JBR 2011-6 by office

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WETTEREN 1

P 702083

Volume 94 Page 309-368

November-December Bimonthly

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2011

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

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

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

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JBR-BTR ♦ 94/6 ♦ 2011 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

Small bowel ischemia caused by strangulation in complicated small bowel obstruction. CT findings in 20 cases with histopathological correlation. W. Wiesner, K.Mortelé . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309 MDCT imaging before transcutaneous aortic valve implantation: rationale and measurements. L. Ardies, Th. Vancauwenberghe, T. De Beule, M. de Booij, P.K. Van hoenacker . . . . . . . . . . . . . . . . . . . . . . . . . . 315 Non-invasive grading of astrocytic tumours from the relative contents of myo-inositol and glycine measured by in vivo MRS. A.P. Candiota, C. Majos, M. Julià-Sapé, M. Cabanas, J.J. Acebes, A. Moreno-Torres, J.R. Griffiths, C. Arus . . 319 Metastatic renal cell carcinoma presenting as a breast mass in a woman with history of primary breast cancer. C. Balliauw, B. Termote, A. Van Steen, P. Moerman, M.R. Christiaens, C. Van Ongeval . . . . . . . . . . . . . . . . . . . . 330 Diastematomyelia: pre- and postnatal multimodal diagnostic approach. V. Passoglou, M. Tebache, L. Collignon, E. Weerts, J.P. Misson, L. Rausin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333 Secondary retroperitoneal teratoma. Ph. Grandjean, E. Danse, F. Thys, J.P. Cosyns, F.X. Wese . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 336 Retention of an ingested small blunt foreign body. K.C. Ng, E. Mansour, E. Eguare . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339 Pott’s puffy tumor: CT and MRI findings. F. Acke, M. Lemmerling, Ph. Heylbroeck, G. De Vos, K. Verstraete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343 Spontaneous soccer-induced pneumomediastinum in a 39-year-old man. K. De Smet, B. Ilsen, J. De Mey, M. De Maeseneer, W. Vincken . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346 Cortical associated diverticular perforation. L. Goethals, K. Nieboer, K. De Smet, F. De Geeter, N. Hosseinpour, E. Van Eetvelde, J. de Mey . . . . . . . . . . . . 348

IMAGES IN CLINICAL RADIOLOGY Unsuspected case of congenital bronchial atresia in work-up for supposed pulmonary AVM. J. Toirkens, B. Op de Beeck, M. Spinhoven, A. Snoeckx, R. Salgado, T. Van der Zijden, P.M. Parizel . . . . . . . . . 350 A complicated fourth branchial fistula. N. Bottossso, C. Coibion, M. Dirix, J. Khamis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351 Particular location of a cardiac pacemaker lead. V. Hamoir, X. Hamoir, J. Kirsch . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 352 Selective spleen SPECT/CT. G. Ceulemans, A. Sermeus, D. Verdries, M. Keyaerts, B. Ilsen, M. Kichouch, M. De Ridder, H. Everaert . . . . . 353 Enchondroma protuberans of the rib. L.J. Ceulemans, L. Verheyen, F.M. Vanhoenacker, R. De Wyngaert, J. De Leersnyder . . . . . . . . . . . . . . . . . . . . . 354 Unexpected pyomyositis of right buttock. S. Van Nieuwenhove, F. Haven, L. Ghijselings, J. Pringot, P.Matthys . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355 Focal infarction of lesser omentum. M. Bersou, Ch. Heylen, P. Matthys, J. Pringot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 356 Typical CT and MRI features of cortical laminar necrosis. J.L. Samain, F. Haven, M. Gille, P. Matthys . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357

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Proceedings of RBRS section Breast Imaging, Leuven, 07.06.2011 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358 News from the Universities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 362 SRBR-KBVR General Assembly, Brussels, 19.11.2011 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363 Honorary Membership Nominees . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363 President-Elect Address . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363 Forthcoming Courses and Meetings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 367 Instructions to Authors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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

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

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02-voorblz-11-6_Opmaak 1 16/12/11 09:02 Pagina 2

Editor: J. Pringot

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

Managing Editor: P. Seynaeve

President: B. Desprechins Vice-presidents: J.F. De Wispelaere, R. Hermans

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

Past-President: M. Lemort General Secretaries: F. Avni, J. Verschakelen Executive Secretaries: D. Henroteaux, M. Spinhoven Treasurers: D. Brisbois, A. Van Steen Coordinators of continuing education: E. Coche, G. Villeirs Coordinators of professional defence: C. Delcour, D. Bielen Webmasters: J. de Mey, J. Struyven

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

B. Op de Beeck, E. Danse

Bone and joints

P. Van Dyck, J.F. Nisolle

Breast imaging

C. Van der Merckt, A. Van Steen

Cardiac imaging

R. Salgado, O. Ghekière

Cardiovascular and interventional radiology

G. Maleux, M. Laureys

Chest radiology

B. Ghaye, W. De Wever

Head and neck radiology

J. Widelec, R. Hermans

Neuroradiology

P. Demaerel, N. Sadeghi

Pediatric radiology

B. Desprechins, L. Rausin

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

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

–

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

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

(continued on p. 368)

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

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

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

Dynamische tomografie:

Onmiddellijk na een bolus injectie.

Vertraagde tomografie:

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

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

Imagerie dynamique

Immédiatement après l’injection en bolus

Imagerie retardée

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

Hersenen en ruggenmerg

Tot 60 minuten na toediening.

Système nerveux central

Jusqu’à 60 minutes après administration

MRA

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

ARM

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

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

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

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

www.bayerhealthcare-diagnostics.be

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 309-314.

SMALL BOWEL ISCHEMIA CAUSED BY STRANGULATION IN COMPLICATED SMALL BOWEL OBSTRUCTION. CT FINDINGS IN 20 CASES WITH HISTOPATHOLOGICAL CORRELATION W. Wiesner1, K. Mortele2 Purpose: To analyze the CT findings in 20 cases of complicated small bowel obstruction with surgically and histopathologically proven small bowel ischemia, caused by extrinsic venous outflow obstruction of the affected bowel loops and to discuss the question, if bowel wall thickening, abnormal bowel wall enhancement, ascites and mesenteric stranding correlate with the severity of bowel wall damage. Methods: CT scans of 20 patients with surgically an histopathologically proven isolated small bowel ischemia caused by strangulation (10 patients with only partial mural, still potentially reversible small bowel ischemia and 10 patients with transmural irreversible small bowel infarction) were analyzed retrospectively with special emphasis on the presence and degree of small bowel wall thickening, enhancement of the bowel wall, ascites and/or mesenteric stranding at CT and the question whether these findings correlated with the severity of ischemic small bowel wall damage in these patients. Results: Small bowel wall thickening, local mesenteric stranding and ascites were equally common in both groups of patients, regardless of whether obstruction and strangulation related small bowel ischemia was transmural or only partial mural. Out of those patients who were examined by contrast enhanced studies no patient showed lack of enhancement along the ischemic bowel loops. Conclusion: Although highly sensitive and specific for small bowel ischemia in complicated small bowel obstruction, the presence and degree of bowel wall thickening, ascites or local mesenteric stranding at CT do not correlate with the severity of ischemic small bowel wall damage and even the presence of bowel wall enhancement does not exclude severe and potentially transmural bowel infarction in these patients. Key-words: Intestines, stenosis or obstruction â&#x20AC;&#x201C; Intestines, CT.

Acute bowel ischemia is a complex entity that may affect both the large and the small bowel and that can result from a variety of different conditions that critically disturb intestinal perfusion (1, 2). The clinical, radiological and histopathological presentation of bowel ischemia may show a wide range. In partial mural bowel ischemia the ischemic damage of the intestine may be limited to the mucosa, or it may be more pronounced and affect also the submucosal space or the muscularis propria. Contrarily, in transmural bowel ischemia (ie. bowel infarction) the ischemic bowel wall damage involves all layers and typically represents a full thickness necrosis of the affected bowel wall. While mild ischemic bowel lesions involving only the mucosa are typically self limiting and reversible, more pronounced ischemic bowel wall damage involving also the submucosal space or the muscularis propria may lead to scarring and strictures as a late complication. Therefore, surgical bowel resection is not absolutely necessary

in mild and only partial mural bowel ischemia, whereas transmural bowel infarction definitely requires surgical resection of the necrotic bowel segments. Over the past years CT has become the key imaging modality for the detection of acute bowel ischemia. It is well known that bowel ischemia may present with a wide range of imaging findings at CT including bowel wall thickening, absent or heterogeneous bowel wall enhancement, hypo- or hyperattenuating bowel wall thickening, mesenteric fluid and ascites, pneumatosis or even mesenteric or portal venous gas (2-9). Although many of these CT findings are not highly specific, the diagnosis of intestinal ischemia can be made with a high accuracy by CT if there are additional radiological or clinical findings suggesting the diagnosis of acute bowel ischemia. In cases of arterial bowel ischemia these include severe arteriosclerosis, occlusion of visceral vessels, aortic dissection, severe mural thrombosis of the aorta, infarctions in other organs such as spleen or kidneys

From: 1. Klinik Stephanshorn, St.Gallen, Kantonal Hospital Herisau, Herisau, Kantonal Hospital Heiden, Heiden, Radiologie Nordost, Heerbrugg, Switzerland, 2. Brigham and Women`s Hospital, Harvard Medical School, Boston, USA. Address for correspondence: Pr Dr med. W. Wiesner, M.D., Klinik Stephanshorn, Brauerstrasse 95, CH-9016 St.Gallen, Switzerland. E-mail: wwiesner@bluewin.ch

(suggesting thromboembolic disease), or just a typical and suggestive clinical setting such as a positive medical history of prior abdominal aortic surgery, retrograde angiography, atrial fibrillation, cardiovascular disease, hypotensive episodes, hematological disorders, vasculitis or known administration of certain drugs (10-21). However, the majority of histopathologically proven cases of small bowel ischemia in our daily routine represent venous ischemia, caused by extrinsic compression of mesenteric veins in patients with complicated small bowel obstruction, in which the presence of bowel ischemia usually represents only an additional, but surely important finding, since it strongly influences the further management of these patients. It is known, that in context with clinical and radiological findings of acute small bowel obstruction the presence of small bowel wall thickening, ascites and mesenteric stranding at CT has a high sensitivity and specificity for the diagnosis of strangulation induced venous small bowel ischemia (22-24). However, differentiation between partial mural and transmural bowel ischemia is difficult by CT as long as perforation has not yet occurred and as long as pronounced pneumatosis or portal venous gas do not indicate a more severe and potentially

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Table I. â&#x20AC;&#x201D; Results. Imaging findings (n = 20)

Partial mural ischemia (n = 10)

Transmural infarction (n = 10)

Bowel wall thickening Mesenteric stranding Peritoneal fluid / ascites

5 (50%) 8 (80%) 7 (70%)

6 (60%) 8 (80%) 8 (80%)

One or two findings All three findings

5 (50%) 5 (50%)

3 (30%) 6 (60%)

4-7 mm (mean 5.8 mm) 5/5 (100%)

4-12 mm (mean 7.2 mm) 4/4 (100%)

The patients were divided into two groups based on the severity of small bowel ischemia. Group 1 consisted of 10 patients with isolated transmural small bowel infarction secondary to strangulation obstruction. Group 2 consisted of 10 patients with isolated, but only partial mural small bowel ischemia secondary to strangulation obstruction. 9 patients were male, 11 were female. The age of our patients ranged from 28 to 89 years with a mean age of 62.75 years. 15 patients underwent surgery within 12 hours after their CT examination. 2 patients of group 1 were operated the next day (within 24 hours) after their CT examination and one patient of group 1 even with a delay of 3 days. However, these patients were not excluded from our study since they had shown positive findings of bowel ischemia (wall thickening, stranding and ascites in two and pronounced ascites in one of these patients) already at the time of their CT examination. In 2 patients of group 2 the time delay between CT and abdominal surgery was also 1224 hours, but these patients were also not excluded from our study since one of them showed wall thickening, ascites and stranding and the other pronounced ascites already at the time of their CT examination and since they both showed subacute partial mural bowel ischemia at the time of surgery. In all patients the ischemic parts of the small bowel were resected and histopathological analysis was therefore available in all cases (Table I).

trast was administered with a volume of 100 ml and an injection rate of 2 ml/second. If intravenous contrast was given, image acquisition was performed at a portal venous phase with a scan delay of 70 seconds. Slice thickness and table feed ranged from 8/8 mm to 10/10 mm and window/center was 350/50. All patients received oral contrast prior to their CT examination although in the majority of cases opacification of the entire small bowel and especially of those segments that were strangulated was not reached at the time of scanning. All CT scans were analyzed retrospectively by two experienced radiologists with special interest in gastrointestinal radiology who were unaware of the surgical and histopathological results. Special emphasis was given to describe abnormal small bowel wall thickening of more than 2 mm, local mesenteric stranding and ascites if present and to determine the degree of each one of these findings. Bowel wall enhancement and presence or absence of mesenteric venous engorgement were analyzed only in nine patients according to the fact that eleven CT examinations were performed as unenhanced studies only. Finally, all surgical and histopathological reports on the resected small bowel wall segments were reviewed. Transmural small bowel infarction was defined as continuous ischemic full thickness necrosis of the affected small bowel wall with or without serositis, whereas partial mural small bowel ischemia was defined as ischemic necrosis limited to the mucosa and submucosa with or without parts of the muscularis propria but without continuous necrosis of all bowel wall layers and without serositis. Finally the presence and degree of bowel wall thickening, ascites and mesenteric stranding at CT was compared to the severity of small bowel ischemia as determined by histopathology in all patients.

Bowel wall thickness Bowel wall enhancement

transmural infarction. Furthermore, absence of bowel wall enhancement seems to be a highly specific CT finding in cases of arterio-occlusive bowel infarction but, this is probably not valid for cases of venous ischemia without thrombosis of the mesenteric veins. Therefore the present study was initiated to evaluate retrospectively if the presence and degree of bowel wall thickening, bowel wall enhancement, mesenteric stranding or ascites correlate with the severity of ischemic bowel wall damage in cases of obstruction and strangulation related small bowel ischemia. Material and methods Patients 20 consecutive patients with histopathologically proven isolated small bowel ischemia were included into our study. Patients were identified by reviewing the histopathological reports of all patients who underwent small bowel resection due to small bowel obstruction and who showed ischemia or infarction. Patients in whom ascites could have had other causes, such as liver cirrhosis or peritoneal carcinomatosis and patients with focal or diffuse neoplastic or inflammatory diseases affecting the bowel, the mesentery or the peritoneal cavity were not included into our study as well as patients in whom transmural bowel infarction could be suspected by CT already on the basis of pronounced pneumatosis and/or portal venous gas or free intraperitoneal air and/or peritonitis indicating intestinal perforation. Therefore, our study population consisted exclusively of patients with non-perforated complicated obstruction of their small bowel, caused by adhesions or herniations with or without volvulus, and with subsequent also purely mechanically induced extrinsic venous small bowel ischemia.

Image acquisition and image analysis CT scans were performed using a Somatom Plus 4 scanner (Siemens, Erlangen, Germany). 9 CT examinations were contrast enhanced studies, while 11 CT examinations were unenhanced studies. In contrast enhanced studies, intravenous con-

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SMALL BOWEL ISCHEMIA CAUSED BY STRANGULATION — WIESNER et al

Fig. 1. — Unenhanced spiral CT of the abdomen in a patient with acute small bowel obstruction shows thickened small bowel loops (small arrows), local mesenteric stranding (arrowheads) and small amounts of free intraperitoneal fluid (large arrow). Surgery confirmed strangulation obstruction with ischemic small bowel loops and histopathological analysis showed transmural small bowel infarction with full thickness necrosis of the affected small bowel walls.

Results In those 10 patients who presented with transmural small bowel infarction secondary to complicated small bowel obstruction (Group 1), bowel wall thickening was present in 6 patients (60%) and ranged from 412 mm (mean 7.2 mm). Ascites was present in 8 patients (80%) and mesenteric stranding was present in 8 patients (80%). 6 patients (60%) showed all 3 of above findings, 1 patient (10%) showed two of above CT findings and 2 patients (20%) only one of above CT findings. One patient of group 1 showed neither wall thickening, nor mesenteric stranding nor ascites at CT. However, in all four patients from group 1 who received intravenous contrast the bowel walls showed contrast enhancement. In those 10 patients who presented with only partial mural small bowel ischemia secondary to complicated small bowel obstruction (Group 2), bowel wall thickening was present in 5 patients (50%) and ranged from 4 mm to 7 mm (mean 5.8 mm). Ascites was present in 7 patients (70%) and mesenteric stranding was present in 8 patients (80%). 5 patients (50%) showed all 3 of above findings and 5 patients (50%) presented with only one of

311

Fig. 2. — Contrast enhanced spiral CT of the abdomen in a patient with acute small bowel obstruction shows thickened small bowel loops (small arrows), local mesenteric stranding (arrowheads) and free intraperitoneal fluid (large arrows). Surgery confirmed strangulation obstruction with ischemic small bowel loops but histopathological analysis showed only early ischemia limited to the mucosa and submucosa of the affected small bowel walls.

above CT findings. However, in all five patients from group 2 who received intravenous contrast the bowel wall showed contrast enhancement. Overall small bowel wall thickening, bowel wall enhancement, mesenteric stranding and/or ascites were comparably common in those patients who proved to have transmural small bowel infarction secondary to complicated small bowel obstruction as compared to those patients who had only partial mural small bowel ischemia (Figs. 1-5). Differentiation between transmural and partial mural small mall bowel ischemia in strangulation obstruction was not possible by CT since some patients with mild bowel ischemia limited to the inner layers (mucosa and submucosa) showed already very pronounced bowel wall thickening, ascites and mesenteric stranding at CT, comparable to the findings of some patients with transmural ischemia, whereas others with transmural ischemia presented with much less pronounced CT findings (Fig. 5). Discussion Over the past years the value of CT in diagnosing acute bowel ischemia has been well estab-

lished (1-9). The causes for acute bowel ischemia range from embolic, thrombotic or atherosclerotic occlusion of the mesenteric arteries (10, 11), primary or secondary thrombotic occlusions of the mesenteric veins (12, 13) certain hematological disorders (12-14), various forms of vasculitis (14-18) to various nonocclusive conditions (19-21). Nevertheless, one of the more common reasons for small bowel ischemia encountered in our daily routine is complicated small bowel obstruction including closed loop obstruction with strangulation by adhesions, incarceration in internal or external hernias or small bowel volvulus in which the involved small bowel may show venous or hemorrhagic ischemia and/or infarction that is caused by mechanically induced extrinsic occlusion of the mesenteric veins with or without subsequent mesenteric venous thrombosis (22-23). In cases of small bowel obstruction patients are often not able to drink enough contrast material prior to their CT – examination and administration of oral contrast is also not absolutely necessary for the CT diagnosis under such circumstances, since the orally ingested contrast material will often not reach the point of obstruction in these cases

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JBR–BTR, 2011, 94 (6)

Fig. 3. — Contrast enhanced spiral CT of the abdomen in a patient with acute small bowel obstruction shows thickened small bowel loops (small arrows), local mesenteric stranding (arrowheads) and small amounts of free intraperitoneal fluid (large arrow). Surgery confirmed strangulation obstruction with ischemic small bowel loops and histopathological analysis showed transmural small bowel infarction with full thickness necrosis of the affected small bowel walls.

Fig. 5. — Contrast enhanced spiral CT of the abdomen in a patient with acute small bowel obstruction shows only dilated bowel loops without bowel wall thickening, but large amounts of free intraperitoneal fluid (large arrows). Surgery confirmed strangulation obstruction with ischemic small bowel loops and histopathological analysis showed transmural small bowel infarction with full thickness necrosis of the affected small bowel walls.

Fig. 4. — Contrast enhanced spiral CT of the abdomen in a patient with acute small bowel obstruction due to an abdominal wall hernia shows thickened small bowel loops (small arrows), local mesenteric stranding (arrowheads) and free intraperitoneal fluid (large arrow). Surgery confirmed strangulation obstruction with ischemic small bowel loops but histopathological analysis showed only early ischemia limited to the mucosa and submucosa of the affected small bowel walls.

anyway. However, since it is not easy to know in advance what`s awaiting you, administration of some oral contrast prior to the CT – examination may be helpful for detection of perforations and especially also to pronounce the prestenotic dilatation of bowel loops and to depict the

exact level and degree of obstruction. In contrast to inflammatory bowel wall thickening, in which oral opacification of thickened and hyperemic bowel walls may be even contraproductive, since it may sometimes masquerade the hyperdense thick-

ening of the bowel walls, this problem does usually not occur in strangulation related small bowel ischemia, where the thickened bowel walls are relatively hypodense due to edema, and therefore, may be usually well depicted – regardless if the lumen of the affected bowel loops is filled with contrast material or not. Intravenous contrast administration on the other hand is important in this setting, and although many patients of our retrospective study had been examined unfortunately by unenhanced CT only, one should at least try to perform such CT – studies as unenhanced and contrast enhanced studies with acquisition of a portal – venous scan with a time delay of around 70 seconds in order to be able to analyze the enhancement pattern of the bowel walls and also not to miss potentially important additional findings, inlcuding for example an associated secondary mesenteric venous thrombosis. Although many CT findings may be encountered in acute bowel ischemia, unfortunately most of them are non-specific since bowel wall thickening, hypo- or hyperattenuating bowel walls, inhomogeneous bowel wall enhancement, mesenteric stranding and ascites may occur in many non-ischemic conditions as well. Therefore, acute bowel ischemia may be diagnosed by CT with a higher accuracy only if CT

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SMALL BOWEL ISCHEMIA CAUSED BY STRANGULATION — WIESNER et al

also shows the primary cause of bowel ischemia (such as occlusions of mesenteric vessels or infarctions of other organs suggesting embolic disease), more specific signs of bowel ischemia (such as pneumatosis or portal-venous gas) or if there is a highly suggestive patients history or a very typical clinical setting. Therefore, if small bowel wall thickening, mesenteric stranding and/ or ascites are encountered in a clinical and radiological setting of acute small bowel obstruction, the reported specificities of each one of these CT findings for strangulation obstruction with associated small bowel ischemia may rise as high as to 78%, 90% and 76%, respectively, and the presence of two of these CT findings may even further increase the specificity of CT for the diagnosis of bowel ischemia in small bowel obstruction to 94-99% (23). Nevertheless, although the overall sensitivity and negative predictive value of helical CT in diagnosing strangulation obstruction and bowel ischemia in complicated small bowel obstruction has been reported to be as high as 96% and 99%, respectively, it is very difficult, if not impossible to estimate the severity of bowel ischemia as long as transmural bowel infarction with perforation has not yet occurred under these conditions and as long as there is absence of free intraperitoneal air, signs of diffuse peritonitis or pronounced pneumatosis intestinalis and portal-venous gas (24-26). Unfortunately in cases of complicated small bowel obstruction bowel wall thickening, mesenteric stranding and ascites do result from venous congestion and transudation, which is caused by mesenteric venous outflow obstruction caused by compression and/or strangulation of mesenteric veins with or without subsequent mesenteric venous thrombosis. Therefore, and since it is impossible to estimate the degree of compromise of the mesenteric venous circulation as well as the duration of preexistent mesenteric venous outflow obstruction at the time of the CT examination the presence of above CT findings can not allow to estimate the severity of the ischemic damage to the small bowel wall according to the fact, that edema of the bowel wall, intramural hemorrhage and edema within the adjacent mesentery as well as fluid in the mesentery and in the peritoneal cavity may develop earlier under these circumstances than subsequent transmural infarction and

full thickness necrosis of the involved bowel segments. This is shown by our findings, where the presence of bowel wall thickening, mesenteric stranding and ascites at CT was equally encountered in both groups of patients, regardless whether their obstruction related small bowel ischemia was transmural or only partial mural. The fact that the time delay between CT and surgery was more than 12 hours in three patients of group 1 and in two patients from group 2 may be a limitation of our study, but we can argue that the three cases of group 1, in whom the time delay between CT and surgery has been more than 12 hours might have had only partial mural bowel ischemia at the time of their CT examination and that their ischemic bowel wall damage just progressed to transmural bowel infarction in the meantime. This would only support our results which show that the CT findings of strangulation obstruction and subsequent bowel ischemia may be observed in earlier stages allready – at a time when the obstruction related bowel ischemia is only partial mural and, therefore, still potentially reversible. According to the studies of Balthazar and Zalcman CT has a sensitivity of 83% and 96%, a specificity of 93% and 93%, a positive predictive value of 79% and 72% and a negative predictive value of 95% and 99% for the diagnosis of strangulation related small bowel ischemia in complicated small bowel obstruction. Although small bowel ischemia in strangulation obstruction may be missed by CT as shown by older studies including non-helical CT scans, the latest study of Zalcman et al, including only results from helical CT scans shows that the sensitivity, specificity and negative predictive value of CT in diagnosing strangulation obstruction range from 93-99%. The significantly lowest value of this study is found in the positive predictive values (72%) and according to our findings it may be speculated if this result is probably underestimated. The study of Zalcman showed that out of those 23 patients with true positive CT scans for strangulation obstruction only 14 patients needed bowel resection, which means that the remaining 9 patients with proven bowel ischemia must have had reversible ischemia which did not request bowel resection. Therefore, one may further speculate that those cases from the stud-

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ies of Balthazar and Zalcman, who have shown CT findings of bowel ischemia but who did not undergo surgery and who therefore were counted as „false positive“ did probably not represent false positive cases throughout, but probably at least partially also cases with partial mural and reversible bowel ischemia. Taking these considerations into account, the high specificity of CT in diagnosing strangulation obstruction would not further increase singificantly according to the fact that the majority of patients with small bowel obstruction do not have bowel ischemia. In contrast, the positive predictive value of CT in the detection of strangulation obstruction might increase if those cases that were not operated and therefore interpreted as false positive (5/24 patients in the study of Balthazar and 7/32 patients in the study of Zalcman) could be counted as false positive for bowel infarction but as true positive for partial mural bowel ischemia. However, it is suggestive that the occurrence of bowel wall thickening, mesenteric stranding and ascites preceeds the occurrence of bowel ischemia in certain cases of strangulation obstruction and, therefore, some of these “false positive cases” reported by Balthazar and Zalcman could represent really false positive cases, similarily as it is also surely possible that some of our patients from group 2 might have developed partial mural bowel ischemia only in the meantime between CT-examination and surgery. Nonetheless, the bowel wall mucosa is very sensitive to ischemia and a venous outflow obstruction, that causes transudation into the bowel wall, into the mesentery and/or the peritioneal cavity will quite rapidly also induce some ischemic changes of the inner bowel wall layers. Therefore, neither the presence of bowel wall thickening nor the presence of mesenteric stranding or ascites will allow clear differentiation between transmural small bowel infarction and only partial mural small bowel ischemia in complicated small bowel obstruction. Although absence of bowel wall enhancement is one of the most specific CT findings in arterioocclusive small bowel infarction, this is obviously not always valid for cases of venous ischemia, where the arterial perfusion of affected bowel loops seems to be maintained for a quite long time – regardless whether

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partial mural bowel ischemia has already progressed to hemorrhagic necrosis â&#x20AC;&#x201C; and the crucial differentiation between potentially reversible partial mural bowel ischemia and irreversible transmural bowel infarction can obviously be made only intraoperatively under these circumstances. References 1. Wolf E.L.: Ischemic diseases of the gut. In: Gore R.J., Levine M.S., Laufer I. eds. Textbook of gastrointestinal radiology. Philadelphia, Pa: Saunders, 1994, 2694-2706. 2. Haglund U., Bergqvist D.: Intestinal ischemia - the basics. Langenbecks Arch Surg, 1999, 384: 233-238. 3. Alpern M.B., Glazer G.M., Francis I.R.: Ischemic or infarcted bowel: CT findings. Radiology, 1988, 166: 149-152. 4. Klein H.S., Lensing R., Klosterhalfen B., Toens C., Guenther RW. Diagnostic imaging of mesenteric infarction. Radiology, 1995, 197: 79-82. 5. Rha S.E., Ha H.K., Lee S.H., Kim J.H., Kim J.K., Kim J.H., Kim P.N., Lee M.G., Auh Y.H. CT and MR findings of bowel ischemia from various primary causes. Radiographics, 2000, 20: 29-42. 6. Taourel P.G., Deneuville M., Pradel J.A., Regent D., Bruel J.M. Acute mesenteric ischemia: diagnosis with contrast enhanced CT. Radiology, 1996, 199: 632-636. 7. Ha H., Rha S.E., Kim A.Y., Auh Y.H.: CT and MR diagnoses of intestinal ischemia. Semin Ultrasound CT MR, 2000, 21: 40-55. 8. Perez C., Llauger J., Puig J., Palmer J.: Computed tomographic findings in

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lupus erythematosus: massive mesenteric infarction. Hepatogastroenterology, 2000, 47: 761-762. Mirvis S.E., Shanmuganathan K., Erb R.: Diffuse small-bowel ischemia in hypotensive adults after blunt trauma (shock bowel): CT findings and clinical significance. AJR, 1994, 163: 1375-1379. John A.S., Tuerff S.D., Kerstein M.D.: Nonocclusive mesenteric infarction in hemodialysis patients. J Am Col Surg, 2000, 190: 84-88. Kornecki A., Shemie S.D., Daneman A., Ein S.: Nonocclusive small bowel infarction in familial dysautonomia syndrome. J Pediatr Surg, 1999, 34: 623-625. Balthazar E.J., Liebeskind M.E., Macari M.: Intestinal ischemia in patients in whom small bowel obstruction is suspected: evaluation of accuracy, limitations, and clinical implications of CT in diagnosis. Radiology, 1997, 205: 519-522. Zalcman M., Sy M., Donckier V., Closset J., Van Gansbeke D.: Helical CT signs in the diagnosis of intestinal ischemia in small bowel obstruction. AJR, 2000, 175, 1601-1607. Wiesner W., Mortele K.J., Glickman J.N., Ji H., Ros P.R.: Pneumatosis intestinalis and portomesenteric venous gas in intestinal ischemia: Correlation of CT findings with severity of ischemia and clinical outcome. AJR, 2001, 177: 1319-1323. Wiesner W., Khurana B., Ji H., Ros P.R.: CT of acute bowel ischemia. Radiology, 2003, 226: 635-50 Wiesner W., Hauser A., Steinbrich W.: Accuracy of Multidetector Row Computed Tomography for the diagnosis of acute bowel ischemia in a non selected study population. Eur Radiol, 2004, 14: 2347-56.

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MDCT IMAGING BEFORE TRANSCUTANOUS AORTIC VALVE IMPLANTATION: RATIONALE AND MEASUREMENTS L. Ardies1, Th. Vancauwenberghe1, T. De Beule1, M. de Booij2, P.K. Vanhoenacker1 Since its introduction in 2002, transcatheter aortic valve implantation (TAVI) has assumed growing importance in the treatment of patients with severe aortic stenosis (AS), because it offers a much less invasive alternative for those in high risk for surgery. Good early results and advances in percutaneous valve technology have led to a substantial increase in procedural success rate and number of patients undergoing this less invasive treatment. Pre-procedural screening of several anatomic factors to assess the feasibility of this technique is important. Multidetector row computed tomography (MDCT) is the technique of choice in assessing these factors. This technical note aims to describe and illustrate the key elements that need to be evaluated before the procedure. Key-word: Aortic valve.

Aortic valve stenosis is one of the most frequent causes of valvular disease in the elderly population and is often associated with other cardiovascular comorbidities causing these patients to be at high risk for surgery. A study by Iung et al. (1) showed us that about 33% of patients with severe AS and severe symptoms are high-risk candidates for surgery. This emphasizes the need for a minimal invasive technique in this population of patients. Since its first use in 2002 (2), TAVI has become a good alternative for high-risk patients. Procedural success rates between 93-95% and low 30 day mortality rate (3) have led to a dramatic increase in percutaneous procedures and development of new devices. Although TAVI is less invasive than conventional valve replacement, it needs an accurate preprocedural workup and patient selection to minimize complications and maximize success. Cardiovascular imaging plays an important role in screening and optimal patient evaluation. At the moment 2 TAVI technologies have received CE-approval (Fig. 1): the CoreValve technology and the Cribier Edwards SAPIEN valve. The CoreValve technique uses a self-expanding valve with an 18 French delivery system, which allows access to the femoral or subclavian artery. The Edwards SAPIEN on the other hand is a balloonexpendable valve with a 24-26 French delivery system, thus only suitable for a retrograde transfemoral or anterograde transapical approach.

B Fig. 1. — A. CoreValve. B. Edwards SAPIEN

Pre-operative imaging As mentioned before, preprocedural TAVI planning heavily relies on imaging for patient selection and sizing (4). However, to date there isn’t a gold standard for evaluating the aortic valve (5). Echocardiography has emerged as the method of choice in evaluating hemodynamic status and severity of aortic stenosis. However, transthoracic echocardiography may lead to suboptimal results in patients with poor acoustic windows (thick or deformed chest walls, small hearts, obesity, and pulmonary disease). In addition, echocardiography is very operator dependent and limited in quantifying aortic valve calcification, since only indirect signs, such as increased echogenicity and thickening of the aortic valve leaflets are usable. Further, echocardiography is limited by its 2-dimensional character, making it difficult to make correct calculations of the aortic root diameters. Due to the complex anatomy of the aortic root and

From: 1. Department of Radiology and Imaging, OLV Ziekenhuis, Aalst, Belgium and 2. Department of Radiology, Atrium MC Parkstad, Heerlen, The Netherlands. Address for correspondence: Dr L. Ardies, M.D., OLV Ziekenhuis Aalst, Moorselbaan 164, B-9300 Aalst, Belgium. E-mail: lenz_ardies@hotmail.com

annulus an adequate 3D imaging modality is required for accurate reproduction of aortic root and annulus measurements (6). Multidetector computed tomography (MDCT) has the advantage of providing reproducible 3-dimensional images with a high spatial and temporal resolution, emerging it as a promising method for non-invasive valve and coronary imaging. Further MDCT has the merit of evaluating peripheral artery and thoracic aorta anatomy and morphology and revealing several incidental nonvascular findings. Still, the major drawback of using MDCT for imaging is the limitation in repetitive scanning because of the hazardous radiation, although development of the new generation MDCT’s has led to significant reduction in radiation dose (7-9). Scan protocol All our pre-TAVI examinations are performed with a 128 multi-detector row computed tomography (CT) scanner (Somatom Definition Flash, Siemens Erlangen, Germany), upgraded to allow low-dose acquisitions (Caredose4D, Siemens). Collimation was 128 x 0,6 mm. Tube voltage was 120 kV and current 340 mAs. At our institution we seper-

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Fig. 2. — A: The lateral angulation (alpha angle, red line), measured on the coronal view. B: The cranio-caudal angulation (beta angle, blue line), measured on the sagittal view.

atly aqcuire images of the the heart and iliac arteries, instead of scanning them in one volume. Cardiac images are obtained with prospective triggering at the 70% phase of R-R cardiac cycle to ensure minimum motion artifacts, under electrocardiographic gating and with longitudinal coverage of the entire thoracal aorta. Gantry rotation time was 280 ms. For the aqcuisition of the iliac arteries, we use a longitudinal coverage of the infrarenal aorta, iliac and common femoral arteries and a gantry rotation time of 500 ms. A bolus of 100 ml contrastmedium (Iopromide 370 mg/ml <Ultravist, Bayer Schering Pharma AG, Berlin, Germany>) was given intravenously at 5 ml/s for scanning of the heart, followed by a second bolus of 20 ml for scanning of the infrarenal aorta and iliacs. To ensure optimal contrast enhancement bolus tracking was used at the aorta ascendens level, with the trigger at 100 HU. No beta-blockers were administered. Computed data were processed using a B30f medium-smooth kernel. Thickness of reconstructed images was 0.6 mm. Data were sent to an external workstation (Vitrea Core 1.3, Vital) where images were analyzed. Image analysis We first measured the angulation of the aortic valve plane, combining the lateral angulation calculated from the coronal plane, and craniocaudal angulation from the sagital view, as described by Decramer et al (10) (Fig. 2). To measure the aortic annulus diameter we used a 2-step method. The first step was based on a double oblique transverse view with reconstruction of a plane including the aortic root, the left ventricular outflow tract, and the left atrium and ventricle (3-chamber view), where

Fig. 3. — Double oblique transverse view, 1: Ascending aorta maximum diameter, 2: Sino-tubular junction maximum diameter, 3: Sinus of Valsalva maximum diameter, 4: Aortic valve annulus maximum and minimum diameter. 5: double oblique transverse view, left ventricle outflow tract maximum and minimum diameter. 6: coronal view in systole of the height of the coronary ostia relative to the aortic valve annular plane.

we could measure the diameter of the annulus at the hinge points of the leaflets. Second, we obtained a slice perpendicular to the aortic root and measure the diameters of the ascending aorta, the sino-tubular junction, the sinus of Valsalva, the aortic valve annulus and the left ventricle outflow tract (Fig. 3). Contribution of MDCT to preoperative screening and presurgical work-up Adequate sizing and probe selection are required for correct apposition of the prosthesis into the native aortic root leading to optimal prosthesis stability post-deployment and minimal potential paravalvular leakage or prosthesis migration. Due to the complex anatomy of the aortic root and aortic annulus an accurate 3D imaging technique will be mandatory to acquire sufficient data for reliable reconstruction of the aortic anatomy. In contrary to 2D TTE and TEE, MDCT offers superb spatial and temporal resolution needed for precise reconstruction of the several anatomic dimensions important for preprocedural TAVI planning (11). Several studies (12,13) have revealed that the annulus has an oval shape instead of a circular one, which might help explain differences in measured aortic annular diameters using TEE, TTE and calibrated angiography (14). These findings

suggest that minimum and maximum diameters should be taken in the axial plane to calculate the mean diameter or area of the aortic valve annulus providing more accurate selection of the prosthesis size. Determining inclination of the aortic valve (angle α and β) (Fig. 2) will also be of importance for successful percutaneous aortic valve replacement. Defining the correct plane with MDCT avoids having multiple “trial and error” angiographic series before the optimal plane is found. Exact anatomical knowledge of the aortic root is needed for accurate positioning of the prosthesis in the aortic annulus, especially when using the corevalve prosthesis, as an extremely narrow or wide aortic root might be a contraindication for this type of probes (15). Measurements of the aortic root dimensions include maximum diameters of the ascending aorta, the sino-tubular junction, the sinus of Valsalva, and maximum and minimum diameters of the aortic valve annulus and the left ventricle outflow tract (Fig. 3). It is also important to measure the height of the coronary ostia relative to the aortic valve annular plane to avoid covering of the coronary ostia by the upper part of the prosthesis or one of the native leaflets (Fig. 3) (15,16). Furthermore, location and quantifying the degree of aortic valve calcifications (Fig. 6) is important,

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Fig. 4. — MDCT images. A. Normal iliofemoral arteries, (B) Circumferential iliofemoral calcification. (C) Severe iliofemoral tortuosity. B and C are illustrations of iliac arteries which are considered as a contra-indication for TAVI placement, as they don’t allow safe passage of the prosthesis into the aorta and increase the risk of local vascular complications and formation of emboli.

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Fig. 6. — The axial reformat, showing us the 3 aortic cusps in one plane. A: normal valve without calcifications. B: mild calcifications. C: moderate calcifications. D: severe calcifications, which hamper the prosthesis deployment and increase the risk of paravalvular leakage.

Fig. 5. — Example of a tortuosity index that exceeds 1.5 (= total length of the external iliac artery (lines ABC) divided by the shortest possible distance between the common iliac artery and the femoral artery (line D), indicating that the course of the iliac artery is too tortuous for the prosthesis to safely pass the iliac artery.

because heavily calcified valves may hamper the prosthesis in crossing the native valve in percutaneous valve replacement or may interfere with stent expansion and cause paravalvular leakage (17). Willmann et al describes a good correlation between nonenhanced and contrastenhanced CT and surgical findings, with regard to quantification of the degree of aortic valve calcification (18). As mentioned above, precise preoperative workout will not only reduce procedural complications, it will also speed up the TAVI procedure and minimize the amount of contrast used during the procedure. One bolus of contrast on ventriculogram/aortogram will be sufficient in most cases, hereby effectively reducing the dose of contrast from an average of 250 ml to 60 ml (10).

Preoperative anatomic screening variables Further knowledge of vascular anatomy and existing comorbidities is needed in determining which way of access is most desirable. MDCT is the imaging modality of choice for evaluating these variables. First the luminal diameters, tortuosity and wall calcifications of the ilio-femoral arteries should be accurately assessed (Fig. 4, 5). Concentric or circumferential calcifications and complex plaques with thrombus formation are considered as relative contra-indications for the transfemoral approach, as they hamper the advancement of the catheter and increase the risk of inducing emboli (19). Extremely tortuous and small iliacs (diameter smaller than 6 mm) are also a contra-indication,

because they don’t allow safe manipulation of the rigid catheter past the iliac artery into the aorta and hereby enlarge the risk of local vascular complications (19). To make an estimation of the tortuosity of an iliac artery we can calculate it’s tortuositiy index, which is total length of the external iliac artery divided by the shortest possible distance between the common iliac artery and the femoral artery (Fig. 5) (20). In such cases, a transapical approach can be considered, hereby access to the left ventricle is achieved through a minithoracotomy with needle puncture, which is a viable alternative for patients who also have advanced peripheral vascular disease, but might be contraindicated in patients with lung disease, pericardial calcifications, extensive epicardial fat, previous left ventricular surgery and dysmorphic chest anatomy (19, 21). This TAVI approach may become an attractive alternative in the future, especially if the incidence of cerebrovascular accidents is significantly smaller compared to the retrograde approach. Another valuable alternative in patients with unsuitable femoral access includes the subclavian approach with high success rates showed by several small studies (21). Second, MDCT may serve as an alternative to invasive coronary angiography to rule out significant coronary artery disease, as most practitioners feel compelled to assess coronary anatomy ahead of valve surgery, as severe coronary artery disease might be a relative contraindication (4). As expected,

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coronary calcifications are very frequent in patients with aortic valve stenosis. Complications related to percutaneous valve implantation The fast growing number of patients treated with TAVI and data provided by longer follow-up studies have resulted in a better knowledge of the complications. Again MDCT is an important tool in preventing the majority of these complications. A detailed insight in vascular anatomy can reduce vascular injuries, such as aortic rupture and iliac perforation. Obtaining accurate measurements of the aortic root and annulus will prevent valve malpositioning, which can lead to coronary obstruction, significant paravalvular leakage and prosthesis migration. Other complications, such as cardiac perforation and tamponade, conduction abnormalities, myocardial infarction, and stroke with a reported rate of 3% to 9% (11), are procedure related and are therefore more difficult to prevent. Concluding, a detailed evaluation of different anatomical variables is mandatory before any implant.

Conclusion TAVI has become a widely accepted alternative to conventional openheart surgery for selected high-risk patients with severe symptomatic aortic stenosis. As techniques and devices evolve, the procedure will become suitable for a wider range of candidates. Pre-surgical work-up is of major importance in reducing complications related to the procedure. Due to its superb spatial and temporal resolution and accurate 3D imaging, MDCT is emerging as the best preprocedural imaging modality, and will inevitably play a vital role in facilitating the selection and evaluation of candidates. So, radiologists should familiarize themselves in using MDCT as a standard workup tool preceding the TAVI procedure to succeed future demands.

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NON-INVASIVE GRADING OF ASTROCYTIC TUMOURS FROM THE RELATIVE CONTENTS OF MYO-INOSITOL AND GLYCINE MEASURED BY IN VIVO MRS A.P. Candiota1,2, C. Majós3,1, M. Julià-Sapé1,2,4, M. Cabañas5,1, J.J. Acebes6,1, A. Moreno-Torres7,1, J.R. Griffiths8, C. Arús2,1,4 MRI and MRS are established methodologies for evaluating intracranial lesions. One MR spectral feature suggested for in vivo grading of astrocytic tumours is the apparent myo-Inositol (mI) intensity (ca 3.55ppm) at short echo times, although glycine (gly) may also contribute in vivo to this resonance. The purpose of this study was to quantitatively evaluate the mI + gly contribution to the recorded spectral pattern in vivo and correlate it with in vitro data obtained from perchloric acid extraction of tumour biopsies. Patient spectra (n = 95) at 1.5T at short (20-31 ms) and long (135-136 ms) echo times were obtained from the INTERPRET MRS database (http://gabrmn.uab.es/interpretvalidateddb/). Phantom spectra were acquired with a comparable protocol. Spectra were automatically processed and the ratios of the (mI + gly) to Cr peak heights ((mI + gly)/Cr) calculated. Perchloric acid extracts of brain tumour biopsies were analysed by high-resolution NMR at 9.4T. The ratio (mI + gly)/Cr decreased significantly with astrocytic grade in vivo between low-grade astrocytoma (A2) and glioblastoma multiforme (GBM). In vitro results displayed a somewhat different tendency, with anaplastic astrocytomas having significantly higher (mI + gly)/Cr than A2 and GBM. The discrepancy between in vivo and in vitro data suggests that the NMR visibility of glycine in glial brain tumours is restricted in vivo. Key-words: Astrocytoma - Magnetic resonance (MR), spectroscopy.

Abbreviation List A2 A3 GBM mI Gly Cr NAA Cho SW TR TE STE LTE PCA HR-MAS wtw

Low-grade astrocytoma Anaplastic astrocytoma Glioblastoma Multiforme Myo-inositol Glycine Creatine N-acetyl aspartate Choline Sweep width Recycling time Echo time Short time of echo Long time of echo Perchloric acid High resolution magic angle spinning Wet tissue weight

MRI and MRS are well established methodologies for evaluating intracranial lesions (1,2). MRS is nowadays receiving increasing attention from radiologists and neurologists, and its use to help MRI in

the clinical decision making process is increasing. MRS of brain tumours is currently used for diagnosis, grading, assessing therapeutic response and providing prognostic information on survival (3-4). According to Stewart et al (5), approximately 60% of all intracranial tumours are of neuroepithelial origin (gliomas). Among the glioma subtypes, Chamberlain and Kormanik (6) have reported percentages of 4050% for glioblastomas (GBM), 3035% for anaplastic astrocytomas (A3), and 15-20% for low grade astrocytoma (A2). Proper grading of astrocytic tumours is important for the clinician to decide upon treatment and patient care (4, 6). Current radiological methods do not distinguish adequately between the large number of recognised types of brain tumours, and histopathological diagnosis from a biopsy remains the gold standard for diagnosis and grading, although

From: 1.Centro de Investigación Biomédica en Red en Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), Cerdanyola del Vallès, Spain, 2. Departament de Bioquímica i Biologia Molecular, Unitat de Bioquímica de Biociències, Edifici Cs, Universitat Autònoma de Barcelona, 08193, Cerdanyola del Vallès, Spain, 3. Institut de Diagnòstic per la Imatge (IDI), CSU de Bellvitge, Autovia de Castelldefels km 2.7, 08907, L’Hospitalet de Llobregat, Barcelona, Spain, 4. Institut de Biotecnologia i de Biomedicina (IBB). Universitat Autònoma de Barcelona, 08193, Cerdanyola del Vallès, Spain, 5. SeRMN, Edifici Cs, Universitat Autònoma de Barcelona, 08193, Spain, 6. Department of Neurosurgery, Hospital Prínceps d’Espanya, CSU de Bellvitge, Feixa Llarga s/n, 08907, L’Hospitalet de Llobregat, Barcelona, Spain, 7. Research Department, Cetir Centre Mèdic SL-Unitat Esplugues, C/ Josep Anselm Clavé 100, 08950 Esplugues de Llobregat, Spain, 8.Cancer Research UK, Cambridge Research Institute, Robinson Way, Cambridge CB2 ORE, UK. Address for correspondence: Dr C. Arús, Departament de Bioquímica i Biologia Molecular, Unitat de Bioquímica de Biosciènces, Edifici Cs, Universitat Autonoma de Barcelona, 08193, Cerdanyola del Vallès, Spain. E-mail: carles.arus@uab.es

even here accuracy is not perfect (7). Neuroimaging-based classification (defined as the assignment of type and grade) is frequently reported to be unreliable, especially for certain lesions such as gliomas (8, 9). An additional non-invasive method for accurately diagnosing and grading brain tumours would be a major advance, particularly in those cases. As MRS spectra of brain tumours and other focal lesions are often quite distinctive, 1H-MRS is a very promising non-invasive method for brain tumour diagnosis, and it is becoming widely acknowledged as a useful complement to MRI. Several in vivo diagnostic approaches for MRS have been tested, such as spectroscopic imaging (10) or single voxel MRS (11, 12). Previous studies with MRS have suggested correlations between metabolic features in vivo and the histopathological grade of astrocytic tumours (4, 13, 14), but they were generally concerned with the NAA, Cr and Cho resonances. In addition to those resonances, MRS produces much more information of potential interest for astrocytic tumour grading, e.g. the myo-inositol resonance (ca 3.55 ppm) which can be measured at short echo times (15-18). It had earlier been realized that the J-modulation dependent effect on mI resonances would strongly decrease the apparent mI peak intensity at ca. 3.55 ppm (19). In contrast, since the gly resonance is a singlet and shows no J-dependent modulation, the ca. 3.55 ppm peak intensity will not be affected by echo time

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when gly is its major contributor. Barba et al (20) utilised this echo time J-coupling modulation-dependent effect to estimate the relative mI and Gly content in human brain tumours in vivo. This approach was extended using a two-phantom protocol to produce an expression that should allow estimation of the MRS visible mI/gly content ratio (21). We now report the use of a simple expression for mI + gly content relative to creatine content for astrocytic tumour grading from in vivo MRS data, and an investigation of a biochemical rationale for this method, based on the analysis of biopsy metabolite extracts by high field NMR spectroscopy. Methods Patients The in vivo MRS data from patients involved in this study were acquired by the INTERPRET project (http://azizu.uab.es/INTERPRET) at the following centres: St George’s Hospital Medical School (SGUL), Institut de Diagnòstic per la Imatge CSU Bellvitge (IDI), Centre Diagnòstic Pedralbes (CDP), Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia (FLENI), Medical University of Lodz (MUL). The Institutional Review Board of each institution approved the study and patients gave signed informed consent prior to the MRS exploration.

Biopsy samples (n = 74; A2 n = 7, A3 n = 8, GBM n = 59) were collected after surgical resection of tumours at Hospital Universitari de Bellvitge. The Institutional Review Board approved the study and patients gave signed informed consent prior to surgery. Samples were frozen in liquid nitrogen within 5 minutes of collection and maintained in those conditions until processing at the Universitat Autònoma de Barcelona (UAB). The Anatomical Pathology department of the hospital provided the diagnosis of the patient. For the in vivo MRS cases, the histopathological diagnosis was achieved by examination of a biopsy sample from the tissue excised at operation. Diagnostic agreement was required between a minimum of two of the consultant neuropathologists involved in the INTERPRET project (see (11) for further details). For the unpaired cases (no MRS, but biopsy collected), the local pathologist’s diagnosis was used.

Samples were centrifuged to eliminate precipitated potassium perchlorate (40,000 x g for 15 min), reextracted once and supernatants combined and freeze-dried. All operations were performed at 4ºC. The PCA-insoluble pellet was kept for further protein analysis. Prior to NMR acquisition, samples were resuspended in 400 ml of D2O. The pH* (pH meter reading uncorrected for the deuterium isotope effect) was adjusted to 7.06 ± 0.22 and TSP (3trimethylsilyl2,2,3,3sodium tetradeuteropropionate) was added as chemical shift and concentration standard (final concentration of TSP proportional to the initial frozen sample weight). Some samples had been analysed by the group previous to the introduction of the internal standard into the extraction protocol; they were corrected for the mean losses (25%) observed in our present PCA protocol which includes an internal standard (24). In vivo MRS spectra

Perchloric acid extraction of biopsies Perchloric acid (PCA) extracts were carried out essentially as in (22). Frozen samples were pulverized with a pre-cooled mortar and pestle. The fine powder obtained was transferred into a tube containing 0.5 M PCA (6 ml/g wet weight) and homogenized. External fumarate (ca. 5 µmol/g wet weight) was added as an internal standard to account for extraction process losses (23).

Patient spectra (n = 95; A2 n = 18, A3 n = 7, GBM n = 70) were obtained from the INTERPRET validated database (http://gabrmn.uab.es/interpretvalidateddb <accessed on 2011-0121>). The consensus protocols developed by the INTERPRET project for acquisition of MRI and MRS data (25) are shown in Table I. Gadolinium contrast agents, when used, were given prior to MRS measurements. The MRS voxel was

Table I. — Consensus acquisition protocols for new data and also ranges (in italics) used for retrospective data accepted into the INTERPRET database. Mixing time in STEAM sequences (short echo time) varied and was the standard for the different systems used. PARAMETER

STEAM (SHORT TE)

PRESS (SHORT TE)

PRESS (LONG TE)

20 ms (20-32 ms)

30 -32 ms (30-32 ms)

136 ms (135-144 ms)

2000 ms (1600-2000 ms)

Volume

4-8 cm3

N. averages metabolites

256

192-128

N. averages water

8 to 32

8 to 16

N. points

512 [Philips] 1024 [Siemens] 2048 [GE]

Bandwidth

1000 Hz [Philips] 1000 Hz [Siemens] 2500 Hz [GE]

Dummy scans

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Table II. — Glycine, myo-Inositol and creatine concentrations in the phantom used for the calibration curve. Phantom number

[mI] (mM)

[Gly] (mM)

Ratio [mI/Gly]

[Cr] (mM)

1 2 3 4 5 6 7 8 9 10

0 12 16 27 40 54 60 70 80 80

80 78 64 54 40 27 12 7 5 0

0 0.15 0.25 0.5 1 2 5 10 16 ⬁

10 10 10 10 10 10 10 10 10 10

placed on the cellular part of the tumour, according to the previous MRI exploration. Phantom studies at clinical field Phantom studies were planned from calculations based on the concentration ranges and T2 of brain metabolites (mI, gly, Cr) reported by others (26-28), as well as previous experimental data from our group (20), and were devised in order to estimate by previous external calibration the mI/gly ratio in vivo. The calibration curve solution had a constant creatine concentration (10 mM) and variable mI and gly concentrations (Table II). The phantom used in these acquisitions was based on the EUROSPIN phantom, and is described in more detail in (29). Acquisition of phantom spectra (inner phantom cube containing the model solutions described in Table II) was carried out in a Philips scanner (ACS NT) operating at 1.5 T. MRS; acquisition parameters were: PRESS sequence, 512 data points, SW 1000 Hz, TR 2 s, TE 30 and 136 ms. The number of acquisitions was 96 for short TE (STE) and 128 for long TE (LTE), except in the case of the phantom with a lower concentration of mI (12 mM) in which the number of acquisitions was increased to 768. The single voxel (SV) volume was placed inside the inner cube of the phantom and the voxel size was fixed to 1.5 cm3. Unsuppressed water reference spectra were also acquired with the same parameters except that the number of acquisitions was 16. In vitro high resolution NMR spectroscopy Pulse-and-acquire spectra were acquired in an ARX - 400 spectrometer operating at 9.4 T (Bruker SADIS, Wissembourg, France) at the UAB

facility ‘Servei de Ressonància Magnètica Nuclear’ (SeRMN) at 298 K. Acquisition parameters were: time domain 16 k (8 k complex points), sweep width 4854 Hz, recycling time 10 s, and water presaturation with 0.05 mW power for 1 second. Initially, a short spectrum (16 scans) with 30s of recycling time was acquired to allow for fumarate quantification and loss-related corrections. The number of acquisitions was between 64 and 4096 scans, depending on the initial biopsy sample weight. Spectra were processed with DC correction, zero filling to 16 K and 0.3 Hz line broadening before Fourier transformation with WINNMR version 6.1.0.0 (Bruker Daltonik, GmbH) in a PC. Peaks of interest were fitted to Lorentzianshaped curves, quantified with respect to the TSP reference with WINNMR, and finally corrected for the percent losses measured or estimated from fumarate content in the final extract sample. Processing of in vivo MR spectra In vivo and phantom spectra were automatically processed with a software module derived from the INTERPRET data manipulation software (11, 12). This module carried out the required functions such as Fourier transform, residual water filtering by HLSVD between 4.3 and 5.1 ppm, offset correction, zero order (Klose algorithm) phase correction, setting the 4.2 to 5.0 ppm range to zero, exponential apodisation result-

[ [

] ]

321

ing in a line broadening of 1Hz and normalization of the spectra to Euclidean unit length (eq.1), with X being the height of any point in the spectral vector. Next, the signal-tonoise ratio (SNR) for the tallest peak in the 0-3.4 ppm range was also calculated (see (11) and (12) for further details). The noise level was defined as the average standard deviation of noise between 9 to 11 ppm. The resulting processed file had 512 points and ranged from -2.7 to 7.1 ppm. Astrocytoma cases in the database were only used if they had available both one short echo and one long echo time spectrum, which had both passed spectroscopic quality control criteria (water linewidth at half height < 8 Hz and SNR > 10, and lack of visible spectral artifacts (11)). X2 i=n 苴 ⌺ X2

冪

[1]

i=l

An additional inclusion criterion for this work (but see also (29)) was that only spectra with SNR higher than 5 for the 3.55 ppm (mI + gly) and 3.03 ppm (creatine) signals at short echo time (STE) spectra were used. Following these restrictions, 9 spectra (1 A2 and 8 GBM) were discarded. In order to make the (mI + gly)/Cr function simple to measure, we used peak heights rather than peak areas. In principle a non-specialist user of the method could measure them with a pencil and ruler. In the present study, a modified processing module was developed to calculate SNR and peak heights for in vivo and phantom spectra. The 3.03 and 3.55 peak heights and their SNR (range -2 to -1 ppm as basis) were automatically calculated for STE and long echo time (LTE) for the resulting processed file derived from the INTERPRET data manipulation software (DMS). Before peak height measurement in phantom spectra, a 4 Hz line broadening was applied to mimic the linewidth effects in in vivo brain tumour spectra. After that, the (mI + gly)/Cr ratio (eq.2) was calculated.

(3.55 ppm height STE) (3.03 ppm height STE) (3.55 ppm height LTE) (3.03 ppm height LTE)

= (mI + gly)/Cr

[2]

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A B Fig. 1. — Spectra at STE (top) and LTE (bottom) at 1.5 T of phantom solutions of two calibration curve points. A) phantom #1: creatine 10 mM, gly 80 mM and B) phantom #2: creatine 10 mM, mI 12 mM. The mI/gly peak at ca 3.55 ppm is labelled with an arrow. Phantom spectra were scaled to approximately constant creatine peak height for each pair of STE/LTE spectra.

Simulation of expected (mI + gly)/Cr from in vitro PCA extract calculated values The (mI + gly)/Cr that would be expected in vivo was simulated from in vitro PCA extract sample data. This simulation was based in data obtained with the phantom calibration curve and an equation (equation 3, see results) was adjusted to give curve points that correlate the (mI + gly)/Cr in vivo to mI and gly concentrations measured in vitro.

more than two comparisons were carried out) the ANOVA test. For values with normal distribution but inhomogeneous variance, Student’s t-test was carried out. Values with non-normal distribution were evaluated with the nonparametric Mann-Whitney’s U test. Significance level was set to 0.05, and all analyses were carried out with SPSS version 11.5.1 and 14.0 (SPSS Inc, Chicago, IL). Results

Statistical analysis Statistically significant differences were evaluated as follows: the normal distribution of values was assessed with the KolmogorovSmirnov test and the variance homogeneity with the Levene's test. Values with a normal distribution and homogeneous variance were compared with Student’s t test or (if

Phantom studies and calculation of (mI + gly)/Cr Phantom spectra were acquired under conditions of good SNR, which allowed clear identification of peaks of interest (see figure 1). The SNR range obtained for the signals of interest was 30-122 (STE) and 5178 (LTE).

The mI signal at LTE was attenuated when compared to the creatine signal, due to mI J-coupling induced phase modulation, whereas glycine remained practically isointense with respect to creatine at 3.03 ppm (Fig. 1). Values of calculated mI and gly concentrations used in the phantom and the resulting (mI + gly)/Cr ratio were used to devise the calibration curve shown in figure 2. From these values, an asymptotic equation was obtained from fitting the calculated (mI + gly)/Cr for each (mI)/[gly) ratio (eq. 3), with the SIGMAPLOT (Systat Software) program. y=

5.02 1 + exp

(

– (x – 2.77) 3.11

)

[3]

From equation [3], (mI + gly)/Cr (y) values in vivo can be predicted

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Gly and mI content in biopsies from in vitro measurements of PCA extracts and calculation of the predicted (mI + gly)/Cr in vivo

Fig. 2. — Calibration curve (semilogaritmic plot) obtained with phantom measurements. For proper fitting, an arbitrary value of 500,000 was used in place of “⬁” for (mI)/[gly) in phantom solution #10, for which two different acquisitions were performed. The value for phantom #1 is not shown in the plot.

from assumed mI and gly content ratios (x), and vice versa mI/gly ratios calculated from in vivo measured (mI + gly)/Cr. In vivo measurement of (mI + gly)/Cr for calculation of (mI)/[gly) The initial set of in vivo spectra (n = 95) available in the database was reduced to n = 86 by application of the criteria mentioned previously: unsuppressed water linewidth and SNR for the whole spectral pattern, and for the individual 3.55 and 3.03 peaks. Variations due to short echo time STEAM or PRESS sequences (STE) were assessed by separating cases according to acquisition conditions and testing (t-test) for differences between groups (data not shown), and no significant differences were found. This observation agrees with that of Ernst and Hennig (19), who reported differences in modulations between metabolites measured with STEAM and PRESS sequences, but only at higher echo times (> 50 ms). Slight differences in echo time (20-35ms for STE or 135-136 ms for LTE) were assumed to be negligible for the purposes of this work with respect to MRS pattern effects in the mI/gly or Cr regions. Table III summarizes (mI + gly)/Cr and (mI)/[gly) calculation from equation 3 for the studied groups (A2, A3 and GBM).

The distribution of glial cases in the validated INTERPRET database that fulfilled the inclusion criteria for this analysis partially agrees with the distribution reported in (6), in which of 86 astrocytoma cases, 72.1% were glioblastomas, 8.1% were anaplastic astrocytomas and 19.8% were diffuse astrocytomas. The agreement is even more complete if high grade (GBM + A3) tumours are compared with low grade (A2) tumours; the numbers are then 80.2% vs. 19.8% in the INTERPRET data and 70-85% vs. 15-20% in (6). In typical in vivo spectra (Fig. 3A and 3B, mean spectra), the attenuation of the 3.55 ppm signal at LTE is higher in low-grade tumours, whereas in glioblastomas, there is usually little attenuation. Furthermore, the boxplot in figure 4A shows that (mI + gly)/Cr tends to be inversely correlated with grade, achieving statistically significant differences between A2 and GBM. The (mI + gly)/Cr values obtained for paired in vivo/in vitro cases (most of which, 15/16, were GBMs, Table IV) were variable; some cases presented similar values and some cases did not. These values were statistically compared with Student’s “t” test and significant differences (p = 0.02) were found. The (mI + gly)/Cr value tended to be higher in vivo, suggesting a lower apparent glycine content in vivo.

Typical PCA extract spectra from biopsies can be seen in figure 5, with examples of spectra from A2 and GBM. Values for (mI)/[gly) were calculated for each in vitro spectrum, and equation 3 was used for predicting the expected (mI + gly)/Cr value in vivo. Average values for gly and mI concentration ratios obtained from biopsies are summarized in Table V. The total number of paired cases (MRS and biopsy extraction) is summarized in Table IV. The boxplot for the calculated (mI + gly)/Cr is shown in figure 4B and in Table III a statistically significant decrease in (mI + gly)/Cr between A3 and GBM can be seen, while the reverse tendency is observed between A2 and A3, the former presenting lower values. While the (mI + gly)/Cr values for GBM and A3 are not significantly different when comparing values measured in vivo with values calculated from extract data, (mI + gly)/Cr values for A2 are significantly different, being 3-fold lower for in vivo data with respect to ratios calculated from in vitro data (Table III). Discussion Quantification of the mI/gly ratio in vivo by combining data acquisition at two echo times Several approaches have been used to evaluate the mI and/or gly content of the human brain and of human brain tumours using data obtained in vivo in clinical scanners (1.5-7T) (20, 30-35). This measurement is difficult, especially at low field, because of the co-resonance at ca. 3.55 ppm of the singlet resonance of glycine with the J-coupled resonances from the protons of myo-inositol (protons 1, 3, 4 and 6). Most authors have usually resorted to independent gly and mI quantification at a single echo time (between 30 and 144 ms (31, 33, 34)) or have used a method based on averaging echo time results in the 30-284 ms range (31, 36), and using frequency domain fitting and quantification with LCModel. The method described in (31, 36) was also based on the well known fact that the Jmodulation dependent effect on mI resonances would strongly decrease the apparent mI peak intensity at ca. 3.55 ppm at short TE (15, 19, 20). Additionally, since the gly resonance

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Table III. — Measured (mI + gly)/Cr (in vivo) or calculated from biopsy data (in vitro) and (mI)/[gly) calculated (in vivo) or measured from biopsies (in vitro). Values are mean ± SD. In vivo (mI + gly)/Cr [mI]/[gly]

d,e,f

a,b,c

In vitro

A2 n = 17

A3 n = 7

GBM n = 62

A2 n = 7

A3 n = 8

GBM n = 59

6.08 ± 3.42

4.28 ± 2.30

2.91 ± 3.00

2.36± 0.62

3.53± 1.14

2.12 ± 0.60

17.06 ± 9.49

10.10 ± 9.90

5.35 ± 8.67

2.39 ± 1.59

6.28 ± 3.90

1.89 ± 2.23

(a) p < 0.05 for in vivo/in vitro comparisons (A2 x A2 values) (b) p < 0.05 for in vivo comparisons (A2 x GBM values) (c) p < 0.05 for in vitro comparisons (A2 x A3 and A3 x GBM values) (d) p < 0.05 for in vivo/in vitro comparisons (A2 x A2 values) (e) p < 0.05 for in vivo comparisons (A2 x GBM values) (f) p < 0.05 for in vitro comparisons (A2 x A3 and A3 x GBM values)

B Fig. 3. — In vivo mean spectra + /- SD (shading) at STE (left) and LTE (right) for A) A2 cases (n = 17) and B) GBM cases (n = 62). Note that for the A2 cases, the 3.55 ppm signal (arrows) is high at STE and much lower at LTE, whereas for the GBM the relative signal height with respect to creatine at 3.03 ppm remains high. Spectral intensity was set to zero after 4.2 ppm to avoid contribution of artefactual signal due to suboptimal water suppression (11).

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Fig. 4. â&#x20AC;&#x201D; A) Boxplot for (mI + gly)/Cr automatically calculated from actual in vivo spectra ($) labels significant differences using an ANOVA test between the A2 and GBM groups. Number of cases for each group is given on the abscissa axis. B) Boxplot obtained for predicted (mI + gly)/Cr in vivo, calculated from values obtained from PCA extracts of biopsies. ($) labels significant differences between the A3 and the other two groups. In these boxplots, upper and lower box limits represent 3rd and 1st quartiles, respectively. The central thick line is the median. Whiskers label maximum values comprised between the quartile and the product Interquartile Range (IQR) x 1.5. Outliers are represented as circles when value is within the 1.5 and 3.0 x IQR. Extreme outliers (higher than 3.0 x IQR) are represented as *.

is a singlet and shows no J-dependent modulation, the ca. 3.55 ppm peak intensity is not affected by echo time when gly is its major contributor. This effect had already been noticed in studies of glial tumours in vivo (15, 20). Barba et al (20) used the echo time J-coupling modulation-dependent effect to estimate the relative mI and gly content of human brain tumours (hemangioperycitomas and meningiomas) in vivo. In that study, mI/gly content was estimated from a two phantom protocol. This approach has been extended in our present work (see also (21) for a preliminary description) to produce an expression (equation 3) that allows MRS-visible mI/gly content ratio estimation under our experimental conditions. No correction was applied in our work for possible differences in T1 or T2 values between the phantom solution and brain tumour tissue. Accordingly, the mI/gly ratio calculated for the tumour tissue should be considered an approximation to the real tissue mI/gly. If T1 or T2 values differentially change for mI and gly, this could produce an apparent mI/gly ratio derived from the measured ratio, weighted by the relative NMR visibility of the two compounds, and compared with the height of a singlet resonance which is not affected by the echo time modulation (creatine). A similar approach to the present one was described by Hattingen et al. (35) for MRSI dataset grids. They also used the change in pattern produced by recording spectra from

human brain tumours at two echo times (30 and 144 ms), time domain data fitting using AMARES and QUEST, and phantom spectra, to calculate mI/gly ratios for low grade astrocytomas (A2), high grade astrocytomas (A3 + GBM) and control subjects (35). Their results, which would be qualitatively equivalent to 1/(mI + gly)/Cr using the terminology in our study, also showed a trend to increasing apparent gly content in high grade tumours, although a full quantitative comparison between both studies is made difficult by the different phantom approach used and their combination of A3 (n = 10) and GBM (n = 5) in a single high grade group. The approach described herein may have some advantages with respect to other previously developed approaches in its relative simplicity, which should allow its use with SV MRS data acquired at any clinical centre. Monitoring of the relative mI/gly content in vivo may also be of interest for other clinical conditions in which changes in the relative contents of mI or gly are expected (20, 34, 36). Relevance of the apparent mI and gly content detected by MRS in vivo for non-invasive astrocytic tumour grading The relative content of mI and gly in tumours was calculated ((mI + gly)/Cr) from the quantitative pattern change caused by the MRS visibility of mI varying at increasing echo times (19, 20). The apparent mI/gly

ratio obtained in vivo (Fig. 4A) by substituting the experimental values into equation 3 has allowed us to demonstrate statistically significant differences in calculated mI/gly ratios between low grade astrocytic tumours (n = 17) and glioblastoma multiforme (n = 62) (Table III). This would agree with previous work (17) in which a tendency for a higher mI/Cr to be associated with lower grade had already been described at a single echo time (20 ms) in a smaller cohort of patients (n = 34), albeit without statistical analysis of the differences described. However, even though a trend towards a decrease in mI/gly ratio with grade exists (Fig. 4A) and statistically significance can be demonstrated for the difference between A2 and GBM, there is a great deal of overlap among grades. Therefore, if the (mI + gly)/Cr value is to be used for tumour grading, it should be combined with other relevant spectral features that have already been described (11, 37, 38). Indeed, the mI + gly peak height or peak area have already been used for classifier development at short (ca. 30 ms) or long (ca. 136 ms) echo times (11, 16, 37), and a joint classifier that uses information from the two echo times has recently been developed (39). We have already pointed out (37) that the manual combination of data obtained at short and long echo time significantly improves human brain tumour classification, and also the grading of astrocytic tumours. The (mI + gly)/Cr factor described here would

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Table IV. — Number of paired cases (in vivo MRS + in vitro biopsy extract) in this study. Pathology

Total number of cases

Number of paired cases (%)

A2 A3 GBM

17 7 62

1 (5.8%) 0 (0%) 15 (24%)

Table V. — In vitro (PCA extracts) values of glycine and myo-Inositol (mean ± standard error of the mean, µmol/gtw) calculated for biopsies.

A2 (n = 7) A3 (n = 8) GBM (n = 59)

Glycine

myo-Inositol

1.98 ± 0.54 1.06 ± 0.29** 3.28 ± 0.66

5.22 ±2.46 4.54 ± 0.75 3.92 ± 0.55

**p < 0.05 for the comparison A3 vs GBM.

effectively combine the information contained in spectra obtained at the two echo times in the 3.55 ppm mI + gly region. Using a single echo time for astrocytic tumour grading may be misleading when using the 3.55 ppm region since, for instance, a signal that is high at short echo time would modulate and almost disappear at long echo time if it were due to mI, whereas it would be constant if it were due to gly. This confusion disappears if two echo times are used, as has previously been proposed (15, 20, 35). Noisy spectra can also cause overlap in calculated (mI + gly)/Cr -factor values , since the value of (mI + gly)/Cr will then approach one, independently of the grade investigated. In order to reduce the contribution of “bad quality” cases we therefore restricted our analysis to short TE spectra with SNR values for the 3.55 and 3.03 ppm resonances that were larger than 5. A further reason for overlap in (mI + gly)/Cr data is that GBM is not a homogeneous tumour type: both tumour evolution and genetic data suggest that GBMs can be divided into primary and secondary groups (40), while transcriptomic studies have demonstrated three molecularly differentiated primary GBM subtypes (41). Although a detailed in vivo analysis of the MRS pattern of these GBM subtypes is still lacking, ex vivo data obtained by HR-MAS analyses of tumour biopsies suggest that secondary GBM could display a much higher mI content than primary ones (42). This would point to the possibility that the GBM outliers with a high (mI + gly)/Cr value in figure 4A could correspond to secondary GBMs. Further studies comprising survival data may be helpful in this respect. Comparison of mI/gly calculated from in vivo data and mI/gly measured from biopsies in vitro

Fig. 5. — Typical biopsy extract spectra of a grade II astrocytoma (gly 1.34 µmol/gtw and mI 2.59 µmol/gtw) (top) and a glioblastoma multiforme (gly 2.18 µmol/gtw and mI 1.17 µmol/gtw) (bottom). Arrow points to part of the mI doublet of doublets (3.53/3.55 ppm) while star labels the gly singlet (3.56 ppm).

We were interested in validating the in vivo estimated mI/gly with in vitro data obtained from high resolution NMR spectra of PCA extracts from brain tumour biopsies. The glycine and mI contents in Table V show a similar trend compared to other reported studies (43-48): mI content decreased with astrocytic grade, albeit non-significantly, in agreement with (43-48). Furthermore, gly content increases with grade, in agreement with previous studies (43, 44, 46, 48) (gly was detected only in one out of five low grade astrocytoma cases analyzed

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in (43)), and the same trend in gly increase with tumour grade was observed in (47 and 50) (HRMAS studies). In this respect, we are confident that our results from astrocytic tumour PCA extracts, obtained from the largest biopsy dataset yet described (n = 74), represent the expected metabolite pattern of the tumour grades investigated here. With respect to the discrepancy between (mI + gly)/Cr measured in vivo and calculated from in vitro data, there are several possible explanations. As biopsies and in vivo spectra were not matched (Table IV) it could be argued that sampling was somewhat biased. Furthermore, the biopsy sample may not necessarily represent the average spectral pattern sampled from a much larger voxel by the SV in vivo MRS approach. The rather large number of cases investigated (86 in vivo and 74 in vitro) makes this unlikely, as bias should not be coherent. Another possibility to take into account would be post-ischaemic changes in mI and or gly content between the in vivo tumour pattern and the pattern obtained from the PCA extract after open surgery resection of the biopsy. We are not aware that such changes have been described after the short ischaemia experienced by biopsies during the pre-freezing time (ca. 5 min) after surgical excision. One further possibility to take into account would be a reduced in vivo NMR visibility of gly in A2. If this were to be the case, the in vivo (mI + gly)/Cr value would be providing an apparent mI/gly ratio contributed only by the NMR-visible mI and Gly pools. One of the accepted causes of NMR invisibility of a small molecular weight metabolite is binding to macromolecular structures, with concomitant reduction of its T2 value (e.g. ADP bound to F-actin in muscle microfilaments). In this respect, binding of gly to multimeric channel proteins in the plasma membrane of PC-12 cells (50) or to a glycine-sensitive anion death channel in sinusoidal endothelial cells (51) have been proposed. Increased gly content protects various types of cells from necrotic or apoptotic death induced by ATP depletion (PC12 cells, (51)), hypoxia (hepatic sinusoidal cells, (52)) or ischaemia-reperfusion derived reoxygenation injury (cardiomyocytes, (53)). As these are physiological situations usually encountered by tumours during progression, it would make sense if similar gly-derived effects were taking place. Then, since the gly pool in A2

tumours is smaller than in GBM, most gly would remain NMR invisible, bound to those plasma membrane proteins, perhaps due to a lower requirement for its protective effect. Once gly content increased above a certain threshold, or it was extracted by PCA, the NMR visibility would be recovered and the (mI + gly)/Cr would be correspondingly affected. In relation to this, it is worth mentioning here the recently described increase in apparent detection of Gly by HRMAS with increased recording time in GBM biopsies (48), which was also interpreted by the authors as suggesting higher gly visibility in GBM ex vivo with respect to the in the in vivo tumour MRS pattern. The concentration of gly that displays a protective effect in the various cell systems mentioned above is in the 3-5 mM range (51-53). This value is very close to the gly content found by us in GBM (3.28 µmol/gtw, Table V). Both explanations, the post-ischaemia changes and the reduced NMR visibility, could also account for some discrepancies observed between the expected (mI + gly)/Cr (deduced from in vivo data) and the calculated (mI + gly)/Cr (from in vitro data) for some of the paired cases in Table IV (results not shown). It may be relevant to mention here that the mI/gly ratio has been analyzed in PCA extracts of rat glioma C6 cells (54) and has been found to be 3.2 times higher in postconfluent cells (mI/gly = 7.2, proliferation slowed down) than in log phase cells (mI/gly = 2.23, active proliferation). In this respect, actively proliferating C6 cells in culture would parallel the GBM behaviour, whereas proliferation-arrested C6 cells would partially mimic the situation in low grade astrocytic tumours. Therefore, changes in the mI/gly ratio in an astrocytic tumour in vivo with location (tumour heterogeneity) or progression towards malignancy could well be accessible noninvasively by monitoring changes in the (mI + gly)/Cr ratio. Conclusions An experimental protocol and an empirical formula have been developed to allow calculation of the (mI + gly)/Cr ratio from in vivo spectra of astrocytic human brain tumours. The in vivo (mI + gly)/Cr decreases with astrocytic tumour grade, and there is a statistically significant difference between the ratios in low grade astrocytoma and glioblastoma multi-

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forme. The (mI + gly)/Cr ratio simulated from mI and gly concentration measured from PCA extracts of tumour biopsies suggest that part of the gly pool is not NMR visible in vivo in low grade astrocytomas. The (mI + gly)/Cr ratio may have application for astrocytic tumour grading and also for other cellular situations or pathologies in which the mI/gly ratio is expected to change. Acknowledgements: We thank Lluís Martí and Guillem Mercadal for programming the SNR calculation automated module for in vivo spectra being analysed. We also thank Dr. Irene Martínez-Pérez and Dr. Ignasi Barba for the use of unpublished PCA extracts data. Work funded by MEDIVO (MCYT SAF 2002-00440), MEDIVO2 (MEC SAF2005-03650), PHENOIMA (MICINN SAF 2008-03323), Generalitat de Catalunya (2001 SGR-194, SGR2005 and XT2002-48) and INTERPRET (EU-IST1999-10310). This work was also partially funded by the Centro de Investigación Biomédica en Red – Bioingeniería, Biomateriales y Nanomedicina, which is an initiative of the Instituto de Salud Carlos III (Spain) co-funded by EU FEDER funds. Data providers: Dr. C. Majós (IDI), Dr. A. Moreno-Torres (CDP), Dr. F.A. Howe and Prof. J. Griffiths (SGUL), Prof. A. Heerschap (RU), Prof. L Stefanczyk and Dr. J.Fortuniak (MUL), and Dr. J. Calvar (FLENI); data curators: Dr. A.P. Candiota, Dr. I. Olier, Ms. T. Delgado, Ms. J. Martín, M. Camisón and Mr. A. Pérez (all from GABRMN-UAB).

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METASTATIC RENAL CELL CARCINOMA PRESENTING AS A BREAST MASS IN A WOMAN WITH HISTORY OF PRIMARY BREAST CANCER C. Balliauw1, B. Termote1, A. Van Steen1, P. Moerman2, M.R. Christiaens3, C. Van Ongeval1 Metastatic extramammary breast tumours are uncommon and differential diagnosis with primary breast carcinoma may prove to be difficult. We report a case of a metastasis of a renal cell cancer in the breast in a woman with a history of primary breast cancer. On follow-up of her breast carcinoma, a lump was detected via mammography and ultrasound. Core needle biopsy revealed a metastatic extramammary lesion originating from an asymptomatic renal cell carcinoma. We conclude that the diagnosis of metastasis to the breast from extramammary tumours is important to avoid unnecessary surgery and insure proper treatment of the primary disease. Key-words: Breast neoplasms, metastases – Kidney neoplasms, secondary.

Metastatic extramammary breast lesions are rare. Differential diagnosis with primary breast lesions may be difficult. The following case describes the clinical course of a woman with a breast lesion as initial presentation of a renal cell carcinoma. Case report A 83-year-old caucasian woman developed a ductal breast carcinoma in the right breast (pT2 N0 M0) in 1995. She underwent a tumorectomy and a right axillary lymph node dissection followed by radiotherapy. She had been treated with tamoxifen during five years. The patient had 11 years of followup of her breast carcinoma without severe abnormalities apart from 2 clinically palpable lumps of scar tissue in the right breast which were twice biopsied and histologically negative. In June 2007, the patient was examined and found to be in a good general condition on a routine gynaecological consultation. Clinically, she had a satisfying heart and lung auscultation. Clinical breast examination remained normal. Her laboratory work-up only demonstrated an elevated lactate dehydrogenase (509 U/L (240-480 U/L)). Mammography in June 2007 demonstrated a single well-marginated opacity in the axillary tail of the right breast with a diameter of 6 mm (Fig. 1A,B) and a similar lesion of 7 mm and calcifications (Le Gal type 2) in the left breast (Fig. 2A,B).

Fig. 1. — Mammography of the right breast (mediolateral oblique view) in 2005 (A) and 2007 (B) shows a well-marginated new opacity (arrow) in the axillary tail with a diameter of 6 mm (B).

Ultrasound investigation (Fig. 3) visualised a regular circumscribed nodular hyporeflective lesion in the axillary tail of the right breast. The lesion was evaluated with fine needle aspiration cytology (FNAC). The left side only showed some lymph nodes. On FNAC epithelial cell populations were found. A differentiation between benign and malignant

From: 1. Department of Radiology, University Hospitals Leuven,Leuven, Belgium, 2. Department of Morphology and Molecular Pathology, University Hospitals, Katholieke Universiteit Leuven, Leuven, Belgium, 3. Multidisciplinary Breast Clinic Section, University Hospitals, Katholieke Universiteit Leuven, Leuven, Belgium. Address for correspondence: Dr C. Van Ongeval, M.D., Dpt of Radiology, KULeuven, Herestraat 49, B-3000 Leuven, Belgium. E-mail: chantal.vanongeval@uzleuven.be

pathologies could not be made. Metastasis of the former breast cancer could not be ruled out. Core needle biopsy (CNB) was performed on the lesion in the right breast. In July 2007 CNB (Fig. 4) showed morphologically a metastasis of a renal cell carcinoma (RCC). Immunohistological characterisation indicated a positive staining for CD 10 suggestive of RCC of the clear cell type (Fig. 5) and a negative for cytokeratine CK7 and CK 20. Next, computer tomography (CT) of the thorax and the abdomen illustrated several lung metastasis and a large hypervascular mass in the left kidney, suggestive of RCC (Fig. 6). Due to the patient’s age, the significant comorbidity, and the

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Fig. 2. — Mammography of the left breast (mediolateral oblique view) in 2005 (A) and 2007 (B) demonstrates the apparition of a sharply marginated opacity (arrow) in the axillary tail with a diameter of 7 mm.

asymptomatic state of her disease no therapy was administered with the patient’s consent. A follow-up in October 2007 showed only a slight progression of her disease without manifestation of any symptoms. Actually, in august 2008, the mass in the right breast is growing without progression of the other metastatic lesions and primary tumour. Discussion The diagnosis of renal cell carcinoma can be challenging. It is the most common cancer of the kidney and many have referred to the disease as the ‘internists’ tumour’

because of its multiple presenting symptoms and signs. Metastasis has been described in approximately 30% of the patients at the time of diagnosis. The disease spread can affect almost every organ (1). Metastasis to the breast from extramammary tumours is rare and accounts only for 0,2-1,3% of the breast malignancies (2). The most common primary tumours are melanomas, lymphomas, leukemias, lung cancers, and prostate cancers in men, although nearly all malignancies have been described to metastasise to the breast (3). In general, metastasis to the breast is most frequently due to a primary breast

Fig. 3. — Ultrasound of the right breast shows a nodular hyporeflective lesion in the right axillary tail.

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cancer. There have been 17 cases of metastatic RCC to the breast described in the literature. In only 8 of these cases the breast mass is the presenting sign of metastatic spread of the disease (4-7). In our case, the patient had a history of breast cancer, but none of RCC. The solitary breast mass represented not only the initial sign of metastatic spread of RCC, but also the diagnosis of an RCC, which is even more rare. Clinically there are no significant characteristics to differentiate a primary breast lesion from a metastatic breast mass. At mammography and sonography, however, primary tumours more frequently have microcalcifications or spiculations while metastatic extramammary breast lesions usually are wellcircumscribed without calcifications or an intraductal component. Because of the absence of ductal involvement, nipple retraction and discharge, and skin dimpling are rare. The growth of a breast metastasis usually is more rapid (8). In most cases differentiation between primary breast cancer and metastatic extramammary breast lesions can be made by FNAC. Cytologic features of RCC include a clear or granular cytoplasm with prominent fine vessels. The CD10 staining is positive in 90% of the RCC; CK7 and CK20 are rarely expressed in RCC (3). In difficult cases CNB should be used for diagnosis (9). Reliable and prompt diagnosis is important to avoid unnecessary surgery (i.e. mastectomy) and to treat the patients’ primary disease more

Fig. 4. — Magnification (×400, hematoxylin and eosin stain) of the biopsy specimen showing the typical aspect of renal cell carcinoma with clear cytoplasm and a prominent vascular network.

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Fig. 5. — CD10 is a specific marker for renal cell carcinoma. Immunohistochemical staining with CD10 is highly positive in the tumour cells’ cytoplasm (Magnification × 400).

adequately. Metastatic RCC is a systemic disease and should be treated accordingly. Conclusion Extramammary breast metastasis is an uncommon disease, yet in order to avoid breast surgery, it is important to diagnose it correctly. The diagnosis may be suggested after radiologic work-up; abnormally rapid growth and atypical behaviour may indicate a metastatic disease. Confirmation of the metastatic extramammary breast lesions is obtained with FNAC or CNB. The treatment should be focused on the primary tumour, hence the importance of a correct diagnosis. References 1.

Leibovich B.C., Pantuck A.J., Bui M.H., Ryu-Han K., Zisman A., Figlin R., Belldegrun A.: Current staging of renal cell carcinoma. Urol Clin North Am, 2003, 30: 481-497.

Fig. 6. — Coronal reformation of a contrast-enhanced computed tomography of the abdomen showing a large mass in the left kidney (arrows) suggestive of a renal cell carcinoma.

2. Alvarado Cabrero I., Carrera Alvarez M., Pérez Montiel D., Tavassoli F.A.: Metastases to the breast. Eur J Surg Oncol, 2003, 29: 854-855. 3. Lee A.H.: The histological diagnosis of metastases to the breast from extramammary malignancies. J Clin Pathol, 2007, 60: 1333-1341. 4. Grossklaus D.J., Holzbeierlein J.M., Roth B.J., Smith J.A. Jr.: Abnormal mammogram as the presenting sign of renal cell carcinoma. J Urol, 2000, 163: 1239-1240. 5. Vassalli L. et al: Solitary breast metastases from a renal cell carcinoma. Breast Cancer Res Treat, 2001, 68: 2931. 6. McLauglin S.A., Thiel D.D., Smith S.L., Wehle M.J., Menke D.M.: Solitary

breast mass as initial presentation of clinically silent metastatic renal cell carcinoma. Breast, 2006, 15: 427-429. 7. Alzaraa A., Vodovnik A., Montgomery H., Saeed M., Sharma N.: Breast metastasis from renal cell cancer. World J Surg Oncol, 2007, 5: 25. 8. Vergier B., Trojani M., de Mascarel I., Coindre J.M., Le Treut A.: Metastases to the breast: differential diagnosis from primary breast carcinoma. J Surg Oncol, 1991, 48: 112-116. 9. Chhieng D.C., Cohen J.M., Waisman J., Fernandez G., Skoog L., Cangiarella J.F.: Fine-needle aspiration cytology of renal-cell adenocarcinoma metastatic to the breast: A report of three cases. Diagn Cytopathol, 1999, 21: 324-327.

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DIASTEMATOMYELIA: PRE- AND POSTNATAL MULTIMODAL DIAGNOSTIC APPROACH V. Passoglou1, M. Tebache1, L. Collignon1, E. Weerts1, J.P. Misson2, L. Rausin1 Diastematomyelia is a relatively rare congenital abnormality presenting as a sagittal separation of the spinal cord. Although cases of diastematomyelia have been previously reported, fully documented approaches by both prenatal and postnatal diagnostic workup are rare in the literature. We present a fully studied case of diastematomyelia type I investigated by prenatal US and MRI and postnatal US, MRI and radiography. Key-word: Diastematomyelia.

Diastematomyelia is a form of spinal dysraphism characterised by a cleft in the spinal cord. This abnormality may be diagnosed at first by the obstetric intrauterine US and is confirmed by prenatal MRI which also provides complementary information about the fetal nervous system. Postnatal diagnostic approach refines the diagnosis, providing additional information about skeletal and nervous lesions. We describe a fully documented case of diastematomyelia type I investigated using prenatal US and MRI and postnatal US, MRI and Radiography. Case report At the 25th week of an uncomplicated gestation the routine US raised the suspicion of spina bifida as it showed a spinal abnormality of the fetus consisting of widening of the spinal canal and an abnormal angulation of the spine. Four days later, a fetal MRI was performed on a 1.5 Tesla scanner. The examination acknowledged a split of the spinal cord at the level of lumbosacral junction. A thick septum which separated the spinal cord was present at the same level (Fig. 1, 2A). No brain abnormality was detected. At birth examination a hairy patch at the level of the lower spine was observed. There was no motor abnormality of the extremities. Three months later an ultrasound examination, radiography of the spine and a MRI were performed. The X-Ray exam showed scoliosis of the dorsolumbar region , multiple costovertebral malformations and widening of the spinal canal (Fig. 2B). The ultrasonography of the spine showed precisely the divided spinal cord and the thick septum (Fig. 3).

Fig. 1. — Prenatal sagittal T2 weighted magnetic resonance image showing the thick septum (arrow) which divides the spinal cord at the lower lumbar spine region.

MRI confirmed the presence of diastematomyelia from the T12 to the L5 level with a thick band separating the two hemicords (Fig. 4, 5). Several abnormalities of the vertebras and agenesis of the sacrum were also detected

From: Department of 1. Radiology, 2. Pediatric University, CHR Citadelle, ULG, Liège, Belgium. Address for correspondence: Dr L. Rausin, Dpt. of Radiology, CHR Citadelle, Bld. 12e de ligne 1, B-4000 Liège, Belgium.

Discussion Diastematomyelia is a rare form of spinal dysraphism characterised by a cleft in the spinal cord. As a result is the separation of the spinal cord in a sagittal direction. There are two types of diastematomyelia. Type 1 consists of two hemicords each being surrounded by a separate dural sac and divided by a bony-cartilaginous septum. Type 2 consists of a single dural sac which contains

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B Fig. 2. â&#x20AC;&#x201D; Prenatal axial T2 (A) and postnatal axial T1 (B) weighted magnetic resonance image (lower lumbar spine level) (arrow) showing a thick septum dividing the spinal cord.

both of the hemicords. The two hemicords are separated by a nonrigid septum (1). The first evidence of diastematomyelia is usually described during the intrauterine life by the routine ultrasound. The two main sonographic signs are the widening of the spinal canal in coronal view and the observation of an additional echogenic focus in the posterior part of the spinal column in the axial view (2, 3). The magnetic resonance confirms the diagnosis and sometimes provides important additional information regarding the fetal nervous system although there are some limitations at the description of the exact bone anatomy (4). This is the main reason for which some centers have described the use of intrauterine 3D CT for the diagnosis of fetal anomalies (5-8). This dysraphism is an abdnormal development of the notochord

Fig. 3. â&#x20AC;&#x201D; Radiography of the spine which demonstrates multiple vertebral defects at lower dorsal and lumbar level: hemivertebrae, costovertebral anomalies, widening of the spinal canal and scoliosis.

between the 15th and 18th week of intrauterine life (9). All the reported individuals, including our patient, are females. This may indicate an Xlinked inheritance (10, 11). The signs of diastematomyelia may appear at any time of life. Diastematomyelia has been diagnosed in adult patients with progressive sensimotor symptoms (12, 13). Nowadays, thanks to organized prenatal control in addition to the advanced imaging techniques, diastematomyelia is usually diagnos ed during intrauterine life or childhood. Patients with diastematomyelia may be asymptomatic (10) or present symptoms, usually progressive. The symptoms of diastematomyelia are classified in 4 categories: cutaneous (hypertrichosis, pilonidal cyst, lipoma, naevus, angioma, meningiocele and fistula), orthopedic (feet deformities, scoliosis, and asymmetric limbs), neurological and

radiological.The neurological signs are usually progressive, appear late and are non-specific. The slowly progressive neurological damage is explained by the injury of the spinal cord resulting from tethering or traction (14). It is estimated that diastematomyelia is responsible for 5% of congenital scoliosis (15). The treatment of diastematomyelia necessitates the decompression of neural elements and removal of bony spur. This may be accomplished with or without resection and repair of the duplicated dural sacs (16). Surgical treatment is recommended in patients with progressive neurological symptoms. The reduction of the associated scoliosis in these patients is a complicated and ambiguous issue. The prognosis of diastematomyelia depends on the associated anomalies (congenital scoliosis, kyphosis, spina bifida, myelomenin-

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A B C

Fig. 5. — Postnatal coronal T2 weighted magnetic resonance image showing the division of the spinal cord-already visible at the dorsal level (A) - above the septum (B). The dural sac appears divided below the level of the spur (C).

9. Fig. 4. — Post-natal ultrasound of the spine demonstrates a thick septum (arrow) which divides the spinal canal in two hemicords (arrowheads) and confirms the non-bony nature of this structure. 10.

gocele, hemivertebra). The neurological function may be improved by early surgical removal of the septum. Anderson et al support the opinion that the outcome is excellent in the isolated forms of diastematomyelia (2).

Conclusion 5.

Diastematomyelia is a rare but potentially serious congenital abnormality of the spinal cord. Prenatal and postnatal multimodal imaging is necessary for the early diagnosis and accurate characterization of this complex abnormality.

References 1. Pang D.: Split cord malformation: Part II: Clinical syndrome. Neuro surgery, 1992, 31: 481-500. 2. Anderson N.G., Jordan S., MacFarlane M.R., Lovell-Smith M.: Diastematomyelia: diagnosis by pre-

natal sonography. AJR, 1994, 163: 911-914. Boulot P., Ferran J.L., Charlier C., et al.: Prenatal diagnosis of diastematomyelia. Pediatr Radiol, 1993, 23: 6768. Yuh W.T., Nguyen H.D., Fisher D.J., et al.: MR of fetal central nervous system abnormalities. AJNR Am J Neuroradiol, 1994, 15: 459-464. Harwood-Nash D.C., McHugh K.: Diastematomyelia in 172 children: the impact of modern neuroradiology. Pediatr Neurosurg, 1990, 16: 247-251. Skalej M., Duffner F., Stefanou A., Petersen D.: 3D spiral CT imaging of bone anomalies in a case of diastematomyelia. Eur J Radiol, 1999, 29: 262265. Jaspan T., Worthington B.S., Holland I.M.: A comparative study of magnetic resonance imaging and computed tomography-assisted myelography in spinal dysraphism. Br J Radiol, 1988, 61: 445-453. Ruano R., Molho M., Roume J., Ville Y.: Prenatal diagnosis of fetal skeletal dysplasias by combining

11. 12.

13.

14.

15.

16.

two-dimensional and three-dimensional ultrasound and intrauterine three-dimensional helical computer tomography. Ultrasound Obstet Gynecol, 2004, 24: 134-140. Duczkowska A., BekiesinskaFigatowska M., Herman-Sucharska I., et al.: Magnetic resonance imaging in the evaluation of the fetal spinal canal contents. Brain Dev. Kapsalakis Z.: Diastematomyelia in Two Sisters. J Neurosurg, 1964, 21: 66-67. Balci S., Caglar K., Eryilmaz M.: Diastematomyelia in two sisters. Am J Med Genet, 1999, 86: 180-182. Kramer J.L., Dvorak M., Curt A.: Thoracic disc herniation in a patient with tethered cord and lumbar syringomyelia and diastematomyelia: magnetic resonance imaging and neurophysiological findings. Spine (Phila Pa, 1976), 2009, 34: E484-487. Porensky P., Muro K., Ganju A.: Adult presentation of spinal dysraphism and tandem diastematomyelia. Spine J, 2007, 7: 622-626. Hensinger R.N., Jones E.T.: Developmental orthopaedics. II: The spine, trauma and infection. Dev Med Child Neurol, 1982, 24: 202-218. Barkovich A.J.: Congenital anomalies of the spine. In: Barkovich A.J., ed. Pediatric neuroimaging: Lippincott Williams & Wilkins, 2000. Miller A., Guille J.T., Bowen J.R.: Evaluation and treatment of diastematomyelia. J Bone Joint Surg Am, 1993, 75: 1308-1317.

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SECONDARY RETROPERITONEAL TERATOMA Ph. Grandjean1, E. Danse1, F. Thys2, J.P. Cosyns3, F.X. Wese4 Retroperitonal teratomas are rare. We report on a case of a retroperitoneal secondary localisation of a gonadal teratoma in a patient who had developed primary testicular teratoma 12 years previously. The retroperitoneal mass was detected with an abdominal CT requested for the management of a non-specific abdominal pain. CT and MRI examinations showed cystic retroperitoneal masses combined with calcifications and peripheral enhancement. Review of the literature is presented, including the common differential diagnoses to be considered. Key-word: Teratoma.

Case report A 34-year-old man was admitted in our emergency department for abdominal pain of two weeks duration. The pain had begun slowly for one year but recently increased. An acute renal colic was suspected as the cause for pain in another institution. Spasmolitic therapy was initiated, without success. Upon admission in our hospital, blood tests revealed only a C-Reactive Protein at the upper limit of the normal (1 mg/dl). Abdominal Ct was performed with a multi-detector scanner (40 rows) using a tri-phasic acquisition mode (without and with intravenous iodine contrast injection, and acquisition on arterial and portal time). Two cystic retro-peritoneal masses with septation, multiple calcifications and peripheral enhancement were noted: the first was situated behind the duodenum and pancreas, compressing the vena cava inferior and measures 87 × 35 mm; the second was in front of the aorta, measuring 35 × 20 mm (Fig. 1). MRI was required in order to have a better understanding of the components of the masses. It helped to confirm the information of the CT examinations, showing heterogeneous areas of hypo and hyper intense T2 signal and iso intense T1 signal into the retroperitoneal mass. Calcifications were suspected, and fat component in the masses was ruled out (Fig. 2). A deeper anamnesis revealed a previous history of right orchidectomy for non-seminomatous tumour in 1998, concluding to a teratoma with initial lombo-aortic nodes. At

B Fig. 1. — Axial (A), coronal and sagittal (B) CT views of the two cystic and calcified retro-peritoneal masses.

From: Department of 1. Medical Imaging, 2. Acute Medicine, 3. Pathology, 4. Surgery, St Luc University Hospital, Brussels, Belgium. Address for correspondence: Dr Ph. Grandjean, Dpt of Medical Imaging, UCL Cliniques St Luc, Avenue Hippocrate 10, B-1200 Brussels, Belgium.

the time, surgery was followed by chemotherapy and radiotherapy, without specific follow-up, as far as we know. Biopsy of the retroperitoneal masses was performed under echoendoscopic guidance. Histology

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Fig. 3. â&#x20AC;&#x201D; Heterogeneous hypermetabolic activity of the retroperitoneal masses on Pet-CT (arrows).

B Fig. 2. â&#x20AC;&#x201D; MRI of the abdomen. A. without contrast: transverse view showing an iso-intense signal on T1 weighted image into the mass (arrowhead). B: hypo and hyper intense signal on T2 weighted image of the retroperitoneal mass (arrowheads).

failed to detect malignant cells. Despite this non-contributive result, a Pet-CT was performed, in order to investigate extra-abdominal localisations of the tumour. The examination showed a heterogeneous hypermetabolic activity in the lesion occupying the retroperitoneal area (Fig. 3). Blood tests indicated an increased level of the alpha-protein (590 ng/ml, nl: < 9 ng/mL). Testicular ultrasound did not show any suspicious mass in the unique testis. Lymphadenectomy was performed. Histological findings of the retroperitoneal mass concluded to a mature teratoma and an embryolo gical carcinoma. Chemotherapy was associated in the post-operative period. The long term follow-up was complicated with a progressive disease, including recurrence of retroperitoneal masses, lung metastases and mediastinal lymph nodes. At the present time (two years after the lymphadectectomy), the patient is still under chemotherapy, with persistence of mediastinal lymph

nodes and lung metastases. The level of alpha-protein is still high (4408 ng/mL). Discussion Retroperitoneal teratomas are uncommon in the adult population: primary retroperitoneal teratomas represent 1 to 11% of the retroperitoneal neoplasms (1). There are usually asymptomatic, but can cause non specific abdominal disorders including pain, nausea and vomiting (2). This disorder is important to diagnose because 26% are malignant when there are detected in adults (3). Beside, primary extragonadal germ cell tumours in the retroperitoneum are very rare and should be considered as metastases of an active or burned-out testicular cancer until proven otherwise (4, 5). Alfa-foeto-protein can be increase in case of malignant teratoma (6). In our case, a retroperitoneal mixed mass was detected with CT. This lesion was initially considered as a primary tumour. Detailed

anamnesis revealed a previous testis teratoma 12 years previously, converting the initially primary retroperitoneal mass as a high suspicion of secondary location of the initial teratoma, which was finally confirmed by surgery. As in our case, the review of the literature concludes that the clinical presentation of such a retroperitoneal mass is non specific. The role of imaging is to orientate the diagnosis (5). CT-scan can give information about the structure of the mass, which can be of two types: solid or cystic. CT and MRI contribute to detecting the three components of the solid type (tissular, fatty and calcified components) and to identifying the cystic type (with or without fat or calcium component). The cystic type may contain enhanced septations (7). The presence of the different components help to suggest the correct diagnosis on the basis of imaging, but surgery is required for the final diagnosis. Differential diagnosis includes secondary location of ovarian carcinoma, sarcoma (when fat is present, then liposarcoma has to be evocated), testicular metastases, neurogenic mass, tuberculosis, Kaposi sarcoma, Castelman disease and growing teratoma syndrome (development of a mature teratoma following chemotherapy for non seminomatous tumor, as in our case).

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When we consider retroperitoneal cystic masses, the following possibilities are to be included: the neoplastic conditions include cystic lymphangioma, mucinous cystadenoma, cystic teratoma, cystic mesothelioma, MĂźllerian cyst, epidermoid cyst, tailgut cyst, bronchogenic cyst, pseudomyxoma retroperitonei, and perianal mucinous carcinoma; nonneoplastic disorders include pancreatic pseudocyst, lymphocele, urinoma and hematoma (8). In patients with nonseminomatous germ cell tumours of the testis, retroperitoneal lymphadenectomy is frequently performed after chemotherapy, for resection of residual masses (9, 10). At histology, fibrosis, necrosis or mature teratoma can be observed (10). When residual malignant cells are noted, it is related to a very poor prognosis (9). Retroperitoneal lymphadenectomy is related to per-operative vascular injuries in more than 20 % of the cases, most frequently located to the inferior vena cava, then the renal arteries and the aorta (11). In most of the cases, surgical repair is made immediately, with a good outcome.

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Conclusion Secondary localisation of retroperitoneal teratoma is uncommon. CT is contributive for the suggestion of the correct diagnosis, by showing cystic retro-peritoneal masses with septation, multiple calcifications and parietal enhancement. In patients with previous story of testicular neoplasm, secondary location of the disease is one of the diagnostic possibilities. References 1. Gatcombe H.G., Assikis V., Kooby D., Johnstone P.A.: Primary retroperitoneal teratomas: a review of the literature. J Surg Oncol, 2004, 86: 107-113. 2. Gschwend J., Burke T.W., Woodward J.E., Heller P.B.: Retroperitoneal teratoma presenting as an abdominal-pelvic mass. Obstet Gynecol, 1987, 70: 500-502. 3. Taori K., Rathod J., Deshmukh A., Sheorain VS., Jawale R., Sanyal R., et al.: Primary extragonadal retroperitoneal teratoma in an adult. Br J Radiol, 2006, 79: E120-E122. 4. Scholz M., Zehender M., Thalmann G.N., et al.: Extragonadal retroperitoneal germ cell tumor: evidence of origin in testis. Ann Oncol (England), 2002, 13: 121-124.

5. Coulier B., Lefebvre Y., De Visscher L., et al.: "Metastases of clinically occult testicular seminoma mimicking primary extragonadal germ cell tumors. JBR-BTR, 2008, 91: 139-144. 6. Billmire D.F., Grosfeld J.L.: Teratomas in child hood: analysis of 142 cases. J Pediatr Surg, 1986, 21: 548-551. 7. Bennis S., Lezar., S., Adil A., Kadiri A.: Teratome retroperitoneal de l'adulte: apport de l'imagerie (a propos de deux cas). J Maroc Urol, 2006, 4 : 1721. 8. Yang D.M., Jung D.H., Kim H., et al.: Retroperitoneal Cystic Masses: CT, Clinical, and Pathologic Findings and Literature. RadioGraphics, 2004, 24: 1353-1365. 9. Morin J.F., Provan J.L., Jewett M.A., Ameli F.M.: Vascular injury and repair associated with retroperitoneal lymphadenectomy for nonseminomatous germinal cell tumours of the testis. Can J Surg, 1992, 35: 253256. 10. Luz M.A., Kotb A.F., Aldousari S., et al.: Retroperitoneal lymph node dissection for residual masses after chemotherapyin nonseminomatous germ cell testicular tumor. World J Surg Oncol, 2010, 8: 97. 11. Bassoulet J., du Chatelard P., Auberget J.L., Merrer J., Guillemot M.C., Timbal Y.: Exeresis of residual masses of germinal tumors of the testis after chemotherapy. Ann Urol, 1989, 23: 388-392.

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RETENTION OF AN INGESTED SMALL BLUNT FOREIGN BODY K.C. Ng1, E. Mansour2, E. Eguare2 Foreign body ingestion is a common problem in clinical practice. Majority of foreign bodies, once passed beyond the stomach, will be evacuated through the gastrointestinal tract within days without any difficulty. Retained foreign body is rare and the objects in question are mostly long, large, or have a sharp end. We report a case of retention of a small, blunt, spherical glass-like object in the ileum of an 87-year-old lady having benefited from a Hartmann’s procedure which was incidentally discovered on a computed tomography scan 2 months before its spontaneous evacuation through the stoma. Key-word: Foreign bodies, in air and food passages.

Foreign body ingestion is not an uncommon clinical problem. It is estimated that 1500 people in the United States die annually due to ingestion of foreign bodies in the upper gastrointestinal tract (GI) (1). In about 80% of the cases the foreign bodies passed spontaneously without complication (2). The rest are usually managed endoscopically with less than 1% of the cases requiring surgery (1). In adults, the most common objects are food debris, bones, pills, coins, dentures, safetypin, and razor blade (1). Once the object has negotiated beyond the stomach, it usually passes through the GI tract without difficulty. Longer retention is very rare and only a few cases have been reported (3-7); however, the objects described in those cases are considerably larger possibly preventing their passage through the bowel loops or gastric outlet. Here we report a unique case of retention of a small blunt foreign body in the ileum of an 87-year-old lady and eventually the object was passed out through the stoma 2 months after its first radiological appearance on a computed tomography (CT) scan. Case presentation An 87-year-old Caucasian woman complained to the local general practitioner about finding blood in the colostomy faecal matter and was referred to our hospital for investigation. Her background history includes Hartmann’s procedure for diverticulitis of sigmoid colon 8 years ago. Other comorbidities include left anterior descending

coronary artery occlusion with good collateralization, heart failure, chronic renal failure, hypertension, dyslipidaemia, osteoarthritis and hypothyroidism. Her stoma was not reversed due to cardiovascular comorbidities. Examination revealed a small parastomal hernia with no obvious source of bleeding. A colonoscopy and a rigid sigmoidoscopy of the rectal stump were performed but did not reveal any abnormality other than scattered diverticulae. Seven months later, she re-presented with the same complaint. A repeat colonoscopy revealed a lesion just beyond the stoma site and biopsy from this lesion confirmed the presence of invasive adenocarcinoma. A post oral contrast CT scan of the thorax, abdomen and pelvis done 18 days prior to the hospital admission showed that the tumor is adjacent to the stoma site outside the peritoneum and there was no evidence of enlarged lymph nodes or metastasis. Unexpectedly, the CT scan demonstrated a spherical 1.4 cm x 1.4 cm x 1.4 cm hyperattenuating object, possibly a metallic foreign body (Fig. 1). This object, however, did not cause any symptom or obstruction. The object was not visible on a previous plain film or CT scan dating back 8 years ago. A subtotal colectomy was performed and an ileostomy fashioned at the right iliac fossa. She began to vomit 3 days into her post-operative period. Her vomiting persisted despite nasogastric decompression and there was no output from the stoma 7 days into her recovery while she was on parenteral nutrition. A CT

From: 1. School of Medicine, Trinity College Dublin, Dublin 2, Ireland, 2. Division of Colorectal Surgery, The Adelaide and Meath Hospital, Dublin Incorporating the National Children's Hospital, Tallaght, Dublin 24, Ireland. Address for correspondence: Dr E. Eguare, M.D., Division of Colorectal Surgery, The Adelaide and Meath Hospital, Dublin Incorporating the National Children's Hospital, Tallaght, Dublin 24, Ireland. E-mail: eguaree@hotmail.com

abdomen and pelvis was performed to query for possible ileus and again showed that there was a spherical metallic foreign body in the ileum not causing any obstruction. The scan also showed a small fluid collection adjacent to the afferent limb of the ileostomy with diffuse dilated small bowel suggestive of ileus. Her symptoms were resolved on the ninth post-operative day. The foreign body was spontaneously passed into the stoma bag on the fortieth post-operative day (Fig. 2). It was a glass marble measuring 1.3 cm in diameter. The patient could not recall how long ago she ingested the foreign body and denied any insertion of the foreign body through the stoma. Since the history of ingestion was not available, we can only assume that the foreign body was ingested sometime between its first detection on CT scan and the negative abdominal x-ray 8 years prior; and therefore has been present in her abdomen for at least 2 months. Discussion The majority of foreign bodies pass through the GI without clinical consequences. The properties of the foreign body in relation to the anatomical narrowing determine the likelihood of impaction or other complications. Most blunt objects are passed within 4 to 6 days (8). Impaction usually occurs at a number of anatomical narrowing in the oesophagus, stomach, and intestines. In the oesophagus, transit can be retarded or blocked at the upper oesophageal sphincter, the aortic arch, and the lower oesophageal sphincter. Most foreign bodies pass spontaneously once they reach the stomach. However, objects longer than 5 cm and wider than 2 cm rarely pass through the pylorus (1). Objects longer than 6 cm also have difficulty navigating through the C-curve of duodenum (9).

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Fig. 2. — Image of the foreign body passed out through the ileostomy into the stoma bag 2 months after the initial CT scan showing its presence. The foreign body is a glass marble measuring 1.3 cm in diameter. The object has been cleaned before photographed.

B Fig. 1. — Transverse (A) and coronal (B) views of CT scan with oral contrast showing a hyperattenuating spherical object (arrow) in the ileum with an approximate size of 1.4 cm x 1.4 cm. No bowel obstruction can be seen.

Rarely the foreign body may be entrapped at the ligament of Treitz, Meckel’s diverticulum, or the appendix (10). Downstream from the small bowel, the ileocecal valve and the rectosigmoid junction are the other common areas of impaction due to their acute angulation. In this article we present a rare case of ingested foreign body retention in the ileum and subsequent spontaneous passage of the foreign body through the stoma at least 2 months after ingestion. Our case is unusual because the object is small, measuring only 1.3 cm in diameter, smooth, and spherical, which would predict its passage through the GI without any difficulty. The persistence of any small blunt object longer than 4 weeks is very atypical; and it is likely that the foreign body could have remained in situ had it not been for the surgical manipulation. The possible explanation for the

retention of the foreign body is the presence of adhesion after the previous Hartmann’s procedure 8 years ago resulting in focal narrowing and angulation of bowel loops that was not severe enough to result in obstruction but enough to retard the transit of the foreign body. Another contributing factor to the retention can be the development of postoperative ileus and its effect differs in different segments of the GI tract. The effect on the small intestine is usually transient, recovering within 24 hours of surgery ; and patients undergoing colectomy taking the longest time to recover (11). Postoperative ileus, however, usually do not persist for longer than 5 days. Long term retention of foreign body in the bowel is a rare occurrence. So far only a few cases have been reported in the literature. Lavon et al. (5) reported a case of a

prisoner who intentionally ingested a pack of two AA alkaline batteries which were retained in the stomach for 6 years and were removed laparoscopically. Deeba et al. (4) reported a case of a man who ingested two tea spoons under the influence of alcohol; one of which was adherent to the wall of the ascending colon for 10 years and was retrieved surgically. Endoscopic removal of a toothpick impacted in the wall of rectosigmoid junction causing 18 months history of chronic abdominal pain has been reported (7). A case of ingested sewing needle embedded in the anterior lesser curve of the gastric antrum for 32 years has also been described (6). In all cases, the foreign bodies in question were considerably larger. Some of which were long or even sharp which could easily get stuck at the acute angulation of the GI tract and imbedded into the bowel wall due to mucosal injury and chronic inflammatory process. Though most foreign bodies pass without incident, complications can arise following ingestion of foreign body. Common complications include perforation, haemorrhage, bowel obstruction, and fistula formation to adjacent viscera. Intestinal perforation is quite rare, and accounts for less than 1% (2). However, the signs and symptoms of intestinal perforation can mimic

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other acute abdominal conditions such as acute appendicitis, acute diverticulitis, intra-abdominal abscess or inflammatory mass; and diagnosis is seldom made until laparotomy (10). Perforation is usually caused by thin, pointed objects, although very rare, perforation related to blunt objects have been described (12, 13). Despite the seemingly benign physical properties, it has been suggested that blunt foreign bodies can erode through the intestinal wall through slow pressure necrosis in conjunction with local inflammatory reaction from continual apposition. Foreign body related perforations have occurred throughout the GI tract, but the highest incidence was found to be in the terminal ileum followed by rectosigmoid region owing to the narrower caliber of the intestinal lumen and the acute transition between a mobile portion of mesocolon to a more fixed portion of the retroperitoneum (10, 14). The rate of surgical intervention is significantly higher for longer period of impaction and for objects resided beyond the pylorus (15, 16). Therefore, there is a very small risk of intestinal perforation or other complications for long term retention of foreign body in the ileum. Since the clinical presentation of the complications of foreign body ingestion can be non-specific and a definite history of foreign body is often not available, radiological imaging has become an important modality for the diagnosis. However, localization of the foreign body can be a major challenge. Fish bones, wooden tooth pick, plastic and most thin aluminium objects are radiolucent on routine plain film (17). Barium swallow can be helpful to outline the radiolucent object in selected cases where a suggestive history of foreign body ingestion is available but the object is not visible on radiographs. However it should be used with discretion since it compromises subsequent endoscopic management. Most glass objects of substantial size e.g. 1-2 mm or larger should be visible on radiographs (17). The sensitivity for glass objects is about 86% from a series of seven glass object ingestions (18). Plain film may not be helpful in visualizing pneumoperitoneum in case of perforation since the bowel wall is covered with fibrin due to chronic inflammation progressive impaction and prevent the exit of gas into the peritoneal cavity. CT is superior to plain radiography because of its

capacity to differentiate between tissue densities of 0.5% and is helpful in evaluating foreign bodies which are occult or difficult to localize. In addition, it provides accurate location of the foreign body in cases where surgical retrieval is needed and can be helpful for diagnosing many foreign body related complications. In this case the intra-abdominal foreign body was diagnosed incidentally based on a CT scan. It should be noted that objects may be obscured by the use of contrast media in CT for other purposes and therefore any unsuspected foreign body may be missed. The management of foreign body ingestion is determined by the physical characteristics of the foreign body including the size, shape and type of ingested material, the location of the foreign body in the GI tract, whether the patient is symptomatic and any clinical finding suggestive of complications. A history of ingestion, if available, is important to determine the quantity and the type of ingested material, since urgent intervention may be required for certain foreign bodies like disc battery and drug packet. Physical examination should pay attention to evidence of luminal obstruction or perforation. Conservative management by observation is advocated as the protocol of choice in asymptomatic patients (19, 20). Blunt objects impacted in the oesophagus should be removed as soon as possible to avoid perforation and fistula formation due to pressure necrosis. Once the object is in the stomach, the patient can be managed expectantly because over 90% of cases the object will pass out spontaneously (19, 20). As far as small, blunt object is concerned, the current American Society for Gastrointestinal Endoscopy guideline suggests weekly radiographs to follow the progression of small blunt objects not observed to pass spontaneously and consider surgical removal if objects remain in the same location for more than 1 week (8). We, however, agree with Weiland and Schur (20) that conservative outpatient management by watching and waiting is appropriate in asymptomatic patients even though there is a slight risk of perforation if the object is retained for long term. In their experience, most objects will eventually pass and patients who develop a perforation or acute abdomen can be treated surgically without complications if there is no delay in intervention (20).

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Patients should be instructed to continue a regular diet and observe the stool for the ingested object. They should also be educated regarding the early symptoms of complications and that those symptoms can mimic an acute abdomen. Endoscopic removal is indicated in symptomatic patients who fail to pass foreign bodies out of the stomach within 3 to 4 weeks of observation (8). Flexible endoscopy is the preferred modality of foreign body extraction due to its high efficacy, low morbidity and reduced costs compared to surgical intervention. Surgical intervention is considered if endoscopic removal fails or is not possible when the foreign body has passed beyond the duodenum, or if the patient develops symptoms indicative of complications, or when there is a danger to the patient. In conclusion, long term retention of a small smooth and blunt foreign body that has passed beyond the stomach is very rare. If the patient is asymptomatic, expectant management with patient education regarding the symptoms of complications is the treatment of choice. Acknowledgements We thank Dr. W. Torreggiani, Consultant Radiologist, The Adelaide and Meath Hospital Incorporating the National Children's Hospital, for his review on the radiological images and the manuscript. References 1. Webb W.A.: Management of foreign bodies of the upper gastrointestinal tract: update. Gastrointest Endosc, 1995, 41: 39-51. 2. Velitchkov N.G., Grigorov G.I., Losanoff J.E., Kjossev K.T.: Ingested foreign bodies of the gastrointestinal tract: retrospective analysis of 542 cases. World J Surg, 1996, 20: 1001-1005. 3. Cox D., Donohue P., Costa V.: A swallowed toothbrush causing perforation 2 years after ingestion. Br J Hosp Med (Lond), 2007, 68: 559. 4. Deeba S., Purkayastha S., Jeyarajah S., Darzi A.: Surgical removal of a tea spoon from the ascending colon, ten years after ingestion: a case report. Cases J, 2009, 2: 7532. 5. Lavon O., Lurie Y., Abbou B., Bishara B., Israelit S.H., Bentur Y.: Surgical removal of cylindrical batteries 6 years after ingestion. Isr Med Assoc J, 2008, 10: 799-801. 6. Misra S.P., Dwivedi M., Gupta M.: A needle embedded in stomach for 32 years. Gastrointest Endosc, 2004, 60: 436.

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7. Zezos P., Oikonomou A., Souftas V., Gkotsis D., Pitiakoudis M., Kouklakis G.: Endoscopic removal of a toothpick perforating the sigmoid colon and causing chronic abdominal pain: a case report. Cases J, 2009, 2: 8469. 8. Eisen G.M., Baron T.H., Dominitz J.A., et al.: Guideline for the management of ingested foreign bodies. Gastro intest Endosc, 2002, 55: 802-806. 9. Williams C., McHenry C.R.: Unrecognized foreign body ingestion: an unusual cause for abdominal pain in a healthy adult. Am Surg, 2004, 70: 982-984. 10. Goh B.K., Chow P.K., Quah H.M., et al.: Perforation of the gastrointestinal tract secondary to ingestion of foreign bodies. World J Surg, 2006, 30: 372-377. 11. Holte K., Kehlet H.: Postoperative ileus: a preventable event. Br J Surg, 2000, 87: 1480-1493.

12. Memon M.A., Macafee D., Rattan H.: Accidental ingestion of cotton bud stick during alcohol intoxication: an unusual cause of caecal perforation. Ir Med J, 2002, 95: 19-20. 13. Cross K.M., Holland A.J.: Gravel gut: small bowel perforation due to a blunt ingested foreign body. Pediatr Emerg Care, 2007, 23: 106108. 14. Pinero Madrona A., Fernandez Hernandez J.A., Carrasco Prats M., Riquelme Riquelme J., Parrila Paricio P.: Intestinal perforation by foreign bodies. Eur J Surg, 2000, 166: 307-309. 15. Palta R., Sahota A., Bemarki A., Salama P., Simpson N., Laine L.: Foreign-body ingestion: characteristics and outcomes in a lower socioeconomic population with predominantly intentional ingestion. Gastro intest Endosc, 2009, 69(3 Pt 1): 426433.

16. Chaves D.M., Ishioka S., Felix V.N., Sakai P., Gama-Rodrigues J.J.: Removal of a foreign body from the upper gastrointestinal tract with a flexible endoscope: a prospective study. Endoscopy, 2004, 36: 887-892. 17. Hunter T.B., Taljanovic M.S.: Foreign bodies. Radiographics, 2003, 23: 731757. 18. Cheng W., Tam P.K.: Foreign-body ingestion in children: experience with 1,265 cases. J Pediatr Surg, 1999, 34: 1472-1476. 19. Pavlidis T.E., Marakis G.N., Triantafyllou A., Psarras K., Kontoulis T.M., Sakantamis A.K.: Management of ingested foreign bodies. How justifiable is a waiting policy? Surg Laparosc Endosc Percutan Tech, 2008, 18: 286-287. 20. Weiland S.T., Schurr M.J. Conservative management of ingested foreign bodies. J Gastrointest Surg, 2002, 6: 496-500.

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POTT’S PUFFY TUMOR: CT AND MRI FINDINGS F. Acke1, M. Lemmerling1, Ph. Heylbroeck2, G. De Vos2, K. Verstraete3 Pott’s puffy tumor, a subperiosteal abscess of the frontal bone with cranial osteomyelitis, is a rare complication of frontal sinusitis. In this report, we describe the radiological findings of a 24-year-old man, presenting with swelling of the right upper eyelid. Correct and early diagnosis of this infrequent, but potentially life-threatening condition is of utmost importance. Key-word: Sinusitis.

Pott’s puffy tumor is defined as a subperiosteal abscess of the frontal bone associated with frontal osteomyelitis. It is traditionally considered a complication of frontal sinusitis, but is also occasionally described after head trauma. Spreading of the infection occurs through the venous drainage of the frontal sinus or by direct extension through the bone. In this report, we describe the radiological findings in a patient with frontal sinusitis spreading through the anterior and inferior bony margins of the frontal sinus.

Fig. 1. — This photograph of the patient shows swelling of the right periorbital region (black arrow).

Case report A 24-year-old male patient presented to the emergency department with a recent-onset swelling of the right upper eyelid. The patient complained of headache, but no vision disturbances or fever were present.

Endoscopic examination revealed signs of sinusitis, so the patient was treated with antibiotics, and corticosteroids in a tapering schedule. His complaints disappeared, but after two months he consulted because of

a relapse of the same symptoms. The right periorbital and frontal region was edematous and seemed inflammatory (Fig. 1). A multislice helical computed tomography (CT) scan with axial,

From: 1. Department of Radiology, 2. Department of Otorhinolaryngology, AZ SintLucas, Ghent, Belgium, 3. Department of Radiology, UZ Ghent, Ghent, Belgium. Address for correspondence: Dr F. Acke, Department of Radiology, AZ Sint-Lucas, Groenebriel 1, B-9000 Ghent, Belgium. E-mail: frederic.acke@ugent.be

Fig. 2. — The coronal (A) and parasagittal (B) CT images with bone window setting show osteomyelitis of the frontal bone with bony blurring (black arrow), and with bone erosion of the supraorbital margin (white arrow).

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right frontal bone, and also showed opacification of the subcutaneous fat of the right forehead and upper eyelid. The fat plane surrounding the right superior rectus muscle and levator palpebrae superioris muscle also enhanced (Fig. 4 and 5). Meningeal involvement was however not present. The imaging findings led to the final diagnosis of Pott’s puffy tumor, and a surgical intervention with an appropriate antibiotic treatment was proposed. Discussion

Fig. 3. — Axial CT scan with bone window shows that a soft tissue swelling is present over the right frontal bone (white arrow).

coronal and sagittal reconstructions was performed, and showed bilateral extensive opacification of the frontal and maxillary sinuses, and the anterior ethmoid sinus cells. Bony erosion of the supraorbital margin of the right frontal sinus was present (Fig. 2), as well as soft tissue swelling (Fig. 3).

The patient subsequently underwent magnetic resonance imaging (MRI, 1.5 Tesla) with axial T1- and T2weighted images. After intravenous injection of gadolinium axial and coronal fat-suppressed T1-weighted images were performed. The examination confirmed the presence of sinusitis and osteomyelitis of the

Percivall Pott, an 18th century neurosurgeon, wrote a book about head injuries by means of examples (1). He observed phenomena such as intracranial haemorrhage and infected epidural collections, and treated them with trepanation (2, 3). In 1775, he described a case of frontal sinus infection with a puffy swelling of the forehead. Exploration showed osteomyelitis of the frontal bone, associated with formation of a subperiosteal abscess. The entity became known as Pott’s puffy tumor (4, 5). This condition mostly arises because of the expansion of frontal sinusitis through valveless diploic veins into the marrow cavity of the anterior bony

Fig. 4. — The T1-weighted (A) and T2-weighted (B) axial MRI images show bilateral frontal sinusitis and frontal bone osteomyelitis on the right side, with bone thinning (white arrow).

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Fig. 5. — Axial (A) and coronal (B) fat-suppressed T1-weighted MRI images performed after intravenous injection of gadolinium contrast show inflammation with enhancement of the subcutaneous fat and of the superior periorbital fat (white arrow).

boundary of the frontal sinus. It results in infection, osteomyelitis, bony erosion and finally subperiosteal abscess formation (6). Signs of Pott’s puffy tumor are a soft and fluctuant swelling over the forehead or scalp, headache, photophobia, fever, and symptoms of an underlying subacute or chronic sinusitis. Erythema, warmth and tenderness usually overlie the swelling but may be absent (7). The majority of the reported cases are adolescent males, but cases of young children are also published (7). After the introduction of appropriate antibiotic therapy, this condition has become rare. However, recently there is an increase in cases described in literature, probably because of intranasal drug use (6), HIV pandemic, misdiagnosis and partial treatment (8). The differential diagnosis includes meningitis, especially when there is a delay in appearance of focal symptoms (8). When swelling of the forehead predominates, skin and soft tissue infection should also be considered. A CT scan with intravenous contrast enhancement provides adequate information on the intracranial as well as extracranial complications of frontal sinusitis, but is most of all

superior to MRI in visualisation of the bone. However, MRI after intravenous gadolinium injection provides more detail in the description of the extent of the disease, and enables better evaluation of the underlying subdural space and brain (5, 9). Scintigraphic evaluation can be helpful in the diagnosis of osteomyelitis (10). The cultures of patients with Pott’s puffy tumor often reveal polymicrobial involvement. Streptococci, staphylococci, and some anaerobic bacteria are most frequently found (3, 5). In most cases, there is failure to respond to antibiotics and more aggressive treatment options should be preferred. Surgical intervention is the treatment of choice, including drainage of the abscess and removal of the osteomyelitic bone. Associated sinusitis needs to be addressed at the same time. Postoperatively, the patient should be given appropriate antibiotic medication for a period of 6 to 8 weeks (5, 7). References 1. Pott P.: Observations on the Nature and Consequences of Wounds and Contusions of the Head, Fractures of

4. 5.

10.

the Skull, Concussions of the Brain. Hitch and Howes, London, 1760, p. 38-58. Flamm E.S.: Percivall Pott: an 18th century neurosurgeon. J Neurosurg, 1992, 76: 319-326. Tattersall R., Tattersall R.: Pott’s puffy tumour. Lancet, 2002, 359 (9311): 1060-1063. Ravitch M.M.: Surgery in 1776. Ann Surg, 1977, 186: 291-300. Babu R.P., Todor R., Kasoff S.S.: Pott’s puffy tumor: the forgotten entity. Case report. J Neurosurg, 1996, 84: 110-112. Lamoreau K.P., Fanciullo L.M.: Pott’s puffy tumour mimicking preseptal cellulitis. Clin Exp Optom, 2008, 91: 400-402. Pender E.S.: Pott’s puffy tumor: a complication of frontal sinusitis. Pediatr Emerg Care, 1990, 6: 280-284. Boodhoo H., Karen V.: Pott’s puffy tumour – the tip of an iceberg. S Afr Med J, 2006, 96: 374-376. Huijssoon E., Woerdeman P.A., van Diemen-Steenvoorde R.A., Hanlo P.W., Plötz F.B.: An 8-year-old boy with a Pott’s puffy tumor. Int J Pediatr Otorhinolaryngol, 2003, 67: 10231026. Bagdato ˘ glu ˘ C., Güleryüz A., Ersöz G., Talas D.U., Kandemir O., Köksel T.: A rare clinical entity: Pott’s puffy tumor. A case report. Pediatr Neurosurg, 2001, 34: 156-158.

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SPONTANEOUS SOCCER-INDUCED PNEUMOMEDIASTINUM IN A 39-YEAROLD MAN K. De Smet1, B. Ilsen1, J. De Mey1, M. De Maeseneer1, W. Vincken2 We report on a healthy 39-year-old man who developed spontaneous pneumomediastinum during a soccer game without a traumatic impact. Chest radiography and CT demonstrated the extensive pneumomediastinum and subcutaneous emphysema. Treatment of this rare condition is conservative and prognosis is excellent. Key-words: Pneumomediastinum – Thorax, CT.

Spontaneous pneumomediastinum (SPM) is an uncommon condition defined as the accumulation of free air in the mediastinum without any obvious precipitating cause. The precise nature of this entity is still poorly understood although an abrupt increase in intra-thoracic pressure or volume may play a role in causing this condition. Although usually a benign, self-limiting condition, SPM is not widely recognized by emergency department physicians and should be early differentiated from more serious causes of pneumodiastinum, in particular perforation of the esophagus (Boerhaave’s syndrome), the trachea or a bronchus, severe asthma, blunt or penetrating chest injury or a gasforming mediastinal infection. In this article we report on a case of spontaneous pneumomediastinum, presenting as acute chest pain in a 39-year old man. Case report A 39-year-old man was admitted to the emergency department with acute chest pain and severe subcutaneous emphysema extending up to his chin. He had no other symptoms. The emphysema had occurred during a recreational soccer game. During half-time his fellow players noticed the patient had swelling of the neck. He continued playing the second half of the game, but by that time swelling had further increased and the patient decided to obtain medical advice. He didn’t experience any traumatic impact or angina during the game. Medical history was unremarkable. On physical examination subcutaneous emphysema was apparent especially in the supraclavicular and neck area and the right hemithorax. Hammam’s sign

Fig. 1. — Anteroposterior chest X-ray. Note subcutaneous emphysema in the neck (long black arrows). Also note sharply marginated heart border on the left (closed arrowhead) and continuous diaphragm sign (short arrow). Also note the double bronchial wall sign (white arrow) and the tubular artery sign (open arrowhead).

could not be elicited because subcutaneous emphysema was also present over the chest wall and this caused crepitations masking this classic sign. Hemodynamically the patient was stable. Laboratory findings, including arterial blood gases, and ECG were normal. Radiographs of the chest showed marked subcutaneous emphysema as well as a pneumomediastinum and a continuous diaphragm sign (Fig. 1). These findings were also seen on CT imaging in addition to a limited pneumothorax on the right, and air surrounding the mediastinum (Fig. 2). Noteworthy, the CT scan did

From: 1. Department of Radiology, 2. Department of Pneumology, UZ Brussel, Brussels, Belgium. Address for correspondence: Dr M. De Maeseneer, M.D., Department of Radiology, Laarbeeklaan 101, B-1090 Brussels, Belgium. E-mail: michel.demaeseneer@uzbrussel.be

not show any structural pulmonary disorder such as bullae or blebs. The patient was hospitalized and received oxygen and an NSAID but could be discharged on the next day. He was followed up after 9 days and at that time chest radiography was normal and the subcutaneous emphysema had resorbed (Fig. 3). Discussion Spontaneous pneumothorax with pneumomediastinum is a rare condition. Usually it occurs in people younger than 30 years and is more common in men. It also tends to be more common in drug abusers especially cocaine secondary to inhalation method (1). Spontaneous pneumomediastinum occurs secondary to an abrupt increase in intrathoracic

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Fig. 2. — A. Transverse CT image. Note extensive soft tissue emphysema in the neck (arrows). B. Transverse CT image. Note subcutaneous emphysema along chest wall (arrow). Also seen are air collections surrounding the mediastinum (stars).

Fig. 3. — Anteroposterior chest X-ray after 8 days later. Appearance is normal without evidence of emphysema or pneumomediastinum.

branches of the aorta, both sides of the vessel are depicted creating the tubular artery sign. Occasionally, air can reside next to a major bronchus, allowing clear depiction of the bronchial wall and producing the double bronchial wall sign. On CT imaging pneumomediastinum can be confirmed and CT better shows the distribution of the air (4). Treatment usually is conservative with rest, an NSAID and oxygen to speed resorption of the extrapulmonary air when necessary. A short hospitalisation can be considered. When pneumothorax is associated, insertion of a chest drain may be necessary (3). In summary, spontaneous pneumomediastinum is a benign but rare condition. It is most common in young men. Imaging findings can be very impressive demonstrating mediastinal and subcutaneous air, but treatment is usually conservative and prognosis is excellent. References 1.

pressure or volume with rupture of alveoli or terminal bronchioles. In a first phase this results in interstitial pulmonary emphysema. The air then tracks along peribronchial tissue to the mediastinum. This occurs because the pressure in the mediastinum is lower than in the lung, a phenomenon designated the Macklin effect. Next air frequently decompresses in the soft tissues of the neck (2). Clinical symptoms include retrosternal pain, dyspnea and dysphagia. Pain may irradiate to the back region. In the clinical history a Valsalva manoeuver may be found as a causative factor (3).

Physical examination reveals supraclavicular subcutaneous emphysema with fine palpable crepitations. A clicking sound synchronous with the heartbeat may be evident designated Hamman’s sign (1) Differential diagnosis includes cardiac, pulmonary, musculoskeletal and esophageal disorders (3). On standard chest radiography air is seen outlining the mediastinum and subcutaneous emphysema may also be evident. The continuous diaphragm sign on the anteroposterior view is produced by air trapped posterior by the pericardium. When there is air adjacent to the major

Abolnik I., Lossos I.S., Breuer R.: Spontaneous pneumomediastinum; A report of 25 cases. Chest, 1991, 100: 93-95. 2. Maunder R.J., Pierson D.J., Hudson L.D.: Subcutaneous and mediastinal emphysema. Pathophysiology, diagnosis and management. Arch Intern Med, 1984, 144: 14471453. 3. Koullias G.J., Korkolis D.P., Wang X.J., Hammond G.L.: Current assessment and management of spontaneous pneumomediastinum: experience in 24 adult patients. Eur J Cardio-thorac Surg, 2004; 25: 852-855. 4. Zylak C.M., Zylak C.J.: Pneumomediastinum revisited. Radiographics, 2000, 20: 1043-1057.

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CORTISONE ASSOCIATED DIVERTICULAR PERFORATION L. Goethals1,2, K. Nieboer1, K. De Smet1, F. De Geeter2, N. Hosseinpour Tabrizi3, E. Van Eetvelde4, J. de Mey1 Patients on glucocorticosteroid therapy are at increased risk of gastrointestinal perforation. The associated morbidity and mortality of perforations in this group is increased, compared with normal groups. This difference is due to the delay between onset of clinical symptoms and treatment. In the presence of steroids, gastrointestinal perforation is more difficult to diagnose clinically because signs and symptoms of perforation are masked by the anti-inflammatory effect of the steroids. Key-word: Intstines, perforation.

Steroid associated diverticular perforation is a rare, potentially lifethreatening complication of glucocorticosteroid therapy, associated with a high mortality and morbidity rate. Glucocorticosteroid (GCS) use induces both an increased risk for perforation, and a delay in diagnosis, secondary to the mitigated clinical presentation of peritonitis. Case report A 55-year-old man, who recently received high dose intravenous GCS therapy (3 x 500 mg of methylprednisolone) for an acute relapse of Multiple Sclerosis, presented himself at the emergency ward, suffering from dyspnea and abdominal discomfort. A chest X-ray demonstrated clear signs of a pneumoperitoneum with air under both diaphragms (Fig. 1A, B). The patient had no history of recent abdominal surgery nor blunt or penetrating trauma. C-reactive protein levels were elevated (67 mg/L, normal values < 5 mg/L) and there was a neutrophilic leukocytosis (16 x 103 white blood cells / mm3, 76% neutrophils). An abdominal CT scan, performed after intravenous administration of iodinated contrast, confirmed the presence of free intraperitoneal air and demonstrated diverticulosis of the recto-sigmoid with overt signs of diverticulitis and a pericolic abscess collection due to a ruptured diverticulum (Fig. 2A, B) The patient was treated by emergency Hartmann surgery, confirming the perforated colon and abscess collection. Postoperative recovery and wound healing was without complications, despite the GCS therapy and the

Fig. 1. — Chest X ray, demonstrating signs of free intra-abdominal air densities (white arrows), consistent with pneumoperitoneum on A: lateral X ray, B: frontal image.

Fig. 2. — A. Confirmation of free air surrounding liver falciform ligament (white straight arrows) and in the intra-abdominal fat (curved white arrow). B: Peri-colic abscess collection (arrowhead).

patient returned home 6 days after surgery with planned closure of the colostomy.

From: 1. Department of Radiology, 2. In Vivo Cellular and Molecular Imaging (ICMI) Laboratory, 3. Department of Emergency Medicine, 4. Department of Surgery, UZ Brussel, Vrije Universiteit Brussel (VUB), Brussels, Belgium. Address for correspondence: Dr L.R. Goethals, MD, Department of Radiology, UZ Brussel, Vrije Universiteit Brussel (VUB) Laarbeeklaan 101, B-1090 Brussels, Belgium. E-mail: Lode.Goethals@vub.ac.be

Discussion Although this case demonstrates evident radiological signs of a peridiverticular abscess with perforation, there was a vast radio-clinical discrepancy. Both the etiology of the intestinal perforation and this paucity of symptoms can be explained by the patient’s history. GCSs are known to be positively associated with an increased risk of

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perforated colonic diverticular disease (1, 2). The risk of steroid induced gastric and small bowel perforations was reported soon thereafter (3, 4). The positive relationship between colon diverticular perforation and GCS treatment is described to be more common in patients being treated with steroids for neurological disease, independent of steroid dosage (5). This increased risk, is explained by steroids causing intestinal atrophy, depletion of submucosal lymphoid patches and inhibition of the normal inflammatory reaction, leading to bacterial invasion, lack of containment and subsequent perforation (6, 7, 8). Others have suggested that steroids may cause direct colon mucosal injury (9). Other diseases associated with an increased risk for perforation of the GI system include peptic ulcer disease, necrotic or ulcerated malignancies, iatrogenic injuries, traumatic injuries, diverticulitis, ischemia, inflammatory bowel disease, stercoral perforation or NSAID treatment (10). In GCS treated patients, the mortality rates of intestinal perforation are significantly higher, reported to reach up to 100%, compared with a non-GCS treated group (11). This increased mortality is not only related to the underlying condition for which GCS are given, but mainly to the masking effect of the GCS on the clinical presentation of the perforation, resulting in a longer delay between onset of clinical symptoms and diagnosis or treatment (11). This delay in diagnosis and treatment has been shown to increase as steroid dose increases (12). GCS use can decrease the leukocyte count and cause hypothermia, as well stop the inflammatory process responsible for the clinical expression of peritonitis. This masking effect of GCS appears to work by decreasing the number and availability of immunoreactive participants, depressing the chemotactic homing mechanisms to an area of insult and minimizing the necessary interactions required for cellular immune defense (11). Clinically, abdominal tenderness is the only symptom that is consis-

tently present among GCS treated patients with intestinal perforation. With more pertinent signs and symptoms subdued, the diagnosis of a perforation is often made from a serendipitous roentgenographic finding, as was the case in our patient. The diagnosis of a GI tract perforation is based on direct CT findings, such as discontinuity of the bowel wall and extraluminal air, or indirect findings such as bowel wall thickening, abnormal bowel wall enhancement, abscess and an inflammatory mass adjacent to the bowel (10). If signs of pneumoperitoneum occur on standard chest X-rays, MDCT evaluation should be the next diagnostic step to pinpoint the site of perforation, since it is beneficial to localize the perforation site for planning the correct surgery. MDCT can accurately depict the site of gastrointestinal tract perforation in 86% of cases (13). Extraluminal air bubbles, segmental bowel thickening and focal defect of the bowel wall are strong predictors of the site of perforation (13). The amount and location of free air varies according to the perforation site. If free air is located around the liver and stomach, this most likely indicates a gastroduodenal perforation. Free air detected predominantly in the pelvis and supramesocolic and inframesocolic regions makes perforation of the colon or appendix more likely (14). Conclusion Aggressive diagnostic efforts are mandatory in front of any persisting abdominal pain in patients on systemic steroid therapy. The diagnosis of a diverticular perforation should be considered in any steroid treated patient with abdominal discomfort, fever of unknown origin or unexplained leukocytosis. References 1. Morris C.R., Harvey I.M., Stebbings W.S., Speakman C.T., Kennedy H.J., Hart A.R.: Antiinflammatory drugs, analgesics and the risk of perforated colonic diverticular disease. Br J Surg, 2003, 90: 1267-1272.

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2. Venditti D., Valerio B., Ielpo B., Buonomo O., Petrella G.: Bowel perforations in a patient affected by Churg-Strauss syndrome under highdose steroid treatment: will alternative drugs reduce risk of surgery? Rheumatol Int, 2009 Dec. 12. 3. Glenn F., Grafe W.R., Jr.: Surgical complications of adrenal steroid therapy. Ann Surg, 1967, 165: 10231032. 4. Markowitz A.M.: The less common perforations of the small bowel. Ann Surg, 1960, 152: 240-257. 5. Fadul C.E., Lemann W., Thaler H.T., Posner J.B.: Perforation of the gastro intestinal tract in patients receiving steroids for neurologic disease. Neurology, 1988, 38: 348-352. 6. Rigotti P., Van Buren C.T., Payne W.D., Peters C., Kahan B.D.: Gastro intestinal perforations in renal transplant patients immunocompromised with cyclosporine. World J Surg, 1986, 10: 137-144. 7. Sterioff S., Orringer M., Cameron J.L.: Colon perforation associated with steroid therapy. Surgery, 1974, 75: 5658. 8. Faro R.S., Corry R.J.: Management of surgical gastrointestinal complications in renal transplant recipients. Arch Surg, 1976, 114: 310-312. 9. Warshaw A.L., Welch J.P., Ottinger L.W.: Acute perforation of the colon associated with chronic corticosteroid therapy. Am J Surg, 1976, 131: 442-446. 10. Kim S.H., Shin S.S., Jeong Y.Y., Heo S.H., Kim J.W., Kang H.K.: Gastrointestinal tract perforation: MDCT findings according to the perforation sites. Korean J Radiol, 2009, 10: 63-70. 11. ReMine S.G., McIlrath D.C.: Bowel perforation in steroid-treated patients. Ann Surg, 1980, 192: 581-586. 12. DiSesa V.J., Kirkman R.L., Tilney N.L., Mudge G.H., Collins J.J., Cohn L.H.: Management of general surgical complications following cardiac transplantation. Arch Surg, 1989, 124: 539-541. 13. Hainaux B., Agneessens E., Bertinotti R., De Maertelaer V., Rubesova E., Capelluto E., Moschopoulos C.: Accuracy of MDCT in predicting site of gastrointestinal tract perforation. AJR, 2006, 187: 1179-83. 14. Stoker J., van Randen A., LamĂŠris W., Boermeester M.A.: Imaging patients with acute abdominal pain. Radiology, 2009, 253: 31-46.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 350.

IMAGES IN CLINICAL RADIOLOGY Unsuspected case of congenital bronchial atresia in workup for supposed pulmonary AVM J. Toirkens, B. Op de Beeck, M. Spinhoven, A. Snoeckx, R. Salgado, T. Van der Zijden, P.M. Parizel1 A 58-year-old man was send to our hospital for embolisation of an arteriovenous (AV) malformation of the right lung. This diagnosis was based on a CT made in the referring hospital. Diagnostic pulmonary angiography with catheter placed in the right main pulmonary artery (Fig. A) did not show an AV-malformation. Nevertheless striking was the diminished number of pulmonary vessels in the superior and middle part of the right lung (arrows). When revising the CT scan a hypodense mass was seen in the right hilum (Fig. B, arrow). This lesion was not vascularised and was located near the right upper lobe bronchus (Fig. C, arrow). The lung segment distal to this mass contained little vessels. These findings are compatible with bronchial atresia. Retrospectively this congenital anomaly could already be suggested based on the chest X-ray (Fig. D), which showed a perihilar mass (short arrow) and decreased vascular marking of the right peripheral lung zones (arrows). Comment

Bronchial atresia is defined as congenital atresia of a segmental bronchus with normal distal architecture. Etiology is supposed to be related to bronchial ischemia in utero between 5th and 15th week of gestation. The bronchus loses communication with the bronchial bud. Mucus accumulates and a bronchocele develops. Due to hypoventilation oligemia ensues. Hyperinflation of the alveoli of the effected segment with airtrapping is possible from collateral air drift. The best diagnostic clue is a round, sharply defined perihilar mass with distal hyperinflation. CT is the best diagnostic tool to characterize the bronchocele, airway anatomy, distal hyperinflated lung and other associated anomalies. Because this congenital anomaly in most cases does not cause symptoms, the lesion is only incidently discovered, frequently just in adulthood. Treatment is usually not necessary. Surgical resection is reserved for those with recurrent infection or enchroachment of normal pulmonary structures. The differential diagnosis consists of other lesions with mucoid impaction and hyperinflation as intralobar sequestration and intrapulmonary bronchogenic cyst. In an AV-malformation a contrast study can differentiate this lesion from a bronchocele, which does not enhance after intravenous contrast administration. Congenital lobar emphysema is also associated with hyperinflation but contains no bronchocele and is usually more extensive and diagnosed in infants with respiratory distress. Allergic bronchopulmonary aspergillosis may have mucoid impaction in central bronchiectasis, but is usually bilateral and patients have asthma. In SwyerJames syndrome patients have a history of recurrent infection and bronchiolitis obliterans in childhood. Imaging can look similar due to involvement of only one lung segment, hyperinflation and hypoplasia of the pulmonary artery.

Reference 1.

Gipson M.G., Cummings K.W., Hurth K.M.: Bronchial atresia. Radiographics, 2009, 29: 1531-1535.

1. Department of Radiology, Antwerp University Hospital, University of Antwerp, Edegem, Belgium.

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JBR–BTR, 2011, 94: 351.

IMAGES IN CLINICAL RADIOLOGY A complicated fourth branchial fistula N. Bottosso, C. Coibion, M. Dirix, J. Khamis1

A 5-year-old girl was admitted to our Medical Imaging Departement for ultrasonography of a painful and non-erythematous cervical mass on the left side of the neck. She previously complained of pain and dysphagia for several days. There is no fever and no history of infection. An axial gray-scale US (Fig. A) shows an irregular infiltrative hypo and hyperechoic left cervical mass with adenopathies and deviation of the larynx. Colour Doppler US shows a moderate intralesionnal vascularization (Fig. B). Axial T1 and T2-weighted MR images (Fig. C) show an infiltrative parathyroidian mass of the left lateral neck (hypointense T1 and heterogeneous signal T2) with lateral displacement of the sternocleidomastoid muscle and medial displacement of the larynx, and a communciation with the pyriform sinus . Barium esophagography (Fig. D) shows a left sinus tract from the apex of the pyriform sinus. These examinations confirm the diagnosis of a complicated fourth branchial fistula. Antibiotic therapy and chirurgical resection were performed and confirm the diagnosis. Comment Neck masses are a common finding in children and have a congenital, inflammatory, neoplasic or vascular origin. The fourth branchial arch contributes to the development of the larynx, which derives from the laryngotracheal groove formed during the 4th week of gestation. Anomalies of the branchial arch may appear as a cyst (extending from the apex of the pyriform sinus to the left thyroid lobe), a sinus (one opening-to-skin surface, external auditory canal, pharynx or hypophraynx), a fistula (connecting the skin to the lumen of the foregut) or an ectopic gland. Ninety percent of branchial anomalies arise from the second branchial arch. Anomalies arising from the fourth branchial arch are extremely rare and have been described in children and young adults. They are more common in females. The vast majority of these lesions occur on the left side. A sinus of the fourth branchial arch, following its embryologic origin, forms internally from the apex of the pyriform sinus, crosses the thyrohyoid membrane and the left thyroid lobe. It is sometimes difficult to distinguish a cyst of the third or the fourth branchial arch within the larynx. An internal fistula arising from the apex of the pyriform sinus pleads in favor of a fourth branchial pouch remnant. Clinically, the lesion appears as a painless cervical mass in the posterior triangle area of the neck, anteromedial to the sternocleidomastoidien muscle. It can also manifest itself as a recurrent suppurative thyroiditis sometimes with dysphagia and stridor. Sonography is the imaging method of choice for evaluating congenital neck lesions in children. It shows a thin-walled echolucent cyst if not infected or a thickwalled hyperemic abcess in front of the thyroid. CT and MR are required to define the extent of the lesion. These examinations show either a thin-walled well-defined cyst without significant enhancement, or if infected, a thick-walled cyst with surrounding cellulitis. Barium esophagography or direct laryngoscopy may reveal an outpouching of the pyriform apex. A barium swallowing test can identify a sinus tract extending from the apex of the pyriform sinus to the lower anterior neck. Treatment consist of a chirurgical resection. References 1.

Wang H.-K., et al.: Imaging studies of pyriform sinus fistula. Pediatr Radiol, 2003, 33: 328333.

1. Department of Medical Imaging, CHU Liège, Liège, Belgium.

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JBR–BTR, 2011, 94: 352.

IMAGES IN CLINICAL RADIOLOGY Particular location of a cardiac pacemaker lead V. Hamoir¹, X. Hamoir², J. Kirsch² A dual-chamber pacemaker was implanted in a 69-year-old man. As far as the surgeon was concerned, there were no problems with implantation via a left subclavian transvenous route. The location of the leads seemed to be correct under the fluoroscope. Stimulation thresholds were correct. The chest radiograph was initially considered not revealing anomaly and the position of the electrodes was described as: "ends of leads appear to be correctly placed". On performing precise checks on the pacemaker, the ECG had the appearance of complete right bundle-branch block, during ventricular stimulation, a reason for fearing malpositioning in the left ventricle. The chest X-rays (A) were re-examined. On the lateral X-ray, the lower part of the ventricular lead has a first posterior small kink and is then distinctly directed anteriorly but its end remains clearly distant from the anterior surface. Was it still correctly positioned in the right ventricle? An ultrasound examination (B) was performed: the lead passed from the right atrium to the left atrium through the inter-atrial septum at the foramen ovale (arrow) then it penetrated the left ventricle through the mitral valve (arrow head). Despite the ambiguous appearance of the chest X-rays at the beginning, this lead was therefore malpositioned. A thoracic scan (C) was performed for another indication and also clearly showed the stimulation lead in the left atrium then the left ventricle.

Comment It is important to make sure that a ventricular stimulation lead has been correctly positioned in the right ventricle (the usual position). Indeed its location in the left ventricle is not without consequence (1) because it clearly increases the risk of thromboembolic events and thus requires anticoagulation. Correct positioning of the ventricular electrode is generally checked by frontal plus lateral fluoroscopy during implantation (but lateral fluoroscopy is sometimes difficult to perform in the operating theatre) then by standard post-operative PA and above all, lateral chest radiographs. Usually in the case of normal positioning in the right ventricle, the distal (inferior) part of the lead is directed anteriorly, while if it is positioned in the coronary sinus or the left ventricle, the stimulation lead is directed posteriorly. The chest X-rays are nevertheless sometimes more difficult to interpret, C as in this case with a very slight posterior kink of the ventricular lead before a clear direction forward. An ultrasound examination can solve the problem in a non-invasive way without any radiation. If there is a doubt about the location of the end of a stimulation lead, it should be performed as soon as possible, while the cardiac electrodes are still easily moveable. A thoracic scan is an alternative but involves radiation. Reference 1.

Van Gelder B., Bracke F., Oto A., et al.: Diagnosis and management of inadvertently placed pacing and ICD leads in the left ventricle: a multicenter experience and review of the literature. Pacing Clin Electrophysiol, 2000, 23: 877-883.

1. Cardiology Department, 2. Medical Imaging Department, Centre Hospitalier de Wallonie Picarde, site Clinique Notre-Dame, Tournai, Belgium.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 353.

IMAGES IN CLINICAL RADIOLOGY Selective spleen SPECT/CT G. Ceulemans1, A. Sermeus, D. Verdries2, M. Keyaerts1, B. Ilsen, M. Kichouch, M. De Ridder, H. Everaert1

During virtual colonoscopy, performed for severe constipation in a 77-year-old male, a mass (22 x 51 mm) was detected in the tail of the pancreas. The CT features of the lesion were compatible with a mucous cystadenoma / cystadenocarcinoma: low density (HU: 40), smooth margins and presence of micro-calcifications (Fig. A). The patient's history included: prostatectomy for prostate cancer, splenectomy following trauma, atrial fibrillation for which he was chronically anticoagulated. A biopsy was contraindicated because of anticoagulation, so additional MRI images were acquired. The mass showed heterogenous contrast enhancement in the arterial phase, a contrast enhancing pattern which excludes the diagnosis of cystadenoma / cystadenocarcinoma, and suggests that the lesion could consist of ectopic splenic tissue (Fig. B). A selective spleen SPECT/CT scan showed intense accumulation of heat denaturated 99mTc-labeled red blood cells in the lesion confirming hereby the presence of functioning splenic tissue (Fig. C). Comment

This technique consists of ex-vivo labelling erythrocytes with 99mTc-pertechnetate, heating the cell to 49.5Â°C during 15 minutes and washing the cells prior to intraveous administration. Imaging can be started 30 min after injection. Although selective spleen scintigraphy has been around for more than 3 decades and its yield to detect functional splenic tissue is very high, most nuclear medicine specialists and radiologists are reluctant to use it, largely because most of them are unfamiliar with the technique. However, when ectopic splenic tissue is suspected, and other imaging techniques fail to determine the exact nature of the lesion or when biopsy is contra-indicated or risky, hybrid imaging with heat denaturated 99mTc-labeled red blood cells can lead to the diagnosis. Reference 1. Smith T.D., Richards P.: A simple kit for the preparation of 99MTc-labeled red blood cells. J Nucl Med, 1976, 17: 126-132.

Department of 1. Nuclear Medicine, 2. Radiology, UZ Brussel, Brussels.

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94: 354.

IMAGES IN CLINICAL RADIOLOGY Enchondroma protuberans of the rib L.J. Ceulemans1, L. Verheyen1, F.M. Vanhoenacker2, R. De Wyngaert3, J. De Leersnyder1 A 20-year-old man presented with a hard and painless swelling at the left chest wall. Plain radiographs showed an expansile lesion of the third rib. Most of the lesion was intramedullary located, well-defined and osteolytic, whereas the inner portion (black arrow) was partially calcified and protruding within the chest (Fig. A). The costochondral junction was not involved. Subsequent CT confirmed the eccentric location of the lesion. The inner part contained chondroid-like calcifications and showed intimate relationship with the left lung (white arrow). There was osseous expansion resulting in focal absence of the outer cortex. Sparing of a thin layer of fat adjacent to the outer cortex was indicative of absence of soft tissue extension (Fig. B). On MRI, the outer medullary part of the lesion was of high signal on T2-weighted images, in keeping with cartilaginous matrix. The exophytic inner part (white arrow) was of intermediate signal, with internal foci of low signal due to chondroid calcifications (Fig. C). Based on the imaging findings, the diagnosis of a cartilaginous tumor was made. Because of the marked bone expansion and the central location in the ribs, a chondrosarcoma could not be excluded. Therefore, partial surgical resection of the rib was recommended and histology revealed the diagnosis of an enchondroma protuberans.

Comment Enchondroma is a benign cartilage tumor, derived from displaced embryonic rests in the physis. The lesion typically develops centrally within the intramedullary cavity of the metadiaphysis of the short or long tubular bones. The ribs are only rarely involved. Enchondroma protuberans consists of a morphological variant caused by eccentric osseous expansion beyond the bone surface. This variant had been reported in the humerus, the phalanges of the hand and the ribs. Radiographically, an enchondroma protuberans typically presents as a well-defined intramedullary osteolytic lesion associated with an exophytic component protruding through a focal defect of the cortical bone. CT may better demonstrate lesion extension and the relationship with the adjacent pleura. On MRI, the lesion is of low to intermediate signal on T1-weighted images, whereas T2-weighted images show a hyperintense mass with internal low-intensity septa or nodules, reflecting the cartilaginous matrix with chondroid calcifications. The main differential diagnosis of an enchondroma protuberans of the rib includes a sessile osteochondroma or a chondrosarcoma. The intramedullary location of the cartilaginous matrix on MRI is in favour of a lesion arising from the medullary bone i.e. enchondroma, whereas a sessile osteochondroma is covered by a superficially located cartilage cap. In case of a cartilaginous lesion within the rib, a chondrosarcoma should always be considered, since malignant cartilage tumors are more frequent than benign within the ribs and axial skeleton. Therefore, treatment of choice consists of partial rib resection, allowing accurate histopathological examination and preventing further tumor growth.

C Reference 1.

Keating R.B., Wright P.W., Staple T.W.: Enchondroma protuberans of the rib. Skeletal Radiol, 1985, 13: 55-58.

1. Department of Surgery, AZ Sint-Maarten, Duffel-Mechelen, Duffel, Belgium, 2. Department of Radiology, AZ Sint-Maarten, Duffel-Mechelen, University Hospital Antwerp and University of Ghent, Belgium, 3. Department of Radiology, Regionaal Ziekenhuis Heilig Hart, Leuven, Belgium.

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JBR–BTR, 2011, 94: 355.

IMAGES IN CLINICAL RADIOLOGY Unexpected pyomyositis of right buttock S. Van Nieuwenhove, F. Haven, L. Ghijselings, J. Pringot, P. Matthys1 A 11-year-old boy was admitted to the emergency department complaining of pain in the right hip, fever and had developed a noticeable limp sinds one week. He had fallen on his buttock in the swimming pool a few weeks before. Physical examination revealed pain at the mobilisation of the right hip, without limitation of movement. The laboratory data showed increased value CRP (154 mg/l) and leukocytosis at 11300 WBC/µl. X-ray of the right hip was normal. Ultrasound of the right hip, performed to exclude arthritis, didn’t show any intra articular fluid. Careful anamnesis oriented examination towards his right buttock. The study of the postero internal muscles of the buttock revealed right-left asymmetry. There was heterogeneous tumefaction of the right quadratus femoralis muscle with central hypoechoic collection compatible with an intramuscular abscess (Fig. A, axial view, white arrows, GT: greater trochanter, I: Ischium, GM: Gluteus Maximus muscle). MRI of the pelvis showed an hyperintense aspect of the right quadratus femoris, obturator internus and externus muscles on T2-weighted sequence. It confirmed the presence of multifocal fluid collections hyperintense on T2-weighted sequence (Fig. B, axial view, white arrows) and hypointense with a enhancing rim on T1-weighted sequence after Gadolinium (Fig. C, axial view, white arrows). Aspiration of the target collection of 2,5 cm in diameter under MDCT guidance showed culture positive for Multi Sensitive Staphylococcus aureus. The boy was hospitalized in the pediatric department during a week with intravenous antibiotherapy. The US control 3 weeks after antibiotics per os didn’t show any residual muscle abscess.

C Comment Pyomyositis is the primary acute bacterial infection of the skeletal muscle. It usually affects a group of muscle and mostly the lower extremities. Endemic in tropical countries, it is quite uncommon in temperate areas with an incidence of 1/3000-1/4000. It is commonly associated with immunodeficiency or trauma.The causative agent is Staphylococcus aureus in 85%90%. The clinical history can be divided in three stages. The first stage passes usually unnoticed and consists of general symptoms for a period of two weeks. During the second (or suppurative) stage, the diagnosis is often made. The fever is higher and local symptoms are predominant with swelling, tenderness and myalgia. In the last stage, systemic manifestations are severe and may lead to septic shock with renal failure. Ultrasound shows an enlargement and heterogeneous echo texture of the muscle with or without a central hypoechoic fluid collection (abscess). On CT, pyomyositis is defined as an enlarged muscle with heterogeneous attenuation and a central fluid collection with rim enhancing. The pyomyositis in MRI is described as increase signal intensity on T2-W images corresponding to muscle edema and a central low signal with a hyperintense enhancing rim on T1-weighted images after Gadolinium. MRI is the best technique to determine the localization and extension of abscess. In summary, a child complaining of painful hip, limp, and fever doesn’t always have arthritis. For this reason, ultrasound keeps some advantages ; it can exclude intra articular fluid and can be useful in the suppurative stage of pyomyostis (for guided puncture and follow up). Reference 1.

Gonzalez Moran G., Garcia Duran C., Albinana J.: Imaging on pelvic pyomyositis in children related to pathogenesis. J Child Orthop, 2009, 3: 479-484.

1. Radiology Department, Cliniques de l’Europe, Brussels, Belgium.

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JBR–BTR, 2011, 94: 356.

IMAGES IN CLINICAL RADIOLOGY Focal infarction of lesser omentum M. Bersou, Ch. Heylen, P. Matthys, J. Pringot1

 







A 25-year-old man came to the emergency department complaining of continuous right para-umbilical pain radiating to the epigastric midline since the previous night. Pain was associated with tenderness. He had no fever and the rest of the physical examination was normal. Laboratory studies showed a normal white blood cell count and C-reactive protein level was 11 mg/L (normal < 10 mg/L). Pain was relieved by paracetamol. Abdominal ultrasound (Fig. A) showed a painful incompressible hyperechoic pre-pancreatic ovoid mass (white arrows) about 4 centimeters wide, with low background attenuation, located on the epigastric mid-line between the liver (black star), the pancreas (white star), and left to the duodenum (curved arrow). MDCT (Fig. B) confirmed a slightly hyperdense mass (white arrows) of 2,8 x 1,7 x 3,5 cm with well-defined contours and containing hyperdense streaks (curved arrow), localised in the lesser omentum – contiguous to gastric arteries – on different multiplanar reformated views, along the stomach lesser curvature (white star). The diagnosis of infarction of the lesser omentum was proposed, and conservative treatment was introduced. He received oral analgesic and antiinflammatory drugs, and became asymptomatic in a few days. Comment

In 1999, van Breda Vriesmann et al were the first in defining the concept of intraperitoneal fat focal infarction (IFFI). They described different sites of focal fatty tissue necrosis with similar clinical signs, etiology, radiological features, prognosis and treatment. In the literature, most of the cases of IFFI concern the greater omentum and epiploic appendages, by torsion and/or infarction of fatty appendages. The differential diagnosis is to be made with diverticulitis, appencitis, cholecystitis or gynecological pathologies. In our case, the differential diagnosis included pancreatitis and gastro-duodenal diseases. Usually patients with infarction of lesser omentum present epigastric   pain with tenderness and sometimes signs of peritoneal irritation. Biological parameters are mild elevated white blood cell count and  C-reactive protein or even normal. Like in this case, the ultrasound images show an incompressible, painful, moderatly hyperechogeneic and well-circumscribed epigastric mass (Fig. A). Computed tomography images also show a wellcirconscribed slightly hyperdense mass, along the lesser curvature of the stomach, in the vicinity of the prancreas, containing hyperdense streaks C corresponding to fibrous bands and/or dilated thrombosed veins (Fig. B). US and CT findings contribute to differentiate from other primary bening masses in the lesser omentum like stromal tumor, hemangioma, neurogenic tumor and teratoma, as well as malignant processes such as lymphoma, metastatic diseases and sarcomas. In case of doubt, an imaging follow-up may be necessary. Any kind of IFFI presents the same clinical expression, evolution and conservative treatment (oral analgesic and antiinflammatory drugs). Reference 1.

Contribution of US and CT for diagnosis of intraperitoneal focal fat infarction (IFFI): a pictorial review. JBR–BTR, 2010, 93: 171184.

1. Department of Radiology, Clinique Sainte-Elisabeth, Bruxelles, Belgium.

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JBR–BTR, 2011, 94: 357.

IMAGES IN CLINICAL RADIOLOGY Typical CT and MRI features of cortical laminar necrosis J.L. Samain1 2, F. Haven1, M. Gille3, P. Mathys1

A 47-year-old woman with a prior medical history of SLE and chronic arterial hypertension developed a post-anoxic coma after a prolonged cardiac arrest. She also presented a convulsive status epilepticus. At admission contrast enhanced CT brain (not illustrated) showed minimal loss of gray-white differentiation in the left sylvian region. Due to detoriation of the patient a follow-up CT scan was performed two weeks later. This examination showed hyperdensity in a laminar way, following the cortical gyri, mostly in the temporoparieto-occipital region (Fig. A and B). In the left peri-rolandic region this is associated with low-attenuation sub-cortical edema (Fig. B). Low density of the lentiform nuclei was also observed. Further examination by MRI showed in the same areas thin cortical hyperintensity on sagital T1- and hypo-intense on axial T2-weighted imaging (white arrow in Fig. C). A hyperintense signal in the putamen is seen on T1 weighted imaging (black arrow in Fig. C). T2- and FLAIR- weighted sequence displayed increased signal in the white matter and throughout the subcortical layer, most accentuated in the temporoparietooccipital region (arrow in Fig. D). Diagnosis of advanced cortical laminar necrosis with bilateral deep gray nuclei involvement and encephalomalacia as typical manifestation of anoxic-ischemic brain damage was made. Shortly afterwards the patient passed away. Comment

Several signs of advanced anoxic-ischemic brain damage were observed in our case. The most striking finding is the imaging manifestation of the so called ‘cortical laminar necrosis’. Histological studies demonstrate much more vulnerability of grey matter than white matter to ischaemic necrosis due to hypoperfusion. The third layer of the gray matter is the most vulnerable and the damage is usually greater in the depths and sides of the sulci than over the crest of the gyri. Cortical laminar necrosis is a specific type of cortical infarction, which usually develops as a result of generalized hypoxia rather than a local vascular abnormality. Depletion of oxygen or glucose as in anoxia, hypoglycemia, status epilepticus, ischemic stroke and less common in immunosuppressive therapy and polychemotherapy has been attributed as an underlying cause of cortical laminar necrosis. A hypoxic insult leads to death of neurons, glia and blood vessels along with degradation of proteins. When cortical laminar necrosis is seen on CT imaging, it presents as gyriform linear hyperdensity in the superficial cortex, most frequently located in the medial occipital lobes and perirolandic regions. Mostly this is a subtle finding, but the image can be more spectacular in more severe cases. These areas are often associated with cortical hypoattenuation as presentation of oedema. Cortical enhancement is first seen after 2 weeks, peaks after 1 to 2 months, and is usually resolved after 6 months. Contrast enhancement is present due to disruption of the blood-brain barrier, where loss of neurons and vascular proliferation occur. Initially thought to be caused by hemorrhagic infarction, histopathological examination has demonstrated the cortical short T1 lesions to occur by neuronal damage, reactive tissue change of glia and deposition of fat-laden macrophages. The close interrelation between the protein concentration and free water content makes MR signal changes more complex. Early cortical changes usually show low signal intensity on T1-weighted, which could be due to acute ischemic changes (tissue edema). Usually, cortical high intensity lesions on both T1-weighted and FLAIR-weighted images appear two weeks after the ictus indicating short T1 and long T2 lesions. Protondensity images are even more sensitive than T1-weighted MR images. Cortical diffusion abnormalities in the early postanoxic period are proven to be associated with poor outcome. To conclude, cortical laminar necrosis has no pathognomonic features but shows characteristic chronological signal intensity changes, especially seen on T1-weighted, FLAIR and proton-density MR images. On CT imaging the cortical linear hyperdensities are mostly seen in severe hypoxic-ischemic brain damage.

Reference 1. Siskas N., Lefkopoulos A., Ioannidis I., et al.: Cortical laminar necrosis in brain infarcts: serial MRI. Neuroradiology, 2003, 45: 283-288. 1. Department of Radiology, Europaziekenhuizen/Clinique de l’Europe, Brussels, Belgium, 2. Department of Radiology, UZ Gasthuisberg, Leuven, Belgium, 3. Department of Neurology, Europaziekenhuizen/Clinique de l’Europe, Brussels, Belgium.

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JBR–BTR, 2011, 94: 358-362.

PROCEEDINGS OF THE RBRS SECTION BREAST IMAGING, JUNE 7, 2011, LEUVEN An atypical breast lesion: bilateral multiple myoid hamartoma S. Dekeyzer1, K. Vanwambeke1, C. Petre1, I. Pilate1, F.M. Vanhoenacker1,2, M. Eyselbergs, G. Jacomen3, G. De Praeter1 A 41-year-old female presented at the department of radiology because of multiple slowly growing lumps in both breasts. Mammography showed dense breast tissue with multiple wellcircumscribed round lesions with no calcification. At ultrasound, sharply defined, heterogeneous oval masses were seen. On T2-Weighted Images (WI), the lesions were heterogeneous and hyperintense. T1-WI after intravenous administration of gadolinium contrast showed multiple rapidly and strongly enhancing lesions with type 2 to 3 curves (plateau and wash-out curve). Core needle biopsy reported bilateral multiple myoid hamartoma. Hamartoma of the breast is a benign proliferation of fibrous, glandular, and fatty tissue surrounded by a thin capsule of connective tissue. Breast hamartomas consist of approximately 0.7-5% of all benign breast tumors. The majority of these lesions occur in women over 35 years of age. The myoid or the muscular variant, Myoid Breast Hamartoma (MBH) is exceptionally rare with less than 30 reported cases in the English medical literature. The clinical, radiological and pathological features are discussed. The differential diagnosis includes other benign (e.g. multiple fibroadenomas, leiomyomas) and malignant breast lesions (e.g. leiomyosarcomas). A core biopsy is usually diagnostic for a myoid hamartoma, although excision and subsequent immunohistochemical examination is mandatory for definite diagnosis of this rare lesion. References 1.

Feder J.M., de Paredes E.S., Hogge J.P., et al.: Unusual Breast Lesions: Radiologic-Pathologic Correlation. Radiographics, 1999, 19: S11-S26. 2. Irshad A., Ackerman S.J., Pope T.L., et al.: Rare Breast Lesions: Correlation of Imaging and Histologic Features with WHO Classification. Radiographics, 2008, 28: 1399-1414. 3. Harish M.G., Konda S.D., MacMahon H., et al.: Breast Lesions Incidentally Detected with CT: What the General Radiologist Needs to Know. Radiographics, 2007, 27: S37S51. 1. Department of Radiology AZ St.Maarten, Duffel-Mechelen, Duffel, Belgium, 2. Department of Radiology

Antwerp University Hospital, Edegem, Belgium, 3. Department of Pathology, AZ St.-Maarten, Duffel-Mechelen, Belgium.

Intracystic papilloma of the breast M. Smets, C. Van Ongeval, A. Van Steen1 Background

Do non specific minimal signs in a biennial mammographic breast cancer screening progamme need further diagnostic assessment? R.M. Maes1 This artcle is the inspiration for a presentation on a meeting of the Section Senology RBRS on 7/6/2011 by M. Mortier and P. De Visschere, U GENT. Definition Minimal Signs (MS) in accordance to BIRADS 4th ed.: – – – – –

Asymmetry Global asymmetry Focal asymmetry Microcalcifications with low suspicion Masses, round or oval, sharply circumscribed, slightly lobular – Parenchymal distortion Frequency minimal signs in screening: +/- 10%. Definition of probably benign: ”lesions that carry a less than 2% likelihood of malignancy (lesions for which at least 50 biopsies are needed to identify 1 cancer)” (JWL Leung, Radiol Clinics North Am (2007) 45: 773-789). A developing mammographic sign, when compared with previous films, cannot be interpreted as MS. When developing the likelihood of malignancy is sufficiently high to justify recall and if necessary biopsy. In these cases, normal sonographic findings do not exclude malignancy. RiskFalse Negative (Sickles. Radiology (1991) 179: 463-468): Periodic mammographic follow-up of probably bening lesions: results in 3184 consecutive cases: 17 malignant = PPV 0.5%. Characteristics of missed cancers in screening mammography: – unfulfilled strict probably benign criteria – under- or overexposed films – image unsharpness, motion artifacts – inadequate positioning: lesion not on the film – inadequate compression – artifacts – lesion on the edge of the film: prepectoral, inframammary fold, retroareolar Conclusion The additional risk to that of screened women in general when a minimal sign is present is + 0,5%. When mammography analysis is done correctly and the criteria of probably benign are strictly fulfilled the advice of R. Maes is to invite those women for the next screening round in 2 years.

A 53-year-old woman (1) and a 47year-old woman (2) presented for workup of a painless large breast mass. They both had no significant personal or family history. The mass of the second patient showed distinct progressive growth. Mammography was performed for the first patient (impossible for the second patient due to the extent of the mass) and ultrasound was performed on both patients, as well as additional MRI for the first patient, and CT-scan for the second. Work-up Mammography showed multiple large cysts in the left breast in patient 1. Ultrasound depicted these cystic lesions and showed additional intracystic solid wall proliferations in both women. An MRI examination in the first patient confirmed the large cysts with solid wall components with contrast enhancement of the solid lesions. Since this image was suspect for malignancy, additional fine needle aspiration cytology (FNAC) was performed. A CT-scan performed on the second patient was better able to depict the extent of the mass and its relation to the chest. FNAC of the cystic mass was performed in both patients. Radiological diagnosis Based on the radiological (mainly ultrasound and MRI) and cytological findings, diagnosis of intracystic papilloma was made. Discussion An intracystic papilloma (ICP) is a benign papillary lesion supported by a fibrovascular stalk, growing inside an apparent cystically dilated duct. It may occur at any age but is most commonly seen between 30 and 55 years. It is very difficult to distinguish radiographically between ICP and intracystic papillary carcinoma (ICPC). ICP more often forms a single nodule protruding intracystically, while ICPC usually is larger (> 3 cm) and forms multiple aggregate nodules or even almost solid tumors with a small cystic part. Despite these guidelines, intracystic papillary lesions may be impossible to differentiate. The kinetic features for contrast enhancement on MRI are not helpful either since both the benign and malignant papillary lesions exhibit fast, strong, early enhancement and washout or a plateau enhancement pattern. Therefore, FNAC should be performed on all cystic breast masses with internal

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PROCEEDINGS OF THE RBRS SECTION BREAST IMAGING solid wall proliferations. To start, it can help differentiate between intracystic debris and true solid components. And second, cytologic examination can help evaluate for malignant cells suggestive of ICPC. However, even FNAC as well as core biopsy with pathology of a intracystic papillary lesion can be misleading because cellular atypia is slight in the majority of ICPC’s. For this reason and because several studies have shown that a substantial number of lesions are upgraded in diagnosis at excision, all intracystic papillary lesions diagnosed by either imaging or cytology, should be excised surgically References 1.

Devan J.D., David E.M., Giovanna M.C., et al.: Complex cystic breast masses: diagnostic approach and imaging-pathologic correlation. RadioGraphics, 2007, 27: S53-S64. 2. Uematsu T., Kasami M.: MR imaging findings of benign and malignant circumscribed breast masses: part 2. Cystic circumscribed masses. Jpn J Radiol, 2009, 27: 405-409. 3. Kihara M., Miyauchi A.: Intracystic papilloma of the breast forming a giant cyst. Breast Cancer, 2010, 17: 68-70. 1. Department of Radiology, UZ Leuven, Leuven, Belgium. Unusual breast metastasis M. Walsdorff1, K. Vanden N. Hottat1

Houte2,

Metastatic malignancy in the breast is unusual, especially metastatic spread from extramammary primary tumors. We report a rare case of metastasis to the breast from a renal cell carcinoma. Case presentation A 71-year-old woman consulting for a routine breast cancer screening, with no history of breast cancer, presented with an asymmetric palpation of the upper left quadrants. The mammogram, ultrasound and magnetic resonance imaging suggested a malignant mass at the junction of the upper left quadrants. An ultrasonography-guided core biopsy was taken to assess the nature of the lesion. The histopathological examination and immunohistochemical tests showed it to be a metastasis from a renal cell carcinoma. Consecutive computed tomography of the abdomen confirmed the renal origin of the metastasis. Palliative treatment was recommended based on a multidisciplinary assessment. Conclusion Breast metastases are uncommon but are not to be disregarded as their finding might reveal an aggressive underlying primary tumor. Imaging and histopathology are complementary in diagnosing the disease and evaluating its spread.

References 1. Toombs B.D., Kalisher L.: Metastatic disease to the breast: clinical, pathologic, and radiographic features. AJR, 1977, 129: 673-676. 2. Lee W.K., Cawson J.N., Hill P.A., Hoang J., Rouse H.: Renal cell carcinoma metastasis to the breast: mammographic, sonographic, CT, and pathologic correlation. Breast J, 2007, 13: 316-317. 3. Hajdn S.I., Urban J.A.: Cancers metastatic to the breast. Cancer, 1972, 29: 1691-1696. 4. Maounis N., Chorti M., Legaki S., Ellina E., Emmanouilidou A., Demonakou M., Tsiafaki X.: Metastasis to the breast from an adenocarcinoma of the lung with extensive micropapillary component. Diagn Pathol, 2010, 5: 82-88. 5. Durai R., Ruhomauly S.N., Wilson E., Hoque H.: Metastatic renal cell carcinoma presenting as a breast lump in a treated breast cancer patient. Singapore Med J, 2009, 50: 277-278. 6. Forte A., Peronace M.I., Gallinaro L.S., et al.: Metastasis to the breast of a renal carcinoma: a clinical case. Eur Rev Med Pharmacol Sci, 1999, 3:115118. 7. Vassalli L., Ferrari V.D., Simoncini E., Rangoni G., Montini E., Marpicati P., et al.: Solitary breast metastases from a renal cell carcinoma. Breast Cancer Res Treat., 2001, 68: 29-31. 8. McLauglin S.A., Thiel D.D., Smith S.L., Wehle M.J., Menke D.M.: Solitary breast mass as initial presentation of clinically silent metastatic renal cell carcinoma. Breast, 2006, 15: 427429. 9. Carr B.I.: Renal carcinoma manifesting as a breast mass. Urology, 1983, 21: 166-167. 10. Alzaraa A., Vodovnik A., Montgomery H., Saeed M., Sharma N.: Breast metastasis from a renal cell cancer. World J Surg Oncol, 2007, 5: 25. 11. Mesa Alvarez A., Díaz García A., Nava Tomás E., Calvo Blanco J.: Breast metastasis as initial presentation of renal cell carcinoma. Actas Urol Esp, 2010, 34: 288-303. 12. Torres Muros B., Solano Romero J.R., Rodríguez Baró J.G., Bonilla Parrilla R.: Adenocarcinoma renal metastásico en seno maxilar. Actas Urol Esp, 2006, 30: 954-957. 13. Motzer R.J., Michaelson M.D., Redman B.G., et al.: Activity of SU11248, a multitargeted inhibitor of vascular endothelial growth factor receptor and platelet-derived growth factor receptor, in patients with metastatic renal cell carcinoma. J Clin Oncol, 2006, 24: 16-24. 14. Motzer R.J., Rini B.I., Bukowski R.M., et al.: Sunitinib in patients with metastatic renal cell carcinoma. JAMA, 2006, 295: 2516-24. Department of 1. Radiology, 2. Pathology, Brugmann Hospital and ULB-VUB, Brussels, Belgium.

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Diagnostic accuracy of core biopsy and vacuum assited biopsy in case of atypical hyperplasia of the breast L. Bonne, A. Van Steen, C. Van Ongeval1 Long term follow-up of patients initially diagnosed with atypical hyperplasia of the breast (a collective noun that includes atypical ductal hyperplasia, flat epithelial atypia, atypical lobular hyperplasia and lobular carcinoma in situ) has shown us that it has an increased risk of malignant degeneration. Through improved imaging techniques, organization of breast cancer screening programs and the increasing use of advanced biopsy techniques such as vacuum assisted biopsy, atypical hyperplasia has been diagnosed more and more frequently during recent years. Results of follow-up surgical excision have shown us that core biopsy (CNB) and vacuum assisted biopsy (VAB) are associated with a certain underestimation rate in case of atypical hyperplasia. The purpose of this study was therefore to evaluate the accuracy and diagnostic value of today’s most frequently used biopsy techniques in case of atypical hyperplasia in order to ensure a proper indication for surgical excision. Materials and methods We searched the Pubmed database for following terms: ‘atypical hyperplasia’, ‘atypical ductal hyperplasia’, ‘flat epithelial atypia’, ‘atypical lobular hyperplasia’, ‘lobular carcinoma in situ’, ‘breast’, ‘core biopsy’, ‘vacuum assisted’ for the period 2001-2010. We selected publication that compared the results of CNB/VAB with those of surgical excision. Publications with mixed or synchronous pathology were excluded. Results and discussion 45 publications were selected, representing 176 241 biopsies. The mean prevalence of atypical hyperplasia was 2,2% (ADH 3,6%; ALH/LCIS 0,86%; FEA/FEA+ADH 1,7%). The frequency where the CNB/VAB result was an underestimation of the result of surgical excision (malignancy) was expressed as a percentage (the underestimation ratio or upgrade ratio ‘UR’). We mention four major findings. First, ADH seems to be more frequently underestimated (UR 1/3) than lobular neoplasia (LN = ALH+LCIS) and FEA/FEA+ADH (UR 1/5). Secondly, switching from CNB to VAB in case of atypical hyperplasia implies a reduction of the UR of about 50% (for example for ADH from 43% to 23%). This is probably due to the fact that VAB is able to obtain more and larger tissue fragments, that it uses a single insertion technique and that it is frequently associated with the use of stereotaxis (cfr. infra). Thirdly, needle diameter plays an important role; 11 Gauge needles have an UR that is 5 to 10% lower than the UR of 14 Gauge needles. UR’s of larger needle diameters were probably less reliable because of the limited number of biopsies performed with these diameters. Finally, stereotaxis

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360 seems to be a much more reliable technique than ultrasound (UR 24% and 42% respectively), though this is probably due to the fact that ultrasound is still often used together with CNB, which has an inherently higher UR (cfr. supra). The fact that MRI has a relatively low accuracy (45%) is likely due to the limited number of publications and limited experience. Furthermore, age (> 50 years) and a mass on imaging were two predictive factors of underlying malignancy. Conclusion In case of atypical hyperplasia, ADH is associated with the greatest underestimation ratio (1/3). LN and FEA are underestimated less frequently (1/5). A relatively large needle diameter (11G) is essential for correct diagnosis, as well as a sufficient number of tissue fragments (at least 5). VAB ensures a reduction of the underestimation rate of about 50% compared to CNB. Stereotaxis seems to be more precise than ultrasound. These new imaging and biopsy methods thus imply an important improvement in diagnosis. However, underestimation rates of CNB and VAB in case of atypical hyperplasia are still significantly high, making wider surgical excision recommended, irrespective of the used localization technique and needle diameter. 1. Department of Radiology, UZ Leuven, Leuven, Belgium.

JBR–BTR, 2011, 94 (6) complication (1). The diagnosis is based on the cytological analysis of the periprosthetic liquid showing a silicone leakage. Moreover, no sign of breast implant rupture is observed. Magnetic resonance is the more sensitive exam for the detection of a breast implant rupture (2). In our case, the surgeon has decided to perform a surgical revision of the implant in order to formally exclude a rupture. In this situation, other colleagues propose some repeated fine needle aspirations of the periprosthetic liquid associated with a nonsteroidal anti-inflammatory drug. However, the optimal management of this unusual complication remains unclear. References 1.

O'Neill J.K., Rigby H., Kenealy J.M.: Leakage and osmotic shifts in PIP Hydrogel implants. A case demonstrating increase and decrease of implant volume in the same patient. J Plast Reconstr Aesthet Surg, 2008, 61: 1122-1123. 2. Boutemy R.: Imagerie des prosthèses mammaires. EMC, Radiologie et imagerie médicale – génito-urinaire – gynéco-obstétricale – mammaire. 2010 34-822-A-10. Department of 1. Medical imaging, 2. Pathology. CHR St-Joseph, Mons, Belgium.

Osmotic exchanges through the membrane of a silicone breast implant: an unusual complication S. Murgo1, P. Van Eeckhout2

The risks of radiation therapy of breast cancer R. D’Hauwe, L. De Cocker, C. Van Ongeval1

A 25-year-old woman is addressed for a breast ultrasound. Ten months ago, she had been operated for a bilateral breast augmentation. Two Eurosilicone gel-filled breast implants were inserted in retropectoral position. The patient had no relevant previous medical history and no risk factor of breast cancer. The clinical examination reveals a painful increased of volume of the left breast. The ultrasound demonstrates an echoic liquid surrounding the left breast implant. No sign of breast implant rupture is observed. A fine needle aspiration of periprosthetic liquid is performed under ultrasound guidance. The cultures of the liquid are negatives. The cytological analysis shows histiocystes with cytoplasmic vacuoles of silicone. The patient has been operated in another hospital and her surgeon confirms the absence of breast implant rupture. Thus, we conclude to a phenomenon of osmosis through the membrane of the left breast implant.

Radiation therapy of breast cancer can, in very rare cases, imply some oncologic consequences. We introduce two women with a slightly different presentation of the same radiation induced oncologic pathology. Both women had a broad excision of an intraductal adenocarcinoma (IDA) of the breast with axillary clearance within ten years from now. They both received radiation therapy (25 x 2 Gy) with a radiation boost (16 Gy) of the tumor bed. Our first patient, with a history of IDA of the right breast, presents with a one week lasting sensitive areola, and an induration felt at 5 o’clock, in the right breast. An ultrasound only reveals some postoperative sequelae, and additional biopsy shows no abnormalities. 5 months later, due to persisting pain, with a swollen breast, and a retracted nipple, an MRI of the breasts is performed. In the right breast, two lesions with rapid rim enhancement are visualised, and more caudally there are two zones of contrast captation without clear delineation. Mammography reveals no specificities. A repeated ultrasound shows expansive hyperreflective nodular zones with a hyporeflective border. Biopsy of these zones is performed. Our second patient, with a history of IDA of the left breast, complains of a red,

Discussion The osmotic exchange through the ”semi-permeable” membrane of a silicone breast implant is an unusual

painful left breast, wich feels warm, and is edemateous. To confirm this clinical presentation of peau d’orange, an MRI of the breasts is performed. This shows pathological strong enhancement of the left nipple and areola, as well as a strongly enhancing zone retroareolarly, expanding a few cm posteriorly. A difficult differential diagnosis remains after this examination: inflammatory disease or tumoral pathology, and an ultrasound with puncture is performed. The ultrasound is suggestive of inflammatory changes and the following biopsy shows benign findings compatible with fibrosis. Clinical symptoms remain the same, and two months later the ultrasound is repeated. The imaging findings are now slightly different: a heterogeneous hyporeflective zone retro-areolarly and laterally, and within this zone a small hyporeflective nodular structure with prominent peripherical vascularisation. The biopsy is repeated. Biopsy in the two patients reveals the same pathology: a radiation induced angiosarcoma. Both our patients were treated with a mastectomy. Radiation Induced Angiosarcoma is a high grade tumor with an aggressive nature. The diagnostic criteria include previous radiotherapy with a latency of several years (5 or more), development of sarcoma within a previously irradiated field, and a histologic confirmation. The radiation dose, responsible for the development of this type of angiosarcoma, lies within the total range of 4050 Gy. It is a very rare pathology, with an incidence of 0.05-0.2%, and the average latency period is 12.5 years. Presentation is as a (sub-)cutaneous, painless lesion, flat or nodular, and with a (pathognomonic) bluish or purplish aspect. Hence, differentiation from a benign angioma, or teleangiectasis is sometimes difficult. Diagnosis of this pathology brings some serious challenges as well, first of all due to its rarity. In addition, it has a benign appearance, and is also difficult to differentiate from radio-induced changes. Mammography plays no important role in diagnosis, due to the very aspecific findings, nor does ultrasound. Core needle biopsy with pathologic confirmation is central in the diagnosis. Treatment is never conservative, but consists of mastectomy. References 1.

Tahir M., Hendry P., Baird L., Qureshi N.A., Ritchie D., Whitford P.: Radiation induced angiosarcoma a sequela of radiotherapy for breast cancer folowing coservative surgery. Intern Semin Surg Oncol, 2006, 3: Issue 26. 2. Yi A., Kim H. H., Amraoui A., Shin H.J., Huh M.O., Ahn S.D., Seo B.K.: Radiation induced complications after breast cancer radiation therapy: a pictorial review of multimodality imaging findings. Korean J Radiol, 2009, 10: 496-507.

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PROCEEDINGS OF THE RBRS SECTION BREAST IMAGING 3. Glazebrook K.N., Magut M.J., Reynolds C.: Angiosarcoma of the breast. AJR, 2008, 190: 533-538. 1. Department of Radiology, UZ Leuven, Leuven, Belgium. An uncommon rapid growing breast tumor: phyllodes tumor J. Toirkens, M. Van Goethem, I. Verslegers, L. Hufkens, P.M. Parizel1 We found a rapid growing breast tumor in follow-up of an earlier histologically proven benign small atypical breast tumor suggestive for sclerosed fibroadenoma. Since the small sample size and suspect type 3 kinetic curve on a breast MRI from another hospital we suggested follow up after six months however histology showed no malignant cells. Follow up mammography showed an enlarged lobulated well-circumscribed nodule with heterogeneous density medial in the left breast. A septated heterogeneous mass was seen on sonography with solid and cystic components. Solid components were vascularized as seen on colordoppler imaging. MRI showed on inversion recovery T2-weighted imaging (WI) a heterogeneous mass with overall hyperintense signal intensity with hypointense areas and hypointense septa. The maximum diameter was 3.5 cm versus 2 cm on first sonography. On dynamic contrast enhanced T1-WI the mass showed a marked inhomogeneous enhancement. Kinetic curves displayed a quick intensity rise with wash-out. Because of these malignant characteristics we categorized the mass BI-RADS 4c. Core biopsies were compatible with benign phyllodes tumor. The tumor was surgically removed and histopathology showed a borderline phyllodes tumor. Phyllodes tumor represents less than 1% of all breast tumors. The peak incidence is between 35 and 55 years. The tumor has characteristic leaf-like stromal projections in cystic cavities. The malignancy grade is categorized as benign, borderline or malignant based on tumor margins, stromal cellularity and overgrowth, stromal cell atypia and mitotic activity. Patients typically present with a painless rapid growing breast mass for which imaging is requested. Mammography shows an aspecific well-circumscribed mass. On ultrasound a phyllodes tumor presents as a lobulated well-defined heterogeneous echogenic mass with internal cystic alterations and septations. Vascularisation is usually present in the solid components. Magnetic resonance imaging (MRI) shows a welldefined, lobulated mass with internal septations. The cystic components are hyperintense on T2-WI. The solid components enhance after contrast administration, shown as hyperintensity on T1-WI. Kinetic curve pattern can be gradual slow or rapid enhancement. Primary differential diagnosis consists of fibroadenoma, which is the most frequent fibroepithelial tumor. Clinical arguments for phyllodes are peak incidence at the age of 45 years compared

with fibroadenoma before 30 years. Rapid growth is also suspicious for phyllodes tumor. Mammography and ultrasound are insufficient to differentiate phyllodes tumor from fibroadenoma. The presence of fluid-filled, elongated spaces or clefts within a solid mass are characteristic, but not pathognomic for phyllodes tumor. MRI for differentiation has been suggested in literature with conflicting results. MRI can be useful for evaluation of internal structure, enhancement pattern and kinetic curve assessment when differentiating with other well-circumscribed malignant tumors as intracystic / invasive papillary carcinoma or metaplastic carcinoma. Preoperative MRI studies describe various phyllodes tumor characteristics to correlate with histological grade: tumor size, internal non-enhanced septations, silt-like changes in enhanced images, signal changes from T2-weighted to enhanced images, irregular wall, tumor SI lower than or equal to normal tissue on T2-WI and low ADC (equals stromal hypercellularity). Diagnosis is nevertheless based on anatomopathology and pre-operative tissue sampling is necessary. Fine needle aspiration is inaccurate and even core biopsy has moderate sensitivity due to tumor heterogeneity causing inadequate sampling. These factors render pre-operative diagnosis challenging. Surgery is the only therapeutic option since phyllodes tumor is not proven sensitive to radio- or chemotherapy. Wide resection margin of at least 1 cm is advocated to prevent local recurrence. Breast conservative surgery is preferred if possible. The prognosis is good; the tumor rarely metastasizes. References 1.

Farria D., Gorczyca D., Barsky S., Sinha S., Bassett L.: Benign phyllodes tumor of the breast. AJR, 1996, 167: 187-189 (PubMed 8659370). 2. Tan H., Zhang S., Liu H., Peng W., Li R., Gu Y., Wang X., Mao J., Shen X.: Imaging findings in phyllodes tumors of the breast. Eur J Radiol, 2011, Epub ahead of print (PubMed 21353414). 3. Wurdinger S., Herzog A., Fischer D., Marx C., Raabe G., Scheider A., Kaiser W.: Differentiation of phyllodes breast tumors from fibroadenomas on MRI. AJR, 2005, 185: 1317-1321 (PubMed 16247156). 1. Department of Radiology, University Hospital Antwerp, Edegem, Belgium. Mobile mass in the breast: report of two unusual cases J. Soens, C. Van Ongeval, S. Postema, A. Van Steen1 A 36-year-old and a 35-year-old woman presented with a recently detected palpable and mobile mass in the upper outer quadrant of the right breast. The first patient had no significant personal history though she had two relatives with breast cancer (mother at 51 years, aunt at 50 years). The second woman has had resections of multiple

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bilateral fibro-adenomas but no familial history of breast cancer. Mammography showed no abnormalities in the first case, but a lobulated, nodular lesion with smooth borders and rather low density in the second patient. Ultrasound confirmed the presence of a superficial, hyporeflective, nodular lesion with smooth borders in both women. Although the above mentioned features were reassuring, biopsy was performed and unexpectedly mucinous carcinoma was diagnosed. Comment Mucinous carcinoma counts for 1-7% of all breast carcinomas and is usually seen at post-menopausal age. Clinical, mammographic and sonographic features are benign. Macroscopically, a mucinous tumor is round, well circumscribed and non encapsulated, with pushing margins and a gelatinous surface. Microscopically, groups of uniform epithelial cells floating in large extracellular mucin lakes can be detected. Mucinous carcinomas can be subdivided in a pure form and a mixed type, containing the above mentioned cells combined with nonmucinous components of invasive ductal carcinoma. Our first patient had a mixed tumor, the second patient a pure type of mucinous carcinoma. This division is important regarding prognosis. Pure mucinous carcinomas have a 10 year survival of 87-90.4% and a 14-15% chance of lymph node metastasis unlike the mixed forms which have a poorer 10 year survival of 54-66% and a higher chance of developing lymph node metastasis of about 46%. This higher chance was reflected in our patients: the former had a micrometastasis in the sentinel node, the latter had negative sentinel nodes. On MR images, a lobulated, oval or round mass can be detected with smooth borders, a high T2 signal intensity, due to the mucin components and an iso- to hypointens signal on T1. After admission of gadolinium, heterogenous enhancement is seen, showing different dynamic patterns. A mucinous carcinoma of the pure type, as in our second patient, has a persistent, gradually enhancing pattern. Presence of a large amount of mucin delays the intralesional diffusion of contrast material, unlike in case of higher cellularity earlier enhancement is seen. In a mixed type tumor, as in our first patient, the invasive ductal carcinoma components in between the puremucinous components, cause strong enhancement in early and delayed phase. In conclusion, mammography and ultrasound in patients suffering from mucinous carcinoma, show no morphological signs predictive of malignancy, possibly leading to a delayed diagnosis. MR findings can be crucial in pointing out the correct diagnosis, but biopsy is the only way to confirm and should therefore be considered in case of a new lesion or in case of sudden growth of a known lesion, even when associated with benign features.

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References 1.

Linda A., Zuiani Ch., Giormetti R., et al.: Unusual malignant tumors of the breast: MRI features and pathologic correlation. EJR, 2010, 75: 178184.

2. Harvey J.A.: Unusual Breast Cancers: Useful Clues to Expanding the Differential Diagnosis. Radiology, 2007, 242: 683-694. 3. Lam W., et al.: Sonographic appearance of Mucinous Carcinoma of the Breast. AJR, 2004, 182: 1069-1074.

1. Department of Radiology, UZ Leuven, Leuven, Belgium.

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NEWS FROM THE UNIVERSITIES FEMORAL CONDYLAR OSSIFICATION VARIANTS: MR IMAGING FEATURES, PREVALENCE AND DIFFERENTIATION FROM NORMAL VARIANTS* L. Jans MRI is an excellent modality for the imaging of disorders of the pediatric musculoskeletal system. The knee is the joint which is most commonly imaged by MRI in children. A wide spectrum of conditions may result in osteochondral lesions of the knee in children, including trauma, inflammatory disorders, hematological conditions, osteonecrosis, infection and tumors. These diseases all require early diagnosis and tailormade therapy to prevent life-long disability in affected children. The differential diagnosis is wide and may be challenging, especially since variants of the ossifying process of the knee may mimick osteochondral lesions and should not be mistaken for pathological processes. We sought to review the MR imaging features of conditions that may result in lesions of the bone and/or cartilage of the knee in children, illustrated in a study of juxtaarticular venous malformation. There is a paucity of literature regarding the association of juxtaarticular VM and arthropathy in children. We found that location and size of the VM did not correlate with arthropathy, but the degree of lesion extension into the joint space did. We reported on the MRI features and the prevalence of ossification variants of the femoral condyles in children. It is well- known that agerelated changes and normal variants in the normal maturation process of the distal femoral epiphyseal cartilage may occur. In 22.2% of patients ossification variants were present, early ossification center (18.9%) and

Table I. — MR imaging features that help differentiate femoral condylar ossification variants from OCD. MR Imaging Feature Side Age range

Ossification Variant

Stable OCD

Medial = Lateral

Medial > Lateral

3-13 years (Male) 2-10 years (Female)

8-16 years

7-10 years

11-14 years

Peak age Residual physeal cartilage

100% - > 20%

< 30% - < 10%

Bone marrow edema

93%

Joint effusion

‘Lesion angle’

< 105°

> 105°

Posterior (100%)

Middle (88%) +/Posterior

26%

Location (sagittal plane) Intercondylar location Spiculation (coronal plane)

spiculated secondary ossification center (16.6%) were most commonly seen. As the prevalence of normal ossification variants is higher with greater residual physeal cartilage, these variants were most commonly encountered in young children. We found that MRI can differentiate ossification variants from OCD of the femoral condyles in children. We refined the established criteria and added new criteria that may differentiate normal ossification variants from OCD on MRI, presented in Table I. In conclusion, MRI can help differentiate normal ossification variants from pathologic conditions resulting in osteochondral lesions in the pedi-

From: Faculty of Medicine, Department of Radiology, Ghent University Hospital, De Pintelaan 185, B-9000 Gent, Belgium. * Doctoral thesis submitted in 2011.

atric knee. Accurate diagnosis of normal variants may prevent unnecessary treatment or even surgery; early diagnosis of osteochondral lesions may prevent life-long disability. References 1.

Jans L., Ditchfield M., Jaremko J.L., Stephens N., Verstraete K.: MRI demonstrates the extension of juxtaarticular venous malformation of the knee and correlates with joint changes. Eur Radiol, 2010, 20: 17921798. 2. Jans L., Jaremko J., Ditchfield M., Verstraete K.: Evolution of femoral condylar ossification at MR Imaging: Frequency and Patient Age distribution. Radiology, 2011, 258: 880-888. 3. Jans L., Jaremko J., Ditchfield M., Huysse W., Verstraete K.: MRI differentiates femoral condylar ossification evolution from osteochondritis dissecans. A new sign. Eur Radiol, 2011, 21: 247-251.

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ANNUAL GENERAL ASSEMBLY OF THE ROYAL BELGIAN SOCIETY OF RADIOLOGY (RBRS), Brussels, 19.11.2011 Presidential address

As Chairman of the Royal Belgian Radiological Society, I have the great pleasure to welcome you at its annual symposium, dedicated this year to the spine and spinal cord. Today, we will have the opportunity to listen to various speakers whose expertness is nationally as well as internationally widely acknowledged. I cannot thank them enough for having agreed to share their competence with us.

Here is a rundown of our programme: the clinical introduction, delivered by Professor C. Raftopoulos will be followed by presentations by various renowned radiologists who will provide a comprehensive overview of the topic. I have no doubt that their contribution will make of this symposium an outstanding clinical and radiological experience. We are indeed most fortunate to have among our speakers not only Belgian experts, but also foreign ones from France and Italy. Furthermore, this symposium also intends to reflect upon the necessity for a new approach to the spine and spinal cord imaging, considering the dazzling technological strides forward and their incidences upon fundamental medicine. Such a revisited approach should aim to the most appropriate way to obtain a faster and less invasive diagnosis, while being compatible with the unavoidable financial constraints of public health. I also have the great honour to announce that our Society Board has awarded the title of honorary member to three remarkable practitioners: Professor D. Balériaux, for her

worldwide recognized achievements in neuroradiology – and since collaboration, not only on a national basis but also on an international one, is indeed a ingredient essential to taking up the challenges of modern imaging – to Professor J.P. Pruvo and Dr A. Rossi, for their admirable commitment to adult and paediatric radiology respectively. The main purpose of the session on the “General States of Radiology” is to gather all actors of our profession so that all present and future challenges can be addressed and discussed. We want that professional and health representatives meet and explain in front of all our colleagues what the problems are and what could be thesolutions. We want everybody to participate and to build the radiology of tomorrow. Finally, I would like to express my deep gratitude to Dr Stéphane Allard and his secretary, Mrs Geneviève Maon. Without their help, this symposium could not have been properly organized. Brigitte Desprechins President RBRS 2011

Honorary Membership Nominee of the RBRS in 2011

Andrea ROSSI We are proud to honor Dr A. Rossi for his great contribution, as a

thought leader, to the international promotion of pediatric neuroradiology. On this occasion, we are also delighted to have the opportunity to tighten the links with the Italian Society of Radiology of which he is prestigious representative. Dr Andrea Rossi is nationally and internationally acknowledged for his expertise, scientific skills, fantastic teaching talents and the effective advances he contributes to generate in imaging the central nervous system of children. Dr Andrea Rossi,was born in Genoa, Italy on January 8, 1967, graduated cum laude in Medicine and Surgery at the University of Genoa in 1991 and specialized cum

laude in Radiology at the University of Florence in 1998. Dr Rossi has worked in the Department of Pediatric Neuroradiology of the G. Gaslini Children’s Hospital in Genoa, the largest pediatric institution in Italy, since 1999. In March, 2007 he was appointed as the Head of the Department of Pediatric Neuroradiology. Dr Rossi is currently serving in the Executive Committees of the Italian Association of Neuroradiology (AINR), the European Society of Neuroradiology (ESNR), the European Society of Magnetic Resonance in Neuropediatrics (ESMRN), and the American Society

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of Spine Radiology. He was the Chairman of the Neuro Subcommittee of the European Society of Radiology for year 2010, and is a member of the Program Planning Committee for ECR 2013. He also sits in the Editorial Boards of

Danielle BALERIAUX We are proud and delighted to honour the outstanding achievements and lifetime work of Professor Danielle Balériaux. She was born on 29 January 1945. She obtained a Medical Degree in 1969 and a Degree in Radiology in 1973 at the Université Libre de Bruxelles, Belgium. Professor Balériaux is a national and international renowned expert and teacher in the field of neuroradiology, recognized for her pioneering work in the field of MRI of the central nervous system. She can pride herself on an exceptional curriculum (cfr below). Her carrier is marked by a great number of professional responsibilities, awards, publications, organizations of national and international meetings. Her great, worldwide recognized, innovative skills are also apparent in Belgium where she led the Department of Neuroradiology ULB Erasme for 15 years focusing on the development of the new technologies (essentially MRI) and their implantation in the clinical practice. This enthusiastic voluntary woman has put considerable energy to the development of a world class Academic Department of Neuroradiology at the ULB Erasmus Hospital Brussels. She supported many young radiologists and contributed to create new vocations.

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the “American Journal of Neuroradiology” and “Neuroradiology”. He has authored 177 papers in peer-reviewed scientific journals, of which 122 are listed on Pubmed, and 38 book chapters. He is coeditor of

the book “Pediatric Neuroradiology” published by Springer Verlag in 2005. His main field of interest is the imaging and classification of congenital abnormalities of the spine and spinal cord.

We applaud her for her example and inspiration to us all as a most deserving recipient of an honorary membership.

Past-editor in Chief of Neuroradiology, Past-member of the Editorial Board of Journal of Neuroradiology, Journal Belge de Radiologie, Associate Editor of Quarterly of Magnetic Resonance in Biology and Medicine. Vice-President of the European Society of Neuroradiology (199319960), President of the ESNR ANNUAL Congress (XIX) held in Bruges in 1993. Corresponding member of the French National Academy of Medicine. Member of the Royal Belgium Academy of Medicine. Honorary member of the European Society of Neuroradiology, French Society of Radiology, Japanese Society of Neuroradiology. Consulting Professorship of the Shanghai Second medical University – China.

Appointments Assistant at the Radiological Department of the Jules Bordet Cancer Hospital Dir. Professor I. Jeanmart, from 1969 to end 1981. – From 1976 to end 1981, Head of the Neuro-CT Unit of the Jules Bordet Cancer Hospital, Institute of the Université LIbre de Bruxelles (U.L.B.) – November 1981, Assistant of the Clinique de Neuroradiologie, Radiological Department of Radiology – Hôpital Erasme (Dir. Professor J. Struyven) Université Libre de Bruxelles. – Head of the Clinique de neuroradiologie – Hôpital Erasme : 19852010 (Dir. Prof. J. Struyven – Prof. E.F. Avni) – May 1991, Associated Head Radiological Department of Hôpital Erasme. – February 2010 : senior consultant at the Department of Neuroradiology (Head Pr. R. Lubicz) Honors – Assubel prize winner in 1985 (Prize delivered by the Belgian Royal Academy of Medicine) – Torgny Greitz lecturer in 1995 (Karolinska Hospital, Stockholm, Sweden) – Grand officier de l’Ordre de Léopold (2006) Member of the Belgian Society of Radiology, Belgian Society of Neurology, European Society of Neuroradiology, Society of Magnetic Resonance in Medicine, French Society of Neuroradiology, European Society of Magnetic Resonance in Medicine and Biology, American Society of Neuroradiology, European Chinese Society of Clinical Magnetic Resonance. Corresponding Member of the Radiological Society of North America.

Publications Contributed to: – 36 chapters of books – 187 papers published in radiological or neurosurgical journals More than 500 lectures given at scientific societies and more than 60 invited lectures at conferences or international postgraduate courses. Education Co-founder of the European Course of Neuroradiology (sponsored by the European Society of Neuroradiology) in 1984 with P. Lasjaunias, Cl Marneffe and U. Salvolini) Participated since the beginning to the Erasmus Course in Magnetic resonance imagine (EMRI) founded by Prof. M. Osteaux in 1991 and module Organiser of “Central Nervous system II” European Program “Leonardo”: development of new teaching tools: videoconferences, website and series of educational CD ROMS on neuroradiology

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ANNUAL GENERAL ASSEMBLY – BRUSSELS, 19.11.2011

Jean Pierre PRUVO We are proud to honor professor Jean Pierre Pruvo for his recognized tremendous dedication to excellence within his chosen field of academic neuroradiology pursuing this task with a lot of energy and enthusiasm. As an expert in this field he is a popular and regularly invited speak-

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er at national and international meetings, an outstanding organisator of national and international meetings and courses and greatly contributes to the development of an international reputation of the Department of Neuroradiology of the University Hospital Center of Lille. Last but not least he actively promotes the collaboration between the Belgian and the French Society of Radiology. So we are proud and happy to have him as an Honorary Member. Professor Jean Pierre Pruvo was born on August 03, 1956. He is professor and Head of Department of Radiology, University Hospital Center of Lille. He studied medicine at the Lille School of Medicine. After his graduation in 1982, he obtained a Speciality Board Certification in Radiology in 1987 and a National Board Certification in Medical Research in 1992. After a residency in Radiology and Neuroradiology (CHU Lille), followed by two years fellowship he became Professor of Radiology (1992 – present) at the CHU Lille. Since 1995, he has been coordinator of two MRI’s Hospital Roger Salengro.

Since 1997, he has been working as Chief of Department of Neuroradiology of the CHU Lille and coordinator of the hospital radiology department. Between 2000 and 2003, he was coordinator of the Federation of Cancer. Other roles Professor Pruvo is assuming include research in various fields of interest namely:

Right now I want to thank the founders of the Belgian society of radiologists for the work they accomplished. While we are working on reorganizing this society, we are discovering new challenges: we have to transmit scientific knowledge, but shouldn’t we also defend the professional issues of the radiologists? We have to take the example of other medical associations, because they focus on defending professionnal interests. Why should we be afraid of that? This fear has led to the constitution of other professional organisations, as the “national union of radiologists”. They have accomplished a great deal until now, but their questioning is the same: shouldn’t we join all energies and good wills together, in order to be stronger as a professional representation? The same question occurs with “Concilium Radiologicum” and other radiologists unions. It is a fact: the same persons appear in the different organisations,

but this way of representing weakens us more than it makes us stronger. It seems to me that it is also weakness to elect a president just for one year, rather than for three. How could some good work be done in just one year? So, it is very important to me, that we start this afternoon a questioning about merging the different organisations and end it with a vote of the general assembly. Our issue is that the new “Belgian society of radiologists” will be the only Belgian partner to defend radiological interests. Together with the Flemish, Walloon, Brussels and German-speaking community radiologists. Long live the new “Belgian society of radiologists”.

– Supra-aortic vessels, intracranial vasculature – Gadolinium-enhanced MR angiography – Helical CT angiography – Technical developments – Post processing techniques – Interventional vascular procedures He is the author of 143 Peerreviewed publications and 7 book chapters. Professor Pruvo is member of various societies : – French Society of Radiology, General Secretary since October 2007 – French Society of Neuroradiology : Board Member – French Neurovascular Society – European Society of Radiology

President-elect address

Jean-François DE WISPELAERE Ladies and gentlemen, dear colleagues, First of all, let me thank you for electing me as the president of the royal Belgian society of radiologists. This organism will probably soon be called Belgian society of radiologists because we try to rearrange it.

J.-F. De Wispelaere President RBRS 2012

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JBRâ&#x20AC;&#x201C;BTR, 2011, 94 (6)

Members of the Symposium Faculty and Board of RBRS in 2011

First row in the center (from left to right): F. Avni, D. BalĂŠriaux, B. Desprechins. Second row (from left to right): A. Rossi, J. Struyven, J.F. De Wispelaere, J.P. Pruvo, J. Pringot, J. Verschakelen, R. Hermans, G. Villeirs, C. Delcour.

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JBR–BTR, 2011, 94: 367.

FORTHCOMING COURSES AND MEETINGS NATIONAL MEETINGS 09.02.12 BELGIAN WEEK OF GASTROENTEROLOGY Information: etienne.danse@uclouvain.be 05.03.12 RBRS – Neuroradiology Section Information: nsadeghi@ ulb.ac.be 24.03.12 RBRS – section Bone and Joints, joint meeting with “Nederlandse Vereniging voor Radiologie, sectie Skelet” Mechelen, de Noker

RBRS- Cardiovascular and Interventional Radiology / RBRS – Bone and Joints Imaging 24.03.12

Local organizer: Prof. Dr. F.M. Vanhoenacker Information: filip.vanhoenacker@telenet.be or pieter.van.dyck@uza 21.05.12 RBRS – Neuroradiology Section Information: nsadeghi@ ulb.ac.be

17.09.12 RBRS – Neuroradiology Section Information: nsadeghi@ ulb.ac.be 05.11.12 RBRS – Neuroradiology Section Information: nsadeghi@ ulb.ac.be

03.06.12 Fifth congress of senology Oostduinkerke

RBRS – Abdominal and Digestive Imaging 09.02.12

Miscellaneous 03.06.12

RBRS – Neuroradiology Section 05.03.12, 21.05.12, 17.09.12, 05.11.12

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

INTERNATIONAL MEETINGS

12-14.01.12 MIR WINTER COURSE 2012 Schladming, Austria Information: office@mir-online.org 01-05.03.12 ECR 2012 Vienna, Austria Information: www.myesr.org 30.03.12 JOURNEE DE PRINTEMPS DE LA SIAD Theme : Tumeurs malignes du foie Paris, France Information: siad@sfradiologie.org 15-18.04.12 THE BREAST COURSE 2012 Lisbon, Portugal Information: info@thebreastpractices.com

20-22.04.12 CEUS 2012 Contrast enhanced ultrasound and new technologies Prague, Czech Republic Information: www.crs.cz / www.ceus.cz

03-06.05.12 27TH CONGRESS OF RADIOLOGY ICR 2012 Sao Paulo, Brasil Information: www.icr2012.org

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

22.06.12 ESTI EUROPEAN SOCIETY OF THORACIC IMAGING London, UK Information: www.esti-society.org 15-19.09.12 CIRSE 2012 Lisbon, Portugal Information: www.cirse.org 00.10.12 JOURNÉES FRANÇAISES DE RADIOLOGIE Paris, France Information: sfr@sfradiologie.org 25-30.11.12 RSNA 2012 Chicago, USA Information: www.rsna.org

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

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

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

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Pages III V VI VII, VIII IX X XI XII CIV

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