically represented (Fig. 2). The final CT diagnosis was an early onset type Trocar Site Hernia (TSH) with atypical externalizing in two-step. Emergency laparotomy was immediately performed. Careful dissection through a re-aperture of the fresh cutaneous scar of the right lower quadrant trocar found the suffering dilated intestine loop in the deep subcutaneous fat. The superficial hernial orifice was carefully stretched and the superficial sub cutaneous bowel hernia was reduced. The intestinal loop appeared being viable and segmental resection might be avoided. The intraparietal bowel loops were then pushed within the peritoneal cavity through the other deep hernial orifice. The different orifices were firmly sutured plane by plane. The post-operative period was uneventful. Discussion In 2004 Tonouchi classified TSH into 3 types (1, 5-6). – The Early Onset Type is a dehiscence of anterior and posterior fascial plane and peritoneum characterized by an early onset after surgery. It usually occurs as a small bowel obstruction.

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Fig. 1. — Contrast-enhanced Multidetector Computed Tomographic (MDCT) coronal oblique (A) and sagital oblique (B) multiplanar reconstructions obtained at the level of the deep hernial orifice; sagital (C) and coronal (D) multiplanar reconstructions obtained at the level of the superficial hernial orifice; (E to H) a series of cranio-caudal axial views. The deep “spiegelian like” component of the trocar site hernia (TSH) produces through a 19 mm orifice through the transverse and small oblique muscles (black rings); the entry (white arrow) and output (black arrow) of the interstitially herniated and strangulated loops (white star) are clearly seen protruding with mesenteric fat through this deep orifice. The superficial subcutaneous hernia produces through a 19 mm more superficial anterior orifice (white rings); the entry (small white arrow) and output (small black arrow) of the small superficially strangulated loop (black star) are clearly seen through this orifice. The superficial (white rings) and deep (black rings) orifices of the two steps TSH are clearly anatomically separated and appear perpendicular to each other (H).

Fig. 2. — Schematic transverse illustration of the atypical two step trocar site hernia (TSH): grey star = intra-abdominal dilated small intestine; white star = strangulated loop within the “spiegelian like” deep interstitial component of the TSH; black star = subcutaneous strangulated loop in the superficial component of the TSH.

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– The Late Onset Type is a dehiscence of anterior and posterior fascial plane. Peritoneum constitutes the hernia sac. Hernias usually develop several months after surgery, are not associated with small bowel obstruction and generally appear as an asymptomatic swelling by the wound site. – The Special Type is a complete dehiscence of the whole abdominal wall. Transparietal protrusion of the intestine or omentum produces without any peritoneal sac. The onset is very early, immediately after surgery. – The Early Onset Type and the Special Type represent emergency situations in the majority of cases. Pamela et al. recently reported an extensive literature review. The inci-

dence of TSH ranged from 0.007% to 22% with an average of 1.85% (1). Various interesting and sometimes extensive retrospective reports stressed the importance of predisposing factors. For example an incidence of 0, 02% of herniations was reported from a 4,385,000 estimated laparoscopic procedures by the American Association of Gynecologic Laparoscopists in 1994 (1, 7). 17.9% occurred despite systematic fascial closure and 71, 3% of patients required a following surgical repair. 86.3% of hernias in which the size of the original fascial defect was scrupulously noted occurred in sites where 10 mm or larger diameter trocars had been placed. Only 10.9% were related to the use of 8-10 mm trocars and only 2.7% to minor diameter trocars (7).

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This report stressed the importance of the diameter of the trocar as a predominant predisposing factor but also that TSHs may also produce after systematical surgical fascial closure. In another series of 600 patients, the incidence of incisional hernia was estimated around 2% but exclusively noted in the periumbilical area (8). No case of incisional hernia was registered in extra-umbilical port sites, despite the fact that fascial suture on extraumbilical sites was not performed. This study underlined the fact that particular attention needs to be paid to periumbilical gap suture which is exposed to the trauma of trocar fixing, especially in obese and diabetic patients. But it also explains why no definitive consensus actually exists concerning the necessity of systematic suture of extraumbilical sites. TSH have also been reported with the nearly the same percentages of incidence in pediatric surgery (9). The risk factors classically associated with the occurrence of TSH are related both to the patient’s features but also to the surgical technique (1, 6, 10). When patient’s features are considered, an important predisposing factor is obesity (increased BMI). Obesity is associated with increased morbidity related to port site due to various factors like the need for longer trocars, thick abdominal wall, need for larger skin incision to expose fascia adequately, and limitation in mobility of the instruments due to increased subcutaneous tissue (2, 5-6). Moreover advanced age, sex, nutritional status, smoking status, and other predisposing factors like uncontrolled diabetes mellitus, anemia, steroid therapy, renal insufficiency, but also cancer and portsite infection or pre-existing fascial defects also contribute to the occurrence of TSH (1, 5, 11). When surgical technique is considered other factors may also increase the risk of herniation by widening the fascial defect. They includes the use of “fascial screws” to secure the port within the abdominal wall, long surgical procedures resulting in excessive manipulation of port sites, peritoneal defects larger than the trocar size, large ports, the type and size of trocars (bladed, nonbladed, radially expanding), undetected omentum or bowel entrapment into the intraperitoneal defect after trocar removal and the absence of suture of larger fascial defects (1, 5, 11). Mid-

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line insertion especially near the umbilicus but also other sites of trocar insertion such the lower quadrant port sites (more prone to hernia because of the absence of posterior rectus sheath under the arcuate line of Douglas) also seem more prone to develop TSH (1, 5, 11). Additionally, the stretching of the port site for removal of specimens or organs also represents an etiological factor (5, 11). Since 1999 the attention has been focused on trocar-related problems with the conclusion that port sites created by nonbladed trocars could not require fascial closure because the wounds caused by these types of trocars were presumably narrower, shorter in length and width with less destruction of fascial tissues when compared with bladed trocars (1). Whatever the type of trocar used, there is a significant consensus to consider that the closure of both the fascia and the peritoneum should be recommended if the incision is greater than 7 mm in adult patients and ≥ 5 mm in young children. The insertion of the 10 mm lateral trocar in an oblique way or as a Z-tract is also considered as a method able to reduce hernia formation by placing the external and internal fascias at different levels. Nevertheless systematic closure is not always completely protective and there is no clear consensus that all port sites must be closed (1, 5, and 10). As a general consequence, careful postoperative management is recommended especially for patients with risk factors such as obesity, extensive manipulation of the trocar, and longer procedures (1, 12). A list of tips has been proposed to limit the incidence of TSH (10): – The closing of all port sites despite trocar size, especially if the surgical procedure was prolonged with a probably excessive manipulation of trocars. – The removing of all ports would be performed under visualization. – Careful deflating of the abdomen is necessary when removing ports because escaping CO² can draw bowel loops or omentum through the port sites. – Removal of ports before deflation of CO² is preferable because their removal can be laparoscopically controlled. – A careful examination of all port sites before closing the skin is useful to exclude any potential visceral herniation.

– Obese patients need close attention to closure. – Abnormal slow return of bowel function should alert the physician to a possible bowel hernia. – Placing drains through the port sites should be avoided. Of course, patients can have a port-site hernia, but without bowel involvement and without symptoms. Nevertheless once bowel or omentum gets involved, patients may present with gastrointestinal symptoms (nausea, vomiting, port-site pain, abdominal pain, fever). Either small or large bowel can be involved depending on the site of hernia. Bowel involvement may occur in the form of incarcerated bowel, bowel obstruction, or bowel evisceration. All of these are considered surgical emergencies that can present a few days to weeks after surgery (10). For patients who present with gastrointestinal symptoms after recent laparoscopic surgery, a differential diagnosis should include internal bowel hernia with or without incarceration/strangulation. During the last decades Computed Tomography (CT) has emerged as the gold standard for follow-up after abdominal surgery and for the diagnosis of postoperative complications (13-15). Continuous technical developments have occurred. Today, thanks to its very high performances in term of spatial resolution, table speed and multiplanar reconstructions (MPR), 64-row MDCT offers unrivalled high quality images of the entire abdominal wall (AW) during a single short breath hold. MDCT thus appears particularly useful for the evaluation of AW hernias, allowing accurate identification of their contents, exquisite analysis of their anatomic landmarks, differentiation from other abdominal masses such hematomas or abscesses and planning of optimal surgical re pair (3, 4). The reported case confirms the previous reported performances of CT for the evaluation TSH (3, 11, 16-17). Bowel or omental evisceration, incarceration, and obstruction in cases of TSH scan are managed via laparoscopy or laparotomy, depending on surgeon’s preference. In the reported case the perfect CT diagnosis of an atypical two-step concentric herniation with two distinct orifices appeared of primordial importance for the choice of direct prograde laparotomic dissection rather than retrograde laparoscopic exploration.

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References 1. Pamela D., Roberto C., Francesco L.M., et al.: Trocar site hernia after laparoscopic colectomy: a case report and literature review. ISRN Surg, 2011, 725601. 2. Karthik S., Augustine A.J., Shibumon M.M., Pai M.V.: Analysis of laparoscopic port site complications: A descriptive study. J Minim Access Surg, 2013, 9: 59-64. 3. Coulier B.: Hernias of the greater omentum through the antero-superior abdominal wall: an extensive pictorial MDCT review with emphasis on typical anatomic landmarks. A pictorial essay. JBR-BTR, 2012, 95: 191214. 4. Tonouchi H., Ohmori Y., Kobayashi M., Kusunoki M.: Trocar site hernia. Arch Surg, 2004, 139: 1248-1256. 5. Sharma M.S., Kumar S., Agarwal N.: Trocar site hernia- a case series. Indian J Surg, 2004, 4: 189-190. 6. Montz F.J., Holschneider C.H., Munro M.G.: Incisional hernia following laparoscopy: a survey of the American Association of Gynecologic Laparos-

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copists. Obstet Gynecol, 1994, 84: 881-884. 7. Immè A., Cardì F.: Incisional hernia at the trocar site in laparoscopic surgery. Chir Ital, 2006, 58: 605-609. 8. Paya K., Wurm J., Fakhari M., FelderPuig R., Puig S.: Trocar-site hernia as a typical postoperative complication of minimally invasive surgery among preschool children. Surg Endosc, 2008, 22: 2724-2727. 9. Khurshid N., Chung M., Horrigan T., Manahan K., Geisler J.P.: 5-millimeter trocar-site bowel herniation following laparoscopic surgery. JSLS, 2012, 16: 306-310. 10. Yamamoto M., Minikel L., Zaritsky E.: Laparoscopic 5-mm trocar site herniation and literature review. JSLS, 2011, 15: 122-126. 11. Zemet R., Mazeh H., Grinbaum R., Abu-Wasel B., Beglaibter N.: Incarcerated hernia in 11-mm nonbladed trocar site following laparoscopic appendectomy. JSLS, 2012, 16: 178181. 12. Zappa M., Sibert A., Vullierme MP., Bertin C., Bruno O., Vilgrain V. Postoperative imaging of the peritoneum

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and abdominal wall. J Radiol. 2009; 90:969-979. 13. Gore R.M., Berlin J.W., Yaghmai V., Mehta U., Newmark G.M., G hahremani G.G.: CT diagnosis of postoperative abdominal complications. Semin Ultrasound CT MR, 2004, 25: 207-221. 14. Sandrasegaran K., Maglinte D.D.: Imaging of small bowel-related complications following major abdominal surgery. Eur J Radiol, 2005, 53: 374386. 15. Rammohan A., Naidu R.M.: Laparoscopic port site Richter’s hernia — An important lesson learnt. Int J Surg Case Rep, 2011, 2: 9-11. 16. Cadeddu M.O., Schlachta C.M., Mamazza J., Seshadri P.A., Poulin E.C.: Soft-tissue images. Trocar-site hernia after laparoscopic procedures. Can J Surg, 2002, 45: 9-10. 17. Aguirre D.A., Santosa A.C., Casola G., Sirlin C.B.: Abdominal wall hernias: imaging features, complications, and diagnostic pitfalls at multi-detector row CT. Radiographics, 2005, 25: 1501-1520.

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IMAGES IN CLINICAL RADIOLOGY Diffusion restriction of posterior uveal melanoma on MR imaging R. Semnic1,2, D. Kozic1,2, K. Petrovic2,3, F. M. Vanhoenacker4,5,6 A 55-year-old male with clinical and opthalmological signs of retinal ablation was referred for orbital magnetic resonance imaging (MRI). MR scan revealed a small tumor nodule in the posterolateral part of left eye globe as a cause of ablation. Tumor showed high signal on transverse diffusion weighted image (DWI) (Fig. A, arrow), low signal on apparent diffusion coefficient image (Fig. B, arrow), consistent with restricted diffusion. The nodule had intermediate signal on T1 sagittal weighted unenhanced image (Fig. C, arrow). The patient underwent left eye enucleation with histopathologically proved uveal melanoma.

Comment Uveal melanomas are classified into anterior – when tumor arises from the iris and posterior if arises from the choroid or cilliary body. Origin of the posterior uveal melanoma is choroidal pigment cells. For the diagnosis of these tumors, standard MRI plays a major role, showing in most cases tumor paramagnetic melanin content. However, in case of tumor necrosis or the presence of blood degradation products, DWI, as a non-contrast sequence, may provide additional signal information. DWI is routinely used for brain tumor differentiation but just lately is used for evaluation of orbital masses. Restricted diffusion in uveal melanomas could represent new, potentially reliable signal intensity marker, not yet well known in literature. Reference 1. Erb-Eigner K., Willerding G., Taupitz M., Hamm B., Asbach P.: Diffusionweighted imaging of ocular melanoma. Invest Radiol, 2013, 48: 702-707.

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1. Institute of Oncology, Sremska Kamenica, 2. Faculty of Medicine, University Of Novi Sad, Serbia, 3. Centre of Radiology, Faculty of Medicine, University of Novi Sad, Serbia. 4. Department of Radiology, AZ SintMaarten Duffel-Mechelen, Mechelen, 5. Department of Radiology, Antwerp University Hospital, Edegem, 6. University of Ghent, Faculty of Medicine and Health sciences, Ghent.

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JBR–BTR, 2014, 97: 313.

IMAGES IN CLINICAL RADIOLOGY Delayed onset muscle soreness L. Delcour1, B. Dallaudière1, P. Omoumi1, T. Kirchgesner1, B. Vande Berg1, C. Cyteval2, A. Larbi1

A sportive young woman presents highly painful muscular soreness 48 hours after intensive physical exercise. A first MRI (Fig. A) of her legs is performed during the acute pain period (axial T1 and STIR weighted sequences), which shows on the STIR weighted sequencea diffuse high signal intensity of the muscles groups of the posterior compartment of the left leg (right side of image). Moderate high signal intensity is also showed in both gastrocnemius of the right leg (left side of image) (on the right on Fig. A). No abnormalities are shown on T1 in both legs. A second MRI (Fig. B) of the legs is performed after disappearance of the pain 15 days later, with complete normalization of the muscle signal on both sequences (axial T1 and STIR weighted sequences). Laboratory tests showed a moderate increase in muscle enzymes (Creatine Kinase) in acute phase with normalization 15 days later. Pressure measurements in muscular lodges are normal. Comment

Delayed onset muscle soreness (DOMS) is a clinical entity characterized by heavy muscular pain appearing 48-96 hours after intensive physical exercise, who shows on histology microstructural damages (sarcomeres disorganization) et biologically increased Creatine Kinase enzyme. MRI is the imaging modality of choice. STIR weighted sequence best shows high signal intensity zones in the involved muscle groups. The distribution of high signal intensity is multifocal and reaches the involved overused muscle groups, who can be very limited or extended and diffuse, in relation with the number of involved muscles. The intramuscular distribution of the high signal intensity is often diffuse in the muscle body. A study (1) showed also a correlation between the degree of pain, the elevation of CK enzymes and the volume of muscle edema on MRI. The muscular high signal intensity disappear normally with the resolution of the symptoms, and give residual a normal pattern on MRI. The differential diagnosis of DOMS is large and compatible with these of muscle edema: post-traumatic (strain, contusion, laceration, compartment syndrome), inflammatory (polyomyositis, necrotizing fasciitis, diabetic muscle infarction, sarcoïd myopathy), neuronal denervated muscular territory, post radiation. The clinical context and the medical history and above all the complete return to normality on the MRI images correlated with the clinical status will orientate the diagnosis with DOMS. Reference 1. Nurenberg P., Giddings C.J., Stray-Gundersen J.: MR imaging-guided muscle biopsy for correlation of increased signal intensity with ultrastructural change and delayed onset muscle soreness after exercise. Radiology, 1992, 184: 865-869.

1. Department of Radiology, Cliniques Universitaires St-Luc, Brussels, Belgium, 2. Department of Radiology, CHU Lapeyronie, Montpellier, France.

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IMAGES IN CLINICAL RADIOLOGY Idiopathic intracranial hypertension G. Vandekerckhove1, V. VandeVyver2

A 19-year-old woman consulted the neurologist for headache and diplopia. Physical examination revealed no focal neurological findings except diplopia due to an abducens nerve paresis. Visual acuity and visual field examinations were normal. Fundoscopy showed bilateral papilledema. The patient was referred to our department for an MRI examination. MRI of the brain was revealed no intracranial mass lesion, hydrocephalia or venous sinus thrombosis. Additional T2 high resolution sequences of the orbits showed however tortuosity of the optic nerves with dilatation of the perioptic subarachnoidal spaces (arrows in Fig. A). Also flattening of the posterior sclera and protrusion of the optic nerve papilla into the posterior globes was seen (arrowheads in Fig. A). After gadolinium administration, T1WI of the orbits showed enhancement and protrusion of the prelaminar optic nerve (arrows in Fig. B). Based on the clinical and imaging findings the diagnosis of idiopathic intracranial hypertension was made. The diagnosis was confirmed by lumbar puncture with opening CSF pressure of 38 cm H2O. CSF was evacuated to a closing pressure of 15 cm H2O. The patient was also treated with Diamox and clinical symptoms gradually improved so the patient could be dismissed from hospital. Comment

Idiopathic intracranial pressure is a condition of raised intra cranial pressure of unknown etiology. It is also known as pseudo tumor cerebri or benign intracranial hypertension. It is usually seen in obese young to middle-aged woman who present with headache and papilledema. The headache is mostly generalized and aggravated by Valsalva. Papilledema is nearly always present. Diplopia with abducens nerve paresis can be present. The primary goal of imaging is exclusion of other causes of intracranial hypertension, especially venous sinus thrombosis and space-occupying lesions. CT examination is usually normal, sometimes slit ventricles, an empty sella or enlarged optic nerve sheaths can been seen. MRI is the imaging examination of choice. On MRI of the brain small ventricles and empty sella can been seen. The use of high-resolution, B thin-slice MR imaging improves the visualisation of the optic nerves and nerve papilla. According to literature flattening of the posterior sclera can be seen in 80% of cases, distension of the perioptic subarachnoidal space in 45% and tortuosity of the optic nerves in 40% of cases. After administration of Gadolinium, enhancement of the prelaminar optic nerve can be seen in half of cases. Differential diagnosis should be made with secondary pseudotumor syndromes associated with certain medications (vitamin A derivatives, tetracyclines) or with systemic lupus erythematosus. The imaging findings should also be differentiated with idiopathic empty sella or optic nerve atrophy. In conclusion, in patients with headache, papilledema or abducens nerve paresis, MRI of the brain should be performed to exclude intracranial mass lesion or dural sinus thrombosis. The presence of tortuous optic nerves on high-resolution images of the orbits with perioptic subarachnoid space dilation, flattening of the posterior sclera or enhancement of the prelaminar optic nerve strongly suggests the diagnosis of idiopathic intracranial hypertension. Reference Suzuki H. et al. MR imaging of idiopathic intracranial hypertension. AJNR, 2001, 22: 196-199.

1. Department of Radiology, University of Ghent, Ghent, 2. Department of Radiology, AZ Alma, Eeklo, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Hemangioperiocytoma simulating meningioma in a 41-year-old man E. Rabaey, K. Desmet, M. De Maeseneer, T. Vanderhasselt, T. Stadnik1

A 41-year-old patient was seen in the neurology clinic because of severe memory loss and vision problems. He described his vision problem as “a sail moving in front of his eyes”. He also reported loss of sensation and strength in his right arm and leg. On clinical examination loss of sensation on the right side of his face, arm and leg were evident. This was accompanied by loss of strength in his right arm and leg, and right sided asteriognosia. MR imaging showed a bilobed mass, measuring 3.6 × 6.9 × 4.1 cm, that was in contact with the falx cerebri. There was significant mass effect on adjacent structures in particular the corpus callosum. The diagnosis of meningioma was entertained. On transverse T1 weighted images (A, B) an extra-axial bilobed mass is seen with marked homogenous contrast enhancement. On T2 weighted images (C) flow voids and marked mass effect are present. At surgery the tumor had a highly vascular appearance. It was seen to extend on both sides of the falx. Profuse bleeding occurred during surgery, and hence made complete resection impossible, only the right portion of the tumor was removed. Macroscopically the removed fragments of tumor had a brown color. Microscopically the tumor was of high cellularity. Polymorphic cells with large nuclei were seen. The cells were embedded in a delicate reticulin network. No psammoma bodies were seen. Voluminous vascular structures (‘Staghorn vessels’) were present. On immunohistochemistry the tumor tested positive for vimentin, CD 31, and CD 34, and negative for epithelial membrane antigen and GFAP. These findings were consistent with a hemangioperiocytoma without pathological signs of anaplasia (grade II tumor). Postoperative MR imaging showed presence of residual tumor. Therefore a second surgical procedure was performed during which residual tumor could be removed.

Comment Hemangioperiocytoma is a mesenchymal neoplasm that is histologically unrelated to eningioma. Morphologically it is part of a continuum with solitary fibrous tumors. It arises m from primitive mesenchymal cells throughout the body and most commonly involves soft tissues of the lower extremities, pelvis and retroperitoneum. Approximately 15% of hemangioperiocytomas occur in the head and neck region. Hemangioperiocytomas are classified as mesenchymal, non-meningiothelial tumors, WHO grade II (generally low grade malignant tumors). The average age of onset is 42 years and there is a predilection for men. Headache is a common symptom. Other symptoms related to the mass effect of the tumor also occur. There is only an interval of a few months between the onset of symptoms and diagnosis due to the fast growth rate. Treatment consists of surgery. Chemotherapy has not shown to be effective. There is a 5 year survival rate of 93% following surgery and a disease free survival rate of 89% following surgery. Macroscopically, hemangioperiocytoma presents as a well circumscribed, encapsulated and firm mass with a dural attachment. It is quite vascular and has a tendency to bleed during surgery. Microscopically, hemangioperiocytoma is highly cellular. It is homogenous and consists of randomly oriented plump cells embedded in a dense network of reticulin. A ‘stag horn’ vascular pattern is typical and consists of lobules with tumor cells surrounding wide, branching capillaries. On immunohistochemistry hemangioperiocytoma is positive for vimentin, similar to meningioma. Hemangioperiocytoma is negative for epithelial membrane antigen, whereas meningioma is positive for this antigen. Tumors typically have a supratentorial and occipital location. They involve the falx, tentorium or dural sinuses. Their diameter varies from 2 to 9 cm. The tumor has an extra-axial location with dural attachment. Surrounding edema is common. On non-enhanced CT, a lobulated hyperdense lesion is seen. Bony erosion may be present. Calcifications and hyperostosis are typically absent in contradistinction to meningioma. After contrast administration heterogeneous enhancement is seen. A dural tail sign may be observed. Low density areas corresponding to cysts or necrosis are common. Both on T1- and T2-weighted MR images a heterogeneous mass, isointense to gray matter is seen. Areas of flow void may be apparent. Adjacent edema and mass effect are common. After contrast administration marked and heterogeneous enhancement is seen. A dural tail sign is present in 50% of patients. Central areas of necrosis may be seen. Hemangioperiocytoma and (malignant) meningioma present with similar clinical and MR imaging findings. Hence, differential diagnosis may be difficult. Bone erosion, presence of areas of signal void, and heterogeneous contrast enhancement are more characteristic for hemangioperiocytoma.

Reference 1. Sibtain N.A., Butt S., Connor S.E.: Imaging features of central nervous system haemangiopericytomas. Eur Radiol, 2007, 17: 16851693. 1. Department of Radiology, Vrije Universiteit Brussel-Universitair Ziekenhuis Brussel, Brussels, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Proximal avulsion fracture of the long head of the triceps brachii muscle. M. Vansevenant1,2, F.M. Vanhoenacker1,2,3, T. Wauters4

A 27-year-old male and indoor soccer goalkeeper presented at the private practice of the orthopaedic surgeon with pain in the posterior right shoulder. Two months previously, he felt sudden pain and loss of function in his shoulder when throwing a ball, more specifically during ball release. After 6 weeks of rest, there was almost complete recovery. He started playing indoor soccer again and fell on his right shoulder with relapse of the pain. He never experienced dislocation of the shoulder. Clinically there was full range of motion of his shoulder and no muscle atrophy. Resistance tests of the triceps brachii muscle caused pain in the posterior shoulder. A plain film of the right shoulder showed a bony fragment at the inferior rim of the glenoid (Fig. A, arrow). A CT-arthrography (Fig. B, C) and MR-arthrography showed a sclerotic delineated avulsion fragment at the infraglenoid tubercle, but showed no concomitant lesion of the antero-inferior labrum (Fig. B, arrow). There was no Hill-Sachs lesion and the rotator cuff was normal. There was no tendon retraction of the long head of the triceps brachii muscle (Fig. C, arrow). Based on the clinical presentation and imaging findings, the diagnosis of a proximal avulsion fracture of the long head of the triceps brachii muscle was made. The patient was treated conservatively with relative rest and nonsteroidal analgetics. After 3 months of follow-up, the patient was pain-free during his daily activities and could restart his indoor soccer training with throwing-exercises. Comment

The triceps brachii muscle consists of three muscular heads: a lateral head with its origin on the latero-posterior side of the humeral diaphysis, a medial head originating from the medio-posterior side of the humeral diaphysis and superficial of these two heads the long head with its origin on the infraglenoid tubercle. These three heads join at the distal triceps tendon inserting on the olecranon. The function of the triceps brachii muscle is extension of the elbow and adduction of the arm by the long head. A traumatic tear or avulsion fracture of the triceps tendon is uncommon, accounting for less than 1% of all tendon injuries. Most triceps tendon injuries are located at the distal insertion of the tendon into the olecranon. Proximal triceps tendon injuries are even rarer. The probable trauma mechanism in our case consists of a bony avulsion that occurred when throwing a ball, more specifically at the end of the extension of the elbow. In case of proximal triceps tendon injury, plain films may show an avulsion fragment at the infraglenoid tubercle, which may be confirmed on Computed Tomography (CT) or CT-arthrography. MR-arthrography is less suited for demon strating osseous avulsions without labrum lesions. The differential diagnosis includes a bony Bankart lesion and a Bennet’s lesion. A bony Bankart lesion occurs during an antero-inferior shoulder dislocation and is associated with a lesion of the antero-inferior labrum. A Bennet’s lesion is a calcium deposition in the posterior capsule of the shoulder, seen in professional baseball pitchers. The latter does not provoke acute pain. Typical location at the inferior rim of the glenoid and the absence of a cartilaginous labrum lesion are the clues to the correct diagnosis. Avulsion of the long head of the triceps muscle can be treated conservatively with nonsteroidal analgetics and relative rest. If conservative treatment fails, surgical intervention may be required. Reference

1. Clifford P.D., Posada A., Hancock C.R.: Isolated long-head triceps brachii tendon avulsion in a surfer detected at MR imaging. Skeletal Radiol, 2009, 38: 77-80.

1. Department of Radiology, AZ Sint Maarten, Mechelen-Duffel, 2. Department of Radiology, Ghent University Hospital (UZ Gent), 3. Department of Radiology, Antwerp University Hospital (UZA), 4. Orthopedic Surgery, Mechelen.

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IMAGES IN CLINICAL RADIOLOGY Secondary infertility caused by a midline cyst of the prostate T. Dewaele1, L. D’Hooghe1, K. Everaert2, P. Devisschere1

A 27-year-old male was referred to the urologist for evaluation of secondary infertility. Semen analysis by the referring physician showed a severe oligoastheno teratozoospermia (OAT). The patient had no urinary symptoms or sexual complaints and the past medical history was unremarkable. Physical examination revealed thickened spermatic cords, suggesting a possible obstruction of the vasa deferens. A small varicocele was noticed on both sides. External genitalia and secondary sexual characteristics were otherwise normal. Hormonal laboratory findings were unre markable. An MRI was performed to detect a possible obstructive cause of infertility. T2 weighted images (T2-WI) showed a sharply delineated, homogenous hyperintense cystic structure (c) of 2.5 × 2 cm dorsally at the midline in the prostate (P) (Fig. A). This cyst reached beyond the cranial and dorsal edge of the prostate (Fig. B). Furthermore, significantly swollen seminal vesicles (SV) and vasa deferens (VD) were noted (Fig. C, D). These findings suggested an obstruction of the ejaculatory ducts caused by the prostatic cyst, resulting in distension of the vasa deferens and seminal vesicles. This was considered the probable cause of secondary infertility in this patient. Subsequently, a transurethral unroofing of the cyst was proposed as an attempt to restore fertility. However, this treatment was refused by the patient. Comment

Midline cysts are a common (incidental) finding in the prostate and they may be utricle cysts or müllerian duct cysts. Both are congenital cysts that are remnants of the müllerian duct system. During normal embryogenesis the müllerian ducts form the fallopian tubes, uterus, cervix and upper vagina in the female. In the male embryo the müllerian ducts regress early in embryogenesis under the influence of müllerian regression factor (MRF). Normally, the müllerian system remains rudimentary in males with the appendix testis and prostatic utricle persisting as the only müllerian remnants. Large müllerian duct remnants can cause obstruction of the bladder neck or the seminal vesicles and ejaculatory ducts and therefore they can cause obstructive azoospermia. Müllerian duct cysts are more likely to cause ejaculatory duct obstruction than utricle cysts. Müllerian duct cysts and utricle cysts are separate entities. The müllerian duct cyst is derived from the müllerian duct, whereas the utricle cyst derives from a cystic dilatation of the prostatic utricle. On imaging studies, these two entities can be identical and indistinguishable from one other. However, there are some clinical and morphologic differences that can be used to distinguish them. Müllerian duct cysts are usually discovered in infertile man in the 3rd and 4th decade of life. They are very rarely associated with renal agenesis, but external genitalia are normal. Müllerian duct cysts do not communicate with the prostatic urethra. They extend above the prostate if large. Müllerian duct cysts may cause obstructive azoospermia or severe oligospermia, wich may be progressive in adulthood and preceded by previous fertility. Utricle cysts manifest in the first 2 decades of life and are often associated with hypospadia, intersex disorders, cryptorchidism and ipsilateral renal agenesis. Unlike müllerian duct cysts, utricle cysts do not extend beyond the prostate gland. They are always in the midline and communicate freely with the prostatic urethra. In contrast, müllerian duct cysts can theoretically extend slightly lateral to the midline, since the cephalic portion of the müllerian duct develops lateral to the midline. If we consider the various features discussed above, we can assume that in the presented case we are probably dealing with a müllerian duct cyst. Congenital midline prostatic cysts are easily identified on MR images by their high signal on T2-WI. In müllerian duct cysts, stones are common and virtually diagnostic if found to lie in a retrovesical cavity that is not connected to the bladder. Calculi may cause hemorrhage in a cyst, which can be demonstrated on T1-WI. Congenital midline prostatic cysts should only be treated in symptomatic or infertile patients, and in the latter only when signs of ejaculatory duct obstruction are present. Endoscopic unroofing of the cyst is now the procedure of choice for patients who want to preserve their fertility. Reference 1. Desautel M., Stock J., Hanna M.: Müllerian duct remnants: surgical management and fertility issues. J Urol, 1999, 162, 1008-1014.

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1. Department of Radiology, 2. Department of Urology, University Hospital Gent, Ghent, Belgium.

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IMAGES IN CLINICAL RADIOLOGY Lunate dislocation F. Filippitzi¹, B. Dallaudière¹, P. Omoumi¹, F.E. Lecouvet¹, M. Lefere¹, B. Vande berg¹, A. Larbi¹ A 38 year-old patient was admitted to the emergency department after road accident due to pain on palpation of the right wrist, the 1st and the 2nd finger of the right hand. The patient was subsequently referred for an X-ray. Following the proper positioning of the patient and the systematic analysis of the wrist X-ray (PA and lateral view), a lunate dislocation was diagnosed (Fig. A). A CT scan of the right wrist was then performed, at the request of the surgeon, which clearly demonstrated the lunate dislocation and an additional triquetral fracture (Fig. B).

Comment

The lunate dislocation is one of the most severe carpal instability lesions and it is commonly associated with a trans-scaphoid fracture (Fenton syndrome). It involves all the intercarpal joints and disruption of most of the major carpal ligaments. It produces volar dislocation and forward rotation of the lunatum. The concave distal surface of the lunatum therefore faces anteriorly (Fig. A) and the capitatum drops into the space vacated by the lunate. The capitatum and all the other carpal bones lie posterior to the lunatum on the lateral radiography. On a frontal projection however, the triangular appearance of the lunatum is preserved (Fig. A). When analyzing a wrist radiograph to look for possible carpal instability or fracture dislocation, one should first check the good quality of the picture, in particular the good positioning of the wrist (on the PA and lateral views). Secondly, a systematic analysis is essential. On the PA view the normal alignment between the carpal bones should be verified, as well as the integrity of the three carpal lines (Gilula’s arcs) and the respect of the joint spaces, always < 2 mm. On the lateral view, the alignment of the radius-lunate-3rd metacarpal bone should be verified, as well as the congruity of the capitatum with the cup of the lunatum. The eight carpal bones form an intricately connected unit that allows for three-dimensional movements of the wrist. They are divided into two horizontal rows. The proximal row (scaphoid, lunatum, triquetrum) forms an intercalated segment between the radius and the distal carpal row, and maintains wrist stability. The distal row, supporting the metacarpals, consists of the trapezium, trapezoid, capitatum and hamatum. Both intrinsic and extrinsic ligaments support the wrist. The extrinsic ligaments run between the radius or ulna and the carpal bones, whereas the intrinsic ligaments link adjacent carpal bones. The CT scan is done because in 30% of cases, these lesions were overlooked in the initial posttraumatic setting but could be seen retrospectively. In this case the scaphoïd was intact but there was a triquetral fracture (Fig. B). The treatment consisted to reduce the lunate dislocation and to synthesis the triquetrum fracture; because of the risk of early osteoarthritis. To conclude, in case of doubt during the systematic analysis of the X-ray, a CT-scan should be also performed. Reference 1. Gilula L.A.: Carpal injuries: analytic approach a case exercises. AJR, 1979, 133: 503-517.

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

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JBR–BTR, 2014, 97: 319-320.

LETTER TO THE EDITOR Acute renal failure due to bilateral ureteral stone: a rare occurrence I. Mocanu¹, N. Verbeeck¹, F. Prospert²

Dear Editor, If urolithiasis is a common disease with a lifetime risk of stone develop ment in about 12% of the population, concomitant bilateral obstructing urolithiasis causing acute renal fail ure (ARF) is much rarer (1). ARF is defined as an increase of nitrogenous waste products in serum due to deterioration of renal func tion. There are three kinds of ARF: prerenal failure due to decreased re nal perfusion, intrinsic renal failure due to nephrotoxins and, seldom, postrenal failure due to obstruction of the urinary outflow tract (2). We present such a case of post renal ARF due to bilateral obstructive ureteral stone.

Fig. 1. — Bilateral hydronephrosis demonstrated by unenhanced CT

Case report A 55-year-old man presents to the emergency room complaining of total anuria for two days. He has no other urinary symptom such as renal colic, dysuria or hematuria. He had received a flu vaccine one week pre visouly and has a fever (39°C) with little chills, polyarthralgia and nau sea. His medication is diclofenac, a non-steroidal anti-inflammatory drug (NSAID), occasionally completed with paracetamol and aspirin, for re peated tendinitis. Physical examina tion shows some rhonchi at pulmo nary auscultation, the rest being unremarkable. Digital rectal exam fails to show prostate anomaly. Blood pressure is at 160/60 mm Hg with a heart rate at 84 bpm. Urianaly sis cannot be performed because of the total anuria. The laboratory tests reveal increased uremia (67 mg/dL) and creatinemia (7.42 mg/dL), hyper kalemia (5.4 mmol/L), hyponatremia (126 mmol/L) and hypocalcemia (8.4 mg/dL). Macrocytic anemia and thrombocytopenia are also found.

Fig. 2. — 3D «bone» reconstruction with the red coloured bilateral mid ureteral stone.

From: 1. Dpt of Radiology, 2. Dpt of Nephrology, Centre Hospitalier de Luxembourg, Luxembourg, Grand Duchy of Luxembourg.

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Prostate specific antigen level re mains normal (0.26 ng/mL). A renal ultrasonography (US) is performed and shows a slight right pyelocaliectasis with no other anom aly. Given the chronic intake of NSAID, the ARF with total anuria without re nal colic as well as the anemia and the thrombocytopenia, the patient is diagnosed with acute tubulointersti tial nephritis and likely medullar aplasia secondary to NSAID. A treat ment by dialysis and corticosteroids is started. Two days later, considering the lack of sustained improvement, a second US is done and reveals major bilateral pyelocalyceal dilation. An unenhanced computed tomography (CT) is immediately performed and displays bilateral mid ureteric stone with bilateral hydronephrosis. The patient is then successfully treated by bilateral double J cathe ter. Discussion There are very few publications about bilateral urolithiasis causing ARF in the urological or radiological literatures. Whereas prerenal and in trinsic renal failures are responsible for most episodes of ARF (respec tively 85 and 10%), ARF has a postre nal origin in only 5% of cases (2). In

the majority of the cases, bilateral ureteral obstruction resulting in ARF is due to malignant disorders such as prostate and cervix cancers or be nign disorders like retroperitoneal fi brosis and prostatic hypertrophy (3, 4). Rarer causes are neurogenic blad der and bilateral clots, papillary ne croses or ureteral calculi (2). Our patient has been initially diag nosed with intrinsic ARF because of the nearly normal US and of the known link between NSAID and acute interstitial nephritis (4). Based on a second US and an unenhanced CT, final diagnosis is a rare occur rence of bilateral obstructing ureter al stone in a patient without any pain or history of kidney lithiasis. Ultrasonography is a non irradiat ing technique required in ARF since it can detect stones or signs of ob struction as pyelocalyceal dilation but mid ureters remain hard to ac cess and hydronephrosis can be missing at an early stage. Unen hanced CT of the abdomen has a high sensitivity in the diagnosis of urolithiasis (96%) and is the refer ence-standard examination when li thiasic obstructive uropathy is sus pected (5). Moreover, Dual Energy CT is able to characterize the compo sition of urinary tract stones, which may have an impact for treatment. Since it remains more irradiating, we apply Dual Energy, in our Institution,

only to the segments of the abdo men where the stones are detected. Given the rising stone prevalence due to dietary risks factors (6), ARF secondary to bilateral stone occlu sion will probably become more fre quent, so that we must attentively track it with US examination. Unen hanced CT must be performed in complex cases. References 1. Sierakowski R., Finlayson B., Landes R.R., et al.: The frequency of urolithiasis in hospital discharge diagnoses in the United States. Invest Urol, 1978, 15: 438-441. 2. Thadani R., Pascual M., Bonventre J.V.: Acute renal failure. N Engl J Med, 1996, 334: 1448-1460. 3. Norman R.W., Mack F.G., Awad S.A., et al.: Acute renal failure secondary to bilateral ureteric obstruction: review of 50 cases. Can Med Assoc J, 1982, 127: 601-604. 4. Albright R.C.: Acute renal failure: a practical update. Mayo Clinic Procee dings, 2001, 76: 67-74. 5. Boulay I., Holtz P., Foley W.D., et al.: Ureteral calculi: diagnostic efficacy of helical CT and implications for treat ment of patients. Am J Roentgenol, 1999, 172: 1485-1490. 6. Romero V., Akpinar H., Assimos D.G.: Kidney stone: a global picture of prevalence, incidence, and associated risk factors. Rev Urol, 2010, 12: e8696.

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ABSTRACT OF PAPER PRESENTED FOR FULL MEMBERSHIP AT THE BELGIAN SOCIETY OF RADIOLOGY restriction (N = 14), hippocampal FLAIR hyperintensity and diffusion restriction The seizing brain. A pictorial review of (N = 10), thalamic FLAIR hyperintensity ictal and postictal MR imaging findings and diffusion restriction (N = 5), prominent arterial branches (N = 1), sulcal S. Vanden Bossche, S. Dekeyzer, FLAIR hyperintensity (N = 1), lepto K. Deblaere1 meningeal enhancement (N = 1) and crossed cerebellar diaschisis (N = 1). Purpose: The purpose of this work is Mesial temporal sclerosis could be seen to illustrate the spectrum of seizure- in 4 patients. We could not discriminate related imaging findings on MRI in the between the ongoing status epilepticus ictal and postictal phase and to try to and postictal state based on imaging explain these findings based on the findings. With the exception of temporal presumed underlying pathophysiology. mesial sclerosis and crossed cerebellar Approach: Magnetic resonance imagdiaschisis, these signal alterations ing (MRI) studies were obtained from our disappeared or diminished on follow-up own Picture Archiving and Communicaimaging studies where available. tion System (PACS) from 2005 until 2014. Discussion: The different imaging This way we compiled a database of findings can be explained through the thirty-nine patients. The clinical and elecpresumed pathophysiological cortical troencephalography (EEG) data of these processes during and after seizure. The patients were obtained from the patient’s FLAIR hyperintense signal and diffusion medical file. The clinical data were used restriction seen in most patients most to determine the onset of symptoms and likely reflects focal cytotoxic edema. seizure type. The EEG results of the exFocal cortical hyperexcitability leads to amination closest to the MRI studies were binding of glutamate on postsynaptic noted to determine ictal or postictal state non-NMDA receptors, which results in (mean interval was two days before or afsodium influx and finally cytotoxic ter MRI) Only patients were included (1) edema. The location of these signal with clinical and/or EEG data compatible alterations can be in the focal area of with a ictal or postictal event, (2) with an seizure onset or distant from the focus MRI study prior to or within eight days of due to propagation of seizure activity by the end of symptoms and (3) in whom the known pathways (e.g. through the thalaMRI findings could not be attributed to mo-cortical or cortico-pontine-crebellar other causes. After applying these inclupathway). The propagation of seizure sion criteria 20 patients were withheld for activity to the thalamus or cerebellum further examination. Recent literature explains why in some patients FLAIR was reviewed using the search terms hyperintenisty and diffusion restriction “perfusion CT”, “MRI”, “MR”, “ postictal”, can be seen in these structures. The “ictal”, “todd’s paresis” and “status prominent vasculature can be explained epilepticus”. through distortion of auto-regulation Results: The clinical data, EEG results leading to vasodilatation. The lepto and imaging studies of thirty-nine meningeal enhancement and sulcal patients were reviewed. After applying FLAIR hyperintensity can be attributed to the inclusion criteria, a cohort of twenty the disruption of the blood-brain barrier patients was withheld, of which eight and resulting influx of proteins in the subpatients received their MRI during status arachnoid space. The susceptibility of the epilepticus (ictal phase) and twelve in the hippocampus to these signal alterations postical phase. Eight patterns of signal remains unclear. alterations were recognized: cortical Conclusion: In conclusion, the most FLAIR hyperintensity and diffusion common MR imaging patterns that can NEURORADIOLOGY

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be caused by seizures in the ictal or postictal phase are FLAIR hyperintensity and diffusion restriction in typical locations such as the cortex, hippocampus and thalamus. These signal alterations resolve over time in the great majority of cases. Before attributing the imaging findings to an ictal or a postical event, other possible diagnoses (e.g. arterial ischemia, venous thrombosis, infection, neoplasm, PRES, metabolic encephalo pathies), some of which can also cause seizures, should be excluded since the imaging findings are non-specific. The distribution of signal changes and the evolution over time however can help in making the diagnosis. References 1. Nuno C., Breia P., Soares P., Saraiva P., Calado S., Jordão C., Vale J. The Electroclinical-Imagiological Spectrum and Long-Term Outcome of Transient Periictal MRI Abnormalities. Epilepsy Research, 2010, 91: 240-252. 2. Chatzikonstantinou A., Gass A., Förster A., Hennerici M.G., Szabo K.: “Features of Acute DWI Abnormalities Related to Status Epilepticus. Epilepsy Research, 2011, 97: 45-51. 3. Cianfonia A., Caulob M., Cerasec A., Della Marcad G., Falconee C., Di Lellae G.M., Gaudinoe S., Edwardsf J., Colosimoe C.: Seizure-induced brain lesions: A wide spectrum of variably reversible MRI abnormalities. Eur J Radiol, 2013, 82: 1964-1972. 4. Cole A.J.: Status Epilepticus and Periictal Imaging. Epilepsia, 2004, 45: 72-77. 5. Milligana T.A., Zamani A., B romfields E.: Frequency and patterns of MRI abnormalities due to status epilepticus. Seizure, 2009, 18: 104-108.

1. Department of Radiology, UZ Gent, Ghent, Belgium.

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